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INFORMATION: Pain Reliever
Pain relievers are group of the anti-inflammatory, analgesic and antipyretic drugs. They
are frequently called nonsteroidal antiinflammatory drugs or NSAIDs. NSAIDs find their chief clinical application as antiinflammatory agent in the treatment of musculoskeletal disorder such as rheumatoid
arthritis, osteoarthritis, ankylosing spondylitis and other nonrheumatoid arthropathies. In the treatment of non-articular rheumatic cases NSAIDs are indicated in periarticular conditions eg frozen shoulder
(capsulitis), bursitis, tendinitis, tenosynovitis and low-back pain. NSAIDs can also be used in soft-tissue injuries eg sprains and strains. In general, NSAIDs provide only symptomatic relief from the
pain and inflammation associated with the disease and do not arrest the progression of pathological injury to tissue during severe episodes.
When employed as analgesic, these drugs usually are effective only against
pain of low-to-moderate intensities eg dysmenorrhea, dental and postoperative pain. They lack the unwanted effects the opioids on central nervous system including respiratory depression and the development of
physical dependence. NSAIDs do not change the perception of sensory modalities other than pain. Chronic postoperative pain or pain arising from inflammation is particularly well controlled by NSAIDs,
where as pain arising from hollow viscera usually is not relieved. As antipyretics, NSAIDs reduce the body temperature in febrile states. Although all such drugs are antipyretics and analgesics, some are not
suitable for either routine or prolonged use because of toxicity.
The inhibition of cycloxygenase(COX) activities, and subsequently prostaglandin (PG ) production, is the common basic mechanisms of action of NSAIDs
for their therapeutic benefits.However, PGs have diverse physiological and pathathological functions. Therefore, the inhibition of PG synthesis via COX enzyme was central to both the therapeutic and toxic effects of
NSAIDs. In 1992 two isoforms of COX have been identified. One is a constitutive enzyme (COX-1) producing regulatory prostadinoids under physiological conditions such as maintaining nornal gastric
mucosa,influencing renal blood flow , and aiding in blood clotting by abetting platelet aggregation , where as the other (COX-2) is induced by mitogens and proinflammatory cytokines during pathological states such
as inflamammation. All conventional NSAIDs nonspecifically inhibit both COX-1 and COX-2 at standard antiinflammatory doses. These raise the new concept that the . Side effects of NSAIDs are dued to their
ability to inhibit COX-1, while the anti-inflammatory(therapeutic) effects of these agents are due to their ability to inhibit COX-2. The exact COX-2 inhibitor,has been recently developed based on and understanding of
the differences between COX-1 and COX-2 . Thus, the full criterias of this class are preferential Inhibition of COX-2 than COX-1 in both in vitro and in vivo
test and do not affect on marker of COX-1 In human such as gastric mucosa and platelet functions. It means that the term specific COX-2 inhibitor should be used to describe agents which inhibit COX-2 but have no effect on COX-1 over the whole range of doses used and concentration achieved in clinical usages. At the moment, celecoxib(CELEBREX) and rofecoxib were the excellent hightly selective COX-2 inhibitor.
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