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NSAID와 COX-2 Inhibitor의 비교 jdoe |
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s are indicated for osteoarthritis patients who do not respond to acetaminophen and topical analgesics. NSAIDs were traditionally the drugs of choice in osteoarthritis, and most primary care physicians still choose NSAIDs first. However, the drugs ability to provide symptomatic relief is not necessarily better than that obtained with acetaminophen, probably because inflammation plays little role in osteoarthritis. There is also some concern about deleterious effects on cartilage metabolism. However, the main reason that NSAIDs are not employed as first-line therapy is their toxicity.
There are many NSAIDs to choose from, but no evidence indicates that one is more effective than another in OA. Toxicities are comparable too, but nonacetylated NSAIDs (e.g.,salsalate, choline magnesium trisalicylate) have less renal toxicity and antiplatelet effects. Since intensity of OA pain varies from day to day-and even within a day-using short-acting NSAIDs as needed is a reasonable approach. Low doses of NSAIDs should be used before higher ones are considered.
2.Mechanism of NSAIDs Action
Nonsteroidal anti-inflammatory drugs inhibit the enzyme cyclooxygenase(COX), which is the first enzyme in the pathway that converts arachidonic acid into various prostaglandins. Prostaglandins are locally synthesized chemicals that have a role in inflammation as well as numerous other body processes.
The nonspecific inhibition of prostaglandin synthesis throughout the body causes the wide range of adverse effects associated with NSAIDs.
The greatest problem with NSAIDs is that they may cause gastrointestinal bleeding and ulcers. NSAIDs also interfere with platelet fuction. Inhibition of platelet aggregation may increase the risk of bleeding problems, including GI bleeding.
3.COX-1 VERSUS COX-2
COX-1 is always present at low levels in many organs, including platelets, the kidney and gastrointestinal tract. Under basal conditions COX-2 is present only in a few loci, including th< 저작권자 © 약국신문 무단전재 및 재배포금지 > |
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