Studies on the pathophysiological role of thyroidal prostaglandin E (PGE) in Graves' disease.

A potential role for prostaglandin E (PGE) of thyroid origin in the pathogenesis of the hyperthyroidism of Graves' disease was investigated in vivo. The venous-arterio prostaglandin E (PGE) concentration gradient across the thyroid was measured in 5 patients undergoing subtotal thyroidectomy for Graves' disease. This gradient (161 +/- 14 pg/ml; mean /+- SE) was significantly greater than that found in 11 patients undergoing surgery for hyperparathyroidism and thyroid nodules (64 +/- 20 pg/ml; P < 0.01). This suggests that there is a net increase in PGE output by the thyroid gland in Graves' disease, but the thyroid cell-type responsible for this increased PGE output is unknown. In contrast to previous reports, thyrotropin (TSH) did not stimulate thyroid cell PGE generation in vitro, providing evidence against a role for TSH in this phenomenon. Administration of maximal doses of indomethacin to two thyrotoxic patients did not significantly alter peripheral thyroid hormone concentrations. These data suggest that thyroidal PGE has a function other than to stimulate thyroid hormone secretion in Graves' disease.