The syndromes comprising autoimmune thyroid disease are three intimately related illnesses: (1) Graves' disease with goiter, hyperthyroidism and, in many patients, associated ophthalmopathy (2) Hashimoto's thyroiditis with goiter and euthyroidism or hypothyroidism; and (3) primary thyroid failure or myxedema. Many variations of these syndromes are also recognized, including transient thyroid dysfunction occurring independently of pregnancy and in 5 - 6% of postpartum women, neonatal hyperthyroidism, and neonatal hypothyroidism. The syndromes are bound together by their similar thyroid pathology, similar immune mechanisms, co-occurrence in family groups, and transition from one clinical picture to the other within the same individual over time. The immunological mechanisms involved in these three diseases must be closely related, while the phenotypes probably differ because of the specific type of immunological response that occurs. For example, if immunity against the TSH receptor leads to production of thyroid stimulating antibodies, Graves' disease is produced, whereas if TSH blocking antibodies are formed or a cell destructive process occurs, the result is Hashimoto's thyroiditis or primary myxedema.

Associated with autoimmune thyroid disease in some patients are other organ specific autoimmune syndromes including pernicious anemia, vitiligo, myasthenia gravis, primary adrenal autoimmune disease, ovarian insufficiency, rarely pituitary insufficiency, alopecia, and sometimes Sjogren's syndrome or rheumatoid arthritis or lupus, as manifestations of non-organ specific autoimmunity. Of particular interest recently has been the description of pituitary antibodies and growth hormone deficiency in a around a third of patients with autoimmune hypothyroidism, implying the existence of a substantial reservoir of pituitary autoimmunity in these patients but further work is needed to confirm these findings and to understand the basis for the autoimmune response against the pituitary (39a).