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pubmed:abstractText |
There is considerable circumstantial evidence to support the concept that prostaglandins of the E series can mediate hypercalcemia in neoplastic disease. However, other metabolites of prostaglandin endoperoxides could contribute to the hypercalcemia and the site of the production of prostaglandins is not established. Further analysis of prostaglandin endoperoxide metabolism in tumor and bone tissue and in the circulation will clarify the specific mechanism. The development of quantitative analysis of prostaglandin metabolites had made it possible to identify prostaglandin-dependent hypercalcemia. Therapeutic application of the inhibitors of prostaglandin cyclo-oxygenase in the treatment of patients with prostaglandin-mediated hypercalcemia is feasible, but its general usefulness remains to be evaluated. The development of antagonists to the action of prostaglandin at the affected end organ site, presumably bone, would represent an important therapeutic advance.
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