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ARTICLE

Dose Effects of Aspirin on Gastric Prostaglandins and Stomach Mucosal Injury

Makau Lee; Byron Cryer; and Mark Feldman

1 February 1994 | Volume 120 Issue 3 | Pages 184-189

Objective: To determine if a dose of aspirin exists that might inhibit thromboxane-dependent platelet function without causing gastric mucosal injury, we studied the effects of a wide range of doses of aspirin (3 mg/d to 2600 mg/d) on gastric juice prostaglandins (PGE₂ and PGF₂), on serum thromboxane B₂, and on stomach mucosal injury as reflected by gastric juice hemoglobin and DNA concentrations.

Design: A randomized, placebo-controlled study.

Setting: Research laboratory at a Veterans Affairs medical center.

Participants: 16 healthy volunteers (5 men and 11 women).

Intervention: In the first part of the study, volunteers received placebo; aspirin, 324 mg/d; 1300 mg/d; or 2600 mg/d for 2 days. In the second part, volunteers received placebo; aspirin, 3 mg/d; 10 mg/d; 30 mg/d; or 81 mg/d for 8 days.

Measurements: Gastric juice PGE₂ and PGF₂, hemoglobin and DNA concentrations; gastric juice volume and acidity; and serum salicylate and thromboxane B₂ concentrations.

Results: In the first part, significant and similar (approximately 50%) inhibition of gastric juice prostaglandin output was observed with daily aspirin doses of 324 to 2600 mg. However, a significant increase in gastric juice hemoglobin output occurred only with 2600 mg/d. In the second part, significant inhibition (approximately 50%) of gastric PGE₂ output was noted at a daily aspirin dose of 30 mg. Lower aspirin doses did not reduce PGE₂ output significantly, although these doses did significantly reduce serum thromboxane B₂ in a dose-related manner.

Conclusions: Aspirin can significantly reduce serum thromboxane B₂ at doses of 3 mg/d or 10 mg/d, which are significantly below the threshold dose for significant gastric prostaglandin inhibition and acute stomach mucosal injury.

Author and Article Information

From the University of Texas Southwestern Medical Center and the Veterans Affairs Medical Center, Dallas, Texas.
Requests for Reprints: Mark Feldman, MD, Medical Service (111), Dallas Veterans Affairs Medical Center, 4500 South Lancaster Road, Dallas, TX 75216.
Acknowledgments: The authors thank Cora Barnett, Mary Walker, Dr. V. K. Pillai, and Philip Michaelson for technical assistance.
Grant Support: By a merit grant from the Department of Veterans Affairs and an R01 grant from the National Institute for Diabetes, Digestive and Kidney Disease (DK16816). The study was also supported by the Southland Financial Corporation Chair in Geriatrics (MF).

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