Dermatology

Acquired immune deficiency syndrome (AIDS)

Def: severe irreversible acquired defect in cell-mediated immunity
susceptibility of affected individuals to opportunistic infections & uncommon tumors as Kaposi sarcoma.

Causative agent: human immune deficiency virus (HIV), a retrovirus. Pathogenesis:

-HIV is a sexually transmitted retrovirus. -Its reproduction depends on reverse transcriptase enzyme (RTase). -RTase allows HIV to make a DNA copy of its genome which will be integrated into host cell genetic material. -Division of host cell production of viral copies permanent infection. -HIV attacks T-helper cells its gradual depletion immune deficiency.

Mode of transmission:
-HIV has been detected in blood, semen, cervical & vaginal secretions. -HIV may be found in saliva & tears in small proportion. -Transmission routes: 1-Sexual intercourse: especially with infected homosexuals. 2-Blood & blood product recipients: especially in hemophiliacs. 3-Contaminated syringes & needles: especially in IV drug abusers. 4-Transplacental transmission (mother-to-fetus).

Incubation period:
-about 29 months for adults & 12 months for children. -virus can lie dormant in individual for 5 yrs before producing S. -IP is shorter among cases infected through blood transfusion.

Risk groups:
1-Heterosexual partners of AIDS patients.
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2-Homosexual or bisexual men. 3-IV drug abusers sharing hypodermic needles. 4-Hemophiliacs who have received infected blood products. 5-Infants born to AIDS parents.

Clinical picture:
-Within a period of 2-5 yrs, 2-15% of infected subjects develop AIDS, 23-26% develop AIDS-related complex, 60-70% symptom-free. -Clinical spectrum: 1-Positive individual may remain well but the virus replicates. 2-Persistent generalized Lymphadenopathy (PGL) with no constitutional symptoms. 3-AIDS-related complex: PGL with constitutional symptoms, no tumors or opportunistic infections. 4-Prodromal AIDS: -constitutional illness with serious opportunistic infections. -acute clinical syndrome may develop (fever, night sweats, myalgia, headache, PGL) -usually resolve within 1-2 wks without TTT, of Pts progress to AIDS in 4 months. -Clinical manifestations: 1-Severe persistent fatigue for several wks with unknown cause. 2-Bilateral LNs enlargement usually in cervical, axillary & inguinal regions. 3-Persistent fever or night sweats for several wks (CMV, TB, or atypical pneumonia). 4-Pulmonary: persistent shortness of breath, nonproductive cough, finally pneumonia. 5-GIT: the commonest presentation: -severe extensive oral or esophageal candidiasis. -severe diarrhea. -progressive wasting & cachexia occur over many months.

-genital or perianal herpes simplex lesions that can produce deep ulcerations. 6-Skin: -Kaposi sarcoma: may present as multiple painless purple skin plaques or nodules, few mm in diameter.
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-generalized pruritic dermatitis.

-recurrent herpes zoster.

-seborrheic dermatitis.

-progressive disseminated herpes simplex. -generalized fungal infections & candidiasis. 7-Nervous: occur in 30% of AIDS Pts -lethargy, depression, later on dementia. -Cryptococcal meningitis: has gradual onset with FHMA. 8-Tumors: -Kaposi sarcoma: can occur in any part of the body, commonly affecting GIT. -cerebral lymphomas may occur. -optic retinitis may occur. -folliculitis & eczema.

-lymphoma may present as Lymphadenopathy systemic symptoms. 9-Prolonged unexplained fever may occur especially in central Africa. 10-Uncommon manifestations: -Hepatosplenomegaly. -interstitial pneumonia. -Lymphadenopathy.

-super infection with some bacteria as streptococci, staph epidermidis, E.coli. N.B. death usually occurs within 2 yrs from uncontrolled opportunistic infections or less often from widespread malignancies.

WHO diagnostic criteria of AIDS:

-AIDS in adults is diagnosed by at least 2 major signs + at least 1 minor sign in the absence of other causes of immune suppression as cancer. I-In adults: 1-Major signs: -wt loss > 10% of body wt. -chronic diarrhea > 1 month.

