Alopecia areata (hereinafter: A.a.) is a frequent, usually benign chronic disease of hair the couses of which have not been fully investigated yet. A.a. may appear without any warning in both sexes. It may occur at any age, but it is most frequent between ages 20 and 40. Characteristic symptom of A.a. is appearance of clearly outlined circular spots without hair. In 60% of cases the disease begins in capilicium, with appearance of completely hairless spots with diameter from 0,5 mm to 1 cm. The scalp skin retains the color, and hairs around the affected spot are easily pulled out. After the appearance of the first spots, other spots appear and join into larger bald areas.

Ethiology
Ethiology of alopecia areata is unknown. Although it is certain that alopecia areata often occurs after severe emotional stress, its pathogenesis has not been scientifically proved. Up to some ten years ago, the appearance of alopecia areata had always been examined in relation to focus (dental focus, chronic tonsillitis, and sinusitis). The latest approach hardly considers the FFF to be the cause. Alopecia areata can often be identified within one family. There are different opinions about teating alopecia areata a hereditary disease. Some authors have confirmed that in 27% of the patients had cases of alopecia areata within the family. Yet, some of them denied it.
The modern concept of etiopathogenesis of alopecia areata considers the autoimmune mechanism to be important for the hair follicle. Numerous facts affirm such concept. Hysto pathological finding confirms the existence of the lymphocytic infiltrate around the hair bulbus on alopetic patches. The method of the direct immune fluorescent technique (DIF) finds the C3 component deposit in the hair follicle. Alopecia areata in rare cases appears together with dysfunction of the timulus function, autoimmune tyreoditis, Hashimoto or vitiligo.
The HF finding of antibodies against the hair follicles in patients with alopecia areata in high titre serum, and the finding of decreased values of CD 44 glykoprotein of the cell membrane of sweat glands on alopetic patches, for which it is assumed that they participate immune response regulation, support the autoimmune theory. The newest research performed with monoclonal antibody method has proved the existence of decreased Cytokeratine expression 16 (CK – 16) in hair follicles on alopetic patches in cases of alopecia areata. Since cytokeratine (which is in normal follicles found in the inner membrane of the hair root and dermal papia) is the marker of epithelial differentiation, the significance of the epithelial proliferation dysfunction during the cycles of hair growth is to be taken into account when discussing the alopecia areata pathogenesis.

UNWANTED EFFECTS
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