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In view of the controversy regarding the role of human chorionic gonadotropin as the stimulator of thyroid function in patients with trophoblastic tumors, especially hydatidiform mole, we conducted studies to explore whether a correlation between serum human chorionic gonadotropin levels and thyroid function was demonstrable in such patients. Among 47 patients studied, only one was clinically hyperthyroid, although 10 had serum total thyroxine values exceeding those found in normal pregnancy (8 to 17 micrograms/dl). Among 34 patients in whom free thyroxine indices could be calculated, 18 had elevated values for the free thyroxine index (greater than 10.6), and nine had elevated values for both total thyroxine and free thyroxine index. Serum total 3,5,3'-triiodothyronine concentrations were also measured in 17 patients, and only one of them had a value (400 ng/dl) above the normal limit for pregnancy (greater than 350 ng/dl). Among the 13 patients for whom free 3,5,3'-triiodothyronine indices were calculated, three had values above the normal range (greater than 215). A weakly positive correlation (r = 0.35, p less than 0.05, n = 47) between the serum human chorionic gonadotropin levels and serum total thyroxine concentrations was observed in these patients. However, no correlation was found between serum human chorionic gonadotropin levels and free thyroxine index values (r = 0.32, p greater than 0.05, n = 34). Also there was no correlation between serum human chorionic gonadotropin levels and either serum total 3,5,3'-triiodothyronine concentrations (r = 0.32, p greater than 0.1, n = 17) or free 3,5,3'-triiodothyronine index values (r = 0.27, p greater than 0.1, n = 13). chi 2 Analysis revealed no significant relationship between elevations of serum human chorionic gonadotropin concentration and abnormally high values of the free thyroxine index. These studies do not support the premise that human chorionic gonadotropin per se is the thyroid stimulator of molar pregnancy and suggest that a substance or substances, distinct from human chorionic gonadotropin and elaborated by the gestational trophoblastic tissue, are responsible for thyrotoxicosis observed in patients with trophoblastic tumors.
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