-prolonged fever > 1 month (intermittent or continuous). 2-Minor signs: -persistent cough > 1 month. -recurrent herpes zoster. -generalized pruritic dermatitis.

-oropharyngeal candidiasis.

-chronic progressive & disseminated herpes simplex infection. -generalized Lymphadenopathy.

N.B. The presence of Kaposi sarcoma or cryptococcal meningitis are sufficient for diagnosis. II-In children: like adults + -repeated common infections. -slow growth. -confirmed maternal HIV infection.

Lab investigations:
A-Serological: 1-ELISA: -easy very sensitive screening test commonly used. -occasionally false +ve in pregnant women & liver diseases. -should be repeated for confirmation of diagnosis. 2-Western blot technique: -the most specific test to detect HIV antibodies against P24 & P41 antigens of HIV. 3-Indirect immunoflurescence assay IFA: very sensitive but very expensive test. B-Others: (CBC) 1-Lymphopenia. 2- platelet count. 3- T-helper cells.

4- T-helper/T-suppressor ratio: normally 1.5-2, in AIDS may reach < 0.5.

Markers of HIV infections:

1-Clinical markers: -unexplained fever. -wt loss. -generalized Lymphadenopathy.

-oropharyngeal candidiasis. 2-Lab markers: -inverted CD4/CD8 ratio.

-oral hairy leukoplakia.

-pancytopenia.

TTT of AIDS:
1-Symptomatic TTT. 3-Emotional support. 4-Kaposi sarcoma: -immune-modulating therapy with alpha interferon. -cytotoxic drugs as vinblastine & pentamidine. -drugs should be given in high doses & for prolonged periods. 2-TTT of infections by effective antibiotics.

5-Replacement of factors known to be produced by T4 lymphocytes as IL-2, gamma interferon. 6-Antiviral drugs: Reverse transcriptase inhibitors: as zidovudine prevent viral replication prolonging & improving life quality. Protease inhibitors: as Saquinavir, Ritonavir, Indinavir.

Prevention:
1-Health education. 2-Serological testing of donors blood & human organs before used. 3-Blood transfusions are ordered for Pts only when necessary. 4-Avoid sharing of needles & syringes. 5-Cleaning & disinfecting contaminated surfaces & articles: by -water & soap. -detergents. -1% Na hypochlorite. -25% ethanol.

-2% glutaldehyde solution freshly prepared for 10-15 min. 6-Vaccination: still under research.

Warts (verruca)
General aspects:
-Causative agent: human papilloma virus. -affect any age, may persist in latent form. -IP: few wks to 1 year. -transmission by direct contact or indirect.

Precipitating factors:
-skin abrasion. -swimming pool. -shaving. -sexual contact.

-occupational handlers of meat.

Clinical picture:
1-Verruca vulgaris: the commonest -size: from 1 mm to several cm. -description: symptomless skin-colored or brown papule with rough irregular surface.
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-site: on hands or fingers or any site. -Koebner phenomenon: new warts may form at the site of trauma. -complications: pain & tenderness may occur if warts are under pressure or infected. -fate: 65% of warts disappear spontaneously within 2 yrs. 2-Plane warts (verruca plana): -flat slightly elevated skin-colored or pigmented papules. -site: face, dorsum of the hands, Koebner phenomenon is common. 3-Plantar warts (verruca plantaris): -well-defined, rounded with rough keratotic surface surrounded by smooth collar of thickened horn. -there is abrupt separation between wart & skin around. -site: heel, toes, metatarsal heads. -types: single, small satellite warts, mosaic warts. -pain is common. -DD from callosity.

-callosity: has smooth surface with epidermal ridges continuous over it without interruption. 4-Filiform & digitate warts: -site: face, neck, scalp. -small long elongated or cylindrical papules or digit-like processes. 5-Anogenital warts (condyloma accuminata): -soft, pink, elongated or pedunculated papules. -may cause discomfort, discharge, bleeding. -pregnancy enhances their growth. -large masses may form on vulva. -usually multiple, asymptomatic.

-complications: malignant enlargement, recurrence, laryngeal papillomatosis at birth. -DD: from condyloma lata of 2ry syphilis (table p.38).

