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Graves' Disease with Delayed Hyperthyroidism: Onset After Several Years of Euthyroid Ophthalmopathy, Dermopathy, and High Serum LATS

INDER J. CHOPRA, M.D.; and DAVID H. SOLOMON, M.D., F.A.C.P.
[+] Article and Author Information

Supported in part by grant RR00425, Clinical Research Center, Harbor General Hospital, Torrance, Calif.; grant AM10187, U.S. Public Health Service, Washington D.C.; and by a grant from the John A. Hartford Foundation, Inc., New York, N.Y.

▸Requests for reprints should be addressed David H. Solomon, M.D., Dept. of Medicine, Harbor General Hospital, 1000 W. Carson St., Torrance, Calif. 90509


Torrance and Los Angeles, California


Ann Intern Med. 1970;73(6):985-990. doi:10.7326/0003-4819-73-6-985
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A patient had high serum long-acting thyroid stimulator (LATS) activity and only the ophthalmopathy and dermopathy of Graves' disease for several years and finally developed hyperthyroidism with no increase (actually a decrease) in serum LATS activity. This sequence generates doubt about two prevalent hypotheses: that circulating LATS is the cause of hyperthyroidism in Graves' disease and that the absence of hyperthyroidism in euthyroid Graves' disease is caused by the presence of an additional lesion, such as chronic thyroiditis, limiting the capacity of the thyroid gland to respond to LATS. Alternative hypotheses are discussed.

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