Reumadagarna 2015 - Svensk Reumatologisk Förening
ReumaBulletinen tidskrift för svensk reumatologisk förening • nummer 105 • 4/2015 Reumadagarna 2015 program · abstracts RoACTEMRA förfylld spruta NÄR KOMBINATIONSBEHANDLING INTE ÄR ETT ALTERNATIV FINNS DET EN BIOLOGISK MONOTERAPI SOM UTMÄRKER SIG SE.TOC.1404.10 Referenser: Gabay C et al. Lancet 2013;381;1541-50. Burmester et al, Ann Rheum Dis 2014, 73,69-74. RoACTEMRA® (tocilizumab). Farmakoterapeutisk grupp: Immunosuppressiva medel, interleukinhämmare; ATC-kod L04AC07. Indikationer: RoACTEMRA IV (Rx, F), i kombination med metotrexat (MTX), är indicerat för behandling av måttlig till svår aktiv reumatoid artrit (RA) hos vuxna patienter som antingen inte har haft tillräcklig effekt av eller som inte tolererat tidigare behandling med en eller flera sjukdomsmodifierande antireumatiska läkemedel (DMARDs) eller tumörnekrosfaktor-(TNF)-hämmare. Hos dessa patienter kan RoACTEMRA ges som monoterapi vid intolerans mot metotrexat eller när fortsatt behandling med metotrexat är olämplig. RoACTEMRA är indicerat för behandling av aktiv systemisk juvenil idiopatisk artrit (sJIA) hos patienter som är 2 år eller äldre, som har haft ett otillräckligt svar på tidigare behandling med NSAIDs och systemiska kortikosteroider. RoACTEMRA kan ges som monoterapi (vid intolerans mot metotrexat eller när behandling med metotrexat är olämplig) eller i kombination med metotrexat. RoACTEMRA, i kombination med metotrexat, är indicerat för behandling av polyartikulär juvenil idiopatisk artrit (reumatoidfaktorpositiv eller -negativ samt utvidgad oligoartrit) hos patienter som är 2 år eller äldre, som har haft ett otillräckligt svar på tidigare behandling med metotrexat. RoACTEMRA kan ges som monoterapi vid intolerans mot metotrexat eller när fortsatt behandling med metotrexat är olämplig. RoACTEMRA SC (Rx,F) RoACTEMRA, i kombination med metotrexat (MTX), är indicerat för behandling av måttlig till svår aktiv reumatoid artrit (RA) hos vuxna patienter som antingen inte har haft tillräcklig effekt av eller som inte tolererat tidigare behandling med en eller flera sjukdomsmodifierande antireumatiska läkemedel (DMARDs) eller tumörnekrosfaktor-(TNF)-hämmare. Hos dessa patienter kan RoACTEMRA ges som monoterapi vid intolerans mot metotrexat eller när fortsatt behandling med metotrexat är olämplig. RoACTEMRA har visats reducera progressionshastigheten av ledskadan mätt med röntgen och förbättra den fysiska funktionen, när det används i kombination med metotrexat. Kontraindikation: Överkänslighet mot aktiv substans eller hjälpämne. Aktiv svår infektion. Varning och försiktighet: Tidigare sjukdomshistoria av sår i tarm eller divertikulit. Makrofagaktiverings-syndrom (MAS) kan utvecklas hos patienter med sJIA. Graviditet: Bör undvikas under behandling och i 3 månader efter avslutad behandling. Beredningsform och förpackningar: IV: Koncentrat till infusionsvätska,lösning 20 mg/ml i injektionsflaskor à 4 ml, 10 ml och 20 ml. SC: Varje förfylld spruta innehåller 162 mg tocilizumab i 0,9 ml lösning. Varje förpackning à 4 sprutor. SPC: 2015-03-26. För mer information och aktuella priser se www.fass.se Roche AB, Box 47327, 100 74 Stockholm. Tel 08-726 12 00. www.roche.se ReumaBulletinen ReumaBulletinen är Svensk Reumatologisk Förenings tidskrift och utkommer med sju nummer per år Ansvarig utgivare Ralph Nisell Reumatologiska kliniken Karolinska Universitetssjh 171 76 Stockholm Tel 08-517 760 93 [email protected] Redaktör Tomas Bremell Reumatologi Sahlgrenska Universitetssjh Gröna Stråket 12 413 45 Göteborg Tel 031-342 33 78 [email protected] Innehåll · 4/2015 3 Välkommen till Reumadagarna i Tylösand 4 Brev från vetenskapliga sekreteraren 6 Reumatologin i Halland 10Mötesprogram 12 Reumadagarna 2015 - Abstracts 38 Register - Abstracts 40Reumakalender Red.medlemmar Ido Leden [email protected] Bengt Lindell [email protected] Milad Rizk [email protected] Ioannis Parodis [email protected] Produktion Mediahuset i Göteborg AB Marieholmsgatan 10C 415 02 Göteborg www.mediahuset.se Tel 031-7071930 Annonser Dan Johansson [email protected] Olle Lundblad [email protected] Layout Eva-Lotta Emilsdotter [email protected] Tryck ÅkessonBerg AB Box 148 361 22 Emmaboda www.akessonberg.se Distribution Distribueras som posttidning ISSN 2000-2246 (Print) ISSN 2001-8061 (Online) Utgivningsplan 2015 Nummer Nr 1 RB Nr 2 RB Vetenskap Nr 3 RB Nr 4 RB Nr 5 RB Nr 6 RB Vetenskap Nr 7 RB Manusstopp 30 januari 13 mars 23 april 8 juni 11 september 23 oktober 11 november Utgivning 26 februari 15 april 27 maj 3 juli 16 oktober 26 november 18 december Omslagsbild: Fotolia www.svenskreumatologi.se ReumaBulletinen Nr 105 · 4/2015 1 Bilbo & Co Otezla är den första nya godkända tablettbehandlingen för plackpsoriasis och psoriasisartrit på mer än 15 år 1,2,3 ♦Otezla har bevisad effekt på ett brett spektrum av sjukdoms manifestationer inom godkända indikationer.1 ♦ Otezlas säkerhetsprofil är väldokumenterad i SmPC. Data visar inga tecken på allvarlig infektion, tuberkulos, hjärt kärlhändelse eller malignitet jämfört med placebo.1,4,5 ♦ Otezla är en tablettbehandling utan några krav på föregående screening eller fortgående laboratorieövervakning.1 NS-OTZ150009 feb 2015 Otezla är en ny tablettbehandling som kan förändra sättet att behandla plackpsoriasis och psoriasisartrit.1 Referenser: 1. SmPC Otezla, tillgänglig via www.ema.europa.eu 2. SmPC Arava, tillgänglig via www.ema.europa.eu 3. Sandimmun Neoral, Scientific conclusions and grounds for the variation to the terms of the Marketing Authorisation, tillgänglig via http://www.ema.europa.eu/docs/en_GB/ document_library/Referrals_document/Sandimmun_Neoral_30/WC500158808.pdf. 4. Papp K, et al. Oral presentation #1055 at the 73rd Annual Meeting of the AAD; March 20–24, 2015; San Francisco, CA. 5. Mease P, et al. poster #1564 presented at the 2014 ACR/ARHP Annual Meeting; November 15–19, 2014; Boston, MA. Otezla 10 mg, 20 mg, 30 mg (apremilast) filmdragerade tabletter. ATC kod: L04AA32, Rx, EF. Indikationer: För behandling av aktiv psoriasisartrit hos vuxna patienter som har visat otillräckligt svar eller som har varit intoleranta mot tidigare DMARD-behandling, ensamt eller i kombination med sjukdomsmodifierande antireumatiska läkemedel (DMARDs), för behandling av måttlig till svår kronisk plackpsoriasis hos vuxna patienter som inte svarat på eller som har någon kontraindikation mot eller är intoleranta mot annan systemisk behandling inklusive ciklosporin, metotrexat eller psoralen och ultraviolett A ljus (PUVA). Dosering: Rekommenderad dos är 30 mg två gånger dagligen, morgon och kväll. Se dostitreringsschema för initial titrering, i SPC. Behandling med Otezla ska initieras av specialister med erfarenhet av diagnos och behandling av psoriasis eller psoriasisartrit. Kontraindicerat vid graviditet. Graviditet ska uteslutas innan behandling påbörjas. Ska inte användas under amning. Varningar och försiktighet: Vid gravt nedsatt njurfunktion ges reducerad dos, 30 mg en gång dagligen. Underviktiga bör kontrollera sin vikt regelbundet. Innehåller laktos. Startförpackning 27 tabletter: 4 × 10 mg, 4 × 20 mg och 19 × 30 mg. Standardförpackning (30 mg) 56 tabletter. Texten är baserat på produktresumé: 2015-01-15. För ytterligare information och förmån se www.fass.se. Pris och förmånstyp har ännu inte fastställts. Celgene AB, 164 51 Kista, tel +46 8 703 16 00, www.celgene.se ▼ Detta läkemedel är föremål för utökad övervakning. Celgene AB. Kista Science Tower, 164 51 Kista. Tel: +46 8 703 16 00. www.celgene.se 2 ReumaBulletinen Nr 95 · 1/2014 VÄLKOMMEN · Boel Mörck och Ralph Nisell Välkommen till Reumadagarna i Tylösand 2015 Svensk Reumatologisk Förening (SRF) önskar dig välkommen till Reumadagarna i Tylösand, strax utanför Halmstad, första veckan i september. I år 2015 är det andra gången som Reumadagarna hålls i sin utökade form, dvs under 4 dagar (förra året var vi i Örebro), men det är första gången som dessa dagar är förlagda på andra sidan sommaren. K onferensen har förändrats från att vara ett reumatologiskt vårmöte till ett uppstartmöte inför hösten och för framtiden. Vi i SRFs styrelse hoppas att denna nya ordning ska falla väl ut och bli en extra energi-kick efter sommaren. Tillsammans med SRF har en organisationskommitté med deltagande från Reumasjuksköterskor i Sverige (FRS), Svenskt Reuma Forum (SveReFo), Fysioterapeuterna (Reumasektionen) och Reumatikerförbundet arbetat fram ett spännande program för Reumadagarna. Den lokala värden, Reumatologi Halland, ingår också. Det känns roligt att Reumadagarna i år hålls just i Halland där reumatologin under 2014 fått en organisatorisk nystart och nu har möjlighet att visa upp sig. Mötet innehåller allt man kan tänka sig i form av ny kunskap, praktisk handläggning, registerarbete, nätverksabyggande och blickar mot framtiden. Det finns flera nya inslag i programmet i år såsom Posterutställning om verksamhetsutveckling, post-EULAR föreläsningar och frukostsymposier. Tack till alla ni som på olika sätt har bidragit eller bidrar till programmet och gör att dessa dagar blir möjliga och att de håller hög såväl vetenskaplig, pedagogisk som social kvalitet. Vi riktar även ett tack till Reumadagarnas sponsorer som möjliggör att vi kan träffas och förverkliga allt detta. Vi hoppas på givande och bra Reumadagar 2015 i Tylösand i september. Välkommen och väl mött! Boel Mörck Vice ordf SRF Ordförande i Reumadagarnas programkommitté Ralph Nisell Ordförande SRF ReumaBulletinen Nr 105 · 4/2015 3 FRÅN STYRELSEN · Christopher Sjöwall Dags för årets höjdpunkt! Under årets nationaldag, nyligen hemkommen från Fjällbacka, lyckas jag få lite tid över för att sammanställa dessa rader. Härnäst kan de flesta se fram emot en skön sommarledighet men redan nu har många av oss siktet inställt på årets höjdpunkt – Reumadagarna i Tylösand! Detta blir det andra nationella mötet med nytt upplägg – och det första som tidsmässigt ligger i början av höstterminen, dvs. där det kommer att ligga även framöver. D et vetenskapliga programmet under årets Reumadagar har tagits fram av Svensk Reumatologisk Förenings vetenskaplige sekreterare tillsammans med den regionalt sammansatta vetenskapliga programkommittén. Vi känner oss belåtna och hoppas naturligtvis att programmet ska locka många åhörare. De delar av programmet som fungerade väl på mötet i Örebro ifjol har vi försökt behålla, men årets möte bjuder även på flera nyheter. Och intresset för att delta på årets Reumadagar har hittills överstigit förväntningarna! Årets möten SRF-medlemmar som varit med länge är vana vid ett nationellt möte under vårterminen. Många har kanske till och med upplevt en mer eller mindre uttalad abstinens under den gångna våren då vi inte haft något SRF-möte. Men från och med ”…stolta över att Professor Georg Schett accepterat vår invitation” 2015 har den nya mötesordningen satt sig. Detta innebär regelbundna mötestider för Svensk Reumatologis Registeroch Utvecklingsdagar ( januari), Reumadagarna (september) och Riksstämman (december). Med tanke på de stora förändringar som skett för reumatologin i Halland känns det särskilt roligt att årets Reumadagar förlagts till just Halmstad och Tylösand (läs mer om detta i intervjun med Annika Teleman på annan plats i detta nummer!). Observera att SRFs styrelse naturligtvis var helt ovetandes om vad som skulle ske när reumatologerna på Spenshult tillfrågades om att arrangera mötet för nästan två år sedan! Abstracts på Reumadagarna Antalet insända och accepterade abstractbidrag till SRF under årets Reumadagar är visserligen något färre än vid mötet i Örebro, men glädjande noterar vi att antalet bidrag som inskickats till SveReFo/FRS nästan dubblerats. Samtliga abstracts med tillhörande författare finner Ni längre bak i detta nummer. Vid sidan av dessa bidrag tillkommer ett hittills okänt antal abstracts i kategorin Kvalitets- & Verksamhetsutveckling – en av årets nyheter! SRF-bidragen har bedömts och rangordnats av Professorskollegiet. Denna granskning ligger till grund för utmärkelsen av de två bästa bidragen vilka erhåller diplom och scentid under torsdagen. Ytterligare åtta bidrag som fått goda omdömen ges tid för muntlig presentation under på morgonsessionen samma dag. Nanna Svartz-föreläsare 2015 2015 års Nanna Svartz-föreläsare är österrikaren Georg Schett, verksam i Erlangen, Bayern, Tyskland. Professor Schett har en imponerande merit- och publikationslista som bl.a. rymmer över 70 publikationer inom reumatoid artrit, artros, psoriasisartrit och gikt bara under det senaste året. Schetts intresseområde är huvudsakligen mekanismer bakom uppkomst av strukturella skador i ben, brosk och blodkärl vid artritsjukdom. Vi känner oss mycket stolta över att Professor Georg Schett accepterat vår invitation om att hålla 2015 års Nanna Svartz-föreläsning som ligger redan under tisdagseftermiddagen. Biosimilarer – nya data på Eular? Under några månaders tid har vi nu haft möjlighet att ordinera infliximab biosimilaren CT-P13 (Remsima®/Inflectra®) i Sverige. I början av nästa år kommer sannolikt den första etanercept biosimilaren att finnas tillgänglig, och detta är troligen bara början på en utveckling 4 ReumaBulletinen Nr 105 · 4/2015 FRÅN STYRELSEN · Christopher Sjöwall SRF´s STYRELSE 2015 Ralph Nisell Ordförande Reumatologiska Kliniken Karolinska Universitetssjukhuset 171 76 Stockholm Tel 08-517 760 93 [email protected] Boel Mörck Vice ordförande Reumatologiska kliniken SU/Sahlgrenska 413 45 Göteborg Tel 031-342 10 00 [email protected] Gerd-Marie Alenius Facklig sekreterare Reumatologiska Kliniken Västerbotten Norrlands Universitetssjukhus 901 85 Umeå Tel: 090-785 16 76 [email protected] av ”nya” biosimilarer. Ett drygt år har gått sedan SRFs biosimilararbetsgrupp släppte policydokumentet, vilket fått en stor spridning. I dokumentet framgår att SRFs ståndpunkt att inte kan rekommendera byte från originalprodukt till biosimilar hos patienter där pågående behandling uppnått önskvärd effekt. Vi vet nu att flera oberoende studier på olika indikationer där man prövat ”switch” till biosimilar pågår. Jag förväntar mig att nya resultat kommer att presenteras på Eular-mötet i Rom under nästa vecka. Biosimilararbetsgruppen kommer redan under juni att sammanträda för att diskutera huruvida vårt policydokument behöver uppdateras. Vi ska även diskutera hur vi inom SRQ på ett strukturerat sätt fortlöpande ska kunna utvärdera introduktionen av redan godkända (liksom kommande) biosimilarer i Sverige. Post-Eular – nytt i Tylösand Den avslutande dagen i Tylösand kommer att vara vikt för utbildning och arrangeras av SRF-styrelsens utbildningsansvariga. En ny programpunkt 2015 har tillkommit med anledning av det nya LIF-avtalet, vilket vi befarar kommer att leda till att färre svenska reumatologer ges möjlighet att fortbilda sig genom kunskapsinhämtning på internationella möten som t.ex. Eular och ACR. Tanken med denna programpunkt i Tylösand är således att åhörarna ska kunna få ta del av huvudnyheterna från Eular. Tre bolag har nappat på denna idé från programkommittén och de kommer att belysa nyheter inom varsitt område; reumatoid artrit, psoriasisartrit och systemsjukdomar. Ett av de bolag som deltar är Dagens Medicin. SRF kommer i höst att på försök inleda ett samarbete med Dagens Medicin för återrapportering även från ACR. Detta möte kommer att ligga den 2 december, dvs. precis innan Riksstämman. Jag återkommer med detaljer för detta möte! Väl mött i Tylösand! Detta är mitt sista brev innan sommarledigheten. Jag tillönskar nu alla medlemmar en skön ledighet och ser fram emot att träffa Er på mötet i Tylösand! Christopher Sjöwall Vetenskaplig sekreterare [email protected] Tomas Mandl Kassör Reumatologkliniken Skånes Universitetssjukhus 205 02 Malmö Tel 040-33 23 63 [email protected] Christopher Sjöwall Vetenskaplig sekreterare Universitetsöverläkare IKE, avd f Reumatologi Hälsouniversitetet 581 85 Linköping Tel: 010-1032416 christopher.sjowall@ vastragotaland.se Ann Knight Utbildningsansvarig Verksamhetsområde Reumatologi, Hud- och Könssjukdomar Akademiska Sjukhuset 751 85 Uppsala Tel 018-611 92 29 ann.kataja.knight@ akademiska.se Yulia Stennikova Ledamot, representant för läkare under utbildning Östersunds sjukhus Östersunds rehabcentrum Remonthagen Reumatologmottagningen 831 83 Östersund Tel: 063-153000 [email protected] ReumaBulletinen Nr 105 · 4/2015 5 Reumatologin i Halland · Per Lundblad Reumatologin i Halland För att få en att beskrivning av reumatologin i Halland, stämmer Reumabulletinen träff med Annika Teleman. Hon är synnerligen lämpad för uppgiften. Här har hon arbetat som specialist i reumatologi sedan hon kom hit som ST-läkare (som på den tiden kallades för FV) under mitten av 80-talet. A nnika kom till Spenshult, där alla läkare vid den tiden var anställda av medicinska kliniken vid Halmstad sjukhus. Senare kom Annika även att bli verksamhetschef där. Fick flytta efter upphandling Men på Spenshult arbetar varken hon eller någon annan reumatolog längre. Hur det blev så, är i sig en historia som är värd att berätta. – När jag kom på 80-talet var det Reumatikerförbundet som ägde Spenshult. Men de ville hitta en annan intressent som skulle ta över verksamheten. Orsaken var att de inte tyckte att det var bra att brukarna av anläggningen – patienterna – samtidigt även skulle vara ägare. Då satt man på två stolar ansåg förbundet, berättar Annika. Men sedan dess har ändå alltid reumatologin varit placerad på Spenshult (och Kungsbacka) – via upphandlingar. År 2013 kom en ny upphandling, och den vanns då av Capio Movement. Annika anser att man kan ifrågasätta om en hel länsverksamhet ska vara utsatt för upphandling. – Det innebär att hela verksamheten kan komma att flyttas runt efter ett antal år, med personella och organisatoriska svårigheter som följd. Man kan inte flytta runt en specialitet, säger hon. Tappade läkarkompetens Så blev det dock i alla fall. Hela den reumatologiska verksamheten på Spenshult, som befunnit sig där sedan 1953, flyttades år 2014. – Men man tog samtidigt på sig en ny ”kostym”. Rehabverksamheten minimerades – vilket dock även var en anpassning till modern reumarehabilitering, fortsätter Annika. – På Spenshult kunde vi erbjuda andra regioner rehabilitering för patientgrupper med större vårdbehov, det kan vi inte längre, När man flyttade fick samtliga anställda söka nya tjänster. Alla som arbetade på 6 ReumaBulletinen Nr 105 · 4/2015 Spenshult blev uppsagda. – Alla valde inte att följa med, vilket innebar att vi bl.a. blev underbemannade på läkarsidan – och vi har haft svårigheter att kompensera för det. Vi tappade helt enkelt kompetens! Annika förklarar att det har lett till att åldersstrukturen på läkarna inte är optimal, och att de därför har ett stort behov av nyrekrytering. – Vi fick starta om hela verksamheten på nytt. ISO-certifiering, alla instruktioner, delegeringar etc. fick göras om. Tillgång till tidigare journalinformation blev komplicerad och ett helt nytt journalsystem infördes samtidigt på kliniken. Allt detta har vi lyckats hantera, det vi haft svårt att få till är slutenvårdsrehabiliteringen. Två mottagningar Flytten gick till Halmstad och till Varberg, där Reumabulletinen träffar Annika. Här arbetar hon en dag varannan vecka. Mottagningen i Varberg är belägen inne på området för Varbergs kurort, i vackra, strandnära omgivningar. Mottagningen i Halmstad öppnade i maj 2014, och mottagningen i Varberg i augusti samma år. Här arbetar specialist i reumatologi Per-Erik Rönnborg fast. De övriga reumatologerna i Halland är – förutom Annika själv – Gazmend Abdiu, Ljiljana Stansic Radic samt Dick Sahlberg. Samtliga utom Per-Erik arbetar i Halmstad. – I Halmstad finns röntgen, ortopedisk Annika Teleman och kirurgisk vårdavdelning. Förutom att jag kommer hit till Varberg en dag varannan vecka, så har de konsultläkare som hjälper till på regelbunden basis några dagar i veckan, förklarar Annika. I Varberg köper man öppenvårdsrehabilitering, med möjlighet till övernattning på hotellet som hör till Varbergs Kurort för patienter med lång resväg. Teamet från Halmstad kommer hit en dag varannan vecka, för t.ex. tidig artritmottagning. – En del patienter tycker att det är mer Reumatologin i Halland · Per Lundblad ORENCIA® NU ÄVEN GODKÄND SOM FÖRFYLLD PENNA CLICKJECT ® TILLGÄNGLIG I AUGUSTI 2015 MED ETT KNAPPTRYCK Patienten injicerar dosen med ett knapptryck MED GREPPVÄNLIG FORM Halkfritt material för ett säkrare grepp MED STORT FÖNSTER ORE.SWE.MAY.2015 427SE15PR05599 Blå indikator visar tydligt när hela dosen är injicerad ORENCIA® (abatacept) 125 mg injektionsvätska för subkutan injektion och 250 mg pulver till koncentrat till infusionsvätska för intravenös infusion. Immunosuppressivt medel. Indikation: Subkutan och intravenös beredningsform: Reumatoid artrit - ORENCIA® i kombination med metotrexat är indicerad för behandling av måttlig till svår aktiv reumatoid artrit hos vuxna patienter som svarat otillräckligt på tidigare behandling med en eller flera sjukdomsmodifierande antireumatiska läkemedel (DMARDs), inklusive metotrexat (MTX) eller en TNF-hämmare. Vid kombinations-behandling med abatacept och metotrexat har reduktion av progressiv leddestruktion och förbättring av fysisk funktion påvisats. Endast intravenös beredningsform: Polyartikulär juvenil idiopatisk artrit - ORENCIA® i kombination med metotrexat är indicerad för behandling av måttlig till svår aktiv polyartikulär juvenil idiopatisk artrit (JIA) hos pediatriska patienter från 6 års ålder och uppåt som svarat otillräckligt på andra DMARDs inklusive åtminstone en TNF-hämmare. ORENCIA® har inte studerats hos barn under 6 år. Kontraindikationer: Allvarliga okontrollerade infektioner, som sepsis och opportunistiska infektioner. Överkänslighet mot den aktiva substansen eller mot något hjälpämne. Förpackningar: Fyra förfyllda sprutor med 125 mg abatacept i en ml lösning (förmånsberättigat). Fyra förfyllda pennor med 125 mg abatacept i en ml lösning (ännu ej förmånsberättigat). En injektionsflaska med 250 mg pulver och en silikonfri spruta (förmånsberättigat). Ytterligare information: ORENCIA® är receptbelagt. För fullständig information och pris, se: www.fass.se. Baserad på produktresumé: 23 april 2015. Bristol-Myers Squibb AB, Tel: 08-7047100. www.orencia.se | www.orenciapatient.se | www.bms.se ReumaBulletinen Nr 105 · 4/2015 7 Reumatologin i Halland · Per Lundblad lättillgängligt med mottagning i Varberg och Halmstad, andra saknar Spenshult och det breda omhändertagandet där, påpekar Annika. – Vi har nog blivit mer som andra reumatologiverksamheter nu. Tror på täta kontroller Just tidig artritmottagning är något som reumatologin i Halland valt att satsa på. – I riktlinjerna rekommenderar man det, och det har vi tagit ad notam, säger Annika. Hon berättar att de hade en poster om just detta på förra årets möte i Örebro, där de kunde visa att det går ganska bra för dessa patienter. De har t.ex. inte lika hög förbrukning av biologiska läkemedel. – Vi tror på det här med täta kontroller. Arbetssättet har väckt en nyfikenhet på andra kliniker. Annika förklarar att hon personligen tror att om man träffar patienten en gång i månaden så får de en bättre följsamhet till sin medicinering/ behandling. Men hon understryker att det är hennes egen reflektion. Rent allmänt är Varbergs kurort en trevlig miljö att arbeta i, framhåller hon. 8 ReumaBulletinen Nr 105 · 4/2015 – Det är ganska likt den miljö vi hade på Spenshult. Mottagningen i Halmstad är belägen i lokaler som är en del av Regionen Hallands sjukhus. Forskningsenhet med stark klinisk anknytning På Spenshult fanns tidigare en forskningsenhet vid namn FOU Spenshult, och den har reumatologerna i Halland fortfarande en anknytning till. Enheten har valt att behålla sitt namn efter att den flyttade. – Numera befinner de sig på vårdcentralen Bäckagård, som har ansökt om att få bli en forskningsvårdcentral. FoU Spenshult har en stark klinisk anknytning, där forskarna själva till stor del är verksamma som läkare, sjuksköterskor och sjukgymnaster. Forskningen bedrivs också i nära samverkan med patienter vad det gäller planering och uppföljning av vetenskapliga studier. Chefen för forskningsenheten är Stefan Bergman, som är specialist i allmänmedicin, docent i experimentell reumatologi och professor i hälsa och livsstil. – Han är intresserad av rörelseorganens sjukdomar, och har disputerat på smärta. De projekt som vi arbetar med är ett om spondylartriter (en sjukgymnast) samt omvårdnadsprogram (en sjuksköterska). Samarbete med primärvården Annika förklarar att några läkemedelsprövningar etc. har läkarna inte haft tid att engagera sig i efter flytten. – Vi har på uppdrag av Region Halland ett pågående samarbete med primärvården avseende handläggning av patienter med reumatiska sjukdomar – vad de ska vara vaksamma på, och vem som gör vad, hur och när. (Handläggningsöverenskommelser). Dessutom håller vi – som alla andra – på att diskutera biosimilarer. Hon avslutar med att påpeka att de fortfarande har en decentraliserad läkemedelsbudget i Halland. – Det är ett av de få landsting som inte delat ut kostnaderna till den enskilda kliniken. Dessa kostnader är idag tämligen höga i Halland, avslöjar Annika. Allra sist vill hon också passa på att hälsa alla kollegor från