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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
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
The fascinating history of the first Memorial Hospital patient who was diagnosed as having hyperparathyroidism is reviewed. The illness presented as a cystic mass in a femur in 1929, which was treated with radiation. When the patient was first seen at Memorial Hospital in 1931, the diagnosis of osteitis fibrosa cystica was made; serum calcium was 14 mg/100 ml. In 1932, 6 years after Mandl performed the first parathyroidectomy ever for osteitis fibrosa cystica, this patient's neck was explored, and a right hemithyroidectomy was done, with removal of two normal parathyroid glands. The parathyroid tumor was finally located and partially removed in 1937 after a second failure at neck exploration in 1936. Correspondence between Dr. Edward D. Churchill at the Massachusetts General Hospital and Dr. Bradley Coley at Memorial Hospital indicated the concern at that time about uncontrollable tetany, which had been fatal in some contemporary cases and which had led to the practice of only partially removing the tumor. Following this, the patient was observed with documented hypercalcemia and chemical evidence of hyperparathyrodism until age 79. The physical and chemical abnormalities over the years up to and including her last exam are presented. The case is important not only from the historical viewpoint, but because it lends a perspective to long-term parathyroid disease, which is becoming less appreciated in this day of the routine serum calcium by SMA-12 screening. The question of partial parathyroidectomy for adenoma or hyperplasia is reviewed, and the question of observation of patients with mild hypercalcemia who probably have parathyroid tumors is discussed.
A case of a 26-year-old woman with metastatic choriocarcinoma and clinical and biochemical thyrotoxicosis is described. This represents the eighth reported case of the association of choriocarcinoma and thyrotoxicosis. Serial monitoring of serum thyroxine (T4) and thyroid stimulating hormone (TSH) levels correlated precisely with the beta sub-unit human chorionic gonadotropin (hCG) level and the quantitation of host tumor burden. The development of a hypermetabolic syndrome in patients with choriocarcinoma may be due to secondary thyrotoxicosis from either the TSH-like activity of hCG or from the concomitant production of molar thyrotropin by the tumor.
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