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Adverse Effects of COX-2 Inhibitors
Cyclooxygenase-2 selective inhibitors (COXIBs) were developed with the prime object of minimizing gastrointestinal adverse effects, which are seen with the use of traditional nonsteroidal anti-inflammatory drugs (NSAIDs). Their long-term use is limited by the development of hypertension, edema, and...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
TheScientificWorldJOURNAL
2005
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5936602/ https://www.ncbi.nlm.nih.gov/pubmed/16113940 http://dx.doi.org/10.1100/tsw.2005.82 |
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author | Sharma, Jagdish N. Jawad, Najeeba M. |
author_facet | Sharma, Jagdish N. Jawad, Najeeba M. |
author_sort | Sharma, Jagdish N. |
collection | PubMed |
description | Cyclooxygenase-2 selective inhibitors (COXIBs) were developed with the prime object of minimizing gastrointestinal adverse effects, which are seen with the use of traditional nonsteroidal anti-inflammatory drugs (NSAIDs). Their long-term use is limited by the development of hypertension, edema, and congestive heart failure in a significant proportion of patients. NSAIDs block the activity of both COX isozymes, COX-1 and COX-2, which mediate the enzymatic conversion of arachidonate to prostaglandin H(2) (PGH(2)) and other prostaglandin (PG) metabolites. It is well established that the cardiovascular profile of COX-2 inhibitors can be accounted for by inhibition of COX-dependent PG synthesis. Following the COX-mediated synthesis of PGH(2) from arachidonate, PGH(2) is metabolized to one of at least five bioactive PGs, including PGE(2), PGI(2), PGF(2), PGD(2), or thromboxane A(2) (TXA(2)). These prostanoids have pleiotropic cardiovascular effects, altering platelet function and renal function, and they are acting either as vasodilators or vasoconstrictors. Although COX-1 and COX-2 exhibit similar biochemical activity in converting arachidonate to PGH(2)in vitro, the ultimate prostanoids they produce in vivo may be different due to differential regulation of COX-1 and COX-2, tissue distribution, and availability of the prostanoid synthases. PGs have been established as being critically involved in mitigating hypertension, helping to maintain medullary blood flow (MBF), promoting urinary salt excretion, and preserving the normal homeostasis of thrombosis, and the researchers found that the use of COX-2 inhibitors caused many serious complications in altering the normal body homeostasis. The purpose of the present research is to explain briefly the side effects of COX-2 inhibitors on the renal and cardiovascular system. |
format | Online Article Text |
id | pubmed-5936602 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2005 |
publisher | TheScientificWorldJOURNAL |
record_format | MEDLINE/PubMed |
spelling | pubmed-59366022018-06-03 Adverse Effects of COX-2 Inhibitors Sharma, Jagdish N. Jawad, Najeeba M. ScientificWorldJournal Review Article Cyclooxygenase-2 selective inhibitors (COXIBs) were developed with the prime object of minimizing gastrointestinal adverse effects, which are seen with the use of traditional nonsteroidal anti-inflammatory drugs (NSAIDs). Their long-term use is limited by the development of hypertension, edema, and congestive heart failure in a significant proportion of patients. NSAIDs block the activity of both COX isozymes, COX-1 and COX-2, which mediate the enzymatic conversion of arachidonate to prostaglandin H(2) (PGH(2)) and other prostaglandin (PG) metabolites. It is well established that the cardiovascular profile of COX-2 inhibitors can be accounted for by inhibition of COX-dependent PG synthesis. Following the COX-mediated synthesis of PGH(2) from arachidonate, PGH(2) is metabolized to one of at least five bioactive PGs, including PGE(2), PGI(2), PGF(2), PGD(2), or thromboxane A(2) (TXA(2)). These prostanoids have pleiotropic cardiovascular effects, altering platelet function and renal function, and they are acting either as vasodilators or vasoconstrictors. Although COX-1 and COX-2 exhibit similar biochemical activity in converting arachidonate to PGH(2)in vitro, the ultimate prostanoids they produce in vivo may be different due to differential regulation of COX-1 and COX-2, tissue distribution, and availability of the prostanoid synthases. PGs have been established as being critically involved in mitigating hypertension, helping to maintain medullary blood flow (MBF), promoting urinary salt excretion, and preserving the normal homeostasis of thrombosis, and the researchers found that the use of COX-2 inhibitors caused many serious complications in altering the normal body homeostasis. The purpose of the present research is to explain briefly the side effects of COX-2 inhibitors on the renal and cardiovascular system. TheScientificWorldJOURNAL 2005-08-18 /pmc/articles/PMC5936602/ /pubmed/16113940 http://dx.doi.org/10.1100/tsw.2005.82 Text en Copyright © 2005 Jagdish N. Sharma and Najeeba M. Jawad. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Sharma, Jagdish N. Jawad, Najeeba M. Adverse Effects of COX-2 Inhibitors |
title | Adverse Effects of COX-2 Inhibitors |
title_full | Adverse Effects of COX-2 Inhibitors |
title_fullStr | Adverse Effects of COX-2 Inhibitors |
title_full_unstemmed | Adverse Effects of COX-2 Inhibitors |
title_short | Adverse Effects of COX-2 Inhibitors |
title_sort | adverse effects of cox-2 inhibitors |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5936602/ https://www.ncbi.nlm.nih.gov/pubmed/16113940 http://dx.doi.org/10.1100/tsw.2005.82 |
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