hela landet välkomna till Reumadagarna i Tylösand! Per Lundblad Den första biosimilara monoklonala antikroppen (mAb) för användning inom reumatologi ... ett nytt perspektiv Inflectra™ (Infliximab) är världens första biosimilara mAb. Inflectra har visat likvärdig effekt, säkerhet och kvalitet som referensläkemedlet Infliximab. Doseringen varierar för de olika indikationsområdena: • Reumatoid artrit • Psoriasisartrit • Ankyloserande spondylit • Psoriasis • Crohns sjukdom (även fistulerande) • Ulcerös kolit • Crohns sjukdom hos barn* • Ulcerös kolit hos barn*. Kontraindikationer: Patienter med anamnes på överkänslighet mot infliximab, mot andra murina proteiner eller mot något av hjälpämnena. Patienter med tuberkulos eller andra allvarliga infektioner såsom sepsis, abscesser, och opportunistiska infektioner. Patienter med måttlig eller svår hjärtsvikt (NYHA klass III/IV). Övrigt: Patienter ska testas för HBV och TB-infektion innan behandling med Inflectra påbörjas samt följas noggrant avseende infektion efter insatt behandling. Risk för att utveckla lymfom eller andra maligniteter hos patienter behandlade med TNFhämmande medel kan inte uteslutas. Regelbunden hudundersökning rekommenderas, särskilt hos patienter med riskfaktorer för hudcancer. Kvinnor i fertil ålder måste använda lämpliga preventivmedel för att förhindra graviditet och fortsätta att använda dem i minst 6 månader efter den sista behandlingen med Inflectra. *Inflectra är avsedd för behandling av svår aktiv sjukdom hos pediatriska patienter mellan 6 och 17 år som svarat otillräckligt på konventionell behandling eller har intolerans eller kontraindikationer mot sådan behandling. Inflectra har inte studerats hos patienter yngre än 6 år med ulcerös kolit eller Crohns sjukdom. R x, F: Baserat på produktresumé januari 2015. Detta läkemedel är föremål för utökad övervakning. Rapportering av biverkningar: Om du får biverkningar, tala med läkare, apotekspersonal eller sjuksköterska. Detta gäller även biverkningar som inte nämns i denna information. Du kan också rapportera biverkningar direkt (se detaljer nedan). Genom att rapportera biverkningar kan du bidra till att öka informationen om läkemedels säkerhet. Läkemedelsverket Box 26, 751 03 Uppsala, www.lakemedelsverket.se För ytterligare information om bl.a. effekt och säkerhet, förpackningar och pris, se produktresumé på www.fass.se respektive www.tlv.se Innehavare av godkännande för försäljning: Hospira UK Limited, Queensway, Royal Leamington Spa, Warwickshire CV31 3RW, Storbritannien. Svensk representant: Hospira Nordic AB, Box 34116, 100 26 Stockholm. Tel. 08 – 672 85 00, [email protected] ReumaBulletinen Nr 102 · 1/2015 9 SEADIFX_REUM_April2015 Inflectra ® (Infliximab) är en TNF-hämmare, 100 mg pulver till koncentrat till infusionsvätska, lösning. (R x, F, SmPC jan 2015). MÖTESPROGRAM · Reumadagarna i Tylösand Mötesprogram Tid Tisdag 1 september SRF styrelsemöte 08.30-12.00 Tid för grupper/möten 12.00-13.00Registrering/Lunch 13.00-13.10Introduktion 13.10-14.10 Öppningsföreläsning Hans Winberg, Leading Health Care 14.10-15.40 Värdsymposium Från epidemiologi till klinik Reumatologi Halland 15.40-16.00 Kaffe i utställningen 16.00-17.00 Nanna Svartz föreläsning Georg Schett, FriedrichAlexander Universität, Erlangen, Tyskland 17.30-18.30 Konstvisning på hotellet (2x30 min) 19.00 Mingel på hotellet Tid 07.15-08.15 Onsdag 2 September Parallellt program Frukostsymposium sponsras av AbbVie AB 08.30-10.00 Temasymposium Gikt - vår vanligaste artrit sjukdom, men fortfarande underdiagnostiserad eller bortglömd? Lennart Jacobsson, SU Mats Dehlin, Sahlgrenska akademin Meliha Kapetanovic, Lunds universitet Moderator: Thomas Mandl Teamets olika perspektiv i den kliniska vardagen. Om team Ann Bremander, Halmstad Reumatologen i Falun för patienten i tiden - om hur organisationen kan skapa goda förutsättningar för patienten Elin Löfberg och Cattis Forsberg, Falun Tidigt Team omhändertagandeReumatologen i Lund 10.00-10.30 Kaffe i utställningen 10.30-12.00 Temasymposium Nya möjligheter till diagnostik och behandling av myosit Ingrid Lundberg, Karolinska institutet Johan Rönnelid Uppsala universitet Helene Alexandersson, Karolinska institutet Göran Tornling, KI Moderator: Ann Knight Team vid systemsjukdomar. SLE team från Karolinska universitetssjukhuset Sclerodermi - Eva Severin, Gunnel Sandqvist 12.00-13.00Lunch 13.00-14.30 Temasymposium Smärta vid reumatoid artrit Jon Lampa, Karolinska institutet Stefan Bergman, Reumatologi Halland Tuulikki Sokka-Isler, Jyväskylä Central Hospital, Finland Sofia Hagel, Lunds universitet Moderator: Ralph Nisell 14.30-15.00 Kaffe i utställningen E-hälsa. Var står vi idag? Eva Pihlsäter-Faxner (SLL) Johan Assarsson (Inera) Avslutande debatt 15.00-16.00 Utdelning av priser och föredrag av pristagare 16.10-16.30 Kvalitet och Verksamhetsutveckling Postervandring 16.30-17.30 SRFs årsmöte 18.00-19.00 Konstvisning på hotellet (2x30 min) 19.30 10 ReumaBulletinen Nr 105 · 4/2015 Konferensmiddag på hotellet Fortsatt program för sjuksköterskor Årsmöte SveReFo MÖTESPROGRAM · Reumadagarna i Tylösand Tid Torsdag - 3 September Tid Parallellt program 07.15-08.15 Frukostsymposium sponsras av Bristol-Myers Squibb. The Emerging Role of ACPA in RA Development Chaired by Solbritt Rantapää Dahlqvist, Norrlands Univer sity hospital, Umeå Speakers:Jeremy Sokolove, VA Palo Alto Health Care System, Stanford University School of Medicine, USA Carl Turesson, Skåne Univer sity Hospital, Lund Universi ty, Malmö 08.30-10.00 Utvalda abstracts Moderatorer: Saedis Saevars- dottir och Alf Kastbom 10.00-12.00 Postervandring & kaffe 09.30-09.50 Kaffe i utställningen 09.50-10.50Fortbildning 10.50-11.00Paus Rehabilitering i varmare klimat - Ingiäld Hafström SRQ rehabmodulen - Ingrid Thyberg, Malin Regardt 10.30-12.00 Möjligheter och hinder för dagens reumarehabilitering. Ingiäld Hafström · SRQ rehabmodulen - Ingrid Thyberg, Malin Regardt Rekommendationer för en Modern Reuma Rehabilitering -MORR-gruppen. Paneldebatt kring dagens tema. 12.00-13.00Lunch 13.00-13.30 Pris och föredrag bästa abstracts 13.30-14.15 Stipendieutdelning och föredrag 14.15-14.45 Kaffe i utställningen 14.45-16.45 Axplock avhandlingar 17.00-18.15 Tid för grupper Tid Fredag - 4 September 08.30-09.30post-EULAR 13.00-17.00 Fortsatt program för fysioterapeuter: Tema: Konditionsträning och reumatisk sjd. Gästföreläsare: Hanne Dagfinrud, Fysioterapeut, Dia konihjemmet Oslo, samt sektionen för Reumatologi, . Fysioterapeuterna 13.00-17.00 Fortsatt program för fysioterapeuter: Tema: Konditionsträning och reumatisk sjd. Gästföreläsare: Hanne Dagfinrud, Fysioterapeut, Diakonihjemmet Oslo, samt sektionen för Reumato logi, Fysioterapeuterna. 11.00-12.00Fortbildning Autolog stamcellstransplan tation vid autoimmun sjuk dom, särskilt systemisk skleros Hans Hägglund, hematolog Akademiska sjukhuset Uppsala 12.00-12.30 Summering av mötet 12.30-13.30 Lunch, Grab & Go Ändringar kan förekomma Hitta till Tylösand Tylöhusvägen, 302 73 Halmstad Vägbeskrivning Norrifrån (E6) Sväng av Halmstad N. Kör mot Halmstad centrum och följ lokalslingan mot Tylösand (ca 9 km från centrum). Vägbeskrivning Söderifrån (E6, väg 117) Sväng av Halmstad Södra. Kör mot Halmstad centrum och följ lokalslingan mot Tylösand (ca 9 kilometer från centrum). Övriga transporter till Hotel Tylösand från centralstationen busslinje 30 och taxi, telefon 035-21 80 00. GPS-positioner Lat N 56º 38’ 52” Lon E 12º 43’ 53” 19.00Konferensmiddag ReumaBulletinen Nr 105 · 4/2015 11 ABSTRACTS Reumadagarna 2015 - Abstracts Årets höjdpunkt! Välkommen till Reumadagarna i Tylösand! Det stora nationella SRF-mötet har nu tidsmässigt hittat sin plats – början av höstterminen. Att den vetenskapliga aktiviteten är fortsatt hög inom svensk reumatologi återspeglas inte bara i den nyligen publicerade evalueringen av forskningsintresse hos Sveriges ST-läkare i reumatologi, utan även i antalet insända abstractbidrag till Reumadagarna. I år noterar vi glädjande att antalet inskickade bidrag till SveReFo & FRS nästan dubblerats. Vid sidan av de bidrag som här följer tillkommer ett hittills okänt antal abstracts i kategorin Kvalitets- & Verksamhetsutveckling – en av årets nyheter! SRF-bidragen har bedömts och rangordnats av Professorskollegiet. Denna kvalitetsgranskning ligger till grund för utmärkelsen av de två bästa bidragen vilka erhåller diplom och scentid under torsdagen. Ytterligare åtta bidrag som fått goda omdömen ges tid för muntlig presentation under på morgonsessionen samma dag. På följande sidor finner Ni samtliga abstractbidrag. För några av bidragen visas endast titel, författare och hemvist. Detta är inte något redaktionellt misstag utan svarar mot ett önskemål från flera av forskarna. Genom att bidragen inte publiceras i sin helhet finns inga formella hinder för att de presenteras vid internationella möten som tidsmässigt ligger efter deadline för abstract-inskick till Reumadagarna. På detta sätt kan vi bjudas på nyheter innan de når större reumatologikretsar på t.ex. Eular eller ACR. Än en gång, varmt välkomna! Christopher Sjöwall, Vetenskaplig sekreterare i Svensk Reumatologisk Förening ABSTRACTNUMMER: 1 1 OBESITY AND THE RISK FOR DEVELOPMENT OF RHEUMATOID ARTHRITIS – RESULTS FROM A POPULATION-BASED NESTED CASE-CONTROL STUDY Lotta Ljung1, Solbritt Rantapää Dahlqvist1 Institutionen för Folkhälsa och Klinisk Medicin/Reumatologi, Umeå Universitet, Umeå 1 The authors have chosen not to publish the abstract. ABSTRACTNUMMER: 2 2 ÖKAR RA ELLER TNF-HÄMMARE RISKEN FÖR CERVIXCANCER? Hjalmar Wadström1, Thomas Frisell1, Pär Sparén2, Johan Askling1,3 Enheten för klinisk epidemiologi, Karolinska institutet 2Institutionen för medicinsk epidemiologi och biostatistik, Karolinska institutet 3 Enheten för reumatologi, Karolinska Institutet 1 Bakgrund Immunosuppression spelar en viktig roll vid utveckling av cervixcancer från HPV infektion. Screening I form av cellprovtagning syftar till att upptäcka förstadier till cancer innan de progredierar till invasiv cancer. Vissa rapporter har funnit en ökad risk för cervixneoplasier hos kvinnor med RA jämfört med normalbefolkningen. Beträffande behandling med TNF-hämmare och risk för cervixcancer vet vi lite. Syftet med denna studie var att jämföra följsamheten till screening och risken för cervixneoplasier mellan kvinnor med RA som startar TNF-hämmarbehandling (TNFi), bionaiva kvinnor med RA, samt normalbefolkningen. Material och metoder Genom registerlänkningar, satte vi ihop en kohort av kvinnor som påbörjade TNF-hämmarbehandling (TNFi) (n=9,629), en kohort 12 ReumaBulletinen Nr 105 · 4/2015 med bionaiva kvinnor med RA (n=34,984), och en jämförelsekohort med matchade kontroller (matchade 1:10). Incidenserna för utfallen mellan 2001 och 2012 jämfördes med Coxregression justerat för ålder, utbildningsnivå, tidigare cellprovtagning, komorbiditeter, civilstånd, och sjukhusvistelser i slutenvård under de senaste fem åren innan studiestart. Utfallen var första cellprov med normalt utfall, första låggradiga cellförändring, första höggradiga cellförändring, och första invasiva cervixcancer under uppföljningstiden. Resultat De justerade Coxmodellerna visade på en högre frekvens screening bland kvinnor med RA, Bionaiv RA vs. Normalbefolkningen HR (95% CI) 1.08 (1.06-1.10), en ökad risk för både låggradiga och höggradiga cellförändringar hos kvinnor med RA jämfört med normalbefolkningen, samt en ökad risk för cervixcancer hos de som behandlats med TNF-hämmare, TNFi vs. Bionaiv RA, HR (95% CI) 2.10 (1.04-4.23). Hazardkvoterna påverkades endast måttligt av justering för utbildningsnivå, tidigare cellprovtagning, komorbiditeter, civilstånd, och tidigare sjukhusvistelser. Slutsats Denna studie visar att kvinnor med RA inte löper en ökad risk för cervixcancer men att de som behandlas med TNF-hämmare gör det. Kvinnor med RA screenar sig också i något större utsträckning än normalbefolkningen och löper större risk för att utveckla premaligna cellförändringar. ABSTRACTNUMMER: 3 3 STROKE IN SYSTEMIC LUPUS ERYTHEMATOSUS: A METAANALYSIS OF POPULATION-BASED COHORT STUDIES Marie Holmqvist1, Julia Simard1,2, Kjell Asplund, Elizabeth Arkema1 Clinical Epidemiology Unit, Department of Medicine, Karolinska Institute 2Division of Epidemiology, Department of Health Research 1 ABSTRACTS & Policy, Stanford School of Medicine 3Department of Public Health and Clinical Medicine, Umeå University, Sweden Background Previous studies of stroke in systemic lupus erythematosus (SLE) have had limited statistical power, combined stroke subtypes into composite outcomes and lacked a reference population estimate. We therefore conducted a systematic review and meta-analysis of population-based cohort studies to summarize the risk of stroke by subtype in patients with SLE compared to the general population. Methods A systematic search was performed for cohort studies including a general population comparator which examined the risk of stroke in SLE. A random effects model was used to pool the risk ratio (RR) for stroke. Subgroup analyses were carried out to investigate potential sources of heterogeneity. Results Ten studies were included. Studies reported RRs for overall stroke (n=5), ischemic stroke (n=6), hemorrhagic stroke (n=3) and subarachnoid hemorrhage (n=3). The pooled RR for overall stroke was 2.39 (95%CI 1.86, 3.07), ischemic stroke 2.24 (95%CI 1.80, 2.80) hemorrhagic stroke 2.72 (95%CI 2.15, 3.44) and subarachnoid hemorrhage 3.91 (95%CI 3.27, 4.67) (Figure). Significant heterogeneity among studies for ischemic stroke was detected (p<0.0001). Risk of stroke was highest among individuals younger than 50 years of age. Conclusions Individuals with SLE are at a 2 to 3-fold higher risk of ischemic and hemorrhagic stroke compared to the general population and at a 4-fold increased risk of subarachnoid hemorrhage. Future studies should focus on if and how comorbidity and disease flares are related to stroke and how targeting specific groups of patients with SLE may reduce the risk. Rheumatology and Inflammation Research, Institute of Medecine, Sahlgrenska Academy,, Gothenburg, Sweden 2Section of Rheumatology, SUS, Lund University, Lund, Sweden, The Parker Institute, Dept. of Rheumatology, Copenhagen Universal Hospital, Bispjerg-Fredriksberg, Denmark, Copenhagen, Denmark 3Institute LIME, Solna, Karolinska Institutet, Stockholm, Sweden, Stockholm, Sweden 1 Background Certolizumab pegol(Cimzia®) a Tumor Necrosis Factor inhibitor(TNFi), is one of five TNFi’s presently approved and available in Sweden. Cimzia® was approved for treatment of Rheumatoid Arthritis(RA) 2009, Ankylosing Spondylitis(AS), non-radiographic axial Spondyloarthritis, Psoriatic Arthritis(PsA) 2013. Cimzia® has been used for non-RA diagnoses since 2011, with recordings of treatment in the Swedish Rheumatology Quality Register(SRQ). In longitudinal observational studies, the 6 month adherence for TNFi-naïve patients with AS and PsA treated with other TNFi has ranged from about 78-92%. The aim of this study was to evaluate cumulative survival probability of Cimzia® in clinical practice over the first year of treatment for AS, PsA and undifferentiated Spondyloarthritis(uSpA). Methods Data from all patients with AS/PsA/uSPA initiating Cimzia® treatment before 15 August 2014 were retrieved from SRQ. Follow-up data was available until 30 October. Survival analysis by Kaplan-Meier curves and log-rank test of equality across strata for comparison of bio-naïve patients versus patients with previous treatment with biological Disease-Modifying-Anti-Rheumatic Drugs (bDMARD). Results 541 patients initiated Cimzia®-treatment in SpA. Of those 109(20%) were registered as AS, 276(51%) as PsA and 156(29%) as uSpA, with a mean follow-up time of 9,6/6,9/6,6 months. The proportions of men in AS/PsA/uSpA patient groups were 64/40/44% respectively. Median ages at baseline were 42/51/45 years respectively. In patients with AS/PsA /uSpA the proportions receiving Cimzia® as the first biological treatment were 43/37/38%; and the proportion receiving concurrent conventional DMARDs were 41/53/40%. Cumulative survival probability of Cimzia®-treatment(Table 1), were significantly better(P<0,001) for bDMARD-naïve patients versus others in both AS, PsA and uSpA. ABSTRACTNUMMER: 4 4 SPONDYLOARTHRITIS RECEIVING CERTOLIZUMAB PEGOL. RESULTS FROM THE NATIONWIDE SWEDISH RHEUMATOLOGY QUALITY REGISTER Christina Dackhammar1, Helena Forsblad d’Elia1, Lars-Erik Kristensen2, Ulf Lindström1, Sofia Ernestam3, Lennart Jacobsson1 Table 1. Cumulative survival probability for Certolizumab pegol treatment in AS, PsA and uSpA, stratified by earlier exposure to bDMARDS or not. (% (n=not censored subjects at each time point)) Diagnoses Baseline 3 months 6 months 9 months 12 months and (n) % (n) % (n) % (n) % (n) exposure AS (109) 91(97) 76(70) 72(50) 62(37) Bio-‐naïve (47) 94(44) 89(33) 86(22) 82(16) 89(53) 67(37) 61(28) 50(21) ≥ 1 bDMARD (62) PsA (276) 88(237) 69(163) 59(105) 51/72) Bio-‐naïve (102) 94(92) 91(71) 88(45) 81(32) 83(145) 58(92) 45(59 36(40) ≥ 1 bDMARD (174) uSpA (156) 84(127) 68(87) 58(58) 53(45) Bio-‐naïve (59) 97(56) 92(42) 82(28) 82(25) 76(71) 54(45) 43(30) 38(21) ≥ 1 bDMARD (97) Conclusions Real life experience from this nationwide rheumatology register, demonstrated that drug-survival in bio-naïve patients with SpA receiving CZP-treatment was statistically higher compared to paReumaBulletinen Nr 105 · 4/2015 13 ABSTRACTS tients previously treated with bDMARDs. Adherence rates after 6 and 12 month were within the range of published results for other TNF inhibitors. ABSTRACTNUMMER: 5 5 BIRTH CHARACTERISTICS AND CHILDHOOD INFECTIONS PREDICT ANKYLOSING SPONDYLITIS. A NATIONAL REGISTER BASED NESTED CASE-CONTROL STUDY. Ulf Lindström, Helena Forsblad-d’Elia, Johan Askling, Lars-Erik Kristensen, Elisabeth Lie, Sofia Exarchou, Lennart Jacobsson Institute of Medicine, Sahlgrenska Academy, Rheumatology and Inflammation Research, Gothenburg, Sweden 2Institution of Public Health and Clinical Medicine/Rheumatology, Umeå University, Umeå, Sweden 3Rheumatology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden 4Section of Rheumatology, Department of Clinical Sciences, Lund University, Sweden 5The Parker Institute, Department of Rheumatology, Frederiksberg and Bispebjerg hospital, Denmark 6Diakonhjemmet Hospital, Oslo, Norway lings (OR: 1.3 (95% Cl: 1.1-1.4), and for hospitalization due to infections at age 5-12 (OR: 1.4 (95% Cl: 1.0-1.8) and at age 13-16 (OR: 1.6 (95% Cl: 1.0-1.5)). Similar point estimates were found in a multivariate analysis also including gestational age, mothers’ marital status, mothers’ birth country and size of the delivery unit (fig 1). Point estimates were similar for men and women and in sensitivity analyses excluding subjects with inflammatory bowel disease or psoriasis prior AS diagnosis. Conclusion A diagnosis of AS was predicted by low birth weight, having older siblings and hospitalization due to infection during age 5-16 years, suggesting that these factors may be of importance in the disease pathogenesis. 6 1 Background Ankylosing spondylitis (AS) is strongly associated with genetic factors, but studies on environmental risk factors are few. The objectives were to determine if birth characteristics and childhood hospitalization due to infections predict a later diagnosis of AS. ABSTRACTNUMMER: 6 INCREASED MORTALITY IN ANKYLOSING SPONDYLITIS – RESULTS FROM A NATIONAL POPULATION BASED STUDY. Sofia Exarchou1, Elisabeth Lie2,4, Ulf Lindström2, Johan Askling3, Helena Forsblad-d’Elia2, Carl Turesson1, Lars Erik Kristensen1,5, Lennart Jacobsson1,2 Rheumatology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden 2Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at University of Gothenburg, Sweden 3Clinical Epidemiology Unit & Rheumatology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden 4 Department of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway 5The Parker Institute, Department of Rheumatology, Bispebjerg and Frederiksberg Hospital, the Capital Region of Copenhagen, Denmark 1 Background/Purpose Ankylosing spondylitis (AS) is characterized both by inflammation of the axial skeleton and systemic inflammation, and can also involve joints, entheses and other organs. Information on mortality in ankylosing spondylitis (AS) is scarce. Our study therefore aimed to assess: 1. mortality in AS vs the general population, overall and by gender, and 2. predictors of death in the AS population. Table to abstract A4814: Methods ¨INCREASED MORTALITY SPONDYLITIS – RESULTS FROM A Nationwide cohorts INofANKYLOSING patients with AS diagnosed at a rheumaNATIONAL POPULATION BASED STUDY.¨ Methods The National Patient Register (NPR) was used to identify AS-cases, defined as: born in Sweden after 1972; ≥1 visit to specialized health-care with an AS-diagnosis (ICD-code); first AS-diagnosis at an age of ≥16. Five matched (sex/ age/ county) controls were retrieved from the population register for each case. Cases/controls were linked to the Medical Birth Register and the NPR. Univariate and multivariate conditional logistic regression models were used to assess increased risk for a later diagnosis of AS. Exposures assessed were birth weight, gestational age, type of birth, older siblings and exposure to infections; and the following possible confounders: mothers’ marital status, mothers’ birth country and size of the delivery unit. Results Univariate analyses indicated significantly increased risks for low birth weight (<3000g) (OR: 1.3 (95% Cl: 1.1-1.6)), having older sib14 ReumaBulletinen Nr 105 · 4/2015 Table: Predictors of mortality within the cohort of patients with AS. Higher education (> 12 yrs vs. ≤ 12 yrs) Longer duration (Diagnosis made before 1st Jan 2006 vs. after 1st Jan 2006) General comorbidities# Cardiovascular disease * Diabetes* Chronic lung disease** Malignancy** Infections** AS-related clinical manifestations# Aortic valve insufficiency** Inflammatory bowel disease** Anterior uveitis** Psoriasis** Peripheral arthritis** Joint surgery (small or large joints)# Baseline Hazard frequencies Ratio† (%) 95% CI 2,648 (30.8) 0.67 0.53-0.85 2,954 (34.4) 418 (4.9) 164 (1.9) 427 (5.0) 2,829 (32.9) 1.99 1.92 3.03 1.67 2.01 1.58-2.49 1.51-2.45 2.27-4.05 1.32-2.12 1.68-2.34 5,493 (63.9) 79 (0.9) 644 (7.5) 1,731 (20.1) 512 (6.0) 1,841 (21.4) 645 (7.5) 1.03 1.19 1.23 0.89 1.13 1.17 1.38 0.84-1.36 0.68-2.06 0.92-1.65 0.69-1.13 0.81-1.57 0.95-1.44 1.09-1.73 †age-adjusted and sex-stratified analysis #registered before the start of follow-up *Based on either a visit to physician with such diagnosis (according to ICD-codes – data from the NPR) or on dispensing of pharmacological agents suggesting such diagnosis (according to ATC codes - data from the Prescribed Drugs Register) **Based on a visit to physician with such diagnoses (according to ICD-codes – data from the NPR) CI: Confidence Interval ABSTRACTS Results Among the 8,600 AS patients and the 40,460 controls, there were 496 and 1,533 deaths, respectively, resulting in an age- and sex-adjusted hazard ratio (HR) of 1.60 (95% Confidence Interval (CI): 1.44-1.77), with increased mortality for both men (age-adjusted HR = 1.53, 95% CI: 1.36-1.72) and women (age-adjusted HR = 1.83, 95% CI: 1.50 - 2.22). Cardiovascular disease was the leading cause of death in the AS cohort. Within the AS cohort, statistically significant predictors for death were male sex, higher age, a lower level of education, general co-morbidities (diabetes, infections, cardiovascular, pulmonary and malignant disease) and AS disease severity (previous joint surgery). Conclusion Mortality was increased both for male and female patients with AS. Predictors of death within the AS cohort included socio-economic status, general co-morbidities and disease severity. ABSTRACTNUMMER: 7 7 THE PREVALENCE OF ANKYLOSING SPONDYLITIS IN SWEDEN – A NATIONWIDE REGISTER STUDY Sofia Exarchou, Ulf Lindström, Johan Askling, Jonas Eriksson, Helena Forsblad-d’Elia , Lars Erik Kristensen, Martin Neovius, Carl Turesson, Lennart Jacobsson Section of Rheumatology, Department of Clinical Sciences, Malmö, Lund University, Malmö, Sweden 2Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden 3Clinical Epidemiology Unit, Rheumatology Unit, Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden 4Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden 5The Parker Institute, Department of Rheumatology, Bispebjerg and Frederiksberg Hospital, the Capital Region of Copenhagen, Denmark regarding clinical manifestations, patient demographics, level of education, pharmacological treatment, and geographical region were retrieved from the NPR and other national registers. Results A total of 11,030 cases were identified in the NPR according to our case definition, giving a point prevalence of 0.18% in 2009. The prevalence increased linearly with age up to the age of 55 years, after which it leveled off. Men had overall a higher prevalence compared to women (0.23% vs 0.14%). Prevalence estimates by health care region revealed the highest prevalence in the Northern Health Care Region (0.24%; 95% CI 0.23-0.25). The prevalence of AS was lowest among those with > 12 years of education (0.20%; 95% CI 0.19-0.21), while higher prevalences were observed in the other two strata with a shorter formal education (≤ 9 years and 1012 years) (0.24%; 95% CI 0.22-0.25 and 0.24%; 95% CI 0.23-0.24). Conclusion This nationwide, register-based prevalence estimate of AS in Sweden offers a unique opportunity to better understand the burden of AS to the healthcare system. Moreover, geographic and socio-economic differences in prevalence estimates suggest that genetic and possibly also environmental factors may be important for disease development and detection. Figure to abstract A4813 ¨ THE PREVALENCE OF ANKYLOSING SPONDYLITIS IN SWEDEN – A NATIONWIDE REGISTER STUDY¨ AS prevalence 2009 (%) tology or internal medicine out-patient clinics and age-, sex- and county-matched general population comparators (controls) were identified from the National Patient Register (NPR) between Jan 2001 and Dec 2009 and the census register, respectively. The follow-up period began on January 1st 2006 or at the first date of registered diagnosis thereafter and extended until death, emigration, or December 31st 2012, whichever occurred first. Socio-economic variables, AS-related clinical manifestations, co-morbidities, medication, vital status and causes of death were identified from other national registers. Cox regression models were used to determine mortality and predictors for death in the AS cohort. 