Cox-2 inhibitors and the risk of cardiovascular thrombotic events.

2.50
Hdl Handle:
http://hdl.handle.net/10147/233452
Title:
Cox-2 inhibitors and the risk of cardiovascular thrombotic events.
Authors:
Khan, M; Fraser, A
Citation:
Cox-2 inhibitors and the risk of cardiovascular thrombotic events. 2012, 105 (4):119-21 Ir Med J
Publisher:
Irish Medical Journal (IMJ)
Journal:
Irish medical journal
Issue Date:
Apr-2012
URI:
http://hdl.handle.net/10147/233452
PubMed ID:
22708229
Additional Links:
http://www.ncbi.nlm.nih.gov/pubmed/22708229
Abstract:
In 1971, Vane showed that the analgesic action of traditional NSAIDs relies on inhibition of the cyclo-oxygenase (COX) enzyme, which in turn results in reduced synthesis of proalgesic prostaglandins. Two decades later COX was shown to exist as two distinct isoforms. The constitutive isoform COX-1, supports the beneficial homeostatic functions whereas the inducible isoform, COX-2 becomes up regulated by inflammatory mediators and its products cause many of the symptoms of inflammatory diseases such as rheumatoid and osteoarthritis. Despite the benefits of NSAIDs for acute and chronic pain one of the most clinically significant and well characterized adverse effect is on GI mucosa. The search for NSAIDs with less gastrointestinal toxicity led to the introduction of the selective cyclo-oxygenase-2 (COX-2) inhibitors. The COX-2 selective (COX-1 sparing) inhibitors are associated with reduced GI mucosal damage as demonstrated in several trials. In light of the overwhelming and sometimes contradictory information for patients and physicians regarding the safety of COX-2 agents this article will summarize the available evidence regarding cardiovascular (CV) safety data and contemporary recommendations for prescribing of COX-2-selective NSAIDs.
Language:
en
ISSN:
0332-3102

Full metadata record

DC FieldValue Language
dc.contributor.authorKhan, Men_GB
dc.contributor.authorFraser, Aen_GB
dc.date.accessioned2012-07-12T14:13:49Z-
dc.date.available2012-07-12T14:13:49Z-
dc.date.issued2012-04-
dc.identifier.citationCox-2 inhibitors and the risk of cardiovascular thrombotic events. 2012, 105 (4):119-21 Ir Med Jen_GB
dc.identifier.issn0332-3102-
dc.identifier.pmid22708229-
dc.identifier.urihttp://hdl.handle.net/10147/233452-
dc.description.abstractIn 1971, Vane showed that the analgesic action of traditional NSAIDs relies on inhibition of the cyclo-oxygenase (COX) enzyme, which in turn results in reduced synthesis of proalgesic prostaglandins. Two decades later COX was shown to exist as two distinct isoforms. The constitutive isoform COX-1, supports the beneficial homeostatic functions whereas the inducible isoform, COX-2 becomes up regulated by inflammatory mediators and its products cause many of the symptoms of inflammatory diseases such as rheumatoid and osteoarthritis. Despite the benefits of NSAIDs for acute and chronic pain one of the most clinically significant and well characterized adverse effect is on GI mucosa. The search for NSAIDs with less gastrointestinal toxicity led to the introduction of the selective cyclo-oxygenase-2 (COX-2) inhibitors. The COX-2 selective (COX-1 sparing) inhibitors are associated with reduced GI mucosal damage as demonstrated in several trials. In light of the overwhelming and sometimes contradictory information for patients and physicians regarding the safety of COX-2 agents this article will summarize the available evidence regarding cardiovascular (CV) safety data and contemporary recommendations for prescribing of COX-2-selective NSAIDs.en_GB
dc.language.isoenen
dc.publisherIrish Medical Journal (IMJ)en_GB
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/22708229en_GB
dc.rightsArchived with thanks to Irish medical journalen_GB
dc.titleCox-2 inhibitors and the risk of cardiovascular thrombotic events.en_GB
dc.identifier.journalIrish medical journalen_GB
dc.description.provinceMunsteren

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