STANLEY S. BERGEN, JR. 1960;22:144-150 doi: 10.1161/01.CIR.22.1.144

Pericardial Effusion, a Manifestation of Systemic Lupus Erythematosus
STANLEY S. BERGEN, JR.
Circulation. 1960;22:144-150
doi: 10.1161/01.CIR.22.1.144
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1960 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7322. Online ISSN: 1524-4539
The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://circ.ahajournals.org/content/22/1/144
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles
originally published in Circulation can be obtained via RightsLink, a service of the Copyright
Clearance Center, not the Editorial Office. Once the online version of the published article for
which permission is being requested is located, click Request Permissions in the middle column of
the Web page under Services. Further information about this process is available in the Permissions
and Rights Question and Answer document.
Reprints: Information about reprints can be found online at:
http://www.lww.com/reprints
Subscriptions: Information about subscribing to Circulation is online at:
http://circ.ahajournals.org//subscriptions/
Downloaded from http://circ.ahajournals.org/ by guest on September 9, 2014
Pericardial Effusion, a Manifestation of
Systemic Lupus Erythematosus
By STANLEY S. BERGEN, JR., M.D.
PERICARDIAL effusion can be a striking
physical and radiologic finding, but its
occurrence as a manifestation of disseminated
lupus erythematosus has not been emphasized.
During the last 2 years 4 patients with systemic lupus erythematosus who had an associated pericardial effusion were seen at this
hospital. Two of this group were misdiagnosed
and treated incorreetly, partly because of failure to consider lupus erythematosus as a cause
of pericardial effusion.
On physical examination he appeared well nourished and in no distress. The blood pressure was
120/80, there was no clubbing, the heart was not
enlarged, the lungs were clear, and the abdomen
contained no masses or enlarged organs. There was
generalized lymph node enlargement and swelling
of all the proximal interphalangeal joints of the
hands.
Laboratory data included a normnal urinalysis,
hemoglobin of 10.1 Gm. per cent, white blood cell
count of 9,900 per mnm.3 with a normal distribution, negative serologic test for syphilis, thymol
turbidity of 9.2 units, serum albumin of 3.4 and
serum globulin of 6.4 Gm. per cent, the electrophoretic pattern showing the gamima globulin to
be over 50 per cent. Latex fixation test was normal; all cultures (sputunm, gastric, and urine) for
tuberculosis were negative, and the bone marrow
was within normal limits with negative LE preparation. A sickle-cell preparation was negative and
an electrocardiogram was within normal limits.
Two of LE preparations done on venous blood
were positive, as was the LE precipitin test. Chest
x-ray disclosed a heart of normal size, calcific left
hilar lymph nodes, and linear strand densities at
the right base and left mid-lung. Skin tests for
Case Reports
Case 1
A 39-year-old Negro cook was admitted to St.
Luke's Hospital with swelling of hands and feet
and left-sided chest pain for 3 months. He stated
that he had been hospitalized for 6 weeks while in
mnilitary service with joint pains and "glandular
enlargement." He had also been hospitalized elsewhere 18 months previously following 3 months of
left anterior chest pain, fever to 104 F., night
sweats, joint pains, and weight loss of 15 pounds.
The hospital record noted generalized lymphadenopathy, a hemoglobin of 11.2 Gin. per cent, electrocardiographic "evidence of pericarditis," and an
enlarged heart compatible with pericardial effusion,
and bilateral pleural thickening. Despite negative
cultures of sputum and gastric aspirate, he was
treated with Isoniazid and streptomycin with apparent improvement. He left the hospital against
advice before therapy was completed. He then felt
well, ;but a year before admission to St. Luke's
hospital he noted intermittent swelling and pain
in the proximal interphalangeal joints.
Four months before hospitalization he had a 6day episode of fever, and a chest x-ray disclosed
peribronchial infiltration, both of which cleared
without specific therapy. Three months before admission an epitrochlear lymph node biopsy revealed
"chronic inflammation." Thereafter he experienced
dyspnea on effort, paroxysmal nocturnal dyspnea,
ankle and hand swelling, joint pain, and "feverish-
blastomyeosis,
coccidioidonmycosis
histoplasmosis,
and lymphogranuloma venereum were negative. The
Mantoux test was positive at 1 :1,000 dilution.
