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April 5, 1976

Humoral and Genetic Factors in Thyrotoxic Graves Disease and Neonatal Thyrotoxicosis

Author Affiliations

From the Department of Medicine, University of Washington School of Medicine, Seattle.

JAMA. 1976;235(14):1449-1450. doi:10.1001/jama.1976.03260400015018

WHY IS the thyroid gland hyperactive in Graves disease? Since the demise of the theory that postulated excessive pituitary thyroid-stimulating hormone secretion, most hypotheses have included some type of stimulation by immunoglobulins or activated lymphocytes, with or without a role for an intrinsic abnormality of the thyroid gland.

The presence of autoimmune phenomena in Graves disease is beyond dispute.1 Many patients have demonstrable antibodies to thyroid antigens, and Graves disease has a proved familial association with the archetypal autoimmune endocrine disease, Hashimoto thyroiditis. Graves disease is unique among so-called autoimmune diseases, however, in that an immunoglobulin that has biological effects similar to those of an important hormone, thyrotrophin, is frequently present.

Since the original observation that Graves sera can produce a prolonged stimulation of thyroid secretion in guinea pigs and mice, this "long-acting thyroid stimulator," or LATS, has been the object of intensive study. It is an immunoglobulin of