0,45 0,4 0,35 0,3 0,25 0,2 Total: 0.18% Men: 0.23% Women: 0.14% 0,15 0,1 0,05 0 All age 16-19 20-24 25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 groups 16-64 Men Age groups 2009 Women Total 1 Background/Purpose Prevalence estimates of ankylosing Spondylitis (AS) vary considerably, and there are few nationwide estimates. The present study aimed to describe the national prevalence of clinically diagnosed AS in Sweden, overall as well as stratified according to age, sex, geographical and socio-economic factors, and according to subgroups with AS-related clinical manifestations and pharmacological treatment. Methods According to our case definition, all individuals diagnosed with AS according to WHO International Classification of Disease (ICD) codes between 1967 and 2009, alive and living in Sweden and 16-64 years old in 2009, were identified from the National Patient Register (NPR) (not including primary care and private practice). Data 8 ABSTRACTNUMMER: 8 COMPLEMENT COMPONENT 3 BUT NOT FACTOR B DEFICIENCY AGGRAVATES STAPHYLOCOCCAL AUREUS SEPTIC ARTHRITIS IN MICE Manli Na1, Anders Jarneborn1, Abukar Ali1, Amanda Welin1, Malin Magnusson1, Anna Stokowska2, Marcela Pekna2, Tao Jin1 1 Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska Academy at University of Gothenburg, S-41346 Göteborg, Sweden 2Center for Brain Repair and Rehabilitation, Department of Clinical Neuroscience and Rehabilitation, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden Background The complement system is known to play an essential role in innate immunity to protect against bacterial infections. However, detailed knowledge regarding the role of certain complement pathways/ components in S. aureus septic arthritis is still largely absent. ReumaBulletinen Nr 105 · 4/2015 15 ABSTRACTS Aims To elucidate the role of different complement components in S. aureus septic arthritis. Method Mice lacking the complement component 3 (C3-/-), complement factor B (CfB-/-), or complement component 3a receptor (C3aR-/-) and wild-type (WT) controls were intravenously inoculated with Staphylococcus aureus Newman strain (4x106 CFUs/mouse). The clinical course of septic arthritis were followed for 10 days. Histopathological and radiological changes of joints were compared among the groups. Results C3-/- mice had significantly increased severity and frequency of septic arthritis compared with WT controls and CfB-/- mice, which was in accordance with both histopathological and radiological evaluation. C3 but not CfB deficiency led to more weight loss, more severe kidney abscesses, as well as higher bacterial burden in kidneys. S. aureus opsonised with C3-/- sera displayed decreased uptake by mouse peritoneal macrophages compared with bacteria opsonised with WT sera and CfB-/- sera. C3aR deficiency had no impact on the course of S. aureus septic arthritis. Conclusion C3 deficiency increases the susceptibility to S. aureus septic arthritis, and deteriorates host bacterial clearance, resulting in worse weight development and kidney abscesses. Such effects were not mediated through C3aR but possibly caused by impaired phagocytosis. Keywords Staphylococcus aureus, septic arthritis, mouse, complement component 3, complement factor B, complement component 3a receptor. ABSTRACTNUMMER: 9 9 DIFFERENT SUSCEPTIBILITY OF MICE RECEIVING ANTI-TNF OR CTLA4-IG TREATMENTS TO STAPHYLOCOCCAL SEPTIC ARTHRITIS Abukar Ali1, Amanda Welin1, Manli Na1, Anders Jarneborn1, Malin Magnusson1, Majd Mohammad1, Elisabet Josefsson1, Johan Bylund1, Rille Pullerits1, Tao Jin1 Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska Academy at University of Gothenburg, S-41346 Göteborg, Sweden 1 Background The development of biologics has greatly increased the quality of life as well as the life expectancy of many RA patients. However, a large number of these patients are at an increased risk of developing serious infections. The aim of this study was to examine differential effects of anti-TNF versus CTLA4-Ig treatment on both immunological response and host defense in a murine model of septic arthritis. Method Abatacept (CTLA4-Ig), etanercept (anti-TNF treatment), or PBS were given to NMRI mice intravenously inoculated with Staphylococcus aureus. The clinical course of septic arthritis, histopathological and radiological changes of joints were compared among the groups. 16 ReumaBulletinen Nr 105 · 4/2015 Results Mice receiving CTLA4-Ig treatment had more severe septic arthritis compared with controls and mice receiving anti-TNF treatment. Anti-TNF treatment led to more severe weight loss and kidney abscesses, as well as higher bacterial burden in the kidneys. Mice on CTLA4-Ig therapy had lower serum levels of IL-4, whereas mice receiving anti-TNF therapy had higher levels of TNF- . Both iNOS and arginase-1 expression were reduced in peritoneal macrophages from mice receiving CTLA4-Ig as compared with anti-TNF group. Conclusion CTLA4-Ig therapy significantly increased the susceptibility to S. aureus septic arthritis in mice, whereas anti-TNF therapy deteriorated host bacterial clearance, resulting in worse weight development and kidney abscesses. Keywords Staphylococcus aureus, septic arthritis, mouse, abatacept, etanercept. ABSTRACTNUMMER: 10 10 BOTH ANTI-TNF AND CTLA4-IG TREATMENTS ATTENUATE STAPHYLOCOCCAL DERMATITIS IN MICE Manli Na1, Abukar Ali1, Malin Magnusson1, Elisabet Josefsson1, Tao Jin1 Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska Academy at University of Gothenburg, S-41346 Göteborg, Sweden 1 Background RA patients on biologics were shown to have an increased risk of infections. We have recently shown that both CTLA4-Ig and antiTNF treatment aggravate S. aureus systemic infection in mice. However, the effects of CTLA4-Ig and anti-TNF treatments on a local S. aureus infection e.g. skin infection might differ from their effects on a systemic infection. Aims We aimed to examine differential effects of anti-TNF versus CTLA4-Ig treatment on S. aureus skin infections in mice. Method Abatacept (CTLA4-Ig), etanercept (anti-TNF treatment), or PBS were given to NMRI mice subcutaneously inoculated with Staphylococcus aureus SH1000. The clinical signs of dermatitis, histopathological changes of skin infections were compared among the groups. Results Both CTLA4-Ig and anti-TNF treatment resulted in less severe skin infections and smaller post-infectious pigmentation compared with PBS controls. In accordance with the clinical signs of dermatitis, smaller lesion size, more epithelial hyperplasia and more granulation were found in skin biopsies from mice receiving antiTNF compared with PBS controls. Serum MCP-1 levels were elevated in anti-TNF group compared with CTLA4-Ig and PBS group, whereas IL-6 levels were higher in PBS controls than other two groups. Importantly, no tangible difference was found regarding the bacterial burden in skins among groups. Conclusion Both CTLA4-Ig and anti-TNF therapies attenuate the severity of S. aureus skin infections, and have no impact on bacterial clearance in skin tissues. ABSTRACTS Enbrel finns i olika beredningsformer för att passa patienternas behov INJEKTIONSPENNA 50 mg Varunummer: 06 57 78 Injektionsvätska, lösning förfylld injektionspenna, 50 mg (= 1 ml). 2, 4 eller 12 förfyllda injektionspennor med Enbrel och 2, 4 eller 12 kompresser med alkohol. FÖRFYLLD 25 mg Varunummer: 04 70 42 Injektionsvätska, lösning förfylld spruta, 25 mg (=1 ml). 4 förfyllda injektionssprutor med lösning, 8 kompresser. FÖRFYLLD 50 mg Varunummer: 04 75 60 Injektionsvätska, lösning förfylld spruta, 50 mg (=1 ml). 4 förfyllda injektionssprutor med lösning, 8 kompresser. BLANDBAR 25 mg Varunummer: 55 66 61 Pulver och vätska till injektionsvätska, lösning 25 mg (=1 ml). 4 injektionsflaskor + pulver, 4 förfyllda injektionssprutor med 1 ml lösningsmedel, 4 injektionsnålar, 4 adaptrar, 8 kompresser. BARNBEREDNING 10 mg Varunummer: 48 76 92 Pulver och vätska till injektionsvätska, lösning 10 mg (=1 ml) till barn. 4 injektionsflaskor, 4 förfyllda sprutor med vatten för injektionsvätska, 4 injektionsnålar, 4 adapter till injektionsflaskor och 8 kompresser med alkohol. Gradering på sprutan: 1 ml spruta med 0,1 ml gradering (och fingradering för 0,02 ml). Enbrel är godkänd för förvaring i rumstemperatur max 25° i upp till 4 veckor! ENB20150305PSE04 För fullständig information se www.fass.se Enbrel (etanercept), Rx, F, ATC-kod: L04AB01. Selektivt immunosuppressivt medel. Injektionsvätska i förylld injektionspenna, förfylld spruta, pulver och vätska till injektion i styrkorna: 10 mg, 25 mg och 50 mg. Indikationsområden: Måttlig till svår aktiv reumatoid artrit samt svår, aktiv progressiv reumatoid artrit hos vuxna. Polyartrit och utvidgad oligoartrit hos barn och ungdomar från 2 års ålder med otillräckligt svar på eller intolerans mot metotrexat. Psoriasisartrit hos ungdomar från 12 års ålder med otillräckligt svar på eller intolerans mot metotrexat. Entesitrelaterad artrit hos ungdomar från 12 års ålder med otillräckligt svar på eller intolerans mot konventionell behandling. Aktiv och progressiv psoriasisartrit hos vuxna där svaret vid tidigare behandling med sjukdomsmodifierande antireumatiska läkemedel varit otillräckligt. Svår aktiv ankyloserande spondylit hos vuxna med otillräckligt svar på konventionell terapi. Behandling av vuxna med svår icke-radiografisk axial spondylartrit med objektiva tecken på inflammation genom förhöjt C-reaktivt protein (CRP) och/eller magnetröntgen (MR) och som inte har svarat tillräckligt på icke-steroida antiinflammatoriska läkemedel (NSAIDs).Måttlig till svår plaquepsoriasis hos vuxna som inte svarat på eller som har en kontraindikation mot, eller som är intoleranta mot annan systemisk behandling inkluderande cyklosporin, metotrexat eller psoralen och UVA-strålning (PUVA). Kronisk svår plaquepsoriasis hos barn och ungdomar från 6 års ålder som har otillräcklig effekt av eller som är intoleranta mot andra systemiska behandlingar eller ljusbehandling. Kontraindikationer: Sepsis eller risk för sepsis. Varningar och försiktighet: Allvarliga infektioner, samtidig behandling med anakinra och abatacept, hjärtsvikt, demyeliniserande sjukdomar, återkommande kroniska infektioner. För ytterligare information samt prisuppgift se www.fass.se. Pfizer AB, Vetenskapsvägen 10, 191 90 Sollentuna. Produktresumé: 25 september 2014. Pfizer AB 191 90 Sollentuna Tel 08-550 520 00 www.pfizer.se ReumaBulletinen Nr 105 · 4/2015 17 ABSTRACTS Keywords Staphylococcus aureus, septic arthritis, mouse, abatacept. ABSTRACTNUMMER: 11 11 IL-1 RECEPTOR ANTAGONIST TREATMENT AGGRAVATES STAPHYLOCOCCAL SEPTIC ARTHRITIS AND SEPSIS IN MICE Abukar Ali1, Malin Na1, Mattias Swensson1, Malin Magnusson1, Amanda Welin1, Jan-Christoph Schwarze1, Majd Mohammad1, Rille Pullerits1, Tao Jin1 Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska Academy at University of Gothenburg, S-41346 Göteborg, Sweden 1 Background Interleukin-1 receptor antagonist (IL-1Ra) is the primary therapy against autoinflammatory syndromes with robust efficacy in reducing systemic inflammation and associated organ injury. However, patients receiving IL-1Ra might be at increased risk of acquiring serious infections. Aims To study whether IL-1Ra treatment deteriorates Staphylococcus aureus (S. aureus) septic arthritis and sepsis in mice. Method NMRI mice were treated with anakinra (IL-1Ra) daily for 7 days before intravenous inoculation with S. aureus strain Newman in both arthritogenic and lethal doses. The clinical course of septic arthritis, histopathological and radiological changes of the joints, as well as the mortality were compared between IL-1Ra treated and control groups. Results IL-1Ra treated mice developed more frequent and severe clinical septic arthritis. Also, the frequency of polyarthritis was significantly higher in the mice receiving IL-1Ra therapy. In line with the data from clinical arthritis, both histological and radiological signs of septic arthritis were more pronounced in IL-1Ra treated group compared to controls. Importantly, the mortality of IL-1Ra treated mice was significantly higher than PBS treated controls. Conclusion IL-1Ra treatment significantly aggravated S. aureus induced septic arthritis and increased the mortality in these mice. Keywords Staphylococcus aureus, septic arthritis, mouse, anakinra, IL-1 receptor antagonist ABSTRACTNUMMER: 12 12 STAPHYLOKINASE CONTROLS STAPHYLOCOCCUS AUREUS BIOFILM FORMATION THROUGH HOST PLASMINOGEN ACTIVATION Jakub Kwiecinski1, Marijke Peetermans2, Halla Björnsdottir1, Gunnar Jacobsson, Bengt Johansson, Timothy Foster, Elisabet Josefsson, Johan Bylund, Peter Verhamme2, Tao Jin1 Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, 1 18 ReumaBulletinen Nr 105 · 4/2015 Gothenburg, Sweden 2Center for Molecular and Vascular Biology, Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium 3Department of Infectious Diseases, Skaraborg Hospital, Skövde, Sweden 4Electron Microscopy Unit, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden 5Department of Microbiology, Moyne Institute of Preventive Medicine, School of Genetics and Microbiology, Trinity College, Dublin, Ireland 6Department of Oral Microbiology and Immunology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden Abstract Staphylococcus aureus biofilms, a leading cause of persistent infections, are highly resistant to immune defenses and antimicrobial therapies. In this study, we investigated the contribution of staphylokinase to biofilm formation. In clinical S. aureus isolates, we observed an inverse association between biofilm-associated infections and staphylokinase secretion. High staphylokinase-producing strains formed less biofilm than strains that lacked staphylokinase, suggesting that staphylokinase prevents biofilm formation. This effect depended on plasminogen activation by staphylokinase. Host-derived fibrin, the main substrate cleaved by activated plasminogen, was abundantly present in biofilms and dissolution of the fibrin scaffold greatly increased susceptibility of biofilms to antibiotics and neutrophil phagocytosis. Staphylokinase also attenuated biofilm-associated catheter infections in mouse models. In conclusion, our results reveal a novel role for staphylokinase-induced plasminogen activation that prevents S. aureus biofilm formation and induces detachment of existing biofilms through proteolytic cleavage of biofilm matrix components. Keywords Staphylococcus aureus, biofilm infection, mouse, staphylokinase ABSTRACTNUMMER: 13 KAN EN URINSTICKA UTESLUTA SEPTISK ARTRIT? 13 Per-Johan Hedin Bakgrund Vid misstanke om septisk artrit är det värdefullt med information om antalet leukocyter i ledvätska, eftersom man då vanligen har leukocyter = 50-200 x 10E9/L, medan ett lågt antal leukocyter starkt talar emot en septisk artrit. På vårdcentraler kan man sällan räkna leukocyter i ledvätska, och man måste av den anledningen remittera misstänkta fall med septisk artrit patienter akut. Därför vore det en stor vinst om man med ett snabbtest kunde utesluta, eller minska misstanken på, en septisk artrit. Vår hypotes är att ett lågt - måttligt utslag på urinstickans leukocytfält vid test av ledvätska kan utesluta septisk artrit. Material och metod I samband med ledpunktion tas ofta prov för cellräkning på laboratoriet med frågeställningen inflammatorisk aktivitet. Vid sådana tillfällen har vi vid 72 tillfällen sedan 2001 även analyserat ledvätskan lokalt med urinsticka (Siemens Multstix 5, avläst med Siemens Clinitek Status +). Proven togs när vi kom ihåg det, och det rör sig således om ett godtyckligt urval. Resultat Av 72 prover tagna med olika frågeställningar har det funnits en god korrelation (r=0,61) mellan antalet leukocyter räknade på laboratoriet, och utslaget på urinsticka. 6 fall med odlingsverifierad septisk artrit konstaterades. Samtliga dessa gav maximalt utslag (4+) på urinstickans leukocytfält. ABSTRACTS Slutsats Septiskt artrit förekommer lyckligtvis sällan på reumatologisk klinik. Inget av de 6 fall med septisk artrit vi identifierade gav ett lägre utslag än 4+ för leukocyter på urinsticka. Det vore intressant att undersöka ledvätska från ett större antal patienter med septisk artrit, för att utvärdera urinstickan som en möjlig diagnostisk snabbtest för att utesluta, eller åtminstone minska sannolikheten för, en septisk artrit. ABSTRACTNUMMER: 14 14 RHEUMATOID FACTOR ISOTYPES IN RELATION TO ANTIBODIES AGAINST CITRULLINATED PEPTIDES AND ANTI-CARBAMYLATED ANTIBODIES IN INDIVIDUALS BEFORE THE ONSET OF RHEUMATOID ARTHRITIS Mikael Brink, Monika Hansson, Linda Mathsson-Alm, Priyantha Wijayatunga, Marije Verheul, Leendert Trouw, Rikard Holmdahl, Johan Rönnelid, Lars Klareskog, Solbritt Rantapää Dahlqvist Folkhälsa & Klinisk Medicin, Reumatologi, Umeå Universitet, Umeå Rheumatology Unit, Department of Medicine, Karolinska Institute, Stockholm 3Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala och Thermo Fisher Scientific, Uppsala, 4 Department of Statistics, Umeå University, Umeå 5Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands 6Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands 7Medical Inflammation Research, Medical Biophysics and Biochemistry, Karolinska Institute, Solna, Stockholm, 8Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala 9Rheumatology Unit, Department of Medicine, Karolinska Institute, Stockholm, 10Folkhälsa & Klinisk Medicin, Reumatologi, Umeå Universitet, Umeå 1 Solbritt Rantapää Dahlqvist1, Antonia Boman2, Heidi Kokkonen3, Ewa Berglin4 Institutionen för Folkhälsa och Klinisk Medicin, Reumatologi, Umeå Universitet, Umeå 2Institutionen för Folkhälsa och Klinisk Medicin, Reumatologi, Umeå Universitet, Umeå 3Institutionen för Folkhälsa och Klinisk Medicin, Reumatologi, Umeå Universitet, Umeå 4Institutionen för Folkhälsa och Klinisk Medicin, Reumatologi, Umeå Universitet, Umeå 1 The authors have chosen not to publish the abstract. ABSTRACTNUMMER: 17 17 DOES INDUCTION WITH METHOTREXATE PLUS ANTI-TNF CONFER A LONG-LASTING CLINICAL BENEFIT IN EARLY RA? A SYSTEMATIC REVIEW AND META-ANALYSIS OF INDUCTION-MAINTENANCE TRIALS Sharzad Emamikia1, Elizabeth V. Arkema4, Noémi Györi1, Jacqueline Detert2, Aikaterini Chatzidionysiou1, Maxime Dougados3, Gerd Rüdiger Burmester2, Ronald van Vollenhoven1 2 The authors have chosen not to publish the abstract. ABSTRACTNUMMER: 15 15 PREDICTING RHEUMATOID ARTHRITIS BY MEASURING SURVIVIN IN UNSELECTED SAMPLES - EPIDEMIOLOGICAL STUDY WITHIN TWO UNIVERSITY CITIES OF SWEDEN. Minna Turkkila1, Rille Pullerits1,2, Claes Schiller3, Catharina Eriksson4, Malin Erlandsson1, Solbritt Rantapää-Dahlqvist3, Maria Bokarewa1 Department of Rheumatology and Inflammation Research, Institution of Medicine, The Sahlgrenska Academy at the University of Gothenburg 2Department of Clinical Immunology, Sahlgrenska University Hospital , Gothenburg 3Department of Public Health and Clinical Medicine, Rheumatology, Umeå University Hospital 4Clinical Immunology , University Hospital, Umeå 1 The authors have chosen not to publish the abstract. ABSTRACTNUMMER: 16 16 RECEPTOR ACTIVATOR OF NUCLEAR FACTOR KAPPA-B LIGAND (RANKL) AND SCLEROSTIN ARE RELATED TO JOINT DESTRUCTION IN EARLY RHEUMATOID ARTHRITIS. ClinTRID, Karolinska Institute, Stockholm, Sweden 2Charité - Universitätsmedizin Berlin, Institute of Clinical. Immunology and Rheumatology, Berlin, Germany 3Department of Rheumatology B, Cochin Hospital, Paris, France 4Clinical Epidemiology Unit, Karolinska Institute, Stockholm, Sweden 1 Background The goal of rheumatoid arthritis (RA) treatment is remission or at least low-disease-activity (LDA) when remission is not achievable. Using meta-analysis we compared the efficacy of initial Methotrexate (MTX)-monotherapy versus combination-therapy (MTX plus Adalimumab (Humira)) for clinical remission and LDA among DMARD-naïve early RA-patients. Methods A systematic review was performed for induction-maintenance randomized controlled trials where initial combination therapy was compared with MTX-monotherapy. Our principal outcome was the proportion of patients whose disease could be controlled by MTX alone, comparing patients who started with MTX+ADA to those who started with MTX alone, focusing on achieving LDA (DAS28≤3.2) and/or remission (DAS28<2.6), at 12-52 weeks of follow-up. A random-effects-model was used in this meta-analysis to pool the risk ratio (RR) for clinical remission and LDA at 12-52 weeks of follow-up. Results We found four published randomized trials to include in the meta-analysis, with different study designs and patients’ baseline characteristics, in which MTX+ADA was given as initial therapy and ADA was withdrawn in at least a subset of patients after LDA/ remission had been achieved. For two of these (Guépard and HitHard) the original data were re-examined, for the other two (Optima and Opera) published data were examined. The pooled RR for achieving clinical remission at follow-up was 1.30 (95% CI 0.901.87) and 1.22(95% CI 0.95-1.58) for LDA, with significant heterogeneity (p=0.005 and p=0.016, respectively). Opera featured consistent use of individualized, intra-articular glucocorticoid-injections as part of a treat-to target strategy. A sensitivity analysis excluding Opera was performed to examine the influence of individual studies, where the pooled RR for achieving clinical remission was 1.56 (95% CI 1.21-2.00) and 1.37(95% CI 1.09-1.72) for LDA, with ReumaBulletinen Nr 105 · 4/2015 19 ABSTRACTS non-significant heterogeneity (p=0.320 and p=0.269 respectively) (Figure 1). jury database to identify low-energy fractures. The database (since 1993) covers a population at risk of 118000 adults. DNA was available from 866 RA-patients of whom 244 had a fracture after the diagnosis of RA. Controls were 997 sex and age matched population controls from the same area. The analysed SNPs were; rs3801387 (WNT16), rs6666455 (SOAT), rs3736228 (LRP5), rs4796995 (FAM210A), rs4792909 (SOST), rs2062377 (TNFRSF11B/OPG), rs884205 (TNFRSF11A/RANK), rs9533090 (TNFSF11/RANKL), and rs1373004 (DKK1) using KASPTM genotyping assays (LGC genomics Ltd, Hoddesdon, UK). Conclusions This meta-analysis shows that initial combination therapy may be associated with a higher chance of retaining LDA and/or remission after discontinuation of ADA Results The genotype distribution of rs1373004 differed significantly between RA-patients with fractures and population controls ( 2=8.21, p=0.017, 2df ). Carrier of the rare allele was more common among RA-patients with fractures compared with controls (OR=1.56 [95%CI 1.13-2.16] p=0.007). A difference in genotype distribution for rs4792909 (encoding sclerostin) was found comparing RA patients with and without fracture ( 2=6.66, p=0.036, 2df ). Being homozygous for the major allele was more common among patients with fracture (OR=1.42 [95%CI 1.05-1.93] p=0.023). Carrier of the major allele of rs4796995 was associated with RA (OR=1.48 [95%CI 1.06-2.06] p=0.020), and more strengthened among women (OR=1.62 [95%CI 1.10-2.39] p=0.014). Conclusions Genes related to osteoporotic fractures were associated with increased risk of fractures in RA-patients. The increased risk in RA-patients has besides the disease and its treatment also a contribution of genetic factors. Figure 1A. Forest plot and sensitivity analysis (excluding Opera) of the risk ratio for attaining clinical remission using combination therapy versus monotherapy at follow-up B. Forest plot and sensitivity analysis (excluding Opera) of the risk ratio for attaining LDA using combination therapy versus monotherapy at follow-up. The I2 and p-values for heterogeneity are shown. (Remission=disease activity score (DAS) 28<2.6; low-disease-activity (LDA) = DAS28≤3.2; RR=risk ratio) 18 ABSTRACTNUMMER: 18 ASSOCIATIONS OF OSTEOPOROTIC FRACTURE GENES IN PATIENTS WITH RHEUMATOID ARTHRITIS Kristina Wiberg , Lisbeth Ärlestig , Ulrika Pettersson-Kymmer3, Solbritt Rantapää Dahlqvist4 1 2 Östersunds Remonthagen, Östersund och Institutionen för Folkhälsa & Klinisk Medicin, reumatologi, Umeå Universitet 2Institutionen för Folkhälsa & Klinisk Medicin, reumatologi, Umeå Universitet 3Institutionen för farmakologi och klinisk neurovetenskap, Umeå Universitet 4Institutionen för Folkhälsa & Klinisk Medicin, reumatologi, Umeå Universitet ABSTRACTNUMMER: 19 19 LIPIDOMICS PROFILING DIFFERS IN PATIENTS WITH RHEUMATOID ARTHRITIS AND CONTROLS Anna Södergren, Izabella Surowiec, Ilka Abreu, Rasmus Madsen, Johan Trygg, Solveig Wållberg-Jonsson Department of Public Health and Clinical Medicine/Rheumatology, University of Umeå 2Computational Life Science Cluster, Department of Chemistry, University of Umeå 3Forest Genetics and Plant Physiology, Umeå Plant Science Centre 1 1 Background Patients with rheumatoid arthritis (RA) have increased risk for osteoporosis. An increased incidence of low-energy fractures in RA patients was found in northern Sweden. Increased serum levels and associations with genes encoding proteins involved in the Wnt pathway have been related to joint destruction in RA. Objectives To analyse in RA-patients nine SNPs related to osteoporotic fractures in the general population and to joint destruction in RA. Methods A register of consecutively included RA-patients (ARA criteria) since 1995 (n=1178) was co-analysed with the register of Umeå in20 ReumaBulletinen Nr 105 · 4/2015 Background Patients with rheumatoid arthritis (RA) have an increased mortality and morbidity due to cardiovascular disease (CVD). A premature atherosclerosis can be measured by ultrasound of intima media thickness (IMT). Omics studies such as metabolomics, proteomics and lipidomics have been extensively used to elucidate biological mechanisms of diseases. In this prospective 5-year follow up, we aimed to investigate the plasma lipidomics profiles in patients with RA compared to controls and to analyze the relationship between these profiles and atherosclerosis measured by IMT. Material and methods Patients from northern Sweden diagnosed with early RA are followed in an ongoing prospective study. From these patients a subgroup aged ≤60 years (n=18), was consecutively included for measurements of IMT at inclusion (T0), after 18 months (T18) and after 60 months (T60). 