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The Thyrotoxicosis of Hydatidiform Mole

H. PATRICK HIGGINS, M.D., F.R.C.P.(C.), F.A.C.P.; JEROME M. HERSHMAN, M.D., F.A.C.P.; JAMES G. KENIMER, Ph.D.; ROLAND A. PATILLO, M.D.; T. ARNOLD BAYLEY, M.D., F.R.C.P.(C.), F.A.C.P.; and PAUL WALFISH, M.D., F.R.C.P.(C.), F.A.C.P.
[+] Article and Author Information

Grant support: in part by U.S. Public Health Service Research Grant HD-7181 and Veterans Administration Research Grant 3590-03.

▸Requests for reprints should be addressed to H. Patrick Higgins, M.D., Toronto Professional Building, 123 Edward St., Suite 922, Toronto, Ontario, Canada M5G 1E2.


Toronto,Canada; Los Angeles, California; and Milwaukee, Wisconsin


Ann Intern Med. 1975;83(3):307-311. doi:10.7326/0003-4819-83-3-307
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In 14 women with hydatidiform mole, 9 were hyperthyroid. Serum thyroxine (T4) levels varied between 18 and 34 µg/100 ml, and serum triiodothyronine (T3) levels between 300 and 800 ng/100 ml in the hyperthyroid patients. Bioassayable thyroid-stimulating hormone (molar TSH) was found in high concentrations in the serum of 13 patients in whom preoperative serum was available. There was a close correlation between the serum levels of human chorionic gonadotrophin, molar TSH, and T3. Intravenous sodium iodide caused a fall in serum T3 and, to a lesser extent, in T4 in hyperthyroid patients but not in a euthyroid patient. Removal of molar tissue caused a dramatic fall in the serum levels of T3, T4, molar TSH, and human chorionic gonadotrophin. The close correlation between the serum concentrations of molar TSH and human chorionic gonadotrophin lend support to the suggestion that the human chorionic gonadotrophin molecule itself, when present in large amounts, stimulates thyroid function significantly.

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