Alopecia areata (AA) is a common form of localized, non-scarring hair loss. It is characterized by the loss of hair in patches, total loss of scalp hair (alopecia totalis), or total loss of body hair (alopecia universalis). The etiopathogenesis of the disease is still unclear, but there is evidence that autoimmunity and endocrine dysfunction may be involved. The aim of this study was to determine whether AA is statistically associated with thyroid autoimmunity. In this retrospective epidemiologic study, we compared the frequency of thyroid autoantibodies (thyroglobulin antibody, TgAb, and thyroid peroxidase antibody, TPAb) ATPO) in 70 AA patients and 30 healthy volunteers. Thyroid autoantibodies and thyroid hormones (thyroxine (T4), triiodothyronine (T3) and thyroid stimulating hormone (TSH)) were measured in all subjects. Thyroid functional abnormalities were found in 8 (11.4%) AA patients. Positive autoimmune antibodies were associated with AA in 18 (25.7%) patients, with no significant association between the disease severity and presence of these antibodies. The frequency of thyroid autoantibodies was significantly higher in AA patients than in healthy controls (25.7% vs. 3.3%; p<0.05). Our findings pointed to a significant association between AA and thyroid autoimmunity and showed the tests to detect thyroid autoantibodies to be relevant in AA patients.
Alopecia areata (AA) is a heterogeneous disease characterized by nonscarring hair loss on the scalp or any hair-bearing surface. A wide range of clinical presentations can occur, from a single patch of hair loss to complete loss of hair on the scalp (alopecia totalis, AT) or over the entire body (alopecia universalis, AU). The cause of AA is unknown although most evidence supports the hypothesis that AA is an immunologically mediated disease. The aim of the study was to compare serum levels of total immunoglobulin E (IgE) between patients with AA and healthy subjects, and to assess the difference between the localized form and extensive forms of the disease such as AT and AU. Sixty patients with AA and 50 healthy subjects were enrolled in the study. Fifty patients had localized AA (LAA), and ten patients had AT, AU or AT/AU. Serum levels of IgE were measured using fluoroenzyme immunoassay techniques. Serum levels of total IgE were significantly higher in AA patients than in controls (p<0.05). There was no significant difference in serum levels of total IgE between patients with LAA and those with extensive forms of the disease (p>0.05). The exact role of serum IgE in AA should be additionally investigated in future studies.
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