Autoimmune thyroid disease.

Marked alterations in the level of circulating thyroid hormone frequently induce cutaneous changes. Such visible sequelae of hyperthyroidism or hypothyroidism can be among the first manilestationsot thyroid dysfunction. The etiology of such thyroid dysfunction is frequently attributable to autoimmune thyroid disease, as manifested by Graves' disease (diffuse toxic goiter) or Hashimoto's thyroid it is (chronic lymphocytic thyroiditis). What is the primary immunologic disturbance that induces or facilitates autoimmune thyroid disease? Although many details remain to be elucidated, the hypothesis expounded by Voipe is attractive and appears consistent with the experimental and clinical data available.' In his view, each autoimmune endocrine disorder is due to an organ-specific defect in suppressor T lymphocyte function which allows the survival of a "forbidden" clone of self-reactive T lymphocytes. Having arisen by normal random mutation, the forbidden clone is then free to interact with its antigen, initiating a localized cell-mediated immune process. The same self-reactive T lymphocytes also function as "helper" lymphocytes, influencing the antibodyproducing B lymphocytes to manufacture self-directed antibodies. As suggested by Volpe's hypothesis, both cell-mediated and humoral immunity appear to play a dominant role in the pathogenesis of Graves' disease and Hashimoto's thyroiditis. The specific defect and its sequelae in each disease process will be detailed further under separate headings. Although Graves' disease and Hashimoto's thyroiditis are best viewed as separate entities, both diseases coexist in some patients. The extent of such an association may be dependent upon that patient's specific defect in immune surveillance (suppressor T cell function) and the random appearance ofthe appropriate clone. Why both diseases affect women four times more frequently than men is unknown.