How NSAIDs Work
NSAIDs work by inhibiting the cyclo-oxygenase (COX-1 and COX-2) enzymes. Both the COX-1 and COX-2 enzymes are involved in the production of prostaglandins, which are hormone-like substances produced in various tissues. They mediate a range of physiological functions, such as metabolism and nerve transmissions. The COX-1 enzymes are responsible for making baseline levels of prostaglandins that, among other things, aid in the production of the natural mucus lining that protects the inner stomach from the damaging effects of acid. COX-2 enzymes, however, are implicated in prostaglandin production that causes inflammation.
Since most NSAIDs block both COX-1 and COX-2 enzymes, they can prevent the body from producing prostaglandins that cause pain and inflammation. At the same time, however, NSAIDs also prevent the production of the stomach’s protective mucus lining. As such, taken in high doses or over a long period of time, NSAIDs can lead to stomach irritation that can eventually result in heartburn and gastritis.
About 15 percent of patients on long term NSAID treatment develop stomach ulcers. Many of these patients do not have symptoms and are unaware of their ulcers. However, they are still at risk for developing serious and potentially life-threatening ulcer complications, such as bleeding or perforations of the stomach.
To prevent these gastric side effects, a variety of medicines may be recommended. Antacids, for example, prevent the production of excess stomach acid. Drugs such as sucralfate (Carafate®) help coat and protect the stomach, while medications like misoprostol (Cytotec®) help restore the lost mucus.
