Non-steroidal anti-inflammatory agent: Difference between revisions
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===Gastrointestinal=== | ===Gastrointestinal=== | ||
NSAIDs may contribute to gastrointestinal ulceration including [[peptic ulcer disease]]. A [[meta-analysis]] concluded "[[ibuprofen]] was associated with the lowest relative risk, followed by [[diclofenac]]. Azapropazone, tolmetin, ketoprofen, and [[piroxicam]] ranked highest for risk and [[indomethacin]], [[naproxen]], [[sulindac]], and [[aspirin]] occupied intermediate positions. Higher doses of ibuprofen were associated with relative risks similar to those withnaproxen and indomethacin."<ref name="pmid8664664">{{cite journal |author=Henry D, Lim LL, Garcia Rodriguez LA, ''et al'' |title=Variability in risk of gastrointestinal complications with individual non-steroidal anti-inflammatory drugs: results of a collaborative meta-analysis |journal=BMJ |volume=312 |issue=7046 |pages=1563–6 |year=1996 |month=June |pmid=8664664 |pmc=2351326 |doi= |url=http://bmj.com/cgi/pmidlookup?view=long&pmid=8664664 |issn=}}</ref> | NSAIDs may contribute to gastrointestinal ulceration including [[peptic ulcer disease]]. A [[meta-analysis]] concluded "[[ibuprofen]] was associated with the lowest relative risk, followed by [[diclofenac]]. Azapropazone, tolmetin, ketoprofen, and [[piroxicam]] ranked highest for risk and [[indomethacin]], [[naproxen]], [[sulindac]], and [[aspirin]] occupied intermediate positions. Higher doses of ibuprofen were associated with relative risks similar to those withnaproxen and indomethacin."<ref name="pmid8664664">{{cite journal |author=Henry D, Lim LL, Garcia Rodriguez LA, ''et al'' |title=Variability in risk of gastrointestinal complications with individual non-steroidal anti-inflammatory drugs: results of a collaborative meta-analysis |journal=BMJ |volume=312 |issue=7046 |pages=1563–6 |year=1996 |month=June |pmid=8664664 |pmc=2351326 |doi= |url=http://bmj.com/cgi/pmidlookup?view=long&pmid=8664664 |issn=}}</ref> | ||
The risk of [[peptic ulcer disease]] is higher if NSAIDs are combined with [[corticosteroid]]s.<ref name="pmid2012355">{{cite journal |author=Piper JM, Ray WA, Daugherty JR, Griffin MR |title=Corticosteroid use and peptic ulcer disease: role of nonsteroidal anti-inflammatory drugs |journal=Ann. Intern. Med. |volume=114 |issue=9 |pages=735–40 |year=1991 |month=May |pmid=2012355 |doi= |url= |issn=}}</ref> | |||
===Renal=== | ===Renal=== | ||
Revision as of 09:49, 25 January 2009
Non-steroidal anti-inflammatory agents, also called non-steroidal anti-inflammatory drugs (NSAIDs) are defined as "anti-inflammatory agents that are not steroids. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions. They are used primarily in the treatment of chronic arthritic conditions and certain soft tissue disorders associated with pain and inflammation. They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects. Certain NSAIDs also may inhibit lipoxygenase enzymes or phospholipase C or may modulate T-cell function."[1]
Classification
Non-selective inhibitors of clooxygenase
These drugs inhibit both cyclooxygenase isozymes. An example is aspirin.
Selective inhibitors of cyclooxygenase 2
Adverse reactions
Gastrointestinal
NSAIDs may contribute to gastrointestinal ulceration including peptic ulcer disease. A meta-analysis concluded "ibuprofen was associated with the lowest relative risk, followed by diclofenac. Azapropazone, tolmetin, ketoprofen, and piroxicam ranked highest for risk and indomethacin, naproxen, sulindac, and aspirin occupied intermediate positions. Higher doses of ibuprofen were associated with relative risks similar to those withnaproxen and indomethacin."[2]
The risk of peptic ulcer disease is higher if NSAIDs are combined with corticosteroids.[3]
Renal
NSAIDs may cause acute kidney injury due to acute tubular necrosis. Although this is usually interstitial nephritis, NSAIDS can also cause minimal-change disease in the glomerulus.[4]
Damage from NSAIDS may rarely occur after just a few doses.[4]
References
- ↑ National Library of Medicine. Non-steroidal anti-inflammatory agents. Retrieved on 2007-11-19.
- ↑ Henry D, Lim LL, Garcia Rodriguez LA, et al (June 1996). "Variability in risk of gastrointestinal complications with individual non-steroidal anti-inflammatory drugs: results of a collaborative meta-analysis". BMJ 312 (7046): 1563–6. PMID 8664664. PMC 2351326. [e]
- ↑ Piper JM, Ray WA, Daugherty JR, Griffin MR (May 1991). "Corticosteroid use and peptic ulcer disease: role of nonsteroidal anti-inflammatory drugs". Ann. Intern. Med. 114 (9): 735–40. PMID 2012355. [e]
- ↑ 4.0 4.1 Rabb H, Colvin RB (2007). "Case records of the Massachusetts General Hospital. Case 31-2007. A 41-year-old man with abdominal pain and elevated serum creatinine". N. Engl. J. Med. 357 (15): 1531–41. DOI:10.1056/NEJMcpc079024. PMID 17928602. Research Blogging.