Cardiopulmonary study revealed a defect in
aeration with arterial unsaturation on exercise, reduced vital capacity and minute hyperventilation
at rest, and low bicarbonate serum level. These
findings were believed compatible with pulmonary
fibrosis and an early diffusion block. Lymph node,
skin, and mnuscle biopsies did not reveal any specific
lesions, although perivascular clusters of lymphocytes and plasma cells were noted. Evidence of
tuberculosis or Boeck's sareoid was not seen. Following spontaneous clearing of his chest pain, the
patient was given chloroquine, 250 mg. 3 times a
day, with marked improvement in his joint pain
and swelling.
The patient has been seen in the clinic for the
last 18 months with intermittent exacerbations of
joint pain. LE preparations have been repeatedly
positive and he has required hospital admission on
2 occasions for prednisone therapy for relief of
joint pain and febrile exacerbations. He is at
present doing well on chloroquine and is believed
ness."
From the Department of Medicine, St. Luke's Hios-
pital, New York, N.Y.
144
Circulation, Volume XXII,
Downloaded from http://circ.ahajournals.org/ by guest on September 9, 2014
July
1960
t1\I1 )IA
-PEIIICAI
1~'SI1 N
15
.145-
Figure 1
flfjioc rd(iY)
tffulaion.
IM
Oil
C o
2.
.i
volou/
pcrito itdlot
to hive dissemiiinalted liupus vthetaitosus witl as
p)ilioofina xv fibrosis of mi deterni-ineed etier
sociated
ology.
Case 2
A 2P-vear)-o1(l Negro mierchant seamtam,-in xvlas transferred to St. Luike's hospital forI surgery. He had
s
been ho
ized elsewhxre 39 m-tion-itlhs previously
()pital
following 6 -xveek hI;story of knee, ank1<le, at-nd hand
paint.I)uriang this period the patient hiad also noted
uriaarx
co-ugllh produLcetive of simall
frequenmey atnd
Camimoun0sts of yelloxv nmucoid spuituimn. Five yea rs
earlier thle p}(latient had beeni hospitallized for fex ec
thiat disaIppeavred spontaineously.
On physical examiiination the blood presssure Awas
1,50/90
11910m. lIg, a11d the )atitient ha-id
mnla:rkedlya
I)uffy- facwe \xith
edemna of. thie eyelids. There was
a1 1nicla1hr eruption over hlis forehead, face, and
no,se th.at ha,td ai, "buitter-fly-" distribution. The heart
soullids were quiet, thle healrt seemeid enliared, a-lnd
were
rio murmurs
heard. Bilateral basilar ales
were hiea-rd, and there was edema, of ank-les and
wrists.
Labortaitory datia ine-luded ai negaltixve serologic
test for sy plhilis, tl mviol turbidity of IS units,
hemnoglobin of 'I .9 (Gn. per cent, whiite blood cell
counit of 4,050 per -mnn.3 with. notn-al differenftial
count, serumti. allbumin of 3.2 and seruml. globulin
of 5.1. Giii. prer cent. Ani eleetrocardiogra-m showed
a
low
voltag-e
aind
a.
chest x-rffty
sblowed.
a
large
cardiac silhouette probably duie to p)ericardial effuision, witlh t iriimalblateral pleural effusions. LB
preparations wecre repeatedly positive.
A diagnosis wa,is ii,i.de of systemiic lupiis ery theina tosus tmdthe adret ml ster oid tlerapy- was
started. Veionius pressure at thla.t tim)e was 176 mmni.
of saline nud the a ri -to-tongue circula,tion tilmie
Figure 2
n te)1
o I t/ (')
),
I ?'ff
P,osit i ont
t io) r tOt'
10
of the c /t St If
rmonths ofiti pt ti(lt(f/iott usi inton
c
.
Dveeholin) Nvas -.14 seconds. 2Svpi)toms and p)Ivsilal findings iinprovd duritig thle sUbsequent monthli
the steroid dosag-e wasl., reduced, an.d ehiloroquine
250 mgn-. tw-iice dalilyv was added.
Nexertheless the cardiacie shado-w increased in
1ag"ing Venrlous pressure levels;
size, despite unchat
l
>V
tierefore, r icardiocenit tesis a mdl pericarrabioPS
w\erce reconnmended anid the patient wx as transferred
to St. Luke's hospital xvhere' 1E prepairaItions of
the b)l1oo were agaiin 1o)si-tive, aind an eleetroca(Irdiega reveailed inverted T1 wSxix(vs in leads i, IT,¢aYVI,
and V4 6 A. Angio.ardiogra 111 confirmed the preselee of a p)e'ieardi11 effusioll (0f. 1).
