Autoimmune thyroid disease: an integrated concept of Graves' and Hashimoto's diseases

Graves' disease and Hashimoto's thyroiditis have been previously considered separate clinical and pathologic entities. Current knowledge of the autoimmune cause of specific systemic syndromes has been applied to these seemingly dissimilar diseases and now permit evolution of a unified integrated concept for considering them as two subsets of a single pathologic process. Experimental and clinical data now support the thesis that autoimmune thyroid disease is a genetically conditioned immunologic dysfunction, perhaps an abnormality of suppressor lymphocytes that results in production of humoral and tissue antibodies directed against thyroid gland cells and receptors of other somatic tissues. Thyroid autoantibodies possess hormonally stimulatory qualities and cytotoxic (inflammatory or destructive) properties. They may be present singly or together in the same individual with resulting diverse clinical and biochemical patterns depending upon the predominance or concordance of specific antibodies. Further, antibodies in autoimmune thyroid disease may be directed against other somatic structures such as ocular muscle, skin, hair, pigment cells, hematologic organs, or other endocrine glands. The immune etiology appears to predispose to nonendocrine systemic autoimmune disorders that coincide with thyroid disease. It is not clear at this time how genetic factors influence the onset, course, or ultimate outcome of autoimmune thyroid disease or why certain associated immunopathies tend to cluster with one or the other of these syndromes. Our understanding of the immune etiology common to Graves' and Hashimoto's diseases permits a more precise definition of the terms hyperthyroidism and thyrotoxicosis, the former denoting a pathologic goitrous phenomenon and the latter, a peripheral tissue manifestation of cellular receptor site excess of thyroid hormones.(ABSTRACT TRUNCATED AT 250 WORDS)