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Article
January 27, 1993

Tobacco and Graves' DiseaseSmoking Gun or Smoke and Mirrors?

Author Affiliations

From the Division of Endocrinology, Sinai Hospital of Baltimore (Md) and The Johns Hopkins University School of Medicine.

JAMA. 1993;269(4):518-519. doi:10.1001/jama.1993.03500040084043
Abstract

Graves' disease is an autoimmune disease with a lifetime incidence of 1% to 2% in the general population. Circulating antibodies to the thyrotropin (thyroid-stimulating hormone [TSH]) receptor stimulate growth of the thyroid gland, as well as the synthesis and secretion of excessive amounts of thyroid hormone. These autoantibodies are polyclonal and therefore different clones may have disparate effects on the thyroid gland, possibly by binding and activating different epitopes on the TSH receptor.1 This variety of effects may be one reason why the size of the thyroid and the amount of hormone secreted are not necessarily correlated. The recent cloning and sequencing of the human TSH receptor should enable detailed study of antibody-receptor interactions.2 Despite isolation of the causative antibodies, however, there is little known about the processes that trigger the disease in the first place. Current evidence suggests that a defect in T-cell function or number permits

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