Treatment:
1-Warts may resolve spontaneously. 2-Chemical cautery: using -salicylic acid. -adhesive plaster 40% salicylic acid in plantar warts.

-podophyllin 25%, podophyllotoxin 5% in tincture benzoin in condyloma accuminata (not in pregnancy) applied weekly, should be washed after 4 hours. 3-Cryotherapy. 4-Electrocautery. 5-Laser.

6-For extensive warts: -intra-lesion injection of bleomycin or interferon. -retinoid in immune-suppressed patients.

Scabies
Def: parasitic skin disease caused by sarcoptes scabiei
night itching & multiform lesions

Etiology & pathogenesis:

-Female mite penetrates into stratum corneum, lays 2-3 eggs/day over 4-6 wks before death. -Eggs hatch in 3-4 days larvae maturation after 2 wks. -After copulation, male dies & female excavates burrow. -Skin reacts to parasite, its ova & excreta skin lesions.

Transmission:
1-Direct contact: hands, sexually transmitted. 2-Indirect: clothes, towels, bedding.

Clinical picture:
1-Night itching: due to nocturnal habit of parasites, warmth activates parasites & Pt is alert to himself at night. 2-Distribution of lesions: (delicate skin) -inter-digital spaces. -abdominal. -axilla. -periumbilical. -flexor aspect of forearm. -nipples. -male external genitalia.
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3-Initial lesion: -burrow.

-irregular beaded line. -nodules. -crusts.

-inflammatory papules.

-scratch marks. 4-Secondary lesions: -pustules.

-eczema.

Clinical types:
1-Classical scabies: as described before. 2-Infantile scabies: -pathognomonic sites: hands & feet. -vesicles & bullae may present. -generalized lesions all over the body.

3-Animal scabies: -transmission from cats, dogs & rabbits. -lesions are localized to forearms & legs. -no burrow.

4-Second attack scabies: short incubation period & fewer skin lesions than classical type. 5-Norwegian scabies: -heavy infestations by millions of sarcoptes scabiei in immunocompromised Pts, severe neurological diseases, debilitating diseases & mentally retarded. -warty crusts on elbows, palomplantar keratoderm, nail dystrophy ,mild or no itching, generalized erythema & scaling.

Diagnosis:
1-Clinical: -history of night itching, positive family history. -examination: burrow & multiform lesions on delicate skin. 2-Investigations: -scrapping from burrow on glass slide + 10% KOH or mineral oil microscopic exam.

Differential diagnosis:
1-Papular urticaria. 2-Drug eruption. 3-Chicken pox. 4-Pediculosis. 5-Prurigo.

Treatment:
1-General instructions: -TTT of affected members & animals. -daily hot shower with scrubbing. -disinfection of clothes & bedding.

2-Local TTT: -sulphur 5-10% on 4 successive days. -benzyl benzoate 25-30% for 3 successive d.

-gamma benzene hexachloride 1% single application (CI in pregnant, children). -crotamiton 10% for several applications (weak). -permethrin 5% single application. -malathion 0.5% on 2 successive days.

-monosulfiram 25% solution on 2-3 successive days. 3-Systemic TTT: -Antihistamines. 4-TTT of children: -diluted benzyl benzoate with 2-3 parts water. -permethrin cream or lotion 5%. -sulphur 5%. -Antibiotics. -Ivermectin: tablet = 6 mg/30 kg single dose.

5-TTT of pregnant: sulphur 5-10%.

Pediculosis
Def: severe pruritic skin reaction to bites of insect pediculi. Transmission: head caps, combs, towels, bed linen, clothes, direct contact, STD. Types: 1-Pediculosis capitis. Clinical picture:
1-Pediculosis capitis: -itching, scratching, excoriations. -occipital lymphadenitis. -2ry impetigo. 2-Pediculosis corporis. 3-Pediculosis pubis.

-nits & insects on scalp hair.

2-Pediculosis corporis: -itching, scratching marks, 2ry bacterial infection. -nits & insects on body hair & clothes. 3-Pediculosis pubis: -itching & scratching marks. -nits & insects on pubic or axillary hair or eye lashes. -skin pigmentation.

Diagnosis:
1-Clinical: -history of itching. -examination: see before.