20 age/sex matched controls were included. Blood was drawn at all time points and stored in -80°C. A methanol/chloroform based protocol was used on the plasma samples to extract lipid species, which were then analyzed with LC-Orbi- ABSTRACTS trapMS; compound detection and quantification was performed with Thermo Scientific SIEVE Software. Results At T0, higher levels of lipids were seen in RA patients, whereas at T18 and T60 lower levels of lipids were present in RA patients compared to controls. For RA patients we observed a decrease of lipid levels between T0 and T18, whereas an increase was observed for controls. Regarding the relation to IMT at T0 we could obtain a statistically significant model only for RA samples, here an increase in plasma lipids was observed with increased IMT values. At T60 approximately half of the lipids were positively and half negatively correlated with IMT in RA patients. Conclusion Lipidomics profiling shows that the metabolism of lipid species differs between patients with RA and controls, both at diagnosis and during five years follow up. ABSTRACTNUMMER: 20 20 RESISTIN-INDUCED ACTIVATION OF STAT3 IN SUBCUTANEOUS FAT TISSUE INCREASES CARDIOVASCULAR Mitra Nadali, Rille Pullerits, Karin Andersson, Malin Erlandsson, Sofia Töyrä Silfverswärd, Maria Bokarewa Göteborgs Universitet, Inst för medicin 1 Background RA is risk factor for cardiovascular disease (CVD). Adipokines, signal molecules from adipose tissue exhibit strong proinflammatory effects. Resistin utilizes IGF-1R and TLR4 pathway to induce inflammation in RA leukocytes and synovia. Objectives In the present study we evaluated the role of adipokines and adipokine-related genes on the cardiovascular risk (CVR) in female RA patients. Methods CVR was calculated in 187 female RA patients, using the modified Systematic Coronary Risk Evaluation (mSCORE). Serum levels of adipokines and IGF-1 and transcription of genes affected by Resistin and IGF-1 signalling in peripheral blood leukocytes and in subcutaneous fat tissue were analyzed in relation to mSCORE. To assess the predictive value of adipokines and gene transcription for the increased mSCORE, two independent binary logistic regression models were designed. Results mSCORE was directly related to the age, disease duration, smoking and cholesterol. The patients with mSCORE≥1 (n=96) had significantly higher levels of leptin and resistin but lower levels of IGF-1 compared to the patients with lower CVR (mSCORE<1, n=91). In patients with mSCORE≥1 transcriptional activity in adipocytes was prominently higher compared to peripheral blood leucocytes and the relative transcription of RELA, AKT1 and TLR4 was higher compared to the patients with mSCORE<1.The logistic regression analysis with mSCORE showed that high serum levels of resistin and leptin were independently associated with the increased CVR. Similar associations were observed for adipocyte expression of resistin-triggering genes TLR4 and STAT3 .The model with high serum resistin as a dependent variable revealed an association to high transcription of STAT3 and low transcription of AKT1 in leukocytes and in adipocytes. Conclusions Transcriptional activity of adipose tissue in women with RA is associated with increased CVR. High transcriptional activity of resistin-triggering genes may be a sufficient force driving premature CVD in RA patients. 21 ABSTRACTNUMMER: 21 CD21-/LOW B CELLS IN HEALTHY DONORS AND RHEUMATOID ARTHRITIS PATIENTS Katrin Thorarinsdottir, Alessandro Camponeschi, Lennart Jacobsson, Inga-Lill Mårtensson, Inger Gjertsson Sahlgrenska Universitetssjukhus 2 Göteborgs Universitet 1 Background A unique B cell subpopulation that lack or express low levels of complement receptor 2 (CD21) i.e. CD21-/low is enriched in peripheral blood in conditions with prolonged immune stimulation. Very little is known about the function of CD21-/low B cells. Our aim is to phenotypically and functionally characterize CD21-/low B cells in healthy individuals and patients with reumatoid arthritis (RA) to investigate whether they contribute to disease pathogenesis. Materials and methods We collected PBMCs from healthy women (25-65 years) n=20 and women with RA (30-70 years) n=31. Flow cytometry was used for phenotyping with the markers CD19, CD21, CD23, CD27, CD10, CD38, CD24, CD95, CD40, IgM, IgD, IgG and IgA. Isolated cells were stimulated in vitro for functional analysis. Results Healthy women: The CD21-/low B cell population comprised around 5 % of the total B cells and was present in all individuals. The CD21-/low B-cell population consists mainly of memory B cells and only approx. 10% naïve B cells. In vitro stimulation with anti-Ig/TLR7 ligand/IL-2 of isolated CD21-/low B cells, CD21+ naïve or CD21+ memory B cells showed that CD21-/low (25%) differentiate into plasmablast compared with naïve B cells (1%) and CD21+ memory B cells (15%). RA patients In RA patients the CD21-/low is phenotypically similar to healthy while the proportion is doubled (10%). Patients with joint erosions had significantly lower proportion of CD21-/low B cells than patients without erosions. The frequency of CD21-/low B cells did not differ between seropositive and seronegative patients. Conclusions CD21-/low are mainly memory B cells that easily differentiate into plasmablasts upon stimulation. In RA patients there is an inverse correlation between erosions and proportion of CD21-/low B cells. These findings suggest that CD21-/low B cells is a potentially interesting cell in the pathogenesis of RA and further studies are warranted. ABSTRACTNUMMER: 22 22 ANDELEN TH2-CELLER, TH17-CELLER OCH REGULATORISKA T-CELLER I BLOD ÄR POSITIVT ASSOCIERADE MED REUMATOID ARTRIT JÄMFÖRT MED FRISKA KONTROLLER MEN NEGATIVT ASSOCIERADE TILL SJUKDOMSAKTIVITET ReumaBulletinen Nr 105 · 4/2015 22 ABSTRACTS Magnus Hallström1,2, Jayesh Pandya1, Kerstin Andersson1, Anna-Carin Lundell1, Anna Rudin1,2 Maria Rydholm1,2, Christina Book1,2, Ingegerd Wikström1,2, Lennart Jacobsson1,3, Carl Turesson1,2 Avd för Reumatologi och Inflammationsforskning, Sahlgrenska Akademin 2Reumatologi, Sahlgrenska Universitetssjukhuset 1 1 The authors have chosen not to publish the abstract. ABSTRACTNUMMER: 23 23 REMAINING PAIN IN SPITE OF SUPPRESSED INFLAMMATION IN EARLY RHEUMATOID ARTHRITIS - LONG-TERM STRONGLY INCREASED RISK FOR WIDESPREAD PAIN AND FATIGUE Jon Lampa1, Saedis Saevarsdottir1, Reem Altawil1, Lars Klareskog1, Lars Alfredsson2, Maria EC. Sandberg2 Institutionen för Medicin, Enheten för Reumatologi, Karolinska Institutet 2Institutionen för Miljömedicin, Karolinska Institutet 1 Background/Purpose Pain is common in rheumatoid arthritis (RA), even after adequate inflammatory disease control. Our aim was to investigate the distribution of remaining pain dimension in RA, and whether it is a risk factor for long-term generalized (widespread) pain and fatigue. Methods We used the cases (incident RA patients recruited 1996-2009) from the EIRA study, linked to the SRQ register (N=1633). Three years after diagnosis an additional questionnaire was sent out, assessing fatigue, pain outside joints and sleeping problems (N=186). Remaining pain was defined as pain on visual-analog scale (VAS) ≥20 mm and CRP <10 g/L at the 12 month follow-up visit. Modified Poisson regression was used to calculate the risk ratios (RR) for widespread pain (WSP; pain outside joints in all four quadrants)/ any pain outside joints/sleeping problems/fatigue, as an effect of remaining pain. Results 35% of the patients had remaining pain at 1 year after diagnosis. After 3 years; 7% had WSP, 36% any pain outside joints, 17% sleeping problems and 26% had significant fatigue (VAS ≥40). Remaining pain at 1 year was associated with a strongly increased risk for wide-spread pain; RR=3.07 [95%CI: 1.21-7.81], regional pain RR= 1.74 [95%CI:1.26-2.39], sleeping problems RR=3.11 [95%CI:1.48-6.54] and fatigue RR=1.90 [95%CI:1.18-3.07] at 3 years. All these RRs remained after adjustment for very high baseline pain levels (VAS > 70 mm), indicating that presence of WSP/fibromyalgia at diagnosis had no major impact on the results. Conclusion More than a third of all RA-patients have remaining pain despite satisfactory inflammation control 1 year after diagnosis. This condition is a very strong predictor for development of widespread pain 3 years after diagnosis. Moreover, we found strong associations with long-term non-joint-related pain, sleeping problems and fatigue. These observations stress the importance to optimize pain treatment also in patients with adequate inflammation control early in RA. ABSTRACTNUMMER: 24 24 DESPITE EARLY IMPROVEMENT, PATIENTS WITH RHEUMATOID ARTHRITIS STILL HAVE IMPAIRED GRIP FORCE 5 YEARS AFTER DIAGNOSIS 22 ReumaBulletinen Nr 105 · 4/2015 Reumatologi, Institutionen för Kliniska Vetenskaper, Malmö, Lunds Universitet 2Sektionen för Reumatologi, Skånes Universitetssjukhus, Malmö 3Avdelningen för Reumatologi och Inflammationsforskning, Sahlgrenska Akademin, Göteborgs Universitet Background Objective measures of function are relevant long term outcomes in rheumatoid arthritis (RA). The objective of this study was to investigate grip force in early RA. Methods An inception cohort of patients with early RA (symptom duration ≤12 months), recruited in 1995-2005, was investigated. Grip force (Newton, N) was measured using the electronic instrument Grippit (AB Detektor, Gothenburg, Sweden). Peak grip force values of the right hand were evaluated and compared to the expected, based on age- and sex-specific reference values from the literature. The paired t-test was used for this comparison and for analysis of changes in grip force between visits. Results A total of 223 patients with early RA (71 % women, mean age 60 years, 62 % RF positive, 57 % anti-CCP2 positive) were investigated. At baseline, the mean peak grip force was 128.4 N (standard deviation (SD) 91.2), which was significantly lower than the corresponding expected values (306.4 N (SD 95.4) (p<0.001)). Patients were managed according to usual care, with no pre-specified protocol for pharmacotherapy or rehabilitation. Low disease activity (LDA; DAS28<3.2) was attained in 47 % at 5 years, and 25 % were in clinical remission (DAS28<2.6). Grip force improved significantly from inclusion to the 12 month visit (mean change: 36.1 N; 95 % confidence interval 26.6 -45.6), but there was no consistent change between the 1-year and 5-year follow-up evaluations. At 5 years, grip force was lower than expected overall (mean 168.0 vs 284.2 N; p<0.001), and also among those in LDA (p<0.001) and those in clinical remission (p=0.008). Conclusion Grip force improved during the first year after RA diagnosis, and remained stable thereafter. Patients in LDA or clinical remission at 5 years still had significantly reduced grip force. This suggests that further efforts to improve hand function are important in early RA. ABSTRACTNUMMER: 25 25 IN PURSUIT OF A SHORTER SWEDISH HEALTH ASSESSMENT QUESTIONNAIRE Elin Ros, Gunnel Sandqvist, Anders Gülfe Background Twelve of 20 items of the Swedish HAQ are disregarded in scoring. Shortened versions, e.g. the modified HAQ (MHAQ), have items chosen arbitrarily by investigators and yield lower summary scores (lower disability) than the full HAQ, making comparisons problematic. Purpose 1. Developing a short HAQ (SHAQ) employing the items most often scored high by RA patients in each domain. 2. Testing the SHAQ regarding its agreement with the full HAQ. ABSTRACTS Methods HAQ was filled out by RA patients included in an observational database at start and follow-up of biologic treatment (group A). Response frequencies at item level were analyzed. HAQ and SHAQ summary scores were compared using Pearson correlation and Bland-Altman plots. The findings were validated in an RA cohort evaluated for orthopaedic surgery (group B). MHAQ was included in the analysis for comparison. Results In group A, there were 443 patients (77% female), baseline disease duration was mean (SD)12.5 (11.7) years; in group B, corresponding values were 229 (79%) and 21.5 (14.0) years. In each domain, highest scoring item was selected to form the 8 item SHAQ, excepting one item (tub bath) left out by 20% of patients. Mean (SD) HAQ group A was 1.06 (0.68) and 1.13 (0.69) in group B. SHAQ was 0.86 (0.61) in group A and 0.88 (0.67) in group B. R square (%) comparing HAQ to SHAQ was 95 in group A and 94 in group B; comparing HAQ/MHAQ 84 in both groups and comparing MHAQ/SHAQ 86 in group A and 87 in group B. Discussion SHAQ or MHAQ reduce the “questionnaire burden”. In this study, mean SHAQ scores are lower than HAQ and MHAQ lower than SHAQ. The instruments are not equivalent. Some information on disability is lost with fewer items. SHAQ correlates better with HAQ than does MHAQ. ABSTRACTNUMMER: 26 26 VALIDITY OF GOUT DIAGNOSIS IN SWEDISH PRIMARY AND SECONDARY CARE Mats Dehlin1, Kalliopi Stasinopoulou1, Lennart Jacobsson1 Avdelningen för reumatologi och inflammationsforskning, Sahlgrenska Akademin, Göteborgs Universitet 1 Objective To diagnose gout, the golden standard is detection of monosodium urate (MSU) crystals in synovial fluid. However, while some gout classification criteria include this variable, most gout diagnoses are based on clinical features. This discrepancy between clinical practice and classification criteria hampers gout epidemiological studies. Here, the objective was to validate gout diagnoses (ICD10 gout codes) in primary care and secondary care relative to five classification criteria (Rome, New York, ARA, Mexico, and Netherlands. The frequency with which MSU crystal identification was used to establish a gout diagnosis was also determined. Methods In total, 394 patients with ≥1 ICD-10 gout diagnoses in 2009–2013 in Gothenburg, Sweden were identified from medical records of two primary care centers (n=262) and one secondary care center (n=132). Medical records were assessed for all classification criteria. Results Primary care patients met criteria cut-offs more frequently when ≥2 gout diagnoses were made. However, even then, few PC patients met the Rome and New York cut-offs (19% and 8%, respectively). ARA, Mexico, and Netherlands cut-offs were met more frequently by primary care patients with ≥2 gout diagnoses (54%, 81%, and 80%, respectively). Mexico and Netherlands cut-offs were met frequently by the rheumatology department patients even when patients with only 1 gout diagnosis were included (80% and 71%, respectively). MSU crystal analysis served to establish gout diagnosis in only 27% and 2% of rheumatology department and primary care cases, respectively. Conclusion If a patient is deemed to have gout when ≥2 primary care or ≥1 rheumatology-center visits associate with an ICD-10 gout code, the positive predictive value of this variable relative to the Mexico and Netherlands classification criteria was ≥80% in both primary care and rheumatology care settings in Sweden. MSU crystal identification was rarely used to establish gout diagnoses. ABSTRACTNUMMER: 27 27 PREVALENCE AND TREATMENT OF GOUT IN WESTERN SWEDEN Mats Dehlin1, Panagiota Drivelegka1, Valgerdur Sigurdardottir2, Anna Svärd2, Lennart Jacobsson1 Department of rheumatology and inflammation research, Institute of Medicine, Sahlgrenska Academy at the University of Göteborg, P.O. Box 480, 405 30, Göteborg, Sweden 2Rheumatology Clinic, Falun Hospital, SE-791 82 Falun, Sweden 1 Objective Gout is the most common inflammatory arthritic disease and increasing prevalence is described around the world. Several studies describe unmet needs in treatment and actions on these are required to reduce the impact of gout. The prevalence and treatment pattern of gout has never been studied in Sweden. Here, the objective was to measure the prevalence of gout and its treatment pattern in Västra Götalandsregionen (VGR), a part of western Sweden inhabitating approximately 20% of the Swedish population. Methods All individuals with an ICD-10 diagnosis of gout (M10, M14) in VGR between 2000 and 2012 were identified in the diagnosis register VEGA covering the total population and all caregivers of the region. We defined a strict case of gout as ≥ 2 main diagnoses. For these, all prescribed and dispensed urate lowering drugs (ULT) were identified through Läkemedelsregistret from 2005 to 2012. Results 17438 cases of gout were identified in VGR from 2000 to 2012 rendering an overall prevalence of 1%. When employing the strict case definition, 6368 individuals were identified, giving an overall prevalence of 0,4%”. In both groups, prevalence was higher among males and increased with increasing age. ULT treatment was provided only to a minority of individuals with gout and the most common drug and dose was allopurinol 100 mg per day. Conclusion Gout is the most common arthritic disease in western Sweden with an overall prevalence ranging from 0.4-1 %. ULT treatment is provided only to a minority of patients and at a low dosage according to WHO defined daily doses (DDD). ABSTRACTNUMMER: 28 28 THE VITAMIN D STATUS IN ANKYLOSING SPONDYLITIS IN RELATION TO INTESTINAL INFLAMMATION, DISEASE ACTIVITY AND BONE HEALTH ReumaBulletinen Nr 105 · 4/2015 23 ABSTRACTS Eva Klingberg1, Göran Oleröd2, Ola Hammarsten2, Helena Forsblad-d’Elia1 Avdelningen för reumatologi och inflammationsforskning, Sahlgrenska akademin, Göteborgs Universitet 2Avdelningen för klinisk kemi och transfusionsmedicin, Sahlgrenska akademin, Göteborgs Universitet 1 Background The objectives were to study the vitamin D levels attained mainly by dietary intake in ankylosing spondylitis (AS) in comparison with healthy controls and in relation to gut inflammation, measured indirectly by fecal calprotectin, disease activity, osteoproliferation, bone mineral density (BMD) and vertebral fractures. Methods Serum 25-hydroxy vitamin D (25(OH)D) was measured in 203 AS patients and 120 healthy controls at the end of “the vitamin D winter”, when the out-door UVB irradiation is too low to allow synthesis of vitamin D3 in the skin at the latitude of Gothenburg, Sweden. Fecal calprotectin was measured in stool samples. Disease activity was assessed with CRP, ESR, ASDASCRP, BASDAI, BAS-G, BASFI and BASMI. Lateral spine radiographs were scored for osteoproliferation and vertebral fractures using the mSASSS and Genant scores. BMD was measured in the lumbar spine and femoral neck. Results Vitamin D insufficiency (a serum 25(OH)D <50 nmol/L) was found in approximately 50% of the AS patients, but serum 25(OH)D was not different from healthy controls and not significantly correlated with fecal calprotectin, gastrointestinal symptoms, disease activity parameters, mSASSS, BMD or vertebral fractures. Methods Patients with AS from rheumatology departments in western Sweden were included in 2009 in a longitudinal study. At baseline and after five years BMD was measured with dual enery x-ray absorptiometry (DXA) in hip, radius and lumbar spine in anteroposterior (AP) and lateral projcetions. Lateral spinal radiographs for syndesmophyte grading (mSASSS) were taken. Results At baseline 204 patients were examined, 117 men and 87 women. Median age was 49 years and median duration of symptoms 24 years. 21% used TNF inhibitors (TNFi), 30% conventional DMARDs and 77% NSAIDs. At the follow-up in 2014 165 patients (80%) were reexamined. In the table the results of the changes in BMD ( BMD) at different measuring sites are shown. As secondary aims we investigated how BMD at the various locations were correlated to baseline characteristics as age, duration of symptoms and diagnosis, BAS-indexes, ASDASCRP, mSASSS, CRP, ESR and mean ESR 5 years before baseline and follow-up. Analyses showed that higher mean ESR five years prior to the follow-up correlated with decreased BMD in radius and lumbar spine lateral and volumetric. Patients treated with TNFi had higher BMD in the hip and spine lateral and AP. (p<0,05). Conclusions There were small but significant changes in BMD during five years. BMD increased in the spine and decreased in radius and femoral neck. Treatment with TNFi seemed to increase BMD in both the spine and hip. Prolonged systemic inflammation measured by mean ESR was a risc factor for bone loss. Conclusions The vitamin D status was often poor in the late winter in AS but not different from the healthy controls. No evidence for a connection between subclinical gut inflammation, malabsorption and hypovitaminosis D was found. Serum 25(OH)D was not associated with disease activity, osteoproliferation, BMD or vertebral fractures. We suggest that the lower vitamin D levels in AS, previously found by others, may be caused by reduced out-door UVB exposure. ABSTRACTNUMMER: 29 29 A FIVE YEAR PROSPECTIVE STUDY OF BONE MINERAL DENSITY IN ANKYLOSING SPONDYLITIS Anna Deminger1, Eva Klingberg1, Mattias Lorentzon2, Martin Hedberg3, Eva Rehnberg4, Hans Carlsten1, Lennart T Jacobsson1, Helena Forsblad-d’Elia5 Avdelningen för reumatologi och inflammationsforskning, Göteborgs Universitet, Göteborg 2Center for bone and arthritis research, Göteborgs Universitet, Göteborg 3Reumatologmottagningen, Södra Älvsborgs sjukhus, Borås 4Reumatologmottagningen Alingsås Lasarett, Alingsås 5Institution of Public Health and Clinical Medicine/ Rheumatology, Umeå University, Umeå 1 Background In ankylosing spondylitis (AS) two different bone remodeling processes are taking place; new bone formation and loss of bone. Our aim was to investigate how bone mineral density (BMD) Changes over five years in a group of patients with AS and in addition search for predictors for the change in BMD. 24 ReumaBulletinen Nr 105 · 4/2015 ABSTRACTNUMMER: 30 30 PREVALENCE OF CHRONIC WIDESPREAD PAIN IN WOMEN AND MEN WITH ANKYLOSING SPONDYLITIS AND UNDIFFERENTIATED SPONDYLOARTHRITIS Elisabeth Mogard1, Ann Bremander1, Elisabet Lindqvist2, Stefan Bergman2 SWEREFO 2SRF 1 ABSTRACTS Background Information on pain duration, distribution and intensity in Spondyloarthritis (SpA) is limited and important to recognize for an accurate diagnosis and optimal treatment. Our objective was to estimate the prevalence of self-reported chronic pain, and pain intensity in SpA and for the subgroups, ankylosing spondylitis (AS) and undifferentiated spondyloarthritis (USpA) including gender differences. Methods 3711 subjects from the SpA Scania cohort (AS, USpA, PsA and IBD-related arthritis) were in 2009 included in a postal survey. 2167 (58%) accepted participation, and 940 with AS and USpA were included and responded to questions regarding pain-duration and intensity. Pain was considered chronic when present more than three months. Based on a pain-mannequin the subjects were divided in three groups: chronic widespread pain (CWP), chronic regional pain (CRP) and non-chronic pain (NCP). Pain intensity was measured with numerical rating scale. Proportions and differences between subgroups and gender were calculated with chi-squared and t-test. Results The prevalence of chronic pain in SpA was 63.2% with a mean (SD) pain intensity of 3.8 (2.5), and more common in USpA (69.8%) than in AS (60.0%) (p=0.008). 