Choriocarcinoma as a cause of thyrotoxicosis

Abstract

Three patients with choriocarcinoma had clinical and biochemical evidence of hyperthyroidism. Diminution in the thyrotoxicosis closely paralleled the fall in human chorionic gonadotrophin (hCG) levels. Three patients originally presented to internal medicine units as a problem of hemoptysis. Thyroid-stimulating hormone bioassay activity was demonstrated in the serum of all three patients prior to therapy. Recently evidence has been presented that hCG has intrinsic thyrotropic activity and that in conditions, such as hydatidiform mole, in which serum hCG levels are grossly elevated this thyrotropic activity can be sufficient to produce hyperthyroidism. Two of our cases supported the concept that hCG was also the substance with thyroid-stimulating activity in patients with choriocarcinoma. The third case left open the possibility that, in addition to the thyroid-stimulating activity of hCG, there may also be the production of a true ectopic thyroid-stimulating hormone (TSH). It is considered that the development of biochemical and clinical thyrotoxicosis in patients with choriocarcinoma depends upon the duration of the choriocarcinoma and the level of hCG.

PIP: The cases of 3 patients with advanced metastatic choriocarcinoma and biochemical and clinical evidence of hyperthyroidism are reported. The thyroid-stimulating hormone (TSH) bioassay activity was increased in all 3 patients before chemotherapy. All patients had clinical signs and symptoms of overt thyrotoxicosis although goiter was present in only 1. Sinus tachycardia was present in all. The 1st symptom in all 3 cases was hemoptysis. An X-ray appearance of multiple pulmonary metastases was also present. There was biochemical evidence of improvement in thyrotoxicosis after chemotherapy. This improvement paralleled the fall in urinary human chorionic gonadotropin (HCG). As treatment, intermittent oral 5-day courses of methotrexate and iv actinomycin D were given at 3-week intervals. In 2 of the cases the ratio of bioassayable thyrotropic activity to HCG found in the serum was similar to the ratio in patients with hydatidiform moles. In the other case the ratio was much higher. It appears that the development of biochemical and clinical hyperthyroidism in patients with choriocarcinoma depends on the duration of the choriocarcinoma and the serum level of HCG. Findings suggest that there may be production of another TSH in addition to the thyrotropic activity of high HCG levels.