Clinical endocrine syndromes resulting from production of polypeptide hormones by ectopic tumors have become increasingly well recognized.1 Since the report of Dowling et al2 in 1960, particular attention has been directed to disorders of thyroid function related to ectopic hormonal secretions. These investigators described three patients with hydatidiform moles whohad laboratory evidence consistent with hyperthyroidism. A year later, Myers3 described a woman with metastatic choriocarcinoma who appeared euthyroid but whose laboratory values were consistent with thyrotoxicosis.Odell et al,4 in 1963, described seven of a series of 93 patients with metastatic choriocarcinoma who had elevated thyroidal radioiodine uptakes, increased serum levels of protei n\x=req-\ bound iodine (PBI), and increased basal metabolic rates (BMR) despite the clinical appearance of only minimal hypermetabolism and absence of goiter. These reports established the syndrome of eumetabolic hyperthyroidism associated with biologically active trophoblastic tumors. This syndrome recently was reexamined in detail, and the endocrine aspects of trophoblastic tumors were reviewed.5In 1964, Steigbigel and associates6 described a patient with metastatic embryonal carcinoma of the testis who exhibited both clinical and labo¬ ratory evidence of thyrotoxicosis in