Effects of hydrocortisone on the hypercalcemia and plasma levels of 13,14-dihydro-15-keto-prostaglandin E 2 in mice bearing the HSDM 1 fibrosarcoma

Abstract

In mice bearing the prostaglandin-producing HSDM 1 fibrosarcoma, the plasma concentration of 13,14-dihydro-15-keto-PGE 2 was elevated before the development of hypercalcemia, and the magnitude of the rise was greater than that of PGE 2. When hydrocortisone, which inhibits synthesis of PGE 2 by HSDM 1 cells in culture, was administered to tumor-bearing mice, the steroid hormone prevented the rises in plasma PGE 2 metabolite and calcium concentrations. At the dose levels used, hydrocortisone did not inhibit the calcium-mobilizing action of parathyroid hormone in vivo or the bone resorption-stimulating activity of PGE 2 in vitro . These findings are consistent with our hypothesis that the hypercalcemic syndrome in HSDM 1 tumor-bearing mice is due to the secretion of PGE 2 by the tumor.