Prostaglandins as mediators of hypercalcemia associated with certain types of cancer.

Abstract

We investigated the role of prostaglandins in the hypercalcemia associated with neoplasia. In patients with hypercalcemia and solid tumors the excretion of the major urinary metabolite of the E prostaglandins, 7 alpha-hydroxy-5, 11-diketotetranorprostane-1, 16-dioic acid (PGE-M), was significantly greater than normal, P LESS THAN 0.01 (median of 58.4 and 7.1 ng per milligram of creatinine respectively). Slightly elevated values were seen in normocalcemic patients with solid tumors (14.3 ng per milligram). The levels of the metabolite were normal in hypercalcemic patients with either hematologic neoplasia or primary hyperparathyroidism. Immunoreactive parathyroid hormone was undetectable in the plasma of all hypercalcemic patients with solid tumors. Inhibition of prostaglandin synthesis by aspirin or indomethacin reduced excretion of both the urinary metabolite and serum calcium in six hypercalcemic patients with solid tumors and elevated excretion of the metabolite. These findings support the concept that prostaglandins are mediators of the hypercalcemia caused by certain solid tumors.

• Authors: H W Seyberth, G V Segre, J L Morgan, B J Sweetman, J T Potts Jr, J A Oates
• Journal: The New England journal of medicine (N Engl J Med) Vol. 293 Issue 25 Pg. 1278-83 (Dec 18 1975) ISSN: 0028-4793 [Print] United States
• PMID: 1186822 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Parathyroid Hormone
• Prostaglandin Antagonists
• Prostaglandins
• Prostaglandins E
• Aspirin
• Calcium
• Indomethacin

Topics

• Aspirin (pharmacology)
• Calcium (blood, urine)
• Humans
• Hypercalcemia (etiology, metabolism)
• Indomethacin (pharmacology)
• Male
• Middle Aged
• Neoplasms (complications, metabolism)
• Parathyroid Hormone (blood)
• Prostaglandin Antagonists (pharmacology)
• Prostaglandins (biosynthesis, physiology)
• Prostaglandins E (metabolism, physiology)