2-Investigations: usually not needed.

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DD:
1-Scabies. 2-Flea bites. 3-Bed bug infestations. 4-Impetigo. 5-Lichen planus.

TTT:
1-Pediculosis capitis: -shaving or cutting hair. -frequent hair washing. -TTT of 2ry infection.

-hair disinfection by: permethrin 1% for 10 min the rinsed with water. benzyl benzoate 20% for 12 hrs then rinsed. (repeated weekly for 3 weeks)

2-Pediculosis corporis & pubis: -shaving of body or pubic hair. -local anti-scabies drugs. 3-Eye lashes (pubis): -cutting of eye lashes. -remove nits & insects by forceps. -systemic Ivermectin. -disinfection & boiling of clothes & bed linen. -systemic Ivermectin.

-local anti-pruritic.

-mercury ointment application for eye lashes.

Acne vulgaris
Def:
-chronic inflammatory disease of pilosebaceous units. -characterized by formation of comedones, papules, pustules, nodules, cysts & scars. -usually starts in adolescence. -frequently resolves in mid-twenties.

Etiology: many factors play a role in pathogenesis of acne

1-Genetic factors: -positive family history of acne in 50% of cases. -may play a role in occurrence of acne, its type, course & severity. 2-Hormonal factors: -Androgens are the only stimulus of sebaceous glands.
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-no in serum androgens in acne Pts. -there is evidence of responsiveness of sebaceous glands to dihydrotestosterone. 3-Bacterial factor: -Acne is not infectious. -organisms isolated from ducts of acne Pts are: Propionibacterium acne, Staph epidermidis, Malassezia furfur. -seborrhea activity of P. acne via secretion of inflammatory mediators (lipase, proteases) ductal hypercornification & obstruction comedone formation. 4-Other factors: -Diet: no link between acne & CHO, lipids or chocolates. -Menses: acne flares pre-menstrual in 70% of females. -Sweating: worsens acne in 15% of cases. -UV irradiation: UV rays of sunlight often improves acne while artificial UV may enhance comedones formation. -Stress: may aggravate acne. -Drugs: steroids, testosterone, iodides.

-Occupation: humidity may aggravate acne. Pts dealing with oils may develop acneform oil folliculitis.

Pathogenesis:
-The factors mentioned above contribute in acne formation. -DHT stimulates S.G. sebum secretion (good bacterial medium). -Bacteria present in S.G. produce lipase hydrolysis of TGs in the sebum into free fatty acids (irritant, produces ductal hyperkeratosis & obstruction) comedone formation. -Bacteria also produces proteases (inflammatory mediators & chemotactic) with attraction of polymorphs & pus formation.

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Clinical picture:
-Seborrhea is common. -Polymorphic eruption.

1-Non-inflamed lesion (comedone): -keratotic plug blocking orifices of dilated pilosebaceous ducys. -composed of sebum, bacteria, keratinocytes & melanocytes. -may be open (black heads) or closed (white heads) comedones. -Black color is due to melanin not dirt. 2-Inflammatory lesions: -superficial lesions: papules & pustules. -deep lesions: deep pustules & nodules. 3-Atrophic & hypertrophic scars or keloid: -sites of lesions: face, chest, shoulders & upper back. -acne may be classified according to predominant lesion into comedonal, papular, papulopustular, pustular, nodular, cystic & scar. 4-Nodulocystic acne (acne conglobata): -chronic disorder, common in males. -may last up to 40-50 yrs of age.

-CCCs: nodules with sinus formation in-between, polyporous comedones & scarring. -site: face & trunk. 5-Acne fulminans:(rare) -severe cystic acne with highly inflammatory nodules, plaques on chest & back. -fever & leukocytosis are common.

TTT:
A-Topical TTT: 1-Benzoyl peroxide (2.5, 5, 10%): action: antimicrobial, anti-inflammatory & comedolytic. side effects: -irritant (start with low conc.) -bleaches clothes & hair.
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-photoabsorption (used at night)

2-Antibiotics: -action: number & function of P. acne. -less effective on non-inflamed lesions.

