Risk of Cardiovascular Events in Patients Receiving Celecoxib: A Meta-Analysis of Randomized Clinical Trials

White, William Β.; West, Christine R.; Borer, Jeffrey S.; Gorelick, Philip B.; LaVange, Lisa M.; Pan, Sharon; Weiner, Ethan; Verburg, Kenneth M.

doi:10.1016/j.amjcard.2006.07.069

Cited by 176 publications

(111 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Findings were dissimilar for VIGOR and CLASS, as absolute (nonadjudicated) CV event rates were higher with rofecoxib 50 mg daily than with naproxen 500 mg twice daily in the VIGOR Trial, 2 whereas they were similar for celecoxib 800 mg daily, ibuprofen 2400 mg daily, and diclofenac 150 mg daily in CLASS (Figure 3). 59 The CV event rates in 2 meta-analyses of celecoxib and various NSAIDs 60,61 in the osteoarthritis and rheumatoid arthritis populations confirmed that there were similar rates of Anti-Platelet Trialists' Collaboration (APTC) 62 adjudicated end points.…”

Section: Evaluating CV Events In Clinical Trials Of Arthritis With Comentioning

confidence: 82%

“…The CV event rates in the arthritis trials range from 0.7% in the TARGET 63 treatment arms to Ϸ1% in the CLASS treatment arms 59 and pooled analyses of clinical trials for celecoxib 61 to Ϸ2% in the rofecoxib arm in VIGOR. 2 Whereas the limitations of these trials include a lack of power required for elucidating CV risk in a definitive fashion and maximal treatment exposure of 15 months, the controlled clinical trial data do suggest that supratherapeutic doses of celecoxib (800 mg daily) and lumaricoxib (400 mg daily) have CV risk that is similar to the nonselective NSAIDs.…”

Section: Evaluating CV Events In Clinical Trials Of Arthritis With Comentioning

confidence: 99%

See 1 more Smart Citation

Cardiovascular Effects of the Cyclooxygenase Inhibitors

White

2007

Hypertension

Self Cite

103

View full text Add to dashboard Cite

C yclooxyenase (COX)-2 selective inhibitors were developed to create a new class of nonsteroidal antiinflammatory drugs (NSAIDs) with properties similar to those of nonselective NSAIDS but without their potential COX-1-mediated gastrointestinal toxicities. 1,2 Studies of the various COX-2 selective inhibitors have shown that they are in fact associated with a significantly lower risk of upper and lower gastrointestinal complications than traditional NSAIDs, except in patients who are taking concomitant low-doses of aspirin.Recent evidence also suggests that some doses of the COX-2 selective inhibitors, and perhaps some traditional NSAIDs as well, are associated with an increased risk of adverse cardiovascular (CV) events. Reports of a higher incidence of myocardial infarction (MI) among patients with arthritis taking high doses of the COX-2 selective inhibitor rofecoxib compared with those taking the NSAID naproxen 2-4 have had heightened concerns since 2001 regarding selective COX-2 inhibitor safety. In addition, in early 2005, elevated CV event rates were reported in patients with spontaneous adenomatous polyps who were taking high doses of celecoxib compared with placebo 5 and in patients who received parenteral parecoxib followed by oral valdecoxib versus placebo immediately after coronary artery bypass graft surgery. 6 This article represents a compilation of the data concerning the effects of both nonselective and selective NSAIDs on blood pressure (BP), particularly in patients with hypertension and/or on antihypertensive agents. Subsequently, the impact that the COX inhibitors have on CV events from several recent clinical trials for the treatment of arthritis or for cancer prevention, as well as from selected large observational studies, is discussed. CV Pharmacology of COX InhibitionCOXs participate in numerous physiological functions and human pathological disorders. The COX-1 isoform is constitutively expressed in most tissues where it regulates the synthesis of prostaglandins. COX-1 is the only form of the enzyme in mature platelets and is also expressed in the vascular endothelium, the gastrointestinal epithelium, brain, spinal cord, and kidney. The COX-2 isoform plays an important role in induction of inflammation in response to injury, as well as later repair of inflammation. It is noteworthy that COX-2 may be induced by bacterial endotoxins, cytokines, and growth factors and is expressed in atherosclerotic plaques, during angiogenesis, during wound healing, and in a variety of epithelial cell cancers. [7][8][9] In addition, COX-2 is constitutively expressed in the macula densa and renal medullary interstitium. 10,11 As discussed below, one result of COX-2 inhibition is a reduction in natriuresis and the development of hypertension in susceptible populations. The COX isoenzymes are similar in structure, but the substrate-binding channel of COX-2 contains a side pocket that is absent in COX-1. This structural difference has allowed for the design and development of COX inhibitors with side chains ...

