Choriocarcinoma as a cause of thyrotoxicosis

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.     

Mechanism of pain in diabetic peripheral neuropathy: Effect of glucose on pain perception in humans

Animal studies have suggested an altered response to opiate agonists and antagonists as well as an altered pain threshold in diabetic animals. In the studies reported herein, a 50 g glucose infusion in normal subjects resulted in a significant decrease in both the threshold level of pain and the maximal level of pain tolerated, as measured by responses to electrical pain induced by a Grass stimulator. In addition, patients with diabetes mellitus were hyperalgesic when compared with normal subjects. It is concluded that elevated glucose levels and/or rapid fluxes in glucose levels result in a decrease in pain tolerance. These findings have potential clinical implications in the pathophysiology and management of painful diabetic neuropathy and the use of narcotic agents in diabetes mellitus.     

Thyrotropin-releasing hormone suppressed gastric acid output in patients with Zollinger-Ellison syndrome and systemic mastocytosis

Thyrotropin-releasing hormone administered intravenously was found to be as potent an inhibitor of gastric acid secretion as a conventional dose of oral cimetidine in two patients with Zollinger-Ellison syndrome and one patient with systemic mastocytosis.