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Active Smoking Depresses Prostaglandin Synthesis in Human Gastric Mucosa

G. FOREST QUIMBY, B.A.; CANAN AVUNDUK BONNICE, M.D., Ph.D.; SUMNER H. BURSTEIN, Ph.D.; and GREGORY L. EASTWOOD, M.D.
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▸Requests for reprints should be addressed to Gregory L. Eastwood, M.D.; Gastroenterology Division, University of Massachusetts Medical School, 55 Lake Avenue North; Worcester, MA 01605.


Worcester, Massachusetts


© 1986 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1986;104(5):616-619. doi:10.7326/0003-4819-104-5-616
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To determine the effect of smoking on gastroduodenal mucosal prostaglandin synthesis, endoscopies were done after an overnight fast on 10 nonsmokers, 12 active smokers who smoked four cigarettes in the hour before endoscopy, and then 11 of the smokers who refrained from smoking for 12 hours. Biopsy samples of fundic, antral, and duodenal mucosae were incubated, and the accumulation of prostaglandin E2 and 6-keto-prostaglandin F in the incubation medium was measured by radioimmunoassay. We assumed that accumulation of prostaglandins in the medium reflected mucosal synthesis. Comparison of active and inactive smoking showed that active smoking significantly depressed 6-keto-prostaglandin F synthesis in antral and fundic mucosa and prostaglandin E2 synthesis in antral mucosa. Comparison of nonsmokers and inactive smokers showed no difference in prostaglandin synthesis. Active smoking causes a transient decrease in prostaglandin synthesis in fundic and antral mucosae. This depression of prostaglandin synthesis may help explain slower ulcer healing and predisposition to ulcer recurrence in smokers.

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