Ani ol)pen
icaihocente^sis and pertielalrdial biopsv were performed ad30 ImL of straw colored
fluid were aspirated tnd (lotted quicklv. All cuTltines a-nd LE-eell p)repara.ltions on this fluid were
nieg atix e. The biops;y showed dense fibr-ous tissue
and ai few scattered lymphocytes. The cliest woi-iiid
dra-iinedl pericardial fluid for about 10 dayvv,s and
theji elosed. The eardiae size retairned towaIrd
iormnall after a few dayvs. The venouis pressure
fell to 70 mm. of wtater, whereas the arm-totonlguIe eircul9ation tilme rematined at 14 seconds.
Follo-win surgerv, the dosag-e of prednisone wasi
graduallyv reduced, aind mi-a:iinten,maee therapPy Awithi
chioroquitie xvas reinstituted. Now, 20 nioiitlis
rlaterl the carm-diac exailmination chest x-ray (fig. 2),
a rid lc trocarXd i og)ram aXre normal. Thei patietnt is
working as a mernerchant sea rman and lie is asymptomatie except for mild joint pain tha,t is responsive
to a spirin.
Case 3
A- 37--vear-old Ne-gro wom.la. watris first addmitte(l
to St. Luke's hospital 31/2 eairs ag-o wvithi muiiltiple
ioint painls. A-t that tinie she had (liscrete a:reas
Circulation, Volunme XXII, July 1600
Downloaded from http://circ.ahajournals.org/ by guest on September 9, 2014
N
146
VR(IEIUEN
4
Figure 3
(fase 3. lRo i/gy a)oqramr of the 7hes t, shlowrilj }aobnd
able phleurr
l perik rrbifl cff
nion)Q.s.
of hIyporpig-neatatiorl oxlo tlle tyIrunk alnd extromities, gy?nerirlized lx rrlradeririinrtlr.x arild %spleeomegaIlv. Pertinent laibora"Itory da.1tai rexel,,ed dopressed blood platelet onnits-, rlxcrsal of the niorrualT album1-iiin 'lobuvlinratio, positrive MTazzini and
KNahn tests, a-ga1tive VDR-rL, .anld positive LE-cell
pr-epatrationi,s;. Oni aspirlin a,ind predriisone all Symptom-s eletared and the blood Plteltet counts re-
turned to norm"aL.
Approximaitely 6 months; laiter sh-ie wras re-admitted to the h10spitall bec.aIuse of s':'evere joint pain.
aqnemiaqn aind thromboeNtoaperria. She improved on
pr-ednisone tand, as the dosagi-e wa:s reduced cliloroquiine was bepinr wvithl illailrtenlaIree of imiprovemrerit.
Dur ing this exacerbation a left pleural effusion
nid a splenic infartet oecurred, both of -wlhieh improved by timne of diselha rge.
A thirid admirssion 1 year Iater was prompted
Jbv ataxia, and eon fusion thait el,-ared -when ehloroqutine wais stopped. Three wxeeslaster she suffered
sevexoe rilit upper abdominal paiin. The temperatin1e was 1O0.S F., the heart seemed enulared, a
prade IT apieal sy stolic iiiilrnnr'mr ivras heard,-and
a tender liver edge was felt below the ri-Igt Costal
imargin. LaJ;bor'a-1to-i'v- studies; showed 4+4 albumrirnuria, hm(lo')'O-bin of 9.6 C0i a. per cent, wbite blood
cell eounit of 7, 00 per} 111r113., seri.,um albuinin of
2.7 and serumur globulin of 4.2 Cn. per eemnt. An
electrocardiogram reve; led low v oltage anid inverted
T in le.aids IT II, aVe, and V1 6' A chest x-ray
wrascorISistelrt with peticar;dia.-,dl effusion and a sma111l
righlt pleural<i1 effusion (fig. 3). Transiently on the
thir d hospifital (day pleural aindpler'icardi:il frictioni
rrmlbs wo-rvle hear d. The corigestix failurle uniprioved
folloixvir, digitaliis and diuretie thlerapyv. An increase in predrris:one dosagqe led to imiproveiment
Figure
l?ocrlryer oryaqiant of hte
of intensive
crles
4
ini exsr-
,?
rrftter 4
weeks
tlrthcrap
joinit p1)irrs, skSin raish, and(I graqdualI resolitiorn
of the ffirsinras orveir a 4--week period (fig. 4). The
pulse pres,sur.e did not f.ll below 20 na-in. of p,1-
of
ior did
t(ile venouspl);l'(ssiire exeeed 170 inm. of
ater4. TThe paitient has not been seen since discha-rge.