-include: a-Erythromycin: 2% alone or with zinc or with benzoyl peroxide. b-Clindamycin 1% solution. 3-Azaleic acid 20%: -action: comedones, number & function of P. acne. -less irritant, used in inflamed & non-inflamed lesions. 4-Retinoids: -include: tretinoin 0.01-0.05 %, isotretinoin 0.05%, adapalene 1%. -action: comedolytic, anti-inflammatory, sebum & ductal hypercornification number & function of P. acne. -side effects: irritant (start with low conc.), photoabsorption (used at night only). 5-Sulphur: -comedolytic but may be comedogenic. -not preferred by Pts due to its smell. B-Systemic therapy: 1-Antibiotics: for at least 6 months Indications: combined with topical therapy in: -moderate & severe acne. -mild acne in depressed Pts.

-patients with scarring (bad cosmetic appearance). -Pts with post-inflammatory pigmentation. Preparations: a-Tetracyclines: drug of choice, 1 gm/day. b-Erythromycin: used in pregnancy & lactation, 1 gm/day. mechanism of action of a, b: -large doses are bacteriostatic. -small doses 500 mg: affect function not number of bacteria. side effects of tetracyclines: -GIT upset.
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-vaginal candidiasis.

-Esophagitis.

-photosensitivity. c-Trimethoprim: 400-600 mg/day -similar in efficacy to tetracyclines. d-Clindamycin: 300-600 mg/day -the most effective due to its lipid solubility. -may risk of pseudomembranous colitis. 2-Isotretinoin: -the most effective anti-acne dug but expensive.

- risk of pill failure.

-can be reserved as a 3rd line.

-action: affects all etiological factors involved in acne. -indications: Pts with moderate/severe acne not responding to conventional therapy. -dose: 0.5-1 mg/kg/day for 15-30 weeks. -side effects: dry skin, cheilitis, conjunctivitis, arthralgia, teratogenicity & benign intracranial HTN. 3-Hormonal TTT: -action: reducing sebaceous activity, combined with topical therapy. -indication: in females with: a-failure of antibiotics. b-inappropriate or unavailable oral isotretinoin. -Includes: a-Cyproterone acetate 2 mg + ethinyl estradiol 35 ug. b-spironolactone: 100-200 mg/kg/day for 6 months. -side effects: irregular menses, potential breast cancer. C-Physical modalities: 1-Removal of comedones. 2-Intra-lesional steroid injection for nodulocystic acne.

3-Facial sauna, massage or heat should be avoided (may worsen acne). N.B. 1-Acne conglobata: -isotretinoin is drug of choice, 1 mg/kg/day for 4-6 months. -may be combined with erythromycin or trimethoprim. -short course of oral steroids may be required.
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2-Gram -ve folliculitis: due to long-term use of antibiotics -oral isotretinoin or trimethoprim.

Erythema multiforme (EM)

Def: acute self-limited mucocutaneous hypersensitivity reaction
with CCC target lesions.

Etiology: multi-factorial including

1-Infection: Viral: -the most common is herpes simplex virus infection. -hepatitis B or mycoplasma. Bacterial: streptococci, TB, typhoid. Fungal: some deep fungal infections. 2-Drugs: penicillin, Phenobarbital, sulpha. 3-Others: -collagen diseases as SLE, dermatomyositis. -Pregnancy. -Malignancy.

4-Idiopathic: 50% of cases.

Clinical picture:
-Initial lesion: iris or target lesion. -Clinical types: 1-EM minor: -multiforme lesions in the form of papules or maculopapular or vesiculobullous lesions. -good prognosis within 1-2 weeks. 2-EM major (Stevens-Johnson syndrome): -emergency condition. -severe vesiculobullous lesions of skin, mucus membranes or genitalia.

TTT:
1-TTT of the cause. 2-Symptomatic & soothing agents.
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3-Drugs: -oral antihistamines.

-topical steroids in minor EM.

-systemic steroids in Stevens-Johnson syndrome (prednisone 20-40 mg/day with gradual withdrawal over 2-4 weeks.)

Erythema nodosum
Def: skin hypersensitivity reaction in the form of bilateral erythematous tender
nodules on the extensor aspect of legs.