887 subjects, 536 with AS and 351 with USpA completed the pain-mannequin, and of these almost half reported CWP (AS 45.3%, USpA 49.3%). A smaller group reported CRP (17.7% and 21.9%). More women than men reported CWP in USpA (56.2% vs. 39.2%; p=0.002), and for AS a similar trend was seen (51.6% vs. 42%; p=0.059). For CRP the gender distribution was equal (AS 17.6% vs. 17.9%, USpA 22.4% vs. 21.6%). Women reported higher pain intensity than men in both AS (4.2 vs. 3.4;p=0.001) and USpA (4.2 vs.3.6;p=0.022). Conclusions CWP was common in AS and USpA, indicating the possibility of a concomitant pain syndrome. This could also explain the gender difference with CWP being more common and pain intensity higher in women than in men. ABSTRACTNUMMER: 31 31 DOES A POSITIVE ANTI-CCP TEST IDENTIFY SYSTEMIC LUPUS ERYTHEMATOSUS PATIENTS WITH EROSIVE ARTHRITIS? ANALYSIS OF A REGIONAL SWEDISH REGISTER Philip Wallin1, Michael Ziegelasch1, Thomas Skogh1, Alf Kastbom1, Christopher Sjöwall1 Rheumatology/AIR, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden 1 Background Articular manifestations affect a majority of patients with systemic lupus erythematosus (SLE), at least at some time during the disease course. Several investigators have estimated the frequency of erosive arthritis in SLE to about 5%. Detection of antibodies to ’cyclic citrullinated peptide’ (anti-CCP) is an important diagnostic and prognostic tool in arthritis, since it is highly specific for rheumatoid arthritis (RA) and predictive of erosive disease. While antiCCP reactivity in RA is citrulline-dependent, it has been suggested that anti-CCP in SLE is generally not, and thus also reacts with the corresponding ’cyclic arginine peptide’ (CAP). We analysed antiCCP and anti-CAP in sera from patients in our well-characterized SLE register and related the findings to X-ray data. Materials and methods 245 patients (89% women) in the ’Clinical Lupus Register in Northeastern Gothia’ were included. Cases were classified as SLE according to any of the following criteria sets: ACR-82 (81%), SLICC-12 (95%), or the Fries’ diagnostic principle (100%). IgG anti-CCP and anti-CAP ELISA kits (Euro-Diagnostica) were used. X-ray data (hands, wrists and/or feet) were available in medical records of 111 cases (45%). Results 16 patients (6.5%), all meeting the SLICC-12 critera, were anti-CCP positive, 9 of whom were also anti-CAP positive. 4 of the 7 patients with citrulline-dependent anti-CCP had a history of biopsy-proven lupus nephritis. Anti-CCP did not associate with arthritis judged by physical examination, nor to any other SLE phenotype or immunological disorders. However, X-ray-proven erosions were found in 10 patients (4%). Chi-square test revealed an association between anti-CCP and erosive arthritis (p=0.039). Conclusion Compared to previous reports, we found a slightly lower frequency of anti-CCP in SLE, 44% of whom were citrulline-dependent. Based on our findings, we suggest that anti-CCP could be associated with erosive arthritis, but not with other disease phenotypes, in SLE. ABSTRACTNUMMER: 32 32 HYDROXYCHLOROQUINE (HCQ) INHIBITS TNF-ALPHA PRODUCTION BY PLASMACYTOID DENDRITIC CELLS (pDC) BUT NOT BY NATURAL KILLER (NK) CELLS Karin Hjorton1, Niklas Hagberg1, Olof Berggren1, Maija-Lena Eloranta1, Lars Rönnblom1 Dept. of Medical Sciences, Section of Rheumatology, Uppsala University 1 Background Patients with SLE have an ongoing IFN-alpha production due to the stimulation of endosomal TLRs in pDCs by nucleic acid containing immune complexes (ICs). Such ICs also trigger the production of TNF-alpha by several immune cells. The role of produced TNF-alpha in SLE is complex but a pathogenic role is suggested by the correlation with lupus nephritis and the induction of lupus-like syndrome after TNF-alpha inhibition. HCQ blocks endosomal TLR activation and is routinely used to prevent SLE-flares. We asked how TNF-alpha production was regulated in IC-stimulated pDC and NK cells and if HCQ affects the production. Methods pDC and NK cells were isolated from peripheral blood of healthy individuals. Monocyte depleted PBMCs were used from SLE patients. pDC, NK cells, pDC+NK cells or monocyte depleted PBMCs were stimulated with RNA-containing ICs (RNA-IC) in the presence or absence of 7.8 M HCQ. IFN-alpha and TNF-alpha production was measured after 20 h by an immunoassay or by intracellular staining using flow cytometry. Results Co-cultivation of pDC and NK cells enhanced the IFN-alpha and TNF-alpha production. TNF-alpha was rapidly produced by NK cells (5 h) but exhibited a delayed production in pDC (9 h). All ReumaBulletinen Nr 105 · 4/2015 25 ABSTRACTS IFN-alpha positive pDCs (13.6%) were TNF-alpha positive, 7.1% of pDCs were only TNF-alpha positive. HCQ completely inhibited the IFN-alpha and TNF-alpha production by pDCs, but did not affect TNF-alpha production by NK cells. Cells from HCQ-treated SLE patients produced little IFN-alpha (mean 3 U/ml vs 27 U/ ml) in response to RNA-IC, but TNF-alpha production was intact (mean 542 U/ml vs 340 U/ml). Conclusion RNA-IC stimulated TNF-alpha production is induced by different mechanisms in pDC and NK cells. Furthermore, HCQ strongly inhibits the IFN-alpha synthesis, but only marginally affects the TNF-alpha response. These results may partially explain the varying response to HCQ treatment in SLE patients. ABSTRACTNUMMER: 33 33 DECREASED DISEASE ACTIVITY AND CORTICOSTEROID USAGE AND IMPROVED QUALITY OF LIFE DURING BELIMUMAB TREATMENT IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS Ioannis Parodis1, Christopher Sjöwall2, Andreas Jönsen3, Martina Frodlund2, Daniel Ramsköld1, Anders Bengtsson3, Iva Gunnarsson1 1 Karolinska Institutet 2 Linköping University 3 Lund University Background Belimumab is the first biologic agent approved to treat serologically active Systemic Lupus Erythematosus (SLE). We investigated the effects of belimumab in patients with active SLE despite standard-of-care therapy. Methods Fifty-one patients from Karolinska, Skåne, and Linköping University Hospitals treated with belimumab were enrolled and followed longitudinally. Disease activity was assessed using SLE Disease Activity Index 2000 (SLEDAI-2K) and Physician’s Global Assessment (PGA). Patients reported pain, fatigue and well-being levels using Visual Analogue Scales (VAS), as well as functional status using the Health Assessment Questionnaire (HAQ). Belimumab was mainly chosen for musculoskeletal (n=24), mucocutaneous (n=23), hematological (n=9), renal (n=5), respiratory (n=4), and neurological (n=3) manifestations. Results Treatments at baseline included oral prednisolone (n=47, mean dose 11.36 mg/day), antimalarials (n=38), azathioprine (n=15), mycophenolate mofetil (n=8), methotrexate (n=6), and cyclosporine (n=2). The median SLEDAI-2K score was 7 (2–24). Significant decreases over time were observed for SLEDAI-2K and PGA (p<0.001). Prednisone dosages were decreased significantly (p<0.001), corresponding to a decrease of 4.9 mg/day over a year. C4 levels, but not C3 levels, increased significantly (p<0.001). We observed significant decreases in VAS for well-being (p<0.001), pain (p<0.001) and fatigue (p=0.018), but no significant changes in HAQ (p=0.142). Two patients withdrew due to allergic reactions. Belimumab was discontinued in 7 patients due to inadequate/uncertain effect, in 2 patients due to pregnancy plans, in 5 patients due to flare (increased proteinuria; arthritis, headache; rash, alopecia; lupus nephritis WHO class III; CNS-lupus), and in 3 patients due to adverse events (acute myeloid leukemia; ground glass opacity in computed tomography scan of the lungs, pulmonary arterial hypertension; insomnia, arrhythmia). 26 ReumaBulletinen Nr 105 · 4/2015 Conclusions Belimumab treatment decreased SLE disease activity and reduced corticosteroid usage over time. Moreover, belimumab improved the patients’ quality of life in terms of pain, fatigue and well-being, but had no significant effects on their functional status. ABSTRACTNUMMER: 34 34 LATE-ONSET NEUTROPENIA FOLLOWING RITUXIMAB TREATMENT IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS Ioannis Parodis1, Frida Söder1, Ronald van Vollenhoven1, Elisabet Svenungsson1, Iva Gunnarsson1 Karolinska Institutet 1 Background Late-onset neutropenia (LON) has been described as a side–effect of rituximab. Its incidence and clinical consequences have been studied in various diseases, but data from Systemic Lupus Erythematosus (SLE) cohorts are limited. We studied the prevalence, consequences and predisposing factors for LON following rituximab treatment in SLE patients. Methods Patients from the Karolinska SLE cohort receiving rituximab (patients: N=92; cycles: n=182) were enrolled. Rituximab was mostly given for lupus nephritis (N=49; n=88), arthritis (N=11; n=37), CNS–lupus (N=9; n=15), hemolytic anemia (N=5; n=11), thrombocytopenia (N=5; n=7), and mucocutaneous manifestations (N=6; n=11), either weekly for 4 weeks with or without cyclophosphamide or as intravenous infusions of 1 g at week 0 and 2. LON was defined as a neutrophil count ≤1.5x10^9/L (mild: 1–1.5x10^9/L; moderate: 0.5–1x10^9/L; severe: 0.2–0.5x10^9/L; agranulocytosis: <0.2x10^9/L) occurring four weeks or later following treatment. Four patients with neutropenia during treatment were excluded from this analysis. Results Of 88 patients analysed, 28 (31.8%) developed LON (13 mild, 7 moderate, 8 agranulocytosis; median time after first infusion: 222 days). Eight of these patients were retreated with rituximab after the incidence of LON; three developed LON following these subsequent cycles, and five did not. Ten patients presented with fever (3 with infections: Staphylococcus aureus sepsis, Pseudomonas, Streptococcus fasciitis), and 18 were asymptomatic. The infections resolved with antibiotics. No difference in severity of complications between patients with agranulocytosis and patients with mild/moderate LON was noted. No correlation between incidence of LON and rituximab, prednisone or cyclophosphamide dosages (concurrent/cumulative), other treatments, preceding neutropenia, sex, age, or disease duration was noted. Conclusions SLE patients had a higher prevalence of LON following rituximab than patients with other diseases (e.g. lymphoma, rheumatoid arthritis). However, 64.3% of the cases were asymptomatic and all infections resolved without subsequent complications. No predisposing factors were identified. ABSTRACTNUMMER: 35 35 ANTIPHOSPHOLIPID ANTIBODIES IN LUPUS NEPHRITIS AND ABSTRACTS THEIR ROLE IN LONG-TERM RENAL OUTCOME Background Lupus nephritis (LN) is a major manifestation of Systemic Lupus Erythematosus (SLE). The burden of antiphospholipid antibodies (APLA) in LN has not been clarified. We investigated a potential role of APLA levels as a biomarker of severity in renal lupus. Materials and Methods Sera from 91 healthy donors, 210 SLE, 112 pSS and 69 SSc patients were incubated with untransfected, KIR2DL1-transfected and KIR2DL2-transfected HEK293 cells. Binding of human Ig was detected by flow cytometry. A specific binding ratio was calculated by dividing the median fluorescence intensity (MFI) of transfected cells with the MFI of untransfected cells. Values above the mean+4 standard deviations of healthy donors were considered positive. Clinical data were extracted from medical records and the presence of ACR criteria was compared between SLE patients positive for anti-KIR2DL1 with SLE patients negative for anti-KIR2DL1 and anti-CD94/NKG2A autoantibodies. Methods Serum levels of APLA (antibodies to cardiolipin (aCL) and 2-glycoprotein 1 (anti- 2-GP1); reference <20 IE/mL) were assessed by BioPlex 2200 in 64 patients with biopsy-ascertained active LN before and after induction treatment, and in 295 SLE patients with no history of renal involvement. LN patients were followed for a mean time of 10.9 years. The outcome of kidney function and damage was assessed according to a chronic kidney disease (CKD) grading system based on the estimated glomerular filtration rate, as determined by the Modification of Diet in Renal Disease Study equation. Results Eight SLE patients harbored autoantibodies to the KIR2DL1 receptor, whereas none of the pSS, SSc or healthy donor sera reacted with KIR2DL1. Furthermore, one pSS patient displayed antiKIR2DL4 autoantibodies. None of the anti-KIR positive patients displayed anti-CD94/NKG2A or anti-CD94/NKG2C autoantibodies. Presence of anti-KIR2DL1 autoantibodies were associated with an increased risk for nephritis (62.5% vs. 27.9%; P=0.04 Fischer’s exact test), whereas none of the other ACR criteria were associated with anti-KIR2DL1 autoantibodies Results Percentages of APLA positive patients with active LN (aCL: 12.5% IgG, 9.4% IgM; anti- 2-GP1: 20.3% IgG, 9.4% IgM) were comparable to the ones in patients without renal involvement (aCL: 18.6% IgG, 8.1% IgM; anti- 2-GP1: 19.7% IgG, 8.1% IgM), but lower in LN patients following induction treatment (aCL: 9.4% IgG, 1.6% IgM; anti- 2-GP1: 10.9% IgG, 3.1% IgM). APLA levels decreased significantly following treatment (p<0.001). In patients with proliferative LN, IgM titers decreased significantly in responders but not in non-responders. IgG titers decreased following treatment in all response groups. In the membranous LN subgroup, APLA levels remained unchanged regardless of treatment outcome. CKD stage at discharge correlated significantly with the duration of follow-up, but not with APLA levels/positivity. Conclusion Autoantibodies to NK cell receptors regulating cytotoxicity is a more common phenomenon in SLE patients than previously reported. These autoantibodies are associated with an increased risk for nephritis. Autoantibodies to inhibitory NK cell receptors may conceivably contribute to the disease by increasing the killing of self-cells, which result in the release of necrotic material and the formation of interferon inducing immune complexes. Conclusions APLA levels were comparable in SLE patients without renal involvement and patients with active LN, but decreased significantly following induction therapy. In proliferative LN, IgG and IgM titers were affected differently by immunosuppression with regard to treatment response. Neither APLA levels nor positivity could predict long-term renal outcome. Lina Wirestam1, Helena Enocsson1, Jonas Wetterö1, Thomas Skogh1, Maija-Leena Eloranta2, Lars Rönnblom2, Christopher Sjöwall1 Ioannis Parodis1, Elisabet Svenungsson1, Jakob Gerhardsson1, Agneta Zickert1, Vivianne Malmström1, Iva Gunnarsson1 1 Karolinska Institutet ABSTRACTNUMMER: 36 36 AUTOANTIBODIES TO KILLER IMMUNOGLOBULIN RECEPTORS IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS Niklas Hagberg1, Lars Rönnblom1 Medicinska vetenskaper, Reumatologi, Uppsala Universitet 1 Aim Natural killer (NK) cell cytotoxicity is regulated by multiple activating and inhibitory receptors. Recently, we identified functional autoantibodies to the inhibitory CD94/NKG2A and activating CD94/ NKG2C receptors in systemic lupus erythematosus (SLE) patients. Here, we analyzed sera from patients with SLE, primary Sjögren’s syndrome (pSS) and systemic sclerosis (SSc) for autoantibodies to the inhibitory killer immunoglobulin receptors, KIR2DL1 and KIR2DL4. 37 ABSTRACTNUMMER: 37 INTERFERON-ALPHA MEDIATES SUPPRESSION OF PENTRAXIN 3 IN SYSTEMIC LUPUS ERYTHEMATOSUS 1 Linköpings Universitet 2 Uppsala Universitet The authors have chosen not to publish the abstract. ABSTRACTNUMMER: 38 38 EARLY B CELL FACTOR 1 IS ASSOCIATED TO CLINICAL MANIFESTATIONS IN PRIMARY SJÖGREN’S SYNDROME AND SYSTEMIC LUPUS ERYTHEMATOSUS Dag Leonard1, Iva Gunnarsson2, Christopher Sjöwall3, Per Eriksson3, Helena Forsblad-d’Elia4, Andreas Jönsen5, Elke Theander6, Marie Wahren-Herlenius2, Lars Rönnblom1, Gunnel Nordmark1 Institutionen för medicinska vetenskaper, Reumatologi, Uppsala Universitet, Uppsala 2Institutionen för medicin, Karolinska sjukhuset och Karolinska institutet, Stockholm 3Institutionen för klinisk och experimentell medicin, Reumatologi, Linköpings universitet, Linköping 4Institutionen för folkhälsa och klinisk medicin/Reumatologi, Umeå universitet, Umeå 5Institutionen för kliniska vetenskaper, Reu 1 ReumaBulletinen Nr 105 · 4/2015 27 ABSTRACTS matologi, Lunds universitet, Lund 6Institutionen för kliniska vetenskaper, Malmö, Lunds universitet, Lund Background Early B cell factor 1 (EBF1) is a transcription factor important for B cell development. Genetic variations in EBF1 have been associated with B cell leukemias, multiple sclerosis and primary Sjögren’s syndrome (pSS). Because both pSS and Systemic Lupus Erythematosus (SLE) are characterized by increased activation of B cells, we asked if EBF1 variants associate to disease susceptibility and clinical phenotype. Materials and methods We included 633 patients with pSS from Sweden (n=463) and Norway (n=170), 852 Swedish patients with SLE and 2941 healthy controls from Sweden (n=2760) and Norway (n=181). All patients fulfilled AECG criteria for pSS or the 1982 ACR classification criteria for SLE. Samples were genotyped on the Illumina® ImmunoChip with 200K SNPs. SNPs annotated in or surrounding EBF1 spanning over 1.1 MB were selected where 109 SNPs (pSS) and 145 SNPs (SLE) remained after quality control. Allele frequencies were compared between patients and controls and between patients with or without different clinical manifestations. Benjamini & Hochberg step-up FDR was used for multiple-test correction and pcorr <0.05 was considered significant. Results There were no associations to either pSS or SLE in the case-control analyses. In the pSS case-only analyses one SNP was associated to major salivary gland swelling (npos=183, nneg=312) with pcorr=0.03, OR=1.6(1.2-2.1). In the SLE case-only analyses there was an association to nephritis (npos=293, nneg=559) for 51 SNPs with the top SNP rs116278653 located 8 KB upstream of EBF1 (p=0.03, OR=3.0(1.4-6.5)). After adjusting for rs116278653 no significant signals remained suggesting high linkage disequilibrium within the region. Conclusion Genetic variation in EBF1 might have implications for the clinical manifestations of pSS and SLE, both diseases characterized by B cell activation. The functional consequences of the identified variations remain to be elucidated. 39 ABSTRACTNUMMER: 39 SUSCEPTIBILITY GENES IN SYSTEMIC INFLAMMATORY AUTOIMMUNE DISEASES Johanna K. Sandling , Ingrid E. Lundberg , Ann-Christine Syvänen3, Marie Wahren-Herlenius4, Kerstin Lindblad-Toh5,6, Lars Rönnblom1, the DISSECT consortium 1 2 Rheumatology, Department of Medical Sciences, Uppsala University, Uppsala, Sweden 2Rheumatology Unit, Department of Medicine, Karolinska University Hospital in Solna, Karolinska Institutet, Stockholm, Sweden 3Molecular Medicine and Science for Life Laboratory, Department of Medical Sciences, Uppsala University, Uppsala, Sweden 4Unit of Experimental Rheumatology, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden 5Science for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden 6Broad Institute of MIT and Harvard, Cambridge, Massachusetts, United States of America 1 28 ReumaBulletinen Nr 105 · 4/2015 Background The overall aim of the present study is to identify molecular pathways in sub-phenotypes of three systemic inflammatory autoimmune diseases (SIADs) which share the type I interferon signature in blood and target organs. This will be performed by combining genetic studies with functional cellular studies of shared and disease specific risk genes in well characterized, large cohorts of patients with SAID. The investigators represent three networks: the Swedish SLE network, SweMyoNet linked to EuMyoNet and the Scandinavian Sjögren’s syndrome network. Materials and methods To identify new risk loci for SIAD we are resequencing 1853 genes including their regulatory regions, targeting 32Mb of the genome (~1%), in 3000 patients with SIAD as well as 1000 healthy individuals. The regions are selected to contain genes from pathways known to be involved in canine and human immunological diseases. Capturing of the targeted genes is performed with a NimbleGen custom-made liquid capture library followed by Illumina HiSeq2500 sequencing (SNP&SEQ Technology Platform at SciLifeLab in Uppsala). Results We have so far sequenced 1167 patients with SLE and 904 patients with pSS as well as 1068 healthy individuals to an average sequence depth of 30x generating in excess of 13 tera bases of sequence data. In order to identify rare variants associated with risk for SLE several different approaches are being used with the aim of developing a best practice analysis for the project. Pilot data from a smaller set of patients and genes, has identified several new variants associated with sub-phenotypes of disease, and with validated functional consequences . Conclusion We aim to clarify the function of shared and unique risk genes and the association to clinical phenotypes using targeted sequencing. Our goal is to develop models that can be used to investigate new treatment strategies and identify prognostic biomarkers for these therapies. ABSTRACTNUMMER: 40 40 ACTIVATED PLASMACYTOID DENDRITIC CELLS ALTER THE COMPOSITION OF PERIPHERAL BLOOD B CELL SUBSETS Olof Berggren1, Lars Rönnblom1, Maija-Leena Eloranta1 Department of Medical Sciences, Rheumatology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden. 1 Background Aberrations in the B cell composition and function as well as a continuous IFN-alpha production by plasmacytoid dendritic cells (pDCs) play a central role in the pathogenesis of many systemic rheumatic diseases, e.g. systemic lupus erythematosus (SLE). In the present study we analyzed the phenotype of several peripheral blood B cell subsets upon interactions between B cells and pDCs activated by immune complexes (IC). Methods B cells and pDCs were isolated from peripheral blood of healthy individuals and stimulated with a SLE-related RNA containing IC (RNA-IC), alone or in cocultures for 6 days. Expression of activation markers, cell surface molecules and IL-10 production were analyzed by flow cytometry and immunoassays. ABSTRACTS Results Both B cells and pDCs displayed an increased activation in the stimulated cocultures compared to stimulated cultures of B cells and pDCs alone. Cocultivation with pDCs resulted in a 7-fold increased frequency of CD24hiCD38hi B cells, considered to have a regulatory character. However, the IL-10 production was only moderate in the RNA-IC-stimulated cocultures of pDCs and B cells. Interestingly, we found a decreased frequency of memory and naïve B cells and a remarkable increase of double negative CD27-IgD- B cells, from 7% among fresh B cells to 37% in the RNA-IC-stimulated cocultures of pDCs and B cells. Conclusion The composition of the B cell population described in the present study resembles those found in SLE patients. Interestingly, the frequency of the double negative CD27-IgD- B cells is increased in patients with SLE. Thus, activated pDCs may contribute to the regulation and expansion of potentially pathogenic B cell subpopulations, especially in patients with circulating interferogenic ICs and an ongoing type I IFN production. ABSTRACTNUMMER: 41 41 cal immunology was 72.8% and 45.2%. Concordant results between multiplex and clinical immunology were seen in 88.0% of sera for SSA (r=0.72) and 78.2% for SSB (r=0.56), both p<0.0001. Combined clinical immunology data showed sensitivity, specificity, PPV and NPV for SSA (95.6%, 73.0%, 87.6% and 89.0%) and SSB (79.9%, 77.1%, 69.3% and 85.6%) although the results varied between the four hospitals. Conclusion Analysis in routine clinical care can in most cases be used for dividing pSS patients according to anti-SSA/SSB status. However, in genetic and immunological studies a uniform antibody analysis might be advantageous. ABSTRACTNUMMER: 42 42 SPORADIC OCCURRENCE OF NON-DIAGNOSED IgG4-RELATED DISEASE IN LYMPHOMA PATIENTS WITH A PREVIOUS SJÖGREN’S SYNDROME DIAGNOSIS Lilian Vasaitis1, Christer Sundström2, Carin Backlin1, Gunnel Nordmark1, Eva Baecklund1 COMPARISON BETWEEN MULTIPLEX AND ROUTINE CLINICAL IMMUNOLOGY ANALYSIS OF ANTIBODIES AGAINST SSA AND SSB Section of Rheumatology, Department of Medical Sciences, Uppsala University, Uppsala, Sweden 2Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden Linnea Signér1, Karl Brokstad2, Lilian Vasaitis1, Marika Kvarnström3, Christopher Sjöwall4, Per Eriksson4, Elke Theander5, Roland Jonsson2, Marie Wahren-Herlenius3, Gunnel Nordmark1 Objectives Patients with sicca symptoms can be misdiagnosed as primary Sjögren’s syndrome (pSS) instead of IgG4-related disease (IgG4-RD) because of clinical and histopathological similarities. An increased risk for lymphoma in pSS is reported. Case series have also reported occurrence of lymphoma in major salivary glands in IgG4-RD. The aim of this study was to investigate signs