ACNE SKIP S- Excess sebum production K-altered keratinization I- inflammation P-Proprionibacterium acnes proliferation and activity EPIDEMIOLOGY Worldwide

orldwide distribution Mild degrees seen at birth (from follicular stimulation by adrenal androgens ;) may continue up to neonatal period Greatest prevalence in adolescent population Starts at puberty, incidence decreases by early 20s, may persists until third decade or beyond Disorder of pilosebaceous unit face chest and back Most frequent in adolescents, may persist to adulthood Self-limiting course but with lifelong sequelae ( atrophic/hypertrophic scarring)

CLINICAL PRESENTATION: Morphologic characteristics-non inflammatory: Comedones : (the primary lesions of acne) -inflammatory Papules, pustules, nodules, cysts Locations- areas rich in sebaceous glands-face, chest, upper back, upper arms Symptoms-usually asymptomatic unless inflamed(tender)

DIFFERENTIAL DIAGNOSIS Acneform erosion Gram negative folliculitis Peri-oral dermatitis Rosacea

COURSE AND PROGNOSIS Flares may occur just before the menses Inflammatory type: atrophic/hypertropic scars

MANAGEMENT Tailoring each patients acne regimen: -knowledge of acne pathogenesis -MOA of the available acne treatments Maximum therapeutic response Local therapy Cleansing: Bid washing with gentle cleanser followed by acne treatment application Avoid alkaline soaps- disrupts cutaneous lipid barrier, compound irritancy potential of many topical acne treatments

MILD ACNE Topical Retinols tretinoin adapaline isotretinoin antibiotics erythromycin clindamycin benzoyl peroxide keratolytics salicylic acid resarcinol sulfur sodium sulfacetamide combination: BEST results Oral- not needed

MODERATELY SEVERE ACNE Topical ( as above) Oral Antibiotics Tetracycline 500 mg OD Doxycycline 100 mg OD Minocycline 100 mg OD Lymecycline 300 mg OD Hormonal Cyproterone acetate with ethinyl estradiol Desogestrel with ethinyl estradiol

SEVERE ACNE Oral isotretinoin 0.5-1.0 mkd Teratogenic Do pregnancy test May cause elevation s in lipid profile, liver function test TG, total cholesterol AST, ALT Risk of pseudotumor cerebri if used withtetracycline Local therapy Intralesional steroid injections (ILSI) Comedone extraction Photodynamic therapy Management of sequelae Pigmentation: bleaching agents, peeling, laser Atrophic scarring: fillers, dermabrasion, laser resurfacing Hypertrophic scarring:ILSI

PREVENTION, PATIENT EDUCATION Correct perceived myths - Acne is not due to poor hygiene - Generally unaffected by the diet Discourage squeezing/ pricking pimples at home

SUSPECT PCOS IN ADOLESCENTS Oligomenorrhea- does not correct within 2 years post menarche Acne vulgaris-persistent, severe or of late onset, premature pubarche Hirsutism Steady weight despite caloric intake

PSORIASIS Epidemiology Etiology Autoimmune T-Cell mediated reaction triggered by still unknown factors Heredity; several susceptible genes found Early onset (type 1 psoriasis) Positive family history HLA-CW6 M=F Start at any age ( peak at 2nd and 5th decades) Flare ups during colder months Less frequent in tropics Tends to improve/temporarily disappear but may flare up after delivery

Pathogenesis Autoimmune T-cell mediated reaction -Over expression of pro-inflammatory TH1 and TH17 cytokines (TH 1, IL-1/2/12,TNF , IL 17) -Inflammation -accelerated epidermopoeisis Trigger factors - Stress - Infection( MC streptococcus or HIV) - Trauma(koebners phenomenon) - Drugs(beta- blockers, lithium, anti- malarias, NSAIDS)

Clinical features: Chronic inflammatory lesion on the skin Classic: Circumscribed erythematous plaques covered with thick, silvery white scales May have permanent itching/burning sensation No permanent cure Involves skin and joints - Skin sites of predilection - Deforming arthritis( extremities and spine) Classically begins as erythematous macules covered with dry silvery scales that extend periperhally, coalesce and become thicker May become annular, lobulated, or gyrated with involution at the center

AUSPITZ SIGN Pinpoint bleeding when a psoriatic scale is forcibly removed Severe thinning of the epidermis over the tips of dermal papillae

KOEBNERS PHENOMENON Appearance of typical lesions of psoriasis at sites of even trivial injuries