Etiology: multi-factorial including

1-Infection: -Viral: Cat-scratch fever. -Bacterial: streptococci, TB, leprosy.

-Fungal: some deep fungal infections. 2-Drugs: sulpha, oral contraceptives. 3-Others: -enteropathy & inflammatory bowel disease. -sarcoidosis. -malignancy.

4-Idiopathic: 20% of cases.

Clinical picture:
-Tender painful erythematous nodules. -Nodules heal leaving dark discoloration, never ulcerate. -FHMA.

TTT:
1-TTT of the cause. 2-Symptomatic: topical soothing agents & steroids.

2-Drugs: -systemic KI (potassium iodide) & pentoxyphylline to improve vasculitis. -systemic NSAIDs may help. -systemic steroids in severe cases.

Pigmentary disorders
Leucoderma:
-Def: partial or complete loss of melanin pigment. -Classification: 1-Congenital Leucoderma: -Albinism: total (oculocutaneous) or partial (piebladism).
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-Depigmented nevi. 2-Acquired Leucoderma: a-Primary (idiopathic): vitiligo. b-Secondary: -post-infections: pityriasis versicolor, leprosy, 2ry stage syphilis. -post-inflammatory: eczema, P. alba, P. rosea, psoriasis, LE. -chemicals: phenol, hydroquinone. -systemic causes: endocrinal disturbance, malnutrition.

Vitiligo
Def: acquired idiopathic Leucoderma. Etiology:
1-Genetic factor: plays a role in 1/3 of cases. 2-Autoimmune hypothesis: -vitiligo is frequently associated with other autoimmune diseases as thyroid diseases, type I DM, alopecia areata. 3-Neurogenic hypothesis: -A compound (may be catecholamine) is released at peripheral nerve endings inhibition of melanogenesis & may be destruction of melanocytes. -supported by dermatomal distribution of segmental vitiligo. 4-Self-destruction hypothesis.

Clinical picture:
-Age: occurs at any age. -Lesion: asymptomatic milky white macules of different sizes & shapes. -Site: usually first noticed on sun-exposed areas & areas subjected to repeated trauma as dorsum of hands & feet, elbow, knee, ankle. Koebner phenomenon may occur.

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-Clinical types: 1-Focal. 2-Segmental. 3-Generalized. 4-Acrofacial. 8-Halo nevus. 5-Universal vitiligo.

6-Dichrome vitiligo.

7-Trichrome vitiligo.

Pathology:
-Absent or non-functioning melanocytes.

Prognosis:
-Vitiligo is usually progressive. -Patches with white hair usually have poor prognosis.

TTT:
A-Instructions: -Give Pt idea about the disease (long-term therapy, recurs at any time). -Aim of TTT: to achieve improvement not complete cure. B-Systemic TTT: 1-Systemic Psoralens followed by exposure to UVR (PUVA): Dose: 0.6 mg/kg given 2 hrs before carefully controlled graduated exposure to UVA. Topical psoralens: if used must be diluted with alcohol 50-75% (as they may cause severe phototoxic reactions). Preparations: -8-methoxypsoralen (meladenine). -trimethylpsoralen (trisoralen), less toxic. Contraindications: -children < 13 yrs old. -pregnancy & lactation.

-history of photosensitivity or skin tumors. Side effects: -Acute: nausea, vomiting, GIT upset, Koebner phenomenon. -Chronic: a-accelerate aging of skin. b-premature cataract (proper sun glasses should be used). c-permanent hyper-pigmentation of skin. 2-Narrow band UVB (311 nm): has the following advantages -effective without use of psoralens. -effective & safe in childhood generalized vitiligo. -can be used in pregnant women.

-the only available TTT for eye lids vitiligo.

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-no permanent hyper-pigmentation. -the safest available TTT for vitiligo. 3-Systemic corticosteroids:

-short TTT time (session lasts 30 sec - 2 min).

-short courses of steroids (2 wks) to help control of rapidly progressive vitiligo. 4-Sunscreens: topical sunscreens are necessary for photo-sensitive patients. C-Other lines of TTT: 1-Topical corticosteroid + UVA exposure. 2-Universal vitiligo: topical 20% mono-benzyl ether of hydroquinone to remove pigment from remaining parts (limited use due to severe irritation). 3-Covering of localized resistant lesions with cosmetics. 4-Calcinorin inhibitors (pimicrolimus, tacrolimus). 6-Pseudocatalyses. 5-Excimer laser 308 nm.