of IgG4-RD in a population-based cohort of patients diagnosed with pSS complicated by lymphoma. Dept. of Medical Sciences, Uppsala University,Uppsala, Sweden Dept. of Clinical Science, University of Bergen, Bergen, Norway 3 Dept. of Medicine, Karolinska Institutet, Stockholm, Sweden 4Dept. of Clinical Exp Medicine, Linköping University, Linköping, Sweden 5 Dept. of Rheumatology, Lund University, Malmö, Sweden 1 2 Background Anti-SSA/SSB positivity in primary Sjögren’s syndrome (pSS) is associated with a higher prevalence of extraglandular manifestations, a more distinct type I interferon signature and certain HLA haplotypes. Subdividing patients according to antibody status can be of interest in genetic and immunological studies. Data on antiSSA/SSB collected from medical records include analyses at different clinical immunology laboratories using different methods over time. The aim of this study was to perform a multiplex antibody analysis and compare the anti-SSA/SSB results with the results obtained from routine clinical immunology. Methods Sera from 367 Swedish patients with pSS from four University hospitals were analyzed with a multiplex fluorescent immunoassay. Data on anti-SSA/SSB analyzed in clinical care was retrieved from the patient records. Multiplex and clinical immunology results were compared with Spearman rank correlation test. Sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) with the multiplex analysis as golden standard were calculated. Results Multiplex analysis detected antibodies against Ro60 in 62.1%, Ro52 in 61.3%, any of Ro60/Ro52 (SSA) in 66.8%, La48/SSB in 39.2%, RNP in 4.9%, Sm in 0.5%, Ribosome P in 0.5%, Chromatin in 6.5%, Scl-70 and Jo-1 both in 0%. The frequency of anti-SSA/SSB in clini- 1 Methods Patients with pSS and lymphoma diagnoses and available lymphoma specimens were identified after linkage with the Swedish patient registry 1964-2007 and the Cancer registry 1990-2007 (n=79). Clinical data and lymphomas were reviewed and the diagnoses evaluated. Lymphoma tissues and available biopsies from minor salivary glands (MSGs) (n=11) were immunostained for IgG4+ plasma cells (PCs) and investigated for other specific histopathological features of IgG4-RD. In cases with positive findings, immunostaining for IgG+ PCs was performed for the ratio IgG4+PCs/IgG+ PCs, which was considered significant if above 0.4. Results We identified a positive staining for IgG4 (>10 IgG4+PCs/HPF) in lymphoma tissue from one patient. None of the MSG biopsies showed any IgG4+ PC. The patient with positive findings was a 64-year-old man with idiopathic pulmonary fibrosis and suspected pSS. Unspecified low-grade B-cell lymphoma was diagnosed in the submandibular gland with features of lymphoplasmacytic infiltration and storiform fibrosis. Immunostaining of the lymphoma tissue showed 60 IgG4+ PCs/HPF and the ratio IgG4+/IgG+ was 0.6. Lung biopsy performed 5 years before lymphoma diagnosis showed storiform fibrosis, lymphoplasmacytic infiltration, germinal centers, and 167 IgG4+ PCs/HPF in the lung tissue with a IgG4+/IgG+ ratio of 0.9. The histological findings in both biopsies were highly suggestive of IgG4-RD. With compatible clinical features the patient fulfilled criteria for a previously undiagnosed systemic IgG4-RD. ReumaBulletinen Nr 105 · 4/2015 29 ABSTRACTS Conclusion Sporadic patients with a previous pSS diagnosis complicated by lymphoma may have unrecognized IgG4-RD. ABSTRACTNUMMER: 43 43 EPIGENOME-WIDE DNA METHYLATION ANALYSIS IN MULTIPLE TISSUES IN PRIMARY SJÖGREN’S SYNDROME REVEALS HYPOMETHYLATION IN REGULATORY REGIONS OF INTERFERON INDUCED GENES Gunnel Nordmark1, Juliana Imgenberg-Kreuz2, Jonas Almlöf2, Linnea Signér1, Katrine Norheim3, Roald Omdal3, Lars Rönnblom1, Maija-Leena Eloranta1, Ann-Christine Syvänen2, Johanna Sandling1,2 Rheumatology and Science for Life Laboratory, Department of Medical Sciences, Uppsala University, Uppsala, Sweden 2Molecular Medicine and Science for Life Laboratory, Department of Medical Sciences, Uppsala University, Uppsala, Sweden 3Clinical Immunology unit, Department of Internal Medicine, Stavanger University Hospital, Stavanger, Norway 1 Background Increasing evidence suggests an epigenetic contribution to the pathogenesis of autoimmune diseases, including primary Sjögren’s Syndrome (pSS). The aim of this study was to comprehensively investigate genome-wide DNA methylation profiles in whole blood, CD19+ B cells and minor salivary gland biopsies from patients with pSS and controls. Methods DNA methylation profiles were generated on the HumanMethylation450K BeadChip array for whole blood samples (patients =100, controls =400), CD19+ B cells (patients =24, controls =47) and minor salivary gland biopsies (patients =15, controls =13). After quality control 388,971 CpG sites remained for further analysis. Differential cell count estimations, age and sex were included as covariates in the association model, and a p-value of < 1.3x10-7 was considered significant (Bonferroni correction). Results We identified 11,785 differentially methylated CpG sites in whole blood (6,171 hypo- and 5,614 hypermethylated) annotated to 8,963 genes. The most significantly associated hypomethylated sites were annotated to interferon induced genes (MX1, IFI44L, IFIT1 and IFITM1). The top associated sites showed an even more pronounced difference in methylation between pSS cases and controls in CD19+ B cells. In minor salivary gland biopsies, the most significantly differentially methylated CpG site was in the interferon induced gene OAS2. Hypo- and hypermethylated CpG sites differed in their genomic distribution with hypomethylated sites enriched in enhancer and promoter regions and hypermethylated sites in gene bodies. Pathway analysis resulted in enrichment of antigen presentation and interferon signaling pathways. Differentially methylated sites were also enriched in genes with disease association to lymphoproliferative disorders. Conclusion Our results indicate that epigenetic changes are important in the pathogenesis of pSS. The importance of genes in the interferon system is highlighted, and the enrichment of genes involved in lymphoma is intriguing and warrants further investigation. 30 ReumaBulletinen Nr 105 · 4/2015 ABSTRACTNUMMER: 44 44 RATE OF CO-MORBIDITIES IN GIANT CELL ARTERITIS – A POPULATION-BASED STUDY Aladdin Mohammad1,2, Marin Englund3,4, Carl Turesson5, Gunnar Tomasson6, Peter A Merkel7 Department of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden 2Vasculitis and Lupus Clinic, Addenbrooke’s Hospital, Cambridge, UK 3Orthopaedics, Clinical Sciences Lund, Lund University, Lund, Sweden 4Clinical Epidemiology Research and Training Unit, Boston University School of Medicine, Boston, MA, USA 5 Department of Clinical Sciences, Section of Rheumatology, Malmö, Lund University, Malmö, Sweden 6 Department of Public Health Sciences, University of Iceland, Reykjavik Iceland 7 Penn Vasculitis Center, Division of Rheumatology, University of Pennsylvania, Philadelphia, PA, USA 1 The authors have chosen not to publish the abstract. ABSTRACTNUMMER: 45 45 INCIDENCE AND IMPACT OF SEVERE INFECTIONS IN ANCAASSOCIATED VASCULITIS- A POPULATION-BASED STUDY FROM SOUTHERN SWEDEN Aladdin Mohammad1,2, Mårten Segelmark3, Rona Smith2, Martin Englund4,5, Jan-Åke Nilsson1, Kerstin Westman6, Peter A Merkel7, David Jayne2 Department of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden 2Vasculitis and Lupus Clinic, Addenbrooke’s Hospital, Cambridge, UK 3Department of Medicine and Nephrology, Linköping University, Linköping, Sweden 4Department of Orthopaedics, Lund University Hospital, Lund, Sweden 5Department of Epidemiology, Boston University School of Medicine, Boston, MA, USA 6Department of Clinical Sciences, Section of Nephrology, Lund University, Malmö, Sweden, 7Penn Vasculitis Center, Division of Rheumatology, University of Pennsylvania, Philadelphia, PA, USA 1 The authors have chosen not to publish the abstract. ABSTRACTNUMMER: 46 46 RATE OF CO-MORBIDITIES IN ANCA ASSOCIATED VASCULITIS - A POPULATION-BASED STUDY Aladdin Mohammad1,2, Peter A Merkel3, Gunnar Tomasson4, Mårten Segelmark5, Martin Englund6,7 Department of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden 2Vasculitis and Lupus Clinic, Addenbrooke’s Hospital, Cambridge, UK. 3Penn Vasculitis Center, Division of Rheumatology, University of Pennsylvania, Philadelphia, PA, USA. 4 Department of Public Health Sciences, University of Iceland, Reykjavik Iceland 5Department of Nephrology, Linköping University, Linköping, Sweden 6Orthopedics, Clinical Sciences Lund, Lund University, Lund, Sweden 7Clinical Epidemiology Research and Training Unit, Boston University School of Medicine, Boston, MA, USA 1 ABSTRACTS Objectives To evaluate the rates of selected comorbidities in patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) compared with the general population in Southern Sweden. Methods We used data from a population-based cohort of patients with AAV diagnosed between 1997 and 2010 in southern Sweden (701 000 inhabitants). For each patient we identified four reference subjects randomly sampled from the general population matched for year of birth, sex, area of residence, and date of diagnosis of AAV. Using the population-based Skåne Healthcare Register we identified relevant diagnostic codes for selected comorbidities assigned after the date of diagnosis of AAV or the index date for the reference subjects. We calculated rate ratios for comorbidities (AAV vs. reference subjects). Results The study included 198 patients (98 women, mean age 64.6 years) with AAV and 792 reference persons were included in the analysis. The highest rate ratios (AAV: reference) was obtained for osteoporosis with pathologic fracture (4.5, 95% confidence interval [95% CI] 2.9-6.7), followed by venous thromboembolism (3.5, 95% CI 1.7-6.9), diabetes mellitus (2.1, 95% CI 1.4-3.0), and thyroid diseases (1.9, 95% CI 1.1-2.9). For ischemic heart disease, the rate ratio of 1.5 (95% CI 1.0-2.2) and did not reach statistical significance. No statistically significant differences were found for psychological diagnoses or cerebrovascular accidents. Conclusions AAV is associated with increased rates of several comorbidities including osteoporosis, thromboembolic, and endocrine disorders. Comorbid conditions should be taken in consideration in planning and providing care for patients with AAV. ABSTRACTNUMMER: 47 47 PULMONARY INVOLVEMENT IN ANCA- ASSOCIATED VASCULITIS- A PRELIMINARY REPORT Aladdin Mohammad1,2, Judith Babar3, Kristian Mortensen3, Rona Smith2, Rachel Jones2, Daiki Nakagomi2, Pasupathy Sivasothy4, David Jayne2 Department of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden 2Vasculitis and Lupus Clinic, Addenbrooke’s Hospital, Cambridge, UK. 3Department of Radiology, Addenbrooke’s Hospital, Cambridge, UK 4Department of Pulmonary Medicine, Addenbrooke’s Hospital, Cambridge, UK 1 The authors have chosen not to publish the abstract. ABSTRACTNUMMER: 48 48 IGA - ANCA IN MICROSCOPIC POLYANGIITIS AND GRANULOMATOSIS WITH POLYANGIITIS Aladdin Mohammad1,2, Jörgen Wieslander3, Mårten Segelmark4 Department of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden 2Vasculitis and Lupus Clinic, Addenbrooke’s Hospital, Cambridge, UK 3Department of Nephrology, Lund Uni- 1 versity, Lund, Sweden 4Department of Nephrology and Department of Medicine and Health Sciences, Linköping University, Linköping, Sweden The authors have chosen not to publish the abstract. 49 ABSTRACTNUMMER: 49 LONG-TERM OUTCOMES OF TAKAYASU’S ARTERITIS PATIENTS WITH RENAL ARTERY INVOLVEMENT Corisande Baldwin1, Aladdin Mohammad2,3, David Jayne3 University of British Columbia Faculty of Medicine, Department of Medicine, Division of Rheumatology, Vancouver, Canada 2Department of Clinical Sciences, Rheumatology, Lund University, Lund, Sweden 3Vasculitis and Lupus Clinic, Addenbrooke’s Hospital, Cambridge, UK 1 The authors have chosen not to publish the abstract. ABSTRACTNUMMER: 50 50 PATIENTS´ VERSUS PHYSICIANS´ ASSESSMENT OF DISEASE ACTIVITY USING SYSTEMIC LUPUS ACTIVITY QUESTIONNAIRE Susanne Pettersson1,2, Sonia Möller1, Johanna Gustafsson1,3, Iva Gunnarsson1,3, Elisabet Svenungsson1,3, Elisabet Welin Henriksson1,2 Rheumatology clinic, Karolinska University Hospital. Stockholm, Sweden 2Department of Neurobiology, Care Sciences and Society, Karolinska Institutet. Stockholm, Sweden 3Department of Medicine, Unit of Rheumatology Karolinska Institutet. Stockholm, Sweden 1 Background The aim of this study was to compare patients´ (SLAQ) to physicians´ (SLAM) assessments of disease activity in systemic lupus erythematosus (SLE), and further explore how self-assessed disease activity varied with disease duration. Materials and Methods Patients with SLE filled out the SLAQ questionnaire before meeting the physician. SLAQ scorings explored were, total SLAQ score (0-47), positive symptom responses (Symptom Score, 0-24), Flares (0-3), patients global disease activity (PNRS, 0-10). In addition, corresponding items on SLAQ and SLAM were explored. Spearman´s rho was used for correlations and Mann-Whitney U or chi-square tests for comparisons patients with short disease duration (< 1year) and longer (≥1year). Results 203 patients (79.3% women) were included, median age 45 (IQR 33-57), disease duration 5 years (IQR 0-14). Physician (SLAM-nolab) - patient correlations were; SLAQ score (0.685), Symptom Score (0.651), Flares (0.547), PNRS (0.600). Best correlations between patients and physicians had; fatigue (0.640), seizures (0.635), headache (0.604), Raynaud´s (0.560), alopecia (0.508) and arthralgia/arthritis (0.512). The only symptom item with no correlation was neurological/stroke syndrome (0.109, p=251). The correlations between patients and physicians assessment were lower for the patients with short disease duration SLAQ score (0.606), SLAQ symptom score (0.540), Flares (0.488) and PNRS (0.525). ReumaBulletinen Nr 105 · 4/2015 31 ABSTRACTS Conclusions This study confirms that patients’ assessment by SLAQ can be used to monitor disease activity in SLE. However patients with short disease duration had lower correlations, indicating greater discrepancy between patients and physicians´ assessments. We suggest the SLAQ to be used in rheumatology nursing clinics. Further studies could evaluate if the SLAQ as a base for discussions, can narrow the understanding between patients and health care providers regarding the interpretation of signs and symptoms in SLE. ABSTRACTNUMMER: 51 51 KNOWLEDGE SOURCES FOR EVIDENCE-BASED PRACTICE IN RHEUMATOLOGY NURSING Margit Neher1, Christian Ståhl1, Per-Erik Ellström2, Per Nilsen1 1 Linköpings Universitet,IMH 2 Linköpings Universitet, IBL Background As rheumatology nursing develops and extends, knowledge about current use of knowledge in rheumatology nursing practice may guide discussions about future knowledge needs. Aims To explore what perceptions rheumatology nurses have about their knowledge sources and about what knowledge they use in their practice. Methods and materials Twelve nurses working in specialist rheumatology were interviewed using a semi-structured interview guide. The data were analyzed using conventional qualitative content analysis. Results The analysis yielded four types of knowledge sources in clinical practice: interaction with others in the workplace, contacts outside the workplace, written materials, and previous knowledge and experience. Colleagues, and physicians in particular, were important for informal learning in daily rheumatology practice. Evidence from the medical arena was accessed through medical specialists, while nursing research was used less. Conclusion Facilitating informal learning and continuing formal education is proposed as a way toward a more evidence-based practice in extended roles. Corresponding Author Margit Neher, Division of Social Medicine, Department of Medical and Health Sciences, Linköping University, SE-581 83 Linköping, Sweden. Email: [email protected] ABSTRACTNUMMER: 52 52 LEARNING-OPPORTUNITIES IN RHEUMATOLOGY PRACTICE-A QUALITATIVE STUDY Margit Neher1, Christian Ståhl1, Per Nilsen1 1 Linköpings Universitet Background As rheumatology practice is becoming more complex, there is a growing need to go beyond formal training to develop new skills 32 ReumaBulletinen Nr 105 · 4/2015 and competencies. Learning in health care is also considered by many implementation scientists to be of key importance for achieving a more evidence-based practice and designing interventions towards attaining this goal. While human resource management traditionally focuses on formal education, modern theories about learning in the workplace propose that learning at work is informal, dominated by learning through experience and interactions. Purpose To explore what perceptions professionals working in specialized rheumatology have about their learning opportunities and about what learning activities they use in their practice. Methodology 36 practitioners of different professions were interviewed. Data were analyzed using conventional qualitative content analysis with a directed approach, using a typology of formal and informal learning. Findings The analysis confirms workplace learning theories: interaction with others in the workplace, in most part with professional peers, provided opportunities for learning through informal meetings. Recognized learning opportunities such as continuing professional education and regular participation in rheumatology-specific courses and conferences were perceived as lacking by many, and time for reflection and up-dating knowledge was short. Research- and teaching-roles were drivers for more generic up-dating of knowledge. Value The study confirmed that informal workplace learning is an important part of rheumatology clinical learning. Further studies are needed to clarify in which ways informal and formal learning in the rheumatology clinic may be supported in workplaces with different characteristics. ABSTRACTNUMMER: 53 53 CAN AN EHEALTH SERVICE ENHANCE COMMUNICATION IN EARLY ARTHRITIS? Susanne Pettersson1, Malin Regardt2,3, Svantesson Sofia4, Tarre Tina4, Wretbring Karolina5, Ernestam Sofia1 Rheumatology clinic, Karolinska Univ. Hospital 2Dep. of occupational therapy, Karolinska Univ. Hospital 3Dep. of Learning, Informatics, Management and Ethics, Karolinska Institutet 4Oceans Observations 5Med. Management Inovations, Stockholm, Sweden 1 Background To support patients and guide the general practitioner a web based questionnaire (www.ontilederna.nu) was developed. It includes questions on signs and symptoms of arthritis and generates a summary and depending on the results the respondent is suggested to either contact health care service or not. Materials and methods To evaluate the service a qualitative approach was used at 2 primary care settings and 1 rheumatology clinic for early arthritis. The patients with signs/symptoms of early arthritis were invited to answer the questions prior to their clinical visit. Both health care providers and patients were then invited to participate in an interview. 14 patients and 9 health care providers were interviewed. ABSTRACTS Results The result generated themes. Usability: The e-health service was easy to perform and perceived as innovative. Respondents would have appreciated the opportunity to choose where to answer the questions. It was perceived to be beneficial as part of the medical record or attached to a referral to the specialist. The explanatory text was perceived as valuable and important. Preparation: The questions were perceived as relevant and gave guidance to reflect on symptoms, prepare and organize thoughts before a medical appointment. It gave structure to the meeting which generated time to discuss important topics. Shared communication: The summary offered a common starting point and the health provider could acknowledge the patients symptoms. It helped the patient to describe and communicate symptoms and minimized the risk to miss important aspects. Limitations: The respondents lacked questions regarding neck/back symptoms. The language availability resulted in exclusion of non-Swedish-speaking patients. Conclusions The test was perceived as easy, usable and adds value in the medical consultation for both patients and health care providers. After the result more questions have been incorporated and the translation process initiated. ABSTRACTNUMMER: 54 54 ARBETSFÖRMÅGA, HANDFUNKTION OCH LIVSKVALITET ÄR NEDSATT VID POLYMYOSIT OCH DERMATOMYOSIT Malin Regardt1,2 Arbetsterapikliniken Karolinska Universitetssjukhuset 2Karolinska Institutet, LIME 1 Bakgrund Personer med polymyosit (PM) och dermatomyosit (DM) har muskelsvaghet i de proximala musklerna. Kunskapen är begränsad om hur handfunktion, aktivitetsförmåga och livskvalitet (QoL) är påverkat hos personer med PM och DM. Syfte Syftet var att beskriva handfunktion, aktivitetsförmåga, arbetsförmåga och QoL hos personer med PM och DM. Metod Tvärsnitt, över tid- och intervention pilot design har använts i min avhandling. Totalt inkluderades 143 personer med PM och DM i studierna. Resultat/preliminärt resultat Resultatet visade att både män och kvinnor med PM och DM har nedsatt gripkraft och livskvalitet och att gripkraften korrelerade med QoL. En handträning intervention verkade genomförbar med god följsamhet men med få individuella förbättringar på handfunktion och aktivitetsförmåga varför intervention och design bör modifieras. 44 % av personer med PM och DM i arbetsförålder arbetade heltid medan 25 % var heltids sjukskrivna. Mer än hälften självskattade sin arbetsförmåga som mycket låg eller låg. Arbetsrelaterade riskfaktorer var mer vanligt hos personer som varit heltids sjukskrivna > 2 år. För de personer som var i arbete ansågs arbetsuppgiftens krav, tidskrav och förväntningar på prestation i arbetet utgöra hinder i arbetsmiljön för personens arbetsförmåga. Stödjande faktorer var arbetets värde och betydelse, interaktion med andra och samarbete med arbetskamrater. Låg självskattad arbetsförmåga korrelerade med procent i arbete, förekomsten av arbetsrelaterade riskfaktorer och hinder i arbetsmiljön. Slutsats Personer med PM and DM har nedsatt gripkraft, lägre självskattad livskvalitet, lågt självskattad arbetsförmåga. Den nedsatta gripkraften tycks påverka QoL medan den proximala muskelsvagheten påverkar förmågan att arbeta. Dessa resultat antyder att handfunktion och arbetsförmåga är viktiga aspekter att mäta i det kliniska arbetet med personer med PM och DM. Dessa mätningar kan ligga till grund för arbetsterapeutiska interventioner samt för att utvärdera medicinsk behandling. ABSTRACTNUMMER: 55 55 IMPLEMENTERING AV LEVNADSVANOR VID NYDEBUTERAD RA Malin Regardt1,2, Åsa Lindberg1, Karin Åström1, Anna-Carin Bergström1, Irené Bolander1 Arbetsterapikliniken, Karolinska Universitetssjukhuset 2Karolinska Institutet, LIME 1 Bakgrund Syftet var att utforma, implementera och utvärdera ett arbetssätt där levnadsvanor blir en naturlig del i den arbetsterapeutiska behandlingen av patienter med nydebuterad reumatoid artrit (RA). Metod Totalt har 35 patienter med RA inkluderats. Fyra arbetsterapeuter har utfört implementeringen. Implementering bestod av att patienterna tillfrågades om deras levnadsvanor vid det första besöket hos arbetsterapeuten. Efter besöket fick patienterna svara på hur de upplevde frågorna och i vilken utsträckning frågorna kommer påverka dem. Även arbetsterapeuterna tillfrågades om deras upplevelse. Resultat Arbetsterapeuternas upplevelse: Arbetsterapeuterna upplevde att de flesta var medvetna om vikten av att ha bra levnadsvanor, att patienterna blev bekräftade av ytterligare en yrkesgrupp. En fråga som uppkom var hur man ska ta hand om de svar man får och att de upplevde en kunskapslucka inom kost och rådgivande samtal. De ställde sig också frågande om det var rätt tidpunkt att informera om levnadsvanor när patienten är nydebuterad. De såg en klar koppling mellan arbetsterapi och kost samt fysisk aktivitet/fritid medan de tyckte det var svårare att ställa frågor om alkohol och rökning. Patienternas upplevelse Patienterna blev bekräftade att alkohol och rökning påverkar behandling, att träning och är bra och inte skadligt. Att en upprepning av informationen gav bekräftelse men att det var en balansgång så det inte blev tjat, ”Blir anti om det blir för mycket tjat.” De beskrev att det sår ett frö för förändring men att man ”måste vara motiverad själ.” De beskrev även att de fick en ny identitet med sjukdomen ”kan inte längre vara en festpingla.” Slutsats Majoriteten upplevde det positivt att arbetsterapeuten ställde frågor om levnadsvanor. Arbetsterapeuterna upplevde att levnadsvanor om kost och fysisk aktivitet gav en klar koppling till arbetsterapi. ReumaBulletinen Nr 105 · 4/2015 33 ABSTRACTS ABSTRACTNUMMER: 56 56 WORK DISABILITY IN EARLY SYSTEMIC SCLEROSIS:A LONGITUDINAL POPULATION-BASED COHORT STUDY Gunnel Sandqvist1,2, Roger Hesselstrand1,2, Ingemar F Petersson1,2, Lars Erik Kristensen1,3 1 Lunds Universitet 2Skånes Universitetssjukhus 3Copenhagen University Hospital, Bispebjerg and Frederiksberg, Denmark Background Studies to date indicate that the prevalence of work disability is high in systemic sclerosis (SSc). Therefore, in order to identify patients with needs for early interventions, e.g. medical treatment and rehabilitation, more knowledge about patterns of work disability and its relationship to disease activity in early disease is needed. Objectives To study work disability with reference to levels of sick leave and disability pension in early SSc. Methods Thirty-two SSc patients (26 female, 24 with limited SSc), median age 47.5 years (IQR 43-53), with onset of their first non-Raynaud symptom between 2003 and 2009 and with a follow-up of 36 months were included. Work disability was calculated in 30-day-intervals from 12 months prior disease onset until 36 months after, presented as the prevalence of work disability per year (0 – 3) and as period prevalence of mean net days per month (+/- SD). Comparisons were made between patients with different disease severity and sociodemographic characteristics, and between patients and a reference group from the general population. Results Seventy-eight percent had no work disability one year prior disease onset, which decreased to 47% after 3 years. The relative risk for work disability in SSc patients compared to reference group was 0.95 (95% CI 0.39 – 2.33) at diagnosis, and increased to 2.41 (1.28 – 4.55) after 3 years. There were no significant correlations between work disability and disease severity, but between work disability and years at workplace rs=-.72 (p=0.002), education rs=.51 (p=0.004), and sickness absence the month before disease onset rs=.58 respectively (p=0.001). Conclusions Considerable increase in work disability was noted 3 years after disease onset. Short education, fewer years at workplace, and sickness absence before disease onset may be risk factors for sustained work disability and these patients should be selected for early rehabilitation intervention. ABSTRACTNUMMER: 57 57 ’SOM DEN VÄRSTA TANDVÄRK JAG NÅGONSIN HAFT’ – HUR PERSONER MED REUMATOID ARTRIT BESKRIVER OCH HANTERAR SMÄRTA Maria Bergström1, Inger Ahlstrand1, Ingrid Thyberg2, Torbjörn Falkmer1,3,4, Björn Börsbo4, Mathilda Björk1,4,5 Avdelningen för rehabilitering, Hälsohögskolan i Jönköping 2Reumatologiska kliniken, Region Östergötland 3School of Occupational 1 34 ReumaBulletinen Nr 105 · 4/2015 Therapy & Socail Work, CHIRI, Curtin University, Perth. 