Alopecia Alopecia classified into: Alopecia areata ▪ Non-cicatricial Alopecia : No clinical sign of tissue inflammation, scarring, or atrophy of skin . • A localized loss of hair in round or oval areas with no apparent inflammation of the skin. Most ▪ Cicatricial alopecia : Evidence of tissue destruction such as inflammation, atrophy, and scarring is apparent. common on scalp.

• Nonscarring; hair follicle intact; hair can regrow. Classification of acquired alopecia • Clinical findings: Hair loss ranging from solitary patch to complete loss of all terminal hair. Can occur globally or focally : ( Causes of hair loss ) • Prognosis: good for limited involvement. Poor for extensive hair loss. • Diffuse (global) hair loss Management: intralesional triamcinolone effective for limited number of lesions. Non -scarring PATHOGENESIS DIFFERENTIAL DIAGNOSIS 1- Failure of follicle production • Chronic organ -specific autoimmune disease, Nonscarring Alopecia : 2- Hair shaft abnormality mediated by autoreactive T cells affecting hair • White-patch tinea capitis, 3- Abnormality of cycling (shedding) follicles and nails. • Trichotillomania, • Telogen effluvium • • Early scarring alopecia, • Associated autoimmune disorders: Anagen effluvium • Pattern hair loss, • Loose anagen syndrome Autoimmune thyroid disease in adults. • Secondary syphilis (alopecia areolaris) • Alopecia areata • Follicular damage occurs in anagen followed by (“moth-eaten” appearance ) ‰ rapid transformation to catagen and to ‰ LABORATORY EXAMINATIONS Focal (patchy, localized) hair loss telogen ; then to ‰ dystrophic anagen status . • Serology : Non -scarring Scarring (cicatricial) alopecia While the disease is active, follicles unable to

1- ANA (to rule out SLE); progress beyond early anagen and do not 3- Production decline : 1- Lymphocytic : 2- rapid plasma reagin (RPR) test (to rule • develop normal hair. • Triangular alopecia Chronical cutaneous (discoid) lupus erythematosus out secondary syphilis). • • Lichen planopilaris (LPP) Pattern hair loss (androgenetic alopecia) CLINICAL MANIFESTATIONS • KOH Preparation: Rule out tinea capitis. • Classic pseudopelade of Brocq • Dermatopathology : • Central centrifugal cicatricial alopecia Age: Any age , but peak between 20 – 50 years

4- Hair breakage : Acute lesions show : • Trichotillomania • Alopecia mucinosa Sex : affect both sexes. - peribulbar, perivascular, and outer root • Traction alopecia • Kertosis folliclaris spinulosa decalvans Duration of Hair Loss sheath mononuclear cell infiltrate of T cells • Infection (tinea capitis) Gradual over weeks to months. and macrophages; • Primary or acquired hair shaft abnormality 2- Neutrophilic : • Folliculitis decalvans Skin Symptoms - follicular dystrop hy with abnormal 5- Unruly hair. • Dissecting folliculitis (cellulitis) Disfiguring bald patch. pigmentation and matrix degeneration. MANAGEMENT Associated Findings 6- Abnormality of cycling : 3- Mixed : No curative treatment is currently available. • Autoimmune thyroiditis. • Alopecia areata • Folliculitis keloidalis Treatment for AA is unsatisfactory. • Down syndrome. • Secondary syphilis (alopecia areolaris) • Folliculitis necrotica Treatment directed at inflammatory infiltrate • • Autoimmune polyendocrinopathy - (“moth-eaten” appearance in beard or scalp). Erosive pustular dermatosis and growth inhibitor factors produced by candidiasis –ectodermal dysplasia syndrome. inflammation. 4- Non-specific : Skin Findings • Trauma. 1- General measures : - Usually none. • Chemical or physical burn. • Psychological support ( very important ). • Surgical wound - Possibly minimal erythema in area of hair loss. • Persons with extensive scalp involvement • Neoplasm (Basal cell carcinoma , Squamous cell carcino ma) Hair such as AAT may pr efer to wear a wig or Scarring (cicatricial) alopecia Round patches of hair loss. hairpiece. • • Primary cicatricial alopecia (PCA) results from damage or destruction of the hair follicles stem cells by: • Single or multiple. May coalesce. Makeup applied to eyebrows is helpful. • It's often sharply defined. Eyebrows can be tattooed. - Inflammatory (usually noninfectious) processes - Infection: e.g., “kerion” tinea capitis, necrotizing herpes zoster • Normal -appearing skin with follicular 2- Glucocorticoids - Other pathologic processes: surgical scar, primary or metastatic neoplasm. openings present . • Glucocorticoids Topical : • Manifestations: Effacement of follicular orifices in a patchy or focal distribution, usually in scalp or beard. • “Exclamation mark” hairs (Fig. 32-8) : Superpotent agents not usually effective. • The end result is effacement of follicular orifices & replacement of the follicular structure by fibrous tissue. Diagnostic broken - off stubby hairs • Intralesional Injection : • Scarring is irreversible. Therapies are ineffective. (distal ends are broader than proximal ends) Few and small lesions of AA can be treated TELOGEN EFFLUVIUM ANAGEN EFFLUVIUM seen at margins of hair loss areas. with intralesional triamcinolone acetonide,