Case 4
A 133-yea-old
school girl was a-dmitted to
St. TLuke-'s lospitall -with joilit paiins, fever. a,nd a
diffmrse maculopaplar scalin skin raIsh for 1 week
foIOillo'f a s;ore tlr'at. Phxsical examin"ation revea1led tavelveairdifr of 120, ai irade TT, aipieal systolie hiea1r4t n11rnrinr11q, ar1d mlltiple wTarm, tender,
swx ollen. slimlrtlvcl thematous ioints. Xn electroeai'1dio-r'ar1r1 disclosed tIle Wernekeha,eh phenomenon.
The x'lirito blood eell ,ount wars 5,400 per nim.3,
tie herrroblobii wVas 9 0 GI. per cenlt, and chest
x- "v- reTveanled aii enl'rm'ed nlobul:ar heart eornn'rtqlno w ithl perieaq rld,ial effusion (firr 5).
Tire fatient wu-as believed to have aecute rheinarritic fever wvithi mvoe:arditis, periearditis. and
peric'rm'dirrl effusion. She waqs griven 40 imr. of
redlnisone a daT aiid as she iniproved and her
eleetroeardlionraureinverted toevard norma1l. the doso
was r1m.aduallav redueed. Beeause of the skin ra,sh
and hemnrrtoloic fnding'_s, LE; preparations Were
r positive on many oceasions.
rirde. whliel were
Prednllisoel0 teatri11rent wats eonltinued, hiut the pa tient Tims never' been completelv free of fever and
-joint pairri. Despite intensive theraipy she has exper1ienced 3 ex-aceerbalti.ons of her disease. The periea,-1rdial effusion iezidu,911y resolved over a 3-month
pertiod (fig. 6). Att preselit sIre is fairly well eortralled on moetlh> 1-prednisolone and, ehloroquine buLt
retainis ani e xt\tre1ie "Cushiin-oid" appearance.
Circulation, Volume XXII. July 1960
Downloaded from http://circ.ahajournals.org/ by guest on September 9, 2014
IPERLCA1I1)1A.I EFFUSIUON
147
LE
il
:_AE
A'8
Figure 5
Posterooertrior root/Ify/i ooroln o(f the chest in ctO-Ise
i, s/tol-ing Ce liircjnirnf Of it toe ubhoorfte.
Figure 6
JPosteront eriot lroci
o idgi -nor l l Of] thte iles t iii OSf?
4 offter, re(is sio o! f/IC lap
plis tJffbCiflto sus.
Discussion
Ful pia1tiii1ts with cl Jei(ecatitdlil effu)sion, as
a major. Illtlnifestation oftluips elmx-theiiatosins
(lisseliiiatiis w elre I>11'0enotnnleed.-I. II 2 inistaiees
slig
te
S ifi-i ea11iee of the efflsiIIo was
1 IIIisiIIter.
yrete(l 8111(1 ill 1 8|1 ilC(Ol'e11ei0diaoiliosis waiS
made. 1lii 1he laltter iistiice, )1i)tpl thlelrcapyv
w7a1s (lelaved f-or 18 iioi-itlis.
Thflt all 4 pat ients w eive Ne,irroes is Hotlwortly, s1ilnee less thani 3(0 per eeiit of tlei
genier:al eline p)p)a1t ioI of St. 111ke s liosp|li
tal is -Negro. That 2 ol' the paltieiits ale 11ei is
also strikingy. 'r51wo of the (ri oup) .1W doiltig welI
Cati1d the thir(d hias beeni reporited to he flee of
conimplaiitis witlimut iiiediceitiiiis. ()ily the
Y iiiest i)atieit seeustis to he doilomg. poorly;
ill lher (c/se sile effects oh ftieil)py uel povingI
as (lifficult .1s Ile (1 iswase.
