Rosacea
Seborrhoeic dermatitis, Acne, Rosacea Éva Remenyik Sebaceous gland follicles • Arnosan’s triangle, i.e. central parts of chest and back, face – predilect. sites of acne • to a lesser extent: arms, neck, abdomen • Genitoanal region Sebum / product of sebaceous glands/: Pale yellow, fluid, viscous mixture of glycerides + fatty acids / 65% squalene / 10 % waxesters / 25 % glycerides free fatty acids (bact.lipases) production: high – after birth and for 3-5 months thereafter low-childhood pronounced – before and during puberty less than normal = asteatosis / atopy, ichthyosis/ more than normal = seborrhea / acne, etc./ Seborrheic dermatitis • papulosquamous disorder • sebum-rich areas • Pityrosporum ovale, l – lipase activity—releasing inflammatory free fatty acids (FFA)— – activate the alternative complement pathway • immunologic abnormalities, and activation of complement. Seborrheic dermatitis • aggravated – – – – changes in humidity, trauma (eg, scratching), seasonal changes, emotional stress. • severity – varies from mild dandruff to exfoliative erythroderma. – may worsen in Parkinson disease and in AIDS. Seborrheic dermatitis • Onset: puberty • Peak 40 years • In infants: cradle cap, flexural eruption or erythroderma Course • Intermittent, active phases: burning, scaling, and itching, alternating with inactive periods. • Increased activity is seen in winter and early spring, with remissions commonly occurring in summer Medication may flare or induce seborrheic dermatitis • auranofin, aurothioglucose, buspirone, chlorpromazine, cimetidine, ethionamide, gold, griseofulvin, haloperidol, interferon alpha, lithium, methoxsalen, methyldopa, phenothiazines, psoralens, stanozolol, thiothixene, and trioxsalen Differencial diagnosis • Asteatotic Eczema Atopic Dermatitis Candidiasis, Cutaneous Contact Dermatitis, Allergic Contact Dermatitis, Irritant Dermatologic Manifestations of Gastrointestinal Disease Dermatomyositis Drug Eruptions Drug-Induced Photosensitivity Erythrasma Extramammary Paget Disease Glucagonoma Syndrome • Impetigo Lichen Simplex Chronicus Lupus Erythematosus, Acute Nummular Dermatitis Pemphigus Erythematosus Pemphigus Foliaceus Perioral Dermatitis Pityriasis Rosea Rosacea Tinea Capitis Tinea Corporis Tinea Cruris Tinea Versicolor Treatment • • • • • Topical corticosteroids ( creams, lotions, or solutions) ketoconazole or naftifine creams. sulfur or sulfonamide Systemic ketoconazole (severe or unresponsive) Topical calcineurin antagositák • Dandruff – Salicylic acid, tar, selenium, sulfur, and zinc in shampoos – oil is especially helpful when widespread scalp plaques are present. Acne vulgaris • Lesions: comedones, papules, pustules, and nodules in a sebaceous distribution. • Localisation: face chest, back, and the upper arms Acne vulgaris • Frequency: 85-100% • Consequence: – can cause physical pain and psychosocial suffering – scarring – Acne fulminans, can be associated with fever, arthritis, and other systemic symptoms. Comedo -- Lesions may be "open" or "closed," depending on the presence of a visible black tip resulting from defective keratinization. Papule/pustule -- Inflammatory lesions that if large or persistent may lead to permanent scarring. Nodule -- A deep inflammation, >5 mm in size, guaranteed to produce a scar. Lesions are erroneously termed "cysts." In reality, they are abscesses with no cyst wall present. Conglobate lesions -- Grouped nodules connected by sinus tracts present in the severest forms of acne. Pathomechanism of acne • Sebum production, sebocyte 5 alpha reductase (testosterondihydrotestosterone) – Androgens ↑ estrogen↓ • Hyperkeratinization (follicular) – Androgens (DHEAS) – IL1alpha • Propionibacterium acnes – Proinlammatory cytokines (IL-12, IL-8, TNFa) • Inflammation – Primary or secondary Patomechanizmus Genetikai faktorok Környezeti tényezők androgének Faggyútermelés lipidek Folliculáris keratinizáció citokinek Propionibacterium acnes Gyulladás IgG, lipáz, ROS, kemotaktikus faktorok Citokinek,TLR Clinical findings • primary noninflammatory lesions closed (whitehead) and open (blackhead) comedones • secondary inflammatory lesions papules pustules nodules abscesses • postinflammatory lesions cysts – scars (atrophic, keloidal) Causes: • cosmetic agents, hair pomades • medications: – steroids, lithium, some antiepileptics, and iodides. • endocrine disorders with excess androgens – Congenital adrenal hyperplasia, polycystic ovary syndrome, • genetic factors Clinical Variants of acne Clinical Findings Comments Diagnosis to Consider Erythematous papules and pustules on face of neonate without comedones Neonatal acne May be due to Pityrosporum folliculitis, resolves in days to weeks Inflamed papules and pustules