show abstract

Section: Evaluating CV Events In Clinical Trials Of Arthritis With Comentioning

confidence: 82%

Section: Evaluating CV Events In Clinical Trials Of Arthritis With Comentioning

confidence: 99%

Cardiovascular Effects of the Cyclooxygenase Inhibitors

White

2007

Hypertension

Self Cite

103

View full text Add to dashboard Cite

show abstract

“…I motsetning til dette viste en metaanalyse av White og medarbeidere fra 2007 ingen økt risiko for kardiovaskulaere hendelser etter bruk av celekoksib sammenliknet med placebo eller tradisjonelle ikke-steroide antiinflammatoriske midler (14). Kriteriene for inklusjon i denne samleanalysen var at data blant annet skulle vaere fra celekoksibprodusenten Pfizers egen database og publisert før oktober 2004.…”

Section: Celekoksibunclassified

“…Disse tre studiene ble alle avsluttet tidligere enn planlagt på grunn av økt forekomst av kardiovaskulaere komplikasjoner i celekoksibgruppen i APC-studien. White og medarbeideres analyse (14) inkluderer på den annen side mange studier av kort varighet og/ eller med få deltakere (hvor bivirkningsfrekvensen blir lav) og mange studier med komparatoren diklofenak (se under).…”

Section: Celekoksibunclassified

Hjerte, smerte – kardiovaskulær sikkerhet og ikke-steroide antiinflammatoriske midler

Møllersen¹,

Norgård²,

Spigset³

et al. 2015

Tidsskriftet

View full text Add to dashboard Cite

“…Non-steroidal anti-inflammatory drugs (NSAIDS) such as Ibuprofen, Mefenamic acid and selective cyclo-oxygenase-2 (COX-2) inhibitors are some of the most commonly prescribed medications worldwide, these drugs are used to treat painful inflammatory conditions such as arthritis, traumatic injuries, pain and fever [1]. Non-steroidal antiinflammatory drugs (NSAIDs) are among the most frequently prescribed drugs for treatment of pain, fever, and inflammatory and rheumatic diseases.…”

Section: Introductionmentioning

confidence: 99%

Synthesis and anti-inflammatory evaluation of novel thiadiazol derivatives of Mefenamic acid

Ahmadi¹

2017

Bull. Chem. Soc. Eth.

View full text Add to dashboard Cite

ABSTRACT. In the search for new potential non-steroidal anti-inflammatory agents, some novel Mefenamic acid derivatives were synthesized and confirmed by spectroscopic data. The anti-inflammatory activities of these compounds were evaluated by the croton oil-induced ear oedema test in mice. The preliminary pharmacological evaluations indicate that these new compounds showed potent anti-inflammatory activities compare to control and Indomethacin groups.

show abstract

Risk of Cardiovascular Events in Patients Receiving Celecoxib: A Meta-Analysis of Randomized Clinical Trials

Cited by 176 publications

References 14 publications

Cardiovascular Effects of the Cyclooxygenase Inhibitors

Cardiovascular Effects of the Cyclooxygenase Inhibitors

Hjerte, smerte – kardiovaskulær sikkerhet og ikke-steroide antiinflammatoriske midler

Synthesis and anti-inflammatory evaluation of novel thiadiazol derivatives of Mefenamic acid

Contact Info

Product

Resources

About