Mlany of the e inle(al and laboratorl inani
festatiois of 1lipIs; ervthiemlfat)sus wer-e seen
iin these ptatieits. No eorielatioii of svmi])tolis,
plhysieal fitlitnins, otr al boratotrv tests won (1l
predict the (,leYel)lileiit of p)(eiea1 dial effasioil. The usual phisieal fiiiiliuigs i1l(1 electr-o
cardiograplie evidleiiee of periiear dial disease
Were p)reselit hut wele sinilal to filnilidins ill
i etiologyv.
periCarditis and efflIsioi I of am
(l-rist'Iaii rejoil edi a syii(dltoIIie thcat ineluded
inflaiillamatimii ol'ser1ons
iebtiiibres, and the
samlle year Beli.
}h lKleimpei er, and Schifri1:i
noted the association of a diffuse vcaseular
disease; Awith lupu
1 s eryithelliatosus.
Jarehol reit erat ed that lnlns eryItelicatosus
Wa s a g'eliiel'a lied vasculfar disease aid r-e
l)orted 1 (ease of loeulatedi periearlial effius-ioiil
aid another cease Awith pericardial adhiesioiis. lin 1938 acutte (issenlnli-ated lupus etheniat.osuis Aas replorted in 2 piatients Awho bad
livdopeieadnu.
Contratto and Levine
in 19389, reported a ease ol' aeute 1u1us erv-
Review of Literature
lfii 1924 1ih)mairi and Sacks1 described the
\valvular and eidocaidial iuaiiifestai ionls of
IllpilScse rthlemiatoslis. El('e've1 yea ils I a tI e
theniatosus with a piericardial fr-iction rub and
i}erieardial flnidt. Jhe\ iioted tlhe sinilaritv of
their case to eases oiluaculte rhennatlie e'ver,
iiue1](-]udligr aprolto-ed l1P-4 interval. Thl associatioii of -ver-rueoius eiudoe,ar(Iiti.s aid I)ericar(Ill ilnid iii ae
]merytheniatosus was
By lount ami-l 11carrett in 1.945.
deseribed bNKlelJerer, PO11l(a,l;c aI(n htai1t reviewed
35 eases of dissemintted hi pus eryilieniat osns
aild eoneluded tialt the (diffulse (eoniiee(tive
tissine lesion and its progri essive degenerative
iatnre wvere iiidieadive of a sensitivity ieaetioii. TIis idea reeeirxed su)pp)ort fromi a repIort xy Fox'1 of a patient wiho received ut
tetaiilus seruiii a1m1(1 developed 1111)1,; erytheiiai osiIs.
l
otll(her5]
'
asSociatiol
reports111
wtis
iiotedl
(tallerg-ieo recaetiols ;iiid perioardia)l ablioiial-
(ircufatior, Voiunuc XXJI, July 1960
Downloaded from http://circ.ahajournals.org/ by guest on September 9, 2014
148
BERGEN
ities, both clinically11 12 and experimentally.13
This hypothesis has been further developed by
Dameshek,14 who referred to systemic lupus
erythematosus as "a complex auto-immune
disorder. "
Kleniperer et al.9 noted the frequent occurrenee of fibrinous pericarditis in lupus erythematosus, and a few years later Aegerter and
Longl' called attention to the multiple mesenehymal lesioiis and serous effusions of the collagen diseases. In 1949 Curtis and Horne6
described what they believed were the first
reported cases of lupus erythematosus with
pericardial effusion as the main manifestation.
One of their 2 patients underwent repeated
pericardiocentesis for relief.
Recently there have been many reports of
pericarditis as a manifestation of lupus erythematosus,17-24 with the incidence varyinig
from 1823 to 50 per cent.24 23 Acute pericardial effusion has been noted less frequently, 18 20, 22, 23, 23-27 with an incidence of
826 to 18 per cent.23 Most of the effusions were
small, but occasionally were massive.20 22 23,
25, 28, 29 Pericarditis has also been noted in
discoid lupus.30 Harvey et al.28 emphasized
that pericardial involvement usually occurs
during an acute exacerbation of the illness.