starting 3-6 mo after birth Infantile acne Attributed to early gonadal and adrenal secretion of androgens, especially in boys; may last to age 5; may herald later severe acne Persistent mild acne associated with use of greasy, occlusive cosmetics, sunscreens, or moisturizers Acne cosmetica More common in women Acne associated with use of helmets, shoulder pads, bras, chin rests (e.g., violins) Acne mechanica Suggested by the history and unusual location of skin lesions Typical acne lesions near the hairline; history of applying thick oil to the hair Pomade acne Most common in black women and men Acne associated with ulcers and erosions that heal with scarring; history of picking at the skin Acne excoriee Typically a young woman Large confluent draining nodules and abscesses; severe scarring Acne conglobata A severe scarring form that requires aggressive management An explosive onset of severe widespread nodular lesions with systemic symptoms (e.g., fever, arthralgia, myalgia) Acne fulminans Nodular lesions that contain large quantities of necrotic material may drain, leaving large eroded areas over the face and back; exclusively in males An explosive onset of severe facial nodules and edematous plaques Pyoderma faciale Severe nodular acne occurring exclusively in females, also known as rosacea fulminans Acne associated with drug use Druginduced acne Androgens, corticosteroids, and halogenated medications (e.g., iodides, bromides, lithium, and anticonvulsants) intertiginous areas inversa / = of males a. triad = a. tetrad/ laboratory findings: elevated ESR, leukocytosis Differential diagnosis Clinical Findings Comments Diagnosis to Consider Perifollicular pustules, which may involve unusual sites for acne (e.g., extremities) Folliculitis Usually bacterial; diagnosed by Gram stain and culture of pustules; if Malassezia folliculitis, Gram stain reveals Gram-positive budding yeast Patient on long-term antibiotics develops pustules and nodules at the anterior nares, followed by outward spread on face Gramnegative folliculitis Emergence of antibiotic-resistant bacterial strain; requires switching antibiotics Onset at age >30; history of flushing; erythematous papules, pustules, and telangiectases Rosacea Close exam reveals lack of comedones, the hallmark lesions of acne vulgaris Flat, skin-colored, elevated facial papules Verrucae plana Lack of pustules and comedones helps identify warts Differencial diagnosis Rosacea Pityrosporum folliculitis Perioralis dermatitis Folliculitis Perioralis dermatitis Rosacea Fleshy red papules over the central face Adenoma sebaceum Other skin and central nervous system findings (e.g., seizures) of tuberous sclerosis; lack of comedones and pustules White pinpoint cysts resembling closed comedones on the face Milia Usually around the eyes; not associated with other acne lesions Erythematous, inflamed papules on chin and cheeks; history of longterm use of topical fluorinated corticosteroids on face Perioral dermatitis Periocular lesions may occur concurrently Closed comedones and nodules; history of exposure to halogenated hydrocarbons Chloracne A sensitive indicator of systemic toxicity Inflamed nodules in the axilla and groin with draining sinus tracts Hidradenitis suppurativa Diagnosis suggested by old scars or sinus tracts and sterile cultures Numerous open and closed comedones around the eyes of an elderly person FavreRacouchot disease Most common in men who worked outside for many years; attributed to cumulative sun Differencal diagnosis Cysts (epidermal, trichilemmal) Milia Verruca plana Hydradenitis suppurativa Favre-Racouchot Adenoma sebaceum Consequence – physical pain and psychosocial suffering – Scarring, pigmentation – Acne fulminans, can be associated with fever, arthritis, and other systemic symptoms Treatment Drug Dosage Special considerations Apply to affected area once or twice a day, usually after washing Few side effects, but resistance to erythromycin and clindamycin is becoming a problem Benzoyl peroxide, erythromycin, and clindamycin available in less expensive generic formulations Benzoyl peroxide bleaches clothing and bedding Topical agents Antibiotics Erythromycin Clindamycin topical solution, gel, or lotion Sodium sulfacetamide (Klaron) lotion Benzoyl peroxide Topical therapy Antibiotics Comedolytic agents Azelaic acid (Azelex) cream Retinoids Tretinoin (Retin-A,Avita) cream, gel, microgel, or solution (0.01%-0.1%) Apply twice daily Apply nightly; often used with benzoyl peroxide or an antibiotic Dryness or irritation common; patients may worsen initially; not photosensitizing Skin irritation and photosensitivity are main adverse effects; oxidized if used at the same time as benzyl peroxide; microgel (slow-release) formulation