• • 3–7 mg/mL, which can be very effecve Telogen effluvium (TE) is the transient increased Etiology: See below • Scattered, discr ete areas of alopecia (Fig. 32 -9) shedding of normal club (telogen) hairs from resting temporarily. • Onset is usually rapid & extensive. or

scalp follicles. Confluent with total loss of scalp hair (Fig. 32 -10) , • • Secondary to accelerated shift of anagen (growth • Pathogenesis: Occurs after any insult to hair Systemic Glucocorticoids : phase) into catagen and telogen (resting phase) follicle that impairs its mitotic/metabolic or May induce regrowth, but AA recurs on • Results in increased daily hair loss and, if severe, generalized loss of body hair (including vellus hair). discontinuation; risks of long-term therapy activity. Rapid growth arrest or damage to diffuse thinning of scalp hair. anagen hairs that skip catagen and telogen Diffuse AA of scalp (noncircumscribed) gives the therefore preclude their use.

phases and are shed. appearance of thinned hair; can be difficult to Etiology: differentiate from pattern hair loss of telogen 3- Systemic Cyclosporine • More common and severe with combination A reaction pattern to a variety of physical or mental effluvium, hair loss with thyroid disease. Induces regrowth, but AA recurs when drug is stressors : chemotherapy than with the use of a single discontinued. drug. Severity is generally dose dependent. • With regrowth of hair, new hairs are fine,

often white or gray. 4- Induction of Allergic Contact Dermatitis - • Endocrine : • Manifestations: By Dinitrochlorobenzene ( DNCP ) , but local 1- Hypo- or hyperthyroidism ; Scalp hair : loss is diffuse, extensive; also: Sites of Predilection discomfort due to allergic contact dermatitis 2- postpartum ; eyebrows/lashes, beard, etc. - Scalp ( most commonly ) and swelling of regional lymph nodes poses a 3- discontinuation or changing type of estrogen Nails: show transverse banding or ridging. - Any hair -bearing area : Beard, eyebrows, containing drugs problem. • Regrowth is usually rapid after discontinuation eyelashes, pubic hair. 5- Oral PUVA ( Photochemotherapy) : • Nutritional: of Chemotherapy • Alopecia areata (AA): Entire body must be exposed, 1- Deficiency: biotin, zinc, iron, essential fatty acid Solitary or multiple areas of hair loss. in that the therapy is believed to be a form of 2- Rapid weight loss, Etiology: • AA totalis (AAT): 3- caloric or protein deprivation, systemic immune suppression. Anagen cycle disrupted causing varying degrees Total loss of terminal scalp hair. 4- excessive vitamin A ingestion • AA universalis (AAU): of hair follicle dystrophy : • Patchy alopecia : • Total loss of all terminal body & scalp hair. Physical stress : • o Intralesional corticosteroids : Radiation therapy to head . • Ophiasis: 1- Febrile illnesses, Up to 2 mL injected/session and repeated at 2- catabolic illnesses (e.g., malignancy, chronic • Alkylating agents: Bandlike pattern of hair loss over periphery intervals. infection), busulfan, carboplatin, carmustine, BCNU, of scalp . o Potent topical steroid (1-2×/day). 3- major surgery, o Topical anthralin (0.1%-2.0% once daily) : chlorambucil, cisplatin, dacarbazine, Nails 4- major trauma, estramustine, fotemustine , ifosamide, Wash off after 10-20 min, steadily increase • Fine pitting (“hammered brass”) of dorsal 5- acute or chronic psychological stress lomustine, mechlorethamine, nitrogen contact duration, switch to higher dose if no nail plate. significant irritation. • mustard, melphalan, oxaliplatin, procarbazine, Psychological stress : • mottled lunula, o Minoxidil loon (5%) twice daily. 1- Anxiety, streptozocin, temozolomide, thiotepa. • trachyonychia (rough nails), • Extensive or rapidly progressive alopecia. 2- depression, • onychomadesis (separation of nail from matrix). o Contact immunotherapy. 3- bipolar disorder • Intoxications: o Systemic corticosteroids. mercury, boric acid, thallium, colchicine. FIGURE 32 -8 • Intoxication : Thallium, mercury, arsenic Benefits are uncertain and must be weighed Solitary lesion against risk of systemic corticosteroid therapy. • Drugs : • Severe protein malnutrition. o Wig or hairpiece. 1- Antimitotic agents (dose dependent): cancer The short, broken-off hair • Alopecia totalis/universalis chemotherapy, benzimidazoles. shafts (so-called exclamation point hair) appear as very o Contact immunotherapy. 2- Antihypertensives: captopril short stubs emerging from the o Topical/systemic steroids. 3- Anticoagulants bald scalp. o Wig or hairpiece. 4- CNS drugs: lithium, valproic acid FIGURE 32 -9 5- Cholesterol-lowering drugs multiple, extensive lesions 6- Colchicine COURSE 7- Cytostatic drugs Multiple, confluent, involved • Spontaneous remission is common in patchy AA sites on the scalp with

8- Interferon “exclamation point hairs.” but is less so with AAT or AAU. 9- Penicillamine • Poor prognosis associated with onset in 10- Retinoids: vitamin A excess, retinoids childhood, loss of body hair, nail involvement, (isotretinoin, acitretin, indinavir) atopy, family history of AA. 11- Selective serotonin reuptake inhibitors • If occurring aer puberty, 80% regrow hair. With 12- Inflammatory scalp disease: Seborrheic FIGURE 32-10 extensive AA, AAT, AAU, <10% recover dermatitis, erythroderma AA totalis spontaneously.

• Idiopathic : • Recurrences of AA, however,, are frequent.freq No obvious cause is apparentt in a signsignificant number • Systemic glucocorticoids or cyclosporyclosporine can induce of cases. remission of AA but do not alter the course.