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Donald L. Kaminski, MD; Y. G. Deshpande, MS; Scott Westfall, MD; David Herbold, MD

Arch Surg. 1989;124(3):277-280.

Abstract
• The prostanoids have been demonstrated to be involved in gallbladder physiology and disease. In previous reports, prostaglandin E (PGE) compounds were found to be increased in inflamed human gallbladders. Prostaglandin synthetase inhibition decreased PGE formation by human gallbladders; however, the relief of symptoms of cholecystitis did not correlate well with the decrease in PGE formation. This suggested that other prostanoids may be involved in cholecystitis. The purpose of this study was to evaluate the production of the proinflammatory arachidonic acid metabolite prostacyclin by gallbladders from patients with calculous cholecystitis. The formation of PGE and 6-ketoprostaglandin F₁ (6-keto-PGF₁), the stable metabolite of prostacyclin, in normal human gallbladder mucosal cells and muscle tissue was compared with that produced by diseased mucosal cells and muscle tissue. Normal human gallbladders produced small amounts of 6-keto-PGF₁, and no differences in formation rates were evident when muscle tissue was compared with mucosal cells. Diseased gallbladders produced significantly greater amounts of 6-keto-PGF₁ than did normal gallbladders, and diseased gallbladder muscle produced approximately four times greater amounts of 6-keto-PGF₁ than did diseased gallbladder mucosa. Prostacyclin formation is increased in diseased human gallbladders and may be an important mediator of the inflammatory changes of cholecystitis.

(Arch Surg 1989;124:277-280)

Author Affiliations
From the Department of Surgery, St Louis University Medical Center.

Footnotes
Accepted for publication March 15, 1988.

Reprint requests to Department of Surgery, St Louis University Medical Center, 1325 S Grand Blvd, St Louis, MO 63104 (Dr Kaminski).

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