What precisely is the mechanism of NSAID-induced ulcers? Are NSAIDS direct irritants, or is it a prostaglandin effect?
Consider aspirin. Aspirin plays a dual role in the causation of ulcers. First, there is direct injury to stomach mucosa. Aspirin also inhibits prostaglandins in the stomach, which is one of the important protective mechanisms. If you think about the stomach itself, there is always acid present. What prevents the development of ulcers is the bicarbonate and mucus layers—these are both produced in response to prostaglandins. How much more ulcerogenic is plain aspirin compared to EC ASA, enteric-coated aspirin? We see many ulcer patients who were taking enteric-coated aspirin. The enteric coating prevents the medication from dissolving in the stomach. But once it passes the stomach, reaching the duodenum, it does dissolve, potentially causing an ulcer. The enteric coating may be protective to the stomach. But there is also a systemic effect. Even if you took aspirin intravenously, entirely bypassing the stomach, you would still inhibit the prostaglandin-mediated protection. Are you seeing