PSORIASIS TYPES: A. According to morphology of skin lesions I. Chronic Plaque Type Most common Circumscribed, erythematous, dry plaques covered by silvery white scales

II. Localized pustular type Most common type is palmoplantar Fused putules resemble Lakes of pus Sterile pustules Variant: acrodermatitis continua of Hallopeau ( digits associated with osteolysis)

III. Generalized pustular type (Von Zumbusch) Fever with appearance of skin lesions Erythema in flexures-generalized pustular eruption Lake of pus( periungual, palms, edge of psoriatic plaques) White plaques on mucosa (tongue, mouth) Usually associated with hypocalcemia Maybe triggered by drugs : iodide, coal tar, steroid widrawal,terbinafine, minocycline, hydroxychloroquine, acetazolamide, salicylates Stages: - Exanthematous febrile eruption of pustules - Flare ups of fever and pustules - Continuous fever, erythroderma, cachexia Systemic complications: -pneumonia -CHF -Hepatitis -ARDS

IV. Guttate size of water drops (2-5 mm) acute infection (streptococcal pharyngitis)- abrupt eruption more common in patients under the age of 30

V. Exfoliative dermatitis/ Erythroderma generalized scaling on diffusely erythematous skin no normal skin nor discrete psoriasis plaques maybe accompanied by extropion (eversion of the eyelids)

B. According to location: I. Classic extensor II. Inverse/ Flexural exclusive involvement salmon, red demarcated plaques -eczematized, moist, fissured little scaling Autspitz sign usually negative Napkin psoriasis- usually 2- 8 mos

III. Palmoplantar IV. Nails V. Scalp Most common site of initial involvement Marked prediclection- frontal scalp margin usually no hair loss

D. Psoriatic arthritis Seronegative arthritis Presence of HLA B 27 in nearly half of all patients Sausage shape digits 5 clinical patterns

CO-MORBIDITIES Highly associated with depression Chrons disease Lymphoma

Metabolic syndrome Occurs at higher rate in psoriatic vs. non psoriatic persons Increase risk for DM and atheroscleroticdisease Cluster signs: -obesity (abdominal) -HPN -hyperlipidemia -elevated FBS -pro inflammatory factors (CRP, PAF-1)

DIFFERENTIAL DIAGNOSIS Fungal infections Seborrheic dermatitis Pityriasis rosea Lichen planus Psoriasiform subset of SCLE Contact Dermatitis and dyhidrotic eczema Parapsoriasis and CTCL

Management A. Patient education Nature and course, trigger factors, treatment options and risks Lifestyle modifications to avoid metabolic syndrome B. Screening for comorbidities and appropriate management C. Topical treatment( limited/localized disease) Moisturizers Salicylic acid Keratolytic Widespread dse in pedia group (risk for salicylism) Corticosteroids (topical) Limited quantity/ duration (to avoid atrophy, telangectasias, striae, acne, hirsutism,HPA ax is supression Vit. D Analogs (calcipotriol, calcitriol) Controls keratinocyte proliferation, promotes differeantiation Most common side effect: irritation (face, flexures) Tar Calcineurin inhibitors (Tacrolimus, Pimecrolimus) Malodorous, may stain Free from steroidal side effects, thus safe and effective for facial and flexural

Anthralin Tazarotene

psoriasis Anti-proliferative Irritating( short contact use) may stain Irritating, short contact use

D. Phototherapy (generalized/recalcitrant to topical) Series of controlled exposures to non-ionizing radiation (UV light) to modulate T cell immune mediated reaction Broadband and Narrowband UBV(311 nm wavelength) Psoralen+ UVA (PUVA) Excimer laser therapy targeted at few lesions of localized psoriasis E. Systemic therapy (generalized/recalcitrant to topical) Periodic organ function monitoring required (due to cumulative toxicities) Methotrexate anti- inflammatory & suppresses DNA synthesis Oral DOC for psoriatic arthritis S/E: teratogenicity, hepatotoxicity, bone marrow supression Cyclosporine Immunosuppressive S/E: HPN, Nephrotoxicity Acitretin Anti-proliferative & enhance keratinocyte differentiation S/E teratogenicity, hyperlipidemic, mucocutaneous dryness

Biologic Agents (Ifliximab, Etanercept, Alefacept,Adalimumab, Ustekinumab)

Selectively target a portion of immune reaction leading to psoriasis( thus preventing generalized non selective immunosuppression) May target T- cells or cytokines(TNF) parenteral