4Avdelningen för rehabiliteringsmedicin, Hälsouniversitetet, Linköping 5 Rehabenheten, HMC, Region Östergötland Bakgrund Reumatoid artrit (RA) är en kronisk inflammatorisk sjukdom som ofta leder till funktionsnedsättning. Trots att nya läkemedel introducerats de senast decennierna skattar en majoritet av patienterna fortfarande en hög smärtintensitet. Patienter med RA har identifierat smärta som ett av de viktigaste symtomen att reducera. Idag bedöms smärta ofta genom att använda en visuell analog skala (VAS), vilket inte speglar smärtans komplexitet. Syfte Att beskriva hur män och kvinnor med RA upplever och hanterar smärta Metod Deltagarna rekryterades från tre reumatologenheter i sydöstra Sverige . Inklusionskriterier var diagnostiserad RA sedan minst fyra år samt smärtintensitet >40mm VAS under de senaste två klinikbesöken. 33 av 77 tillfrågade patienter deltog. Deltagarna var mellan 34 och 73 år. Sju semistrukturerade fokusgruppsdiskussioner genomfördes och analyserades genom innehållsanalys. Studien är godkänd av Regionala etikprövningsnämnden. Resultat Fyra kategorier identifierades: (1) Smärta tar sig olika uttryck syftar till patienternas beskrivningar av smärta vid RA som överväldigande, värkande och stelhet i leder. Smärta beskrevs ha en nära koppling till trötthet och stress. (2) Hantering genom att lindra smärtan hänvisar till hur patienterna använde värme och/eller kyla, läkemedel och aktiviteter som distraktion. (3) Hantering genom att anpassa sig till smärtan beskriver patienternas strategier för att lära sig leva med smärtan, att använda hjälpmedel och planera aktiviteter i dagliga livet för att minska smärtan, samt ibland ge upp aktiviteter. (4) Hantering av smärta i ett socialt sammanhang syftar till att den sociala miljön kan vara stöttande men också oförstående, vilket kan leda till att patienten ibland väljer att dölja sin smärta. Slutsats Resultatet visar att smärta vid RA är komplex och mångfacetterad. Bedömning och behandling av smärta bör genomföras med ett biopsykosocialt synsätt inriktat både mot patientens perspektiv såväl som den sociala miljön för att nå ett optimalt resultat. ABSTRACTNUMMER: 58 58 SMÄRTA OCH AKTIVITETSBEGRÄNSNINGAR HOS DAGENS TIDIGA RA-PATIENTER JÄMFÖRT MED TIO ÅR TIDIGARE – TIRA-PROJEKTET Inger Ahlstrand1, Ingrid Thyberg2, Torbjörn Falkmer1,3,5, Örjan Dahlström4, Mathilda Björk1,5,6 Avdelningen för rehabilitering, Hälsohögskolan, Jönköping 2Reumatologiska kliniken, HMC, Region Östergötland, Linköping 3School of Occupational Therapy & Social Work, CHIRI, Curtin University, Perth, Australien 4Linköpings universitet, Linköping 5Avdelningen för rehabiliteringsmedicin, Hälsouniversitetet, 6Rehabenheten, HMC, Region Östergötland, Linköping 1 Bakgrund Smärta och aktivitetsbegränsningar påverkar kvinnor i högre grad än män. Långtidsuppföljningar av tidiga välstrukturerade behand- ABSTRACTS lingsinsatser på 1990-talet visade lägre sjukdomsaktivitet men mindre fördelaktig utveckling för smärta och aktivitetsbegränsningar. Syfte Att studera skillnader i smärta och aktivitetsbegränsningar under de första tre åren efter diagnos hos dagens patienter med Reumatoid artrit jämfört med tio år tidigare. Metod Studien baseras på patienter rekryterade i projektet ”Tidiga Insatser för Reumatoid Artrit (TIRA). I den första kohorten (TIRA-1) inkluderades 320 patienter 1996-1998. I den andra kohorten (TIRA2) inkluderades 463 patienter 2006-2008. Smärtintensitet (VAS), ”bodily pain” (BP) i SF-36 och aktivitetsbegränsningar (Health Assessment Questionnaire, HAQ) rapporterades vid inklusion och vid uppföljningar efter ett, två och tre år. Resultat Det var ingen skillnad i sjukdomsaktivitet vid inklusion, men signifikant lägre vid uppföljningarna efter ett, två och tre år i TIRA2 kohorten jämfört med TIRA-1. Patienterna i TIRA-2 förskrevs i högre grad antireumatiska läkemedel, DMARDs och biologiska läkemedel än TIRA-1. Patienterna i TIRA-2 rapporterade signifikant lägre smärta och aktivitetsbegränsningar vid alla uppföljningar. Män i TIRA-2 rapporterade lägre smärta än kvinnor vid alla uppföljningar medan däremot kvinnor i TIRA-2 rapporterade signifikant större aktivitetsbegränsningar vid alla uppföljningar. Smärta och aktivitetsbegränsningar var signifikant minskad från inklusion till uppföljning efter första året men var fortsatt stabil därefter. Slutsats Både kvinnor och män i dagens tidiga RA-kohort rapporterar lägre smärta och mindre aktivitetsbegränsningar vid uppföljningarna efter diagnos jämfört med deras motsvarighet tio år tidigare. Både aktivitetsbegränsningar och smärta var dock fortfarande uttalade. ABSTRACTNUMMER: 59 59 UPPLEVELSER AV HUR INTIMA RELATIONER PÅVERKAS VID TIDIG REUMATOID ARTRIT. EN INTERVJUSTUDIE INOM TIRA-PROJEKTET Gunnel Östlund1, Mathilda Björk2,3,4, Eva Valtersson5, Annette Sverker3,5 Mälardalens Högskola, Eskilstuna 2Avdelningen för rehabilitering, Hälsohögskolan, Jönköping 3Avdelningen för rehabiliteringsmedicin, Hälsouniversitetet 4Rehabenheten, HMC, Region Östergötland, Linköping 5NSC, Universitetssjukhuset i Linköping, Linköping 1 Bakgrund Reumatoid artrit (RA; ledgångsreumatism) är en kronisk, inflammatorisk sjukdom som i många fall leder till funktionshinder. Vid kronisk sjukdom är tillfredsställelse med sexlivet viktigt för livskvalitet. Vid RA anger drygt 2/3 av patienterna att RA påverkar deras intima relationer negativt. Syfte Syftet var beskriva mäns och kvinnors upplevelser av hur intima relationer påverkas av tidig reumatoid artrit. Metod Studien är associerad till det regionsövergripande projektet ”Tidiga Insatser vid RA” (TIRA) och inkluderar ett urval patienter från de 522 TIRA2-patienter som fick sin RA-diagnos mellan 2006- 2009. Datainsamlingen innefattar 60 intervjuer med (37 kvinnor) i åldrarna 20-63 år. Intervjuerna genomfördes med The Critical Incident Technique” (CIT) och innefattade frågan ”hur påverkar RA ditt sexliv?”. Intervjuerna transkriberades och därefter analyserades med hjälp av innehållsanalys. Resultat Resultat visar att ungefär en tredjedel av patienterna beskrev att RA påverkade deras intima relationer. Trötthet och smärta i kroppen var faktorer som upplevdes som hindrade. Biverkningar av mediciner som bland annat påverkade den sexuella funktionen var en annan aspekt. Några avstod från att ha sex och menade att närhet och smekningar kunde räcka. Många uttryckte emotionell påverkan genom att inte känna sig tillräcklig eller att känna sig mindre attraktiv på grund av RA. Många informanter underströk vikten av att ha en öppen dialog med sin partner för att hitta strategier för ett fungerade sexliv trots RA. Slutsats Trots att omhändertagandet av patienter med RA förbättrats avsevärt de med biologiska läkemedel och ett tidigt multiprofessionellt omhändertagande upplever en tredjedel av patienterna att deras intima relationer påverkas av RA. Resultatet från studien genererar ny och detaljerad kunskap om hur intima relationer påverkas vid tidig RA som underlag för diskussion tillsammans med patienten i den kliniska vardagen. 60 ABSTRACTNUMMER: 60 FYSISK AKTIVITET VID REUMATISK LEDSJUKDOM: VAD HINDRAR OCH VAD UNDERLÄTTAR? Inger Albiin1, Nina Brodin2, Emma Swärdh3 Hälsopoolens Rehabklinik AB, Stockholm 2Karolinska Institutet, Huddinge 3Karolinska Institutet, Huddinge 1 Bakgrund Vilka faktorer som upplevs hindrande och stödjande för att genomföra fysisk aktivitet av personer med reumatisk sjukdom och under modern läkemedelsbehandling i Sverige idag är okänt. Syfte Att beskriva hinder och underlättande faktorer för fysisk aktivitet hos patienter med inflammatorisk reumatisk ledsjukdom. Material och metod 15 patienter med inflammatorisk ledsjukdom intervjuades. Intervjuerna transkriberades ordagrant och innehållet analyserades med innehållsanalys enligt Graneheim och Lundman. Resultat Fem kategorier identifierades: Motivation byggde på mål, samt rutiner och disciplin. Att återfå funktion och att återgå till arbete beskrevs som drivande faktorer. Hemprogram beskrevs vara svårt att genomföra pga bristande disciplin, men vikten av att ta eget ansvar lyftes fram. Resultat av fysisk aktivitet byggde på effekter både kroppsligt och mentalt. Träningen gav en avslappnad känsla i kroppen och skapade ett behov av fortsatt träning. Smärtan och stelheten minskade samtidigt som muskelstyrka och sömn förbättrades. Mentalt gav fysisk aktivitet en positiv kick med ökad livskvalitet. Omgivningen byggde på socialt stöd, tid och tillgänglighet. Stöd från familj, vänner, behandlingsgrupper och behandlande vårdpersonal var särskilt viktiga. Brist av tid relaterat till sociala roller var ett hinder och tillgänglighet till träningslokal och fysioterapeut an- ReumaBulletinen Nr 105 · 4/2015 35 ABSTRACTS sågs viktigt. Fysik byggde på reumatisk sjukdom och läkemedel. Den reumatiska sjukdomen kräver individanpassad träning utifrån smärta och sjukdomsstatus för att vara genomförbar, och adekvat läkemedelsbehandling underlättade fysisk aktivitet. Identitet byggde på självbild, tilltro till egen förmåga och rädsla. Det framkom att ens självbild kan avgöra hur mycket och vilken typ av träning som är accepterbar. Bristande tilltro till egen förmåga att bedöma grad och typ av träning såväl som rädsla för att träna inom friskvården beskrevs som viktiga faktorer för deltagande. Keywords Inclusion body myositis, activity, participation, Questionnaire, ICF. Slutsats Vid initierande och planering av fysisk aktivitet bör vårdpersonal undersöka faktorer relaterade till patientens motivation, resultat av fysisk aktivitet, omgivning, fysik och identitet och individanpassa främjandet av fysisk aktivitet utifrån dessa. Ingrid Thyberg1, Annette Sverker2, Mathilda Björk3, Eva Valtersson2, Gunnel Östlund4 ABSTRACTNUMMER: 61 61 TEST-RETEST RELIABILITY FOR THE MYOSITIS ACTIVITIES PROFILE, MAP, FOR PATIENTS WITH INCLUSIONBODY MYOSITIS. Anna Hallén1, Helene Alexanderson1 Karolinska Universitetssjukhuser 1 Background The Inclusions Body Myositis Functional Rating Scale is the only measure of activity limitation developed for patients for sporadic inclusion body myositis, sIBM, however, it is not validated for Swedish context. Today, the Health Assessment Questionnaire, HAQ, developed for patients with arthritis is the most commonly used instrument to determine activity limitations in myositis, however, HAQ is not validated for patients with sIBM. The Myositis Activities Profile was developed and validated for patients with polymyositis and dermatomyositis in Sweden assessing the ICF domains activity and participation. The psychometric properties of the MAP have not been evaluated for sIBM. Aim To evaluate test-retest reliability of the Myositis Activities Profile for an adult population with sIBM. Method A group of forty five patients with a definite diagnosis of sIBM were identified trough the registry SweMyoNet and some patients were recruited via the department of neurology, Karolinska University Hospital. Thirty four of these patients chose to participate. The patients were asked to fill out the MAP questionnaire twice with one week apart. To determine test-retest agreement the linear weighted kappa coefficient was used. Due to low power for weighted kappa analysis, the method described by Svensson was used as a complement. To determine systematic variations the sign test and the method described by Svensson were used. Results The kappa coefficient of the four sub-scales and the four single items of the MAP ranged from Kw= 0.72 – 0.94 which is regarded as substantial to almost perfect. The percentage agreement, PA, ranged from 70-91% and is regarded as satisfactory to almost perfect. No systematic variations were found with p-values ranging from p=0,62 to p=1. Conclusions The MAP demonstrated good to excellent agreement for test-retest reliability with no systematic disagreements. 36 ReumaBulletinen Nr 105 · 4/2015 ABSTRACTNUMMER: 62 62 AVOIDANCE, ADJUSTMENT, INTERACTION AND ACCEPTANCE STRATEGIES TO HANDLE DILEMMAS IN PARTICIPATION IN MEN WITH EARLY RA. THE SWEDISH TIRA PROJECT. Department of Clinical and Experimental Medicine, Linköping University 2Rehabilitation section NSC, County Council of Östergötland, Linköping, Sweden 3Rehabilitation Medicine, Department of Medicine and Health, Linköping University, Sweden 4Division of Social Work, School of Health, Care and Social Welfare, Mälardalen University, Sweden, Eskilstuna, Sweden 1 Background In spite of early interventions and advancements in medication disability and restricted work capacity is closely related to rheumatoid arthritis (RA). Around 1/3 of diagnosed patients are men, however few studies describe men’s need and experiences of living with RA. Objectives To explore male strategies of handling participating restriction in everyday life. Methods In this study 25 men with early RA from the TIRA2 cohort [1], age 20 – 63, were interviewed about participation restrictions with Critical Incident Technique [2]. Transcribed interviews were synthesized into dilemmas and linked to ICF participation codes and the strategies in handling these dilemmas were analyzed and categorized using content analysis. Results The men described four types of strategies of handling participating restriction in everyday life. Resilience strategies; to find enjoyments, develop self-trust, and a new body-knowledge. Daily routine strategies; use more time on each task and rest in between activities, adjust medication to activity, adjust movements finding new ways to conduct work tasks and physical training. Avoidance strategies; avoid alcohol, social contacts after work, inform of RA and sometimes medicine. Action strategies; continue activities, attend activities as a spectator instead of being an active participant, go home if needed, say no, ask for help, and talk about RA. Acceptance strategies; accept pain, accept less work pace, accept less endurance and fewer activities. Conclusions Men described dilemmas in everyday life due to RA, but not all experienced being restricted in life they rather expressed reorganizing their everyday lives. References 1 Sverker A, Thyberg I, Östlund G, Valtersson E, Thyberg M. (2013). Participation in work in early rheumatoid arthritis: A qualitative interview study interpreted in terms of the ICF. Disability & Rehabilitation May (3); ISSN1464-5165. 2Flanagan, C (1954). The critical incident technique. Psychological Bulletin, 51: p. 327-358. ABSTRACTS ABSTRACTNUMMER: 63 63 INCREASED HEALTH RELATED QUALITY OF LIFE IN EARLY RA TODAY COMPARED TO PATIENTS DIAGNOSED DURING THE 1990´S. THE SWEDISH TIRA PROJECT. Ingrid Thyberg1, Patrik Arvidsson2, Mikael Thyberg3, Mathilda Björk4, Örjan Dahlström5 Department of Clinical and Experimental Medicine, Linköping University 2Centre for Research & Development, Uppsala University/Region Gävleborg, Sweden 3Rehabilitation Medicine, Linköping University, Linköping, Sweden 4Rehabilitation Center and Department of Medical and Health Sciences, Linköping University, Sweden 5 Swedish Institute for Disability Research, Department of Behavioral Sciences and Learning, Linköping University, Sweden 1 Objectives To analyse differences regarding HRQL that were diagnosed during the 2000´s compared to patients diagnosed before the introduction of biological agents. Methods The 276 patients still participating at the three years follow up (included 1996-1998) in the early RA-cohort (TIRA-1) and the corresponding 373 patients included (2005-2008) in the post biological second cohort (TIRA-2). The cohorts showed no significant differences in DAS28 at inclusion but more patients were prescribed DMARD:s. DAS did not differ between sexes in TIRA-1, but men had lower DAS than women at all occasions in TIRA-2. HRQL was reported in Short Form 36 (SF-36) in the subscales Physical Functioning (PF), Role Physical (RP), Bodily Pain (BP), General Health (GH), Vitality (VT), Social Functioning (SF), Role Emotional (RE) and Mental Health(MH) at inclusion (Y0) and after at one year (Y1) , 2 (Y2), and 3 years (Y3). Results Differences between cohorts; for both sexes there were no differences in SF-36 at inclusion between cohorts, but at the follow-ups most scales showed higher HRQL in women and men in TIRA-2 (T1) compared to in TIRA-1 (T1) except for MH and SF which did not differ between cohorts (table). The mean scores at Y3 for women in T1/T2 were; PF 58/69; RP 52/62; BP 52/62; GH 51/63; VT 52/57; SF 79/81; RE 69/7; MH 74/76 and the corresponding for men were PF 66/75; RP 53/64; BP 52/69; GH 55/63; VT 58/66; SF 84/91; RE 75/80; MH 79/84. Differences within cohorts; men had higher HRQL than women at some occasions in TIRA-1 (T1)(Y0 =MH; Y1=GH, MH, SF; Y3=MH, PF) and in some occasions in TIRA-2 (T1) (Y0=PF; Y1=BP, PF, VT; Y2=BP, MH, PF, VT; Y3=BP, MH, PF, SF, VT). Our results indicates continuing needs for multi professional interventions, especially for women, in addition to DMARD:s. ABSTRACTNUMMER: 64 sjukhus, ortopedkliniken, paramedicinska sektionen, Stockholm. 4 Region Östergötland, HMC Rehabenheten, Linköping. 5Hälsouniversitetet, IMH, Avdelningen för Rehabiliteringsmedicin, Linköping. 6 Hälsohögskolan i Jönköping, Avdelningen för rehabilitering, Jönköping Introduktion Handartros medför ofta smärta, nedsatt fingerrörlighet och handkraft vilket påverkar greppförmågan och ger problem med utförandet av dagliga aktiviteter. Åtgärdsprogram för handartrospatienter bör fokusera på handfunktion, aktivitetsutförande och hanteringsstrategier i form av utbildning och träning. Handartrosskola i grupp är en metod som idag används i primärvården. Atrosskola är tidigare utvärderad som effektiv vid knä- och höftartros. Dock är kunskapen om dess effekt begränsad vid handartros. Syfte Syftet var att utvärdera om handartrosskola förändrar handfunktion och aktivitetsförmåga hos handartospatienter i primärvården. Metod Patienter med handartros som påbörjade artrosskola vid en primärvårdsenhet i sydöstra Sverige inkluderades konsekutivt under hösten 2008 till årsskiftet 2011/2012. Totalt tackade 64 personer ja, varav 15 därefter exkluderades utifrån kriterier som att de inte fullföljde interventionen. De 49 studiedeltagarna (92% kvinnor) genomgick artrosskolan med föreläsningar samt paraffinbad och handträning i grupp under en sexveckorsperiod. Data samlades in vid artrosskolans start, efter tre månader samt efter ett år. Instrument som användes för att mäta handfunktionen var Grip Ability Test (GAT), Signal of Functional Impairment (SOFI-hand) och Jamar. För att mäta aktivitetsförmåga användes Patientspecifik Funktionell Skala (PSFS) och Quick-Disabilities of the Arm, Shoulders and Hand (quick-DASH). Studien genomfördes i enlighet med etiska riktlinjer. Resultat Deltagargruppen och bortfallsgruppen var jämförbara gällande ålder, kön, civilstatus och utbildning. Dock arbetade patienter i bortfallsgruppen i signifikant större utsträckning. Resultatet visade att deltagarnas handfunktion, såväl styrka (Jamar) som rörlighet (SOFI-hand) och greppförmåga (GAT) förbättrades signifikant från start till tremånadersuppföljningen samt mellan start och uppföljningen efter ett år. Även aktivitetsförmåga (quick-DASH och PSFS) förbättrades till såväl tremånaders- som ettårsuppföljningen jämfört med start. Mellan tre månader och ett år var det ingen signifikant skillnad förutom på vänsterhandens styrka som förbättrades. Konklusion Resultatet indikerar att handartrosskola i grupp i primärvården är en kostnadseffektiv intervention som förbättrar handfunktion och aktivitetsförmåga med en kvarhållande effekt ett år efter genomgången intervention. 64 ARTROSSKOLA I PRIMÄRVÅRDEN FÖRBÄTTRAR HANDFUNKTION OCH AKTIVITETSFÖRMÅGA HOS PATIENTER MED HANDARTROS. Linda Bjurehed, Nina Brodin, Mathilda Björk Region Östergötland, Rörelse och Hälsa, Linköping. 2Karolinska Institutet, Inst NVS, sektionen för fysioterapi, Huddinge. 3Danderyds 1 ReumaBulletinen Nr 105 · 4/2015 37 Register · Abstracts Register · Abstracts Abreu, Ilka.................................................... 19 Ahlstrand, Inger.......................................... 57 ..........................................................................58 Albiin, Inger.................................................60 Alexanderson, Helene.............................. 61 Alfredsson, Lars.......................................... 23 Ali, Abukar...................................................... 8 ............................................................................ 9 .......................................................................... 10 ........................................................................... 11 Almlöf, Jonas...............................................43 Altawil, Reem.............................................. 23 Andersson, Karin........................................20 Andersson, Kerstin.................................... 22 Arkema, Elizabeth....................................... 3 Arvidsson, Patrik........................................ 63 Askling, Johan............................................... 2 ............................................................................ 5 ............................................................................ 6 ............................................................................ 7 Asplund, Kjell................................................ 3 Babar, Judith................................................47 Backlin, Carin...............................................42 Baecklund, Eva............................................42 Baldwin, Corisande...................................49 Bengtsson, Anders..................................... 33 Berggren, Olof............................................. 32 ..........................................................................40 Berglin, Ewa................................................. 16 Bergman, Stefan.........................................30 Bergström, Anna-Carin............................ 55 Bergström, Maria....................................... 57 Bjurehed, Linda...........................................64 Björk, Mathilda........................................... 57 ..........................................................................58 ..........................................................................59 ..........................................................................62 .......................................................................... 63 ..........................................................................64 Björnsdottir, Halla...................................... 12 Bokarewa, Maria.........................................15 ..........................................................................20 Bolander, Irené............................................ 55 Boman, Antonia.......................................... 