less irritating Adapalene (Differin) gel or Apply twice daily cream Less irritation than with tretinoin or tazarotene; unlike tretinoin; sun precautions as with tretinoin Tazarotene (Tazorac) gel or cream (0.1%) Often quite irritating Apply nightly Antibacterial agent combinations Benzoyl peroxide and erythromycin(Benzamycin) Apply once Effects are synergistic; must be or twice daily refrigerated to retain potency Benzoyl peroxide and clindamycin (BenzaClin) Apply once Must be refrigerated to retain or twice daily potency Benzoyl peroxide with zinc and glycolic acid (Triaz 6% and 10% gels) Apply nightly Oral antibiotics Minocycline (Minocin,Dynaci n) 50, 75, or 100 mg b.i.d. Highly effective, but expensive; early and late severe hypersensitivity reactions, lupus-like syndromes and hepatitis; reversible pigmentation of the skin; irreversible tooth staining with long-term use Tetracycline (Sumycin) 250-500 mg b.i.d. Inexpensive (generic), but compliance a problem because must be taken on an empty stomach to be absorbed Doxycycline (Monodox) 50-100 mg b.i.d. Inexpensive (generic), well tolerated, but is often photosensitizing Erythromycin (PCE and E.E.S.) 250-500 mg b.i.d. (taken with food to reduce GI symptoms) Inexpensive (generic); stomach cramps, diarrhea common, so compliance often poor; bacteria may become resistant Oral hormonal Contraceptives Diane-35 Estrogen Cyproteron acetate Retinoids Isotretinoin 0.5 to 2 mg/kg/day for 4-6 mo (Accutane) Side effects: Teratogenic Mucocutaneous dryness Hyperlipidaemy Arthralgy Liver funciton abnormalities . cumulative dose of 120150 mg/kg Procedural treatments • manual extraction of comedones and intralesional steroid injections. • superficial peels • Phototherapy – red light – blue light – photodynamic therapy • laser treatments Terapeutic steps in acne Primary lesions Forms Mild comedonica papulopustulosa Moderate papulopustulosa Sevre congloblt Teratment Comedo Papula, pustula Heg L BPO L Ret L AB Sz Antiandrogén Sz AB Sz Ret +++ + - ++++ ++++ - +/- - - ++ + - ++++ ++++ ++ +/- + - + ++ - ++++ ++++ ++++ ++ ++ - + +++ + ++++ ++++ +/- ++++ ++++ ++ + + ++++ ++++ +++ ++++ ++++ - ++++ - +/- +/++++ femal ++++ ++++ Rosacea • facial flushing • spectrum of clinical signs, – – – – erythema, (transient, permanent) telangiectasia, coarseness of skin, inflammatory papulopustular eruption resembling acne – no comedones, blepharitis, conjunctivitis – rhinopyhyma: sebaceous gland and connective tissue hyperplasia / bulbous livid-red nose of males/ • central flush/blush areas of the face (ie, forehead, nose, cheeks, chin), – ocular disease and extrafacial • Vascular lability, manifested clinically as intermittent facial flushing, Pathogenesis no definite causative factors • genetic disposition • relationship to systemic diseases / stomach, gut, cholecystopathia, hypertension, etc./ • triggers: – Dietary (eg, hot drinks, alcohol, spicy foods) – environmental triggers (eg, sunlight, temperature changes) Pathomechanism • UV light • Demodex • Innate immunity • Vascular • ROS K. Yamasaki, R.L. Gallo / Journal of Dermatological Science 55 (2009) 77–81 differential diagnosis • • • • • • • • acne vulgaris /comedones/ perioral dermatitis /no telangiect./ boils /solitary/ drug eruptions /widespread/ seborrheic dermatitis /pustules cammon/ rosacea like tuberculid /histology/ LE PLE Treatment topical • metronidazole • Topical keratolytics (eg, benzoyl peroxide, azelaic acid) • shake lotion /sulfur, tetracycline, erythromycin/ • never: steorids! • sun protection • diathermy needle /telangiect./ • surgery /rhinopyma/ Treatment systemic • Systemic antibiotic (Erythema responds poorly.) – tetracycline (250 mg daily to 500 mg) – metronidazole – erythromycin 500 mg bid, – minocycline 50-100 mg, – doxycycline 50-100 mg daily to bid. • Retinoid- isotretinoid • Short course of steroid Perioral dermatitis • Gender: women (The vast majority of patients are aged 20-45 years. ) • Skin lesions: - grouped follicular reddish papules, - papulovesicles, and papulopustules on an erythematous base with a possible confluent aspect - mainly in perioral locations Causes • Drugs: abuse topical steroid • Cosmetics: Fluorinated toothpaste; skin care ointments and creams, especially those with a petrolatum or paraffin base, and the vehicle isopropyl myristate. • Physical factors: UV light, heat, and wind worsen POD. • Microbiologic factors: bacteria, Candida species, Their presence has no clear clinical relevance. • Miscellaneous factors: Hormonal factors. Oral contraceptives. Gastrointestinal disturbances. Treatment • Antiacne drugs • Zero-therapy – initial worsening of the symptoms may occur with treatment
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