Non-steroidal anti-inflammatory agent: Difference between revisions
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'''Non-steroidal anti-inflammatory agents''', also called '''non-steroidal anti-inflammatory drugs''' (NSAIDs) are defined as "anti-inflammatory agents that are not [[glucocorticoid|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 [[prostaglandin]]s 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."<ref name="title-">{{cite web |url=http://www.nlm.nih.gov/cgi/mesh/2007/MB_cgi?term=Non-steroidal+anti-inflammatory+agents |title=Non-steroidal anti-inflammatory agents|author=National Library of Medicine |accessdate=2007-11-19 |format= |work=}}</ref> | '''Non-steroidal anti-inflammatory agents''', also called '''non-steroidal anti-inflammatory drugs''' (NSAIDs) are defined as "anti-inflammatory agents that are not [[glucocorticoid|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 [[prostaglandin]]s 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."<ref name="title-">{{cite web |url=http://www.nlm.nih.gov/cgi/mesh/2007/MB_cgi?term=Non-steroidal+anti-inflammatory+agents |title=Non-steroidal anti-inflammatory agents|author=National Library of Medicine |accessdate=2007-11-19 |format= |work=}}</ref> | ||
The clinical characteristics of NSAISs have been reviewed.<ref>Chou R, Helfand M, Peterson K, Dana T. (2004). [http://derp.ohsu.edu/final/NSAIDS_Final_Report_Update%2032.pdfDrug Class Review of Cyclo-oxygenase (COX)-2 Inhibitors and Non-steroidal Anti-inflammatory Drugs (NSAIDS)]. [http://www.ohsu.edu/ohsuedu/research/policycenter/ Center for Evidence-based Policy]: [http://www.ohsu.edu/ohsuedu/research/policycenter/DERP/Drug Effectiveness Review Project (DERP)]</ref> | |||
==Classification== | ==Classification== | ||
Revision as of 20:54, 16 September 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]
The clinical characteristics of NSAISs have been reviewed.[2]
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.[3][4] 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."[5]
The risk of peptic ulcer disease is higher if NSAIDs are combined with corticosteroids.[6][4]
Non-steroidal anti-inflammatory agents should be avoided in geriatrics according to clinical practice guidelines.[7]
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.[8]
Damage from NSAIDS may rarely occur after just a few doses.[8]
Effectiveness
Combined with acetaminophen
For lumbalgia, acetaminophen one gram orally four times a day combined with diclofenac, a non-steroidal anti-inflammatory agent, was not better than acetaminophen alone in a randomized controlled trial.[9]
For reducing fever, acetaminophen combined with ibuprofen may be better than either drug alone according to a randomized controlled trial.[10]
References
- ↑ National Library of Medicine. Non-steroidal anti-inflammatory agents. Retrieved on 2007-11-19.
- ↑ Chou R, Helfand M, Peterson K, Dana T. (2004). Class Review of Cyclo-oxygenase (COX)-2 Inhibitors and Non-steroidal Anti-inflammatory Drugs (NSAIDS). Center for Evidence-based Policy: Effectiveness Review Project (DERP)
- ↑ Griffin MR, Piper JM, Daugherty JR, Snowden M, Ray WA (February 1991). "Nonsteroidal anti-inflammatory drug use and increased risk for peptic ulcer disease in elderly persons". Ann. Intern. Med. 114 (4): 257–63. PMID 1987872. [e]
- ↑ 4.0 4.1 García Rodríguez LA, Jick H (March 1994). "Risk of upper gastrointestinal bleeding and perforation associated with individual non-steroidal anti-inflammatory drugs". Lancet 343 (8900): 769–72. PMID 7907735. [e]
- ↑ 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]
- ↑ The American Geriatrics Society - Education - AGS Clinical Practice Guideline: Pharmacological Management of Persistent Pain in Older Persons.
- ↑ 8.0 8.1 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.
- ↑ Hancock MJ, Maher CG, Latimer J, et al (2007). "Assessment of diclofenac or spinal manipulative therapy, or both, in addition to recommended first-line treatment for acute low back pain: a randomised controlled trial". Lancet 370 (9599): 1638–43. DOI:10.1016/S0140-6736(07)61686-9. PMID 17993364. Research Blogging.
- ↑ Hay AD, Costelloe C, Redmond NM, et al (2008). "Paracetamol plus ibuprofen for the treatment of fever in children (PITCH): randomised controlled trial". BMJ 337: a1302. PMID 18765450. PMC 2528896. [e]