16 Book, Christina............................................24 Bremander, Ann..........................................30 Brink, Mikael................................................ 14 Brodin, Nina.................................................60 ..........................................................................64 Brokstad, Karl.............................................. 41 Burmester, Gerd Rüdiger..........................17 Bylund, Johan................................................ 9 .......................................................................... 12 Börsbo, Björn............................................... 57 Camponeschi, Alessandro....................... 21 Carlsten, Hans.............................................29 Chatzidionysiou, Aikaterini....................17 Dackhammar, Christina.............................. 4 Dahlström, Örjan........................................58 .......................................................................... 63 38 ReumaBulletinen Nr 105 · 4/2015 Dehlin, Mats.................................................26 .......................................................................... 27 Deminger, Anna..........................................29 Detert, Jacqueline.......................................17 Dougados, Maxime....................................17 Drivelegka, Panagiota.............................. 27 Ellström, Per-Erik.........................................51 Eloranta, Maija-Leena.............................. 37 ..........................................................................40 ..........................................................................43 Eloranta, Maija-Lena................................. 32 Emamikia, Sharzad.....................................17 Englund, Marin...........................................44 Englund, Martin..........................................45 ..........................................................................46 Enocsson, Helena....................................... 37 Eriksson, Catharina.....................................15 Eriksson, Jonas.............................................. 7 Eriksson, Per................................................. 38 .......................................................................... 41 Erlandsson, Malin.......................................15 ..........................................................................20 Ernestam, Sofia............................................. 4 Exarchou, Sofia............................................. 5 ............................................................................ 6 ............................................................................ 7 Falkmer, Torbjörn....................................... 57 ..........................................................................58 Forsblad d’Elia, Helena.............................. 4 ............................................................................ 5 ............................................................................ 6 ............................................................................ 7 ..........................................................................28 ..........................................................................29 .......................................................................... 38 Foster, Timothy........................................... 12 Frisell, Thomas.............................................. 2 Frodlund, Martina...................................... 33 Gerhardsson, Jakob................................... 35 Gjertsson, Inger.......................................... 21 Gunnarsson, Iva.......................................... 33 ..........................................................................34 .......................................................................... 35 .......................................................................... 38 ..........................................................................50 Gustafsson, Johanna................................50 Gülfe, Anders............................................... 25 Györi, Noémi.................................................17 Hagberg, Niklas.......................................... 32 .......................................................................... 36 Hallén, Anna................................................ 61 Hallström, Magnus.................................... 22 Hammarsten, Ola.......................................28 Hansson, Monika....................................... 14 Hedberg, Martin.........................................29 Hedin, Per-Johan.........................................13 Hesselstrand, Roger..................................56 Hjorton, Karin.............................................. 32 Holmdahl, Rikard....................................... 14 Holmqvist, Marie.......................................... 3 Imgenberg-Kreuz, Juliana.......................43 Jacobsson, Gunnar..................................... 12 Jacobsson, Lennart T................................29 Jacobsson, Lennart...................................... 4 ............................................................................ 5 ............................................................................ 6 ............................................................................ 7 .......................................................................... 21 ..........................................................................24 ..........................................................................26 .......................................................................... 27 Jarneborn, Anders....................................... 8 ............................................................................ 9 Jayne, David.................................................45 ..........................................................................47 ..........................................................................49 Jin, Tao.............................................................. 8 ............................................................................ 9 .......................................................................... 10 ........................................................................... 11 .......................................................................... 12 Johansson, Bengt....................................... 12 Jones, Rachel................................................47 Jonsson, Roland.......................................... 41 Josefsson, Elisabet....................................... 9 .......................................................................... 10 .......................................................................... 12 Jönsen, Andreas......................................... 33 .......................................................................... 38 Karolina, Wretbring.................................. 53 Kastbom, Alf.................................................31 Klareskog, Lars............................................ 14 .......................................................................... 23 Klingberg, Eva.............................................28 ..........................................................................29 Kokkonen, Heidi......................................... 16 Abstracts · Register Kristensen, Lars Erik.................................... 6 ............................................................................ 7 ..........................................................................56 Kristensen, Lars-Erik................................... 4 ............................................................................ 5 Kvarnström, Marika.................................. 41 Kwiecinski, Jakub....................................... 12 Lampa, Jon.................................................... 23 Leonard, Dag............................................... 38 Lie, Elisabeth.................................................. 5 ............................................................................ 6 Lindberg, Åsa............................................... 55 Lindblad-Toh, Kerstin............................... 39 Lindqvist, Elisabet......................................30 Lindström, Ulf................................................ 4 ............................................................................ 5 ............................................................................ 6 ............................................................................ 7 Ljung, Lotta.....................................................1 Lorentzon, Mattias....................................29 Lundberg, Ingrid E..................................... 39 Lundell, Anna-Carin.................................. 22 Madsen, Rasmus......................................... 19 Magnusson, Malin....................................... 8 ............................................................................ 9 .......................................................................... 10 ........................................................................... 11 Malmström, Vivianne............................... 35 Mathsson-Alm, Linda............................... 14 Merkel, Peter A...........................................44 ..........................................................................45 ..........................................................................46 Mogard, Elisabeth......................................30 Mohammad, Aladdin................................44 ..........................................................................45 ..........................................................................46 ..........................................................................47 ..........................................................................48 ..........................................................................49 Mohammad, Majd....................................... 9 ........................................................................... 11 Mortensen, Kristian..................................47 Mårtensson, Inga-Lill................................ 21 Möller, Sonia................................................50 Nadali, Mitra................................................20 Nakagomi, Daiki.........................................47 Na, Malin........................................................ 11 Na, Manli......................................................... 8 ............................................................................ 9 .......................................................................... 10 Neher, Margit................................................51 .......................................................................... 52 Neovius, Martin............................................ 7 Nilsen, Per......................................................51 .......................................................................... 52 Nilsson, Jan-Åke.........................................45 Nordmark, Gunnel..................................... 38 .......................................................................... 41 ..........................................................................42 ..........................................................................43 Norheim, Katrine........................................43 Oleröd, Göran..............................................28 Omdal, Roald...............................................43 Pandya, Jayesh............................................ 22 Parodis, Ioannis........................................... 33 ..........................................................................34 .......................................................................... 35 Peetermans, Marijke................................. 12 Pekna, Marcela.............................................. 8 Petersson, Ingemar F................................56 Pettersson-Kymmer, Ulrika..................... 18 Pettersson, Susanne..................................50 .......................................................................... 53 Pullerits, Rille................................................. 9 ........................................................................... 11 ...........................................................................15 ..........................................................................20 Ramsköld, Daniel....................................... 33 Rantapää Dahlqvist, Solbritt....................1 .......................................................................... 14 ...........................................................................15 .......................................................................... 16 .......................................................................... 18 Regardt, Malin............................................. 53 ..........................................................................54 .......................................................................... 55 Rehnberg, Eva.............................................29 Ros, Elin......................................................... 25 Rudin, Anna................................................. 22 Rydholm, Maria..........................................24 Rönnblom, Lars........................................... 32 .......................................................................... 36 .......................................................................... 37 .......................................................................... 38 .......................................................................... 39 ..........................................................................40 ..........................................................................43 Rönnelid, Johan.......................................... 14 Saevarsdottir, Saedis................................ 23 Sandberg, Maria EC................................... 23 Sandling, Johanna K................................. 39 Sandling, Johanna.....................................43 Sandqvist, Gunnel..................................... 25 ..........................................................................56 Schiller, Claes................................................15 Schwarze, Jan-Christoph.......................... 11 Segelmark, Mårten....................................45 ..........................................................................46 ..........................................................................48 Signér, Linnea.............................................. 41 ..........................................................................43 Sigurdardottir, Valgerdur........................ 27 Simard, Julia................................................... 3 Sivasothy, Pasupathy................................47 Sjöwall, Christopher..................................31 .......................................................................... 33 .......................................................................... 37 .......................................................................... 38 .......................................................................... 41 Skogh, Thomas............................................31 .......................................................................... 37 Smith, Rona..................................................45 ..........................................................................47 Sofia, Ernestam........................................... 53 Sofia, Svantesson....................................... 53 Sparén, Pär..................................................... 2 Stasinopoulou, Kalliopi...........................26 Stokowska, Anna......................................... 8 Ståhl, Christian.............................................51 .......................................................................... 52 Sundström, Christer..................................42 Surowiec, Izabella...................................... 19 Swensson, Mattias..................................... 11 Svenungsson, Elisabet.............................34 .......................................................................... 35 ..........................................................................50 Sverker, Annette........................................59 ..........................................................................62 Svärd, Anna.................................................. 27 Swärdh, Emma............................................60 Syvänen, Ann-Christine........................... 39 ..........................................................................43 Söder, Frida...................................................34 Södergren, Anna........................................ 19 the DISSECT consortium ......................... 39 Theander, Elke............................................. 38 .......................................................................... 41 Thorarinsdottir, Katrin............................. 21 Thyberg, Ingrid........................................... 57 ..........................................................................58 ..........................................................................62 ..........................................................................63 Thyberg, Mikael.......................................... 63 Tina, Tarre..................................................... 53 Tomasson, Gunnar.....................................44 ..........................................................................46 Trouw, Leendert.......................................... 14 Trygg, Johan................................................. 19 Turesson, Carl................................................ 6 ............................................................................ 7 ..........................................................................24 ..........................................................................44 Turkkila, Minna............................................15 Töyrä Silfverswärd, Sofia........................20 V. Arkema, Elizabeth..................................17 Wadström, Hjalmar..................................... 2 Wahren-Herlenius, Marie........................ 38 .......................................................................... 39 .......................................................................... 41 Wallin, Philip.................................................31 Valtersson, Eva............................................59 ..........................................................................62 van Vollenhoven, Ronald.........................17 ..........................................................................34 Vasaitis, Lilian.............................................. 41 ..........................................................................42 Welin Henriksson, Elisabet.....................50 Welin, Amanda............................................. 8 ............................................................................ 9 ........................................................................... 11 Verhamme, Peter........................................ 12 Verheul, Marije........................................... 14 Westman, Kerstin......................................45 Wetterö, Jonas............................................ 37 Wiberg, Kristina.......................................... 18 Wieslander, Jörgen....................................48 Wijayatunga, Priyantha........................... 14 Wikström, Ingegerd..................................24 Wirestam, Lina............................................ 37 Wållberg-Jonsson, Solveig..................... 19 Zickert, Agneta........................................... 35 Ziegelasch, Michael....................................31 Åström, Karin.............................................. 55 Ärlestig, Lisbeth.......................................... 18 Östlund, Gunnel......................................... 19 ..........................................................................62 ReumaBulletinen Nr 105 · 4/2015 39 ReumaKalender 2015 2016 8 jul 4th World Psoriasis & Psoriatic Athritis Conference 2015 8-11 juli Stockholm Waterfront Congress Center 27 jan SRFs RESURS-dagar 27-29 januari 8 jun EULAR 2016 8-11 juni London 1 sep Reumadagarna 2015 1-4 september Tylösand 2 sep SLE-mötet i Wien 2-5 september Wien, Österrike 16 sep RULe-internat 3 16-18 september Eklundshof, Uppsala 21 sep SK-Kurs, Akut endokrinologi 21-25 september Stockholm 28 sep Inflammatoriska systemsjukdomar SK-liknande kurs 28 sept-2 okt Göteborg 12 okt SK-kurs, Differentialdiagnostik vid inflammatoriska sjukdomstillstånd 12-16 oktober Stockholm 18 okt 16th EULAR Postgraduate Course 18-21 oktober Prag Post-‐ACR 6 nov ACR/ARHP Annual Meeting 6-11 november San Fransisco 2 december 2015, kl 12.00 - 16.30 9 nov SK-kurs, Akutmedicin och medicinsk intensivvård 9-13 november Stockholm (Rekommenderas av SRF) 12 nov RULe - avslutningsmodul 12-13 november Göteborg 16 nov SK-kurs, Koagulationssjukdomar 16-20 november Malmö Eftermiddagsseminarium (dagen innan Medicinska riksstämman) Arrangeras av SRF i samarbete med Dagens Medicin Agenda. Mer information på svenskreumatologi.se och dagensmedicin.se Information/program/inbjudan återfinnes i Reumakalendern på www.svenskreumatologi.se 40 ReumaBulletinen Nr 105 · 4/2015 Bibehållen effekt vid psoriasisartrit upp till 100 veckor med ® Stelara (ustekinumab) Procentandel av patienterna (%) 80 63.6% 62.7% 56.7% 60 * 40 * * * 20 0 0 4 8 12 16 20 24 28 32 36 40 44 48 52 56 60 64 68 72 76 80 84 88 92 96 100 Tid (veckor) Placebo n= 206 45mg n= 205 90mg n= 204 Placebo 206 205 204 Placebo Stelara® 45mg 185 195 189 Stelara® 45mg 177 178 176 Stelara® 90mg Pilarna indikerar administrationstillfällena för Stelara® och placebo. Referens: McInnes I, et al. Lancet 2013; 382(9894):780–9. Janssen-Cilag AB Box 7073, SE-192 07 Sollentuna, Sweden, Tel +46 8 626 50 00, Fax +46 8 626 51 00, www.janssen.se PHSWE/STE/0015/0001 STELARA® (ustekinumab) Injektionsvätska, lösning i förfylld spruta i doserna: 45 mg/0,5 ml och 90 mg/1ml. ATC kod: L04AC05. Receptbelagt. F. Indikationer: Plackpsoriasis: STELARA är indicerat för behandling av måttlig till svår plackpsoriasis hos vuxna som inte svarat på andra systemiska behandlingar såsom ciklosporin, metotrexat (MTX) eller PUVA, eller när intolerans eller kontraindikationer föreligger mot sådana behandlingar. Psoriasisartrit: STELARA, som monoterapi eller i kombination med MTX, är avsett för behandling av aktiv psoriasisartrit hos vuxna när svaret på tidigare sjukdomsmodifierande antireumatiska läkemedel (DMARDs) har varit otillräckligt. Trafik: STELARA har ingen eller försumbar effekt på förmågan att framföra fordon och använda maskiner. Datum för senaste översyn av produktresumé 2014-11-20. För fullständig produktinformation och aktuellt pris, se www.fass.se JC-140688-1 Effekt mätt i ACR20 vid psoriasisartrit upp till vecka 100 vid behandling med Stelara® Nyhet! Metojectpen® (metotrexat) Metojectpen ® (metotrexat) 50 mg/ml metotrexat förfylld injektionspenna Injektionspennor i 9 olika doser Färdig att använda Enkel att hantera Minskar risken för nålstick Högst koncentration vilket ger lägst volym Instruktionsfilm för subkutan injektion av Metojectpen® 50 mg/ml finner du på www.medicininstruktioner.se En känsla av frihet... Metojectpen® 50 mg/ml Metotrexatfyllda injektionspennor med liten volym (0,15-0,60 ml) Indikationer: Metojectpen® är indicerat för behandling av aktiv reumatoid artrit hos vuxna patienter, polyartritiska former av svår, aktiv juvenil idiopatisk artrit, när behandling med NSAID-preparat (icke-steroida antiinflammatoriska läkemedel) gett inadekvat svar, svår terapiresistent handikappande psoriasis som inte svarar adekvat på andra terapiformer såsom fototerapi, PUVA och retinoider och svår psoriasisartrit hos vuxna patienter. Dosering: Metojectpen® ges som injektion 1 gång per vecka. Individuell dosering. Förpackningsstorlekar: Förfyllda injektionspennor innehållande 0,15 ml (7,5 mg), 0,2 ml (10 mg), 0,25 ml (12,5 mg), 0,3 ml (15 mg), 0,35 ml (17,5 mg), 0,4 ml (20 mg), 0,45 ml (22,5 mg), 0,5 ml (25 mg), 0,55 ml (27,5 mg) eller 0,6 ml (30 mg) lösning finns i förpackningar med 1, 2, 4, 5, 6, 10, 11, 12, 14, 15 och 24 förfyllda injektionspennor. Spritsuddar ingår i förpackningen. Eventuellt kommer inte alla förpackningsstorlekar att marknadsföras. Metojectpen® ingår i förmånssystemet. ATC-kod: L01BA01. Datum för översyn av produktresumé: 2013-08-22. För fullständig produktinformation och priser hänvisas till www.fass.se Medac Box 120, 432 23 Varberg Tel: 0340 - 64 54 70 Fax: 0340 - 64 54 79 [email protected] www.medac.se
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