Open AccessMitigating the Cardiovascular and Renal Effects of NSAID s
Author(s) -
Curiel Rodolfo V.,
Katz James D.
Publication year - 2013
Publication title -
pain medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.893
H-Index - 97
eISSN - 1526-4637
pISSN - 1526-2375
DOI - 10.1111/pme.12275
Subject(s) - medicine , prostacyclin , aspirin , naproxen , cyclooxygenase , celecoxib , pharmacology , ibuprofen , population , renal papillary necrosis , thromboxane , rofecoxib , platelet , kidney , biochemistry , pathology , enzyme , chemistry , alternative medicine , environmental health
Objective Nonsteroidal anti‐inflammatory drugs ( NSAID s) are principal pharmacologic agents for symptom relief in patients with arthritis and other inflammatory conditions. Cardiovascular risk is associated with all NSAID s, excluding aspirin. Selective inhibition of cyclo‐oxygenase‐2 ( COX )‐2 could produce a relative reduction in endothelial production of prostacyclin, while leaving the platelet production of thromboxane A 2 ( TXA 2 ) intact. It has been speculated that this imbalance of homeostatic prostanoids might increase the risk for thrombotic events. The goal of this review is to provide physicians guidelines to mitigate cardiovascular and nephrotoxicity of NSAID s. Methods We conducted a systematic literature review to determine what information is available to guide treatment decisions in this patient population. Results Selective inhibition of COX ‐2 could produce a relative reduction in endothelial production of prostacyclin, while leaving the platelet production of TXA 2 intact. Increasing degrees of selectivity for COX ‐2 are associated with augmented cardiovascular risk, whereas increasing degrees of selectivity for cyclo‐oxygenase‐2 ( COX ‐1) are associated with augmented gastrointestinal risk. Some NSAID s (such as ibuprofen) can interfere with the cardioprotective effects of aspirin by competitively binding to COX ‐1 enzyme, resulting in increased TXA 2 production Naproxen may differ from other NSAID s in sustaining functionally important degrees of inhibition of platelet cyclooxygenase‐1 activity throughout the dosing interval. Conclusion It is of paramount importance to consider individual health factors when choosing therapy with NSAID s.