The most common manifestation of pericardial involvement seems to be pericardial
rub7 22, 23, 25-28, 31, 32 with chest pain,22, 25, 28, 32
gallop,28'
electrocardiographic changes,7 8,
16, 22, 23, 25, 28, 32
failure,28'
cardiomegaly,16' 25, 33 cardiae
and arrhythmias28 also being
noted. In most cases of lupus erythematosus
adhesive fibrinous pericarditis is found
31, 33
at autopsy7' 8, 9, 16, 17, 19, 23, 27, 29, 34, 35 although
Harvey et al.28 reported 2 cases of purulent
pericarditis. No inistance of constrictive
pericarditis has been reported thus far 25, 28
but tamponade has been noted.'6 22 23. 25 The
fluid does not have any special characteristic22' 25 and has been variously described as
turbid,5 34 serosanguineous,28' 29 clear brown,7
and clear, pale yellow.'6 The amount varies
from a few cubic centimeters3' 36 to 3 liters,24
with some cases requiring pericardiocentesis
for relief.'16 23, 24, 32 In at least 3 cases typical
LE cells have been demonstrated in the pericardial fluid.22' 32, 37
Radiologic reviews of the x-ray manifestations of lupus erythematosus usually mentionl
pericardial effusions.20 38 The differentiation
between acute cardiac dilatation and pericardial effusion is often difficult and is frequently
0
resolved only by angiocardiography.20
Pericardial biopsy may also be helpful.41-44
It is well known that lupus erythematosus is
rare in men,'4' 28 and at one time it was felt
to be rare in non-Caucasian races.28 An incidence in Negroes in larger series26 belies this
impression aind is close to the incidence of
Negroes in the gemmeral population.45 Of the
5 case reports of lupus in the male
Negro4 27, 34, 36 (as is true of the 2 Negro men
in this report) pericardial involvement with
effusions of various quantities was present in
all.
The occurrence of false-positive serologic
tests for syphilis, as noted in case 3 of this
group, has been well doeunlented in from 1526
to 44 per cent45 of patients with lupus
erythematosus. The treponerna pallidum immobilization test can be used for differentiation from actual syphilis if necessary.46
Since 3 of the 4 cases in this report were
initially misdiagnosed and 2 were incorrectly
treated, a greater awareness of pericardial effusion as a possible manifestation of lupus
erythematosus may be needed. McKusick and
Harvey25 and McCuiston and Moser22 have
suggested that many so-called idiopathic or
nonspecific cases of pericarditis are actually
cases of lupus erythematosus. In many reports
idiopathic pericarditis is considered a sensitivitv47' 48 or immune reaction.49 If this possibility is kept in mind, a greater effort to secure
tissue or bacteriologic proof is iieeded before
pericarditis is arbitrarily considered to be
idiopathic, viral, or tuberculous in origin. A
recent review22 reveals the similarities and
dissimilarities between idiopathic pericarditis
amid the pericarditis of lupus erythematosus.
Awareness of urinary, hematologic, skin, and
sernum protein changes will help in the differentiation of these 2 types of pericarditis. Angiocardiography, pericardiocentesis, and periCirculation, Volume XXII, July 1960
Downloaded from http://circ.ahajournals.org/ by guest on September 9, 2014
PERICARDIAL EFFUSION
cardial biopsy may aid in making the correct
diagnosis.
Medically, the treatment of choice is administration of the adrenal steroid hormones'8, 31, 32 with whatever maintenance dosage is needed to avoid recurrence. Surgicallv,
pericardiocentesis may prevent tamponade,
and in refractory cases, such as case 1, actual
open drainage or pericardiopexy may be useful.3
Summary
Four cases of systemic lupus erythematosuis
with pericardial effusion as a prominent maniifestation are reported. Lack of awareness of
this finding as a not infrequent part of the
disease entity led to misdiagnosis in 2 instances and incorrect treatment in 1. The
literature on the subject is reviewed and suggestions are offered for diagnosis.
Summario in Interlingua
Es reportate quatro casos de systemic lupus erythematose con effusion pericardial como manifestation
prominente. Non-recognition del facto que effusion
pericardial es un elemento non infrequente in le tableau clinic de systemic lupus erythematose esseva le
causa de un misdiagnose in duo del casos e de unI
incorrecte forma de tractamento in un. Le litteratura
concernite con iste thema es revistate. Suggestiones
pro le diagnose es offerite.
References
1. LIBMAN, E., AND SACKS, B.: A hitherto undescribed form of valvular and mural endocarditis. Arch. Int. Med. 33: 701, 1924.
2. CHRISTIAN, H. A.: Long continued fever with
inflammatory changes in serous and synovial
membranes with essential glomerulonephritis:
A clinical syndrome of unknown etiology. M.
Clin. North America 18: 1023, 1935.
