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Smoking Gun or Smoke and Mirrors?

David S. Cooper, MD

JAMA. 1993;269(4):518-519.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

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

Footnotes
Reprint requests to Division of Endocrinology, Sinai Hospital of Baltimore, Belvedere at Greenspring, Baltimore, MD 21215 (Dr Cooper).

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