Non-steroidal anti-inflammatory drugs are usually the first medicines used to treat arthritis. This article discusses how they work.
Non-steroidal-anti-inflammatory drugs (NSAIDS) block the production of prostaglandins, prostacyclin, and thromboxane by inhibiting an enzyme called cyclo-oxygenase. Prostaglandins are important because they play a major role in the development of fever, pain, and inflammation. Thromboxane is important because it is what makes platelets (the cells in your blood that are responsible for clotting) sticky. Prostacyclins are important for helping produce the mucus lining of the stomach which protects it from injury.
Traditional NSAIDS such as ibuprofen (Motrin), naproxen (Naprosyn), diclofenac (Voltaren), nabumetone (Relafen), and etodolac (Lodine) non-selectively block the formation of prostaglandins, thromboxane, and prostacyclin. In addition to the anti-inflammatory effect, these drugs also have effects on blocking the effects of thromboxane. NSAIDS also inhibit prostacyclin to the point where the mucus lining of the stomach no longer is adequate to protect the stomach. That is why NSAIDS can cause stomach ulcers and bleeding.
Cyclo-oxygenase, the enzyme that is blocked by NSAIDS, comes in two forms. COX-1 and COX-2. COX-2 is the primary form responsible for the production of prostaglandins which lead to inflammation and pain. COX-2 is present at the site of inflammation. COX-1 on the other hand is important for the production of prostacyclin which helps form the protective mucus layer of the stomach and also is responsible for the production of thromboxane. COX-1 is present throughout the body.
COX-2 selective drugs block only the COX-2 pathway and therefore suppress inflammation without damaging the mucus layer of the stomach.
Theoretically all this information should make sense and make it pretty straightforward as to what will happen when these medicines are used. Unfortunately, in real life things don’t work that way. What actually happens is that nonselective NSAIDS do not have any protective effects on prevention of strokes and heart attacks because of their effect on thromboxane.
To make the picture worse, it appears that both non-selective NSAIDS as well as some COX-2 drugs (Vioxx) have the potential for increasing the likelihood of stroke and heart attack. So, the current feeling is that neither non-selective nor COX-2 selective NSAIDS have any protective effects for the heart… and in fact all NSAIDS -as a class -appear to increase the likelihood of cardiovascular events.
COX-2 drugs do appear to be protective against the development of ulcers. When combined with aspirin, the protective gastrointestinal effect of COX-2 drugs also seems to disappear.
So… when deciding whether or not to use NSAIDS for arthritis, a careful analysis of risks and benefits must be made.
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