3. BAEHR, G., KLEMPERER, P., AND SCHIPRIN, A.:
A diffuse disease of the peripheral circulation (usually associated with lupus erythematosus and endocarditis). Tr. A. Am. Physicians
50: 139, 1935.
4. JARCHO, S.: Lupus erythematosus associated with
visceral vascular lesions. Bull. Johns Hopkins
Hosp. 59: 262, 1936.
5. Case Records of the Massachusetts General Hospital: Case # 24201. Acute disseminated lupus
erythematosus; hydropericardium. New England J. Med. 218: 838, 1938.
6. Case Records of the Massachusetts General Hospital: Case # 24341. Acute disseminated lupus
Circulation, Volume XXII, July 1960
149
7.
8.
9.
10.
11.
erythematosus; hydropericardium. New England J. Med. 219: 273, 1938.
CONTRATTO, A. W., AND LEVINE, S. A.: Acute
lupus erythematosus disseminatus report of
a case. New England J. Med. 221: 602, 1939.
BLOUNT, S. G., JR., AND BARRETT, J. T.: Acute
lupus erythematosus disseminatus: A report of
a case in a male with associated atypical verrucous endocarditis (Libman-Sacks). Ann. Int.
Med. 23: 251, 1945.
KLEMPERER, P., POLLACK, A. D., AND BAEHR, G.:
Pathology of disseminated lupus erythematosus. Arch. Path. 32: 569, 1941.
Fox, R. A.: Disseminated lupus erythematosusan allergic disease. Arch. Path. 36: 311, 1943.
CLARK, E., AND KAPLAN, B. I.: Endocardial, arterial and other mesenchymal alterations associated with serum diseases in man. Arch. Path.
24: 458, 1937.
12. HARKAVY, J.: Vascular allergy. Arch. Int. Med.
67: 709, 1941.
13. WILCOX, H. B., AND ANDRUS, E. C.: Anaphylaxis
in the isolated heart. J. Exper. Med. 67: 169,
1938.
14. DAMESHEK, W.: Systemic lupus erythematosus.
Ann. Int. Med. 48: 707, 1958.
15. AEGERTER, E., AND LONG, J. H.: The collagen
diseases. Am. J. M. Sc. 218: 324, 1949.
16. CURTIS, A. C., AND HORNE, S. F.: Disseminated
lupus erythematosus with pericardial effusion.
Ann. Int. Med. 30: 209, 1949.
17. BAGGENSTOSS, A. H.: Visceral lesions in disseminated lupus erythematosus. Proc. Staff Meet.,
Mlayo Clin. 27: 412, 1952.
18. COHEN, H., AND CADMAN, E. F. B.: The natural
history of lupus erythematosus and its modification by cortisone and corticotrophin (ACTH).
Lancet 2: 305, 1953.
19. GOLD, S. C., AND GowING, N. F. C.: Systemic
lupus erythematosus, a clinical and pathological study. Quart. J. Med. 22: 457, 1953.
20. GOULD, D. M.., AND DAVES, M. L.: A review of
roentgen findings in systemic lupus erythematosus (SLE). Am. J. M. Sc. 235: 596, 1958.
21. MEACHAM, G. C., AND WEISBERGER, A. S.: Unusual manifestations of disseminated lupus
erythematosus. Ann. Int. Med. 43: 143, 1955.
22. MCCUISTON, C. F., AND MOSER, K. M.: Studies
in pericarditis. I. Differentiation of the acute
idiopathic form from that occurring in disseminated lupus. Am. J. Cardiology 4: 42, 1959.
23. SHEARN, M. A., AND PIROFSKY, B.: Disseminated
lupus erythematosus. Arch. Int. Med. 90: 791,
1952.
24. TUMULTY, P. A.: The clinical course of systemic
lupus erythematosus. J.A.M.A. 156: 947, 1954.
25. McKUSICK, V. A., AND HARVEY, A. McG.: Diseases of the pericardium. Advances Int. Med.
7: 157, 1955.
Downloaded from http://circ.ahajournals.org/ by guest on September 9, 2014
BERGEN
150
26. JESSAR, R. A., LAMONT-HAVERS, R. W., AND RAGAN, C.: Natural history of lupus erythematosus disseminatus. Ann. Int. Med. 38: 717, 1953.
27. LINDAU, W.: Subacute disseminated lupus erythematosus in the Negro male. Southern M. J.
46: 1099, 1953.
