ETIOLOGY AND PATHOGENESIS
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The cause of AA is obscure. Immune-mediated injury induced by possible infective, chemical, of neuropeptide stimulant is believed to cause damage to hair follicles. There is an increased incidence of autoantibodies directed against gastric parietal cells, thyroid, smooth muscles etc in AA.
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A number of diseases are significantly associated with AA.
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Associations of alopecia areata |
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Vitiligo Thyroid disease Atopy Down syndrome Addison’s disease Pernicious anemia |
Lupus erythematosus Scleroderma Celiac disease Crohn’s disease Lichen planus Rheumatoid arthritis |
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Positive family history points towards a role of genetic factors.
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Damage to hair follicles occurs in the anagen phase of hair cycle with rapid transition to telogen phase before shedding of hairs. Growing, pigmented hairs are usually targeted by the immune process.
CLINICAL FEATURES
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AA is more common in young age, there is no racial, or ethnic predisposition.
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Equally affects both sexes, some reports points to male preponderance.
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There is gradual loss of hair over weeks or months without any discomfort. Mild itching may be reported by some patients.
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Patients are usually very concerned over the prospect of total or permanent baldness and there is a high incidence of depression and social phobias.
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AA mainly affects the scalp, eyebrows, eyelashes, and bearded area, but any hair-bearing area may be affected.
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Single or multiple, roundish or oval areas of total hair loss with smooth, soft skin is noted on examination. Patches may coalesce to form large, diffuse areas of baldness.
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Grey hairs are usually spared.
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Short, broken stubs of hairs with narrow proximal end and broad distal end (exclamation point hairs) may be found at the periphery of expanding patches.
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There may be linear band of hair loss along the periphery of scalp (ophiasis).
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Total loss of hairs from the entire scalp (alopecia totalis) or from all over the body (alopecia universalis) may occur in particularly severe cases.
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Regrowing hairs are thin, lusterless, and white.
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Nail changes are found in up to one fifth of the cases. They take the forms of fine pitting, roughness, horizontal or vertical grooves, thickening, and severe dystrophy.
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Signs of associated diseases may be found.
DIFFERENTIAL DIAGNOSIS
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Trichotillomania (psychogenic hair-pulling)
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Secondary syphilis
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Androgenetic alopecia
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Tinea capitis
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Lupus erythematosus
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Pseudopelade
DIAGNOSIS
AA is easily diagnosed clinically by the features of asymptomatic, non-inflammatory, total loss of hair in patches. Rarely, KOH preparation, syphilis serology, ANA to rule out other causes of patchy alopecia or a scalp biopsy (that shows perivascular, perifollicular lymphocytic and macrophage infiltrate in AA) , may be needed. Thyroid function tests may be done particularly in children to exclude associated thyroid disease.
TREATMENT
Reassurance about the prospect of spontaneous regrowth, simple explanation about the chronic, often recurrent course and prognosis of the disorder.
TOPICAL THERAPY: Although there is a paucity of rigorous double blind studies to confirm their efficacy and safety, a number of topical agents have been found to be effective in AA.
- Corticosteroids: potent topical steroid application once or twice a day. Particularly in children.
- Topical irritant/immune-stimulant: anthralin, squaric acid dibutyl ester (SADBE), dinitrochlorobenzene (DNCB), and diphencyprone have been found to induce regrowth of hairs in a significant proportion of cases.
- Minoxidil: 5% minoxidil solution with or without anthralin may be helpful in a number of cases.
- Topical tacrolimus
INTRALESIONAL STEROID: Intralesional triamcinolone acetonide (diluted to 5mg/ml and injected with a tuberculin syringe) at an interval of 4 to 6 weeks is an effective therapy for small patches particularly of the scalp.
SYSTEMIC THERAPY:
- Prolonged photochemotherapy (psoralen plus ultraviolet A, PUVA) may be effective in a proportion of cases with extensive involvement.
- Systemic steroid: either as continuous low-dose, or pulse therapy, may induce regrowth, but loss of hair following discontinuation usually occur.
- Cyclosporine: oral cyclosporine (6mg/kg/ day) may induce growth of hairs in half of the patients, but relapse is the rule after discontinuation.
COURSE AND PROGNOSIS
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Spontaneous remissions commonly occur in patchy AA, making evaluation of drug therapy difficult. After the first episode of AA spontaneous regrowth occurs within one year in one third of patients. Spontaneous regrowth is rare in alopecia totalis or universalis.
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Poor prognostic factors include: early age of onset, extensive disease (AA totalis or universalis), prolonged history of disease, ophiasis pattern of involvement, history of atopy, rapid progression of disease, and severe associated nail changes.