7-Melanocytes transplantation.

Alopecia
Def: partial or complete loss of hair,
may be congenital or acquired, cicatricial or non-cicatricial.

Classification:
A-Cicatricial alopecia: absence of hair follicle & presence of scarring 1-Developmental: -Aplasia cutis. 2-Physical injury: -birth trauma. -Epidermolysis bullosa dystrophicus. -burns. -radio-dermatitis. -lymphoma.

3-Neoplasm: -basal cell carcinoma. 4-Infection:

-squamous cell carcinoma.

-Bacterial: lupus vulgaris, syphilis, leprosy, deep folliculitis. -Viral: herpes zoster, varicella. -Fungal: kerion, favus. -Discoid LE. -Protozoal: leishmaniasis.

5-Miscellaneous: -Lichen plano-pilaris.

-Cicatricial pemphigoid.

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B-Non-cicatricial alopecia: Localized: 1-Primary: alopecia areata. 2-Secondary: -Traumatic: hair-pulling tick (trichotilomania). -Cosmetic: -permanent waing. -coloring. -straightening.

-Infection: a-bacterial: superficial folliculitis, 2ry syphilis. b-fungal: non-inflammatory Tinea capitis (gray patch, black-dotted). Diffuse: 1-Primary: alopecia areata. 2-Secondary: -Telogen effluvium. -Endocrinal: pattern baldness, hypo or hyperthyroidism, DM. -Systemic diseases: anemia, iron deficiency, malnutrition, chronic liver disease, SLE, malignancy, debilitating diseases. -Drugs: cytotoxic drugs, thiouracil, anticoagulants, retinoid, captopril, cimetidine, anti-psychotic, hypervitaminosis A. -Miscellaneous: seborrheic dermatitis, early 2ry syphilis, diffuse Tinea capitis.

Alopecia areata
Def: common condition with rapid onset of complete hair loss in sharply-defined area
of scalp or other body area.

Etiology:
1-Genetic predisposition. 2-Immunological factors. 3-Emotional stress.

4-Association with autoimmune diseases: vitiligo, thyroid disease, atopy, pernicious anemia.

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Clinical picture:
Age: mostly children & young adults. Site: common on scalp, less common on chin, eye brow, moustache. Lesion: -one or more rounded well-demarcated non-inflamed bald patch of scalp. -pathognomonic exclamation mark, hair tapers near scalp. -nails may be pitted. Clinical varieties: -Patchy. -Reticulate.

-Ophiasis: band-like alopecia at the scalp margin. -Diffuse alopecia areata: diffuse decrease in hair density over the scalp. -Alopecia totalis: total loss of scalp hair. -Alopecia universalis: total loss of body hair.

DD:
-Tinea capitis. -Androgenic alopecia. -Trichotillomania. -2ry syphilis.

-Telogen effluvium.

Prognosis:
-Cause is usually unpredictable. -May recur spontaneously. -Poor prognostic factors: 1-Pre-puberty onset. 4-Ophiasis. 2-Extensive involvement. 6-Alopecia totalis. 3-Frequent recurrences. 7-Alopecia universalis. -May be progressive course.

5-Reticulate.

8-Alopecia with other disease as atopy.

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TTT:
A-General: reassurance. B-Specific: 1-Topical or intra-lesion steroids: 5 mg/ml triamcinolone acetonide for scalp lesion. 2-Topical minoxidil 5%. 3-Topical immune-modulators: -Dinitrochlorobenzene (DNCB). -Diphencyprone. -Squaric acid dibutyl ester (SADBE).

-Anthralin 0.25 - 1 %.

4-Counter irritants: as Tinc capsicum, garlic, iodine, phenol, meladinine, benzyl benzoate. 5-PUVA: topical or systemic psoralene followed by 2hrs with UVA. 6-Systemic steroids: methyl prednisolone 20-40 mg in alopecia totalis.

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