28. HARvEY, A. McG., SHULMAN, L. E., TUMULTY,
P. A., CONLEY, C. L., AND SCHOENRICH, E. H.:
Systemic lupus erythematosus. Reviews of the
literature and clinical analysis of 138 cases.
Medicine 33: 291, 1954.
29. HILL, L. C.: Systemie lupus erythematosus. Brit.
M. J. 2: 655, 1957.
30. DUBOIS, E. L., AND MARTEL, S.: Discoid lupus
erythematosus: An analysis of its systemic
manifestations. Ann. Int. Med. 44: 482, 1956.
31. HASERICK, J. R.: Modern concepts of systemic
lupus erythematosus: A review of 126 cases.
J. Chron. Dis. 1: 317, 1955.
32. SEAMAN, A. J., AND CHRISTERSON, J. W.: Demonstration of L. E. cells in pericardial fluid.
Report of a case. J.A.M.A. 149: 145, 1952.
33. TAUBENHAUS, M., EISENSTEIN, B., AND PICK, A.:
Cardiovascular manifestations of collagen diseases. Circulation 12: 903, 1955.
34. IRBY, R., HENNIGAR, G. R., AND KIK, J.: Acute
disseminated lupus erythematosus in the Negro
male: Report of a case with autopsy findings.
Ann. Int. Med. 37: 1274, 1952.
35. McGuIRE, J., KOTTE, J. H., AND HELM, R. A.:
Acute pericarditis. Circulation 9: 425, 1954.
36. VESEY, J. M., AND NELSON, H. G.: Acute disseminated lupus erythematosus. Report of the
disease in a Negro male. Ann. Int. Med. 32:
565, 1950.
37. COPELAND, G. D., VON CAPELLER, D., AND STERN,
T. N.: Systenmic lupus erythematosus: A clinical report of 47 cases with pathologic findings
in 18. Am. J. M. Se. 236: 318, 1958.
38. GARLAND, L. H., AND SISSON, M. A.: Roentgen
findings in the "collagen" diseases. Am. J.
Roentgenol. 71: 581, 1954.
39. HOLMAN, C. W., AND STEINBERG, I.: The role of
angiocardiography in the surgical treatment
of massive pericardial effusion. Surg., Gynee.
& Obst. 107: 693, 1958.
40. LEVY, L., FOWLER, R., JACOBs, H., LECKERT, J.,
IRION, J., ROSEN, I., AND CHASTANT, H.: Angiocardiographic confirmation of pericardial effusion. Am. Heart J. 43: 59, 1952.
41. BARR, J. F.: The use of pericardial biopsy in
establishing etiologic diagnosis in acute pericarditis. Arch. Int. Med. 96: 693, 1955.
42. EFFLER, D. B., AND PROUDFIT, W. L.: Pericardial
biopsy role in diagnosis and treatment of
chronic pericarditis. Am. Rev. Tubere. 75: 469,
1957.
43. PROUDFIT, W. L., AND EFFLER, D. B.: Diagnosis
and treatment of cardiac pericarditis by peTicardial biopsy. J.A.M.A. 161: 188, 1956.
44. WEINBERG, M., FELL, E. H., AND LYNFIELD, J.:
Diagnostic biopsy of the pericardium and myocardium. Arch. Surg. 76: 825, 1958.
45. DUBOIS, E. L.: Systemic lupus erythematosus:
Recent advances in its diagnosis and treatment. Ann. Int. Med. 45: 163, 1956.
46. MOORE., J. E., AND LUTZ, W. B.: The natural history of systemic lupus erythematosus: An approach to its study through chronic biologic
false positive reactors. J. Chron. Dis. 1: 297,
1955.
47. BARKER, P. S., AND JOHNSTON, F. D.: Chronic
pericarditis with effusion. Circulation 2: 134,
1950.
48. REID, E. A. S., HUTCHISON, J. L., PRICE, J. D. E.,
AND SMITH, R. L.: Idiopathic pericarditis. Ann.
Int. Med. 45: 88, 1956.
49. LEVY, R. L., AND PATTERSON, M. C.: Acute serofibrinous pericarditis of undetermined cause.
Am. J. Med. 8: 34, 1950.
Symposium on Coronary Heart Disease
To Begin in August 1960 Issue
Circulation, Volume XXII, July 1960
Downloaded from http://circ.ahajournals.org/ by guest on September 9, 2014