Rofecoxib, a COX-2 Inhibitor, Lowers C-Reactive Protein and Interleukin-6 Levels in Patients With Acute Coronary Syndromes

Monakier, Daniel; Mates, Michal; Klutstein, Marc; Balkin, Jonathan; Rudensky, Bernard; Meerkin, David; Tzivoni, Dan

doi:10.1378/chest.125.5.1610

Cited by 37 publications

(27 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Aspirin use after colorectal cancer diagnosis has also been associated with lower colorectal and overall mortality (70)(71)(72)(73)(74). Furthermore, in patients with myocardial infarction, use of NSAIDs has been associated with lower CRP concentrations (75,76). These results as well as findings from our study provide further evidence to suggest that CRP levels may help recognize candidates for possible prophylactic and adjuvant therapy with anti-inflammatory drugs in the future.…”

Section: Discussionsupporting

confidence: 70%

C-Reactive Protein and Colorectal Cancer Mortality in U.S. Adults

Goyal¹,

Terry

Jin

et al. 2014

Cancer Epidemiology, Biomarkers &Amp; Prevention

View full text Add to dashboard Cite

Background: Chronic inflammation has been associated with colorectal cancer. Prediagnostic levels of C-reactive protein (CRP), a highly sensitive marker of inflammation, have been weakly associated with increased colorectal cancer incidence, but few data are available examining its relationship with colorectal cancer mortality.Methods: In the Third National Health and Nutrition Examination Survey (NHANES III), 65% of the 15,924 adult participants had CRP levels 0.21 mg/dL. Using this as the reference group, we calculated hazard ratios (HR) for higher CRP categories and colorectal cancer mortality, and compared them with HRs for other mortality causes.Results: Over a median follow-up period of 14.2 years, there were 92 deaths from colorectal cancer. Compared with the reference group, multivariable adjusted HRs for colorectal cancer mortality were 2.66 [95% confidence interval (CI), 1.36-5.20] for CRP levels 0.22-0.50 mg/dL; 3.40 (95% CI, 1.48-7.77) for levels 0.51-1.00 mg/dL; and 3.96 (95% CI, 1.64-9.52) for levels >1.00 mg/dL. Estimates for colorectal cancer mortality did not change appreciably after excluding deaths within the first 3 years or by limiting follow-up to 5 or 10 years.Conclusions: In a large representative study of U.S. adults, we observed strong dose-response associations between CRP levels and colorectal cancer mortality.Impact: Further evaluation of CRP may help identify high-risk groups for colorectal cancer screening and those who might benefit most from prophylactic anti-inflammatory therapy. Cancer Epidemiol Biomarkers Prev; 23(8); 1609-18. Ó2014 AACR.

show abstract

Section: Discussionsupporting

confidence: 70%

C-Reactive Protein and Colorectal Cancer Mortality in U.S. Adults

Goyal¹,

Terry

Jin

et al. 2014

Cancer Epidemiology, Biomarkers &Amp; Prevention

View full text Add to dashboard Cite

show abstract

“…58 However, data about rofecoxib and CRP reduction are controversial. Rofecoxib was found to reduce levels of CRP in a six-month follow-up study of patients with established coronary artery heart disease 62 and in a three-month follow-up study of patients with acute coronary artery syndrome 64 but not in two shorter follow-up studies. 61,65 There are no head-to-head studies that compare this effect between celecoxib and rofecoxib.…”

Section: Effects Of Cox-2-selective Nsaids On Vascular Endothelium: Cmentioning

confidence: 89%

Risks versus benefits of cyclooxygenase-2-selective nonsteroidal antiinflammatory drugs

Chaiamnuay

Allison²,

Curtis³

2006

American Journal of Health-System Pharmacy

View full text Add to dashboard Cite

PURPOSE: A summary of the basic science underlying the current controversies regarding cyclooxygenase-2 (COX-2)-selective nonsteroidal antiinflammatory drugs (NSAIDs), including data on their cardiovascular safety, their gastrointestinal (GI) benefits, cost-effectiveness, physician-prescribing trends, and recommendations for prescribing these agents is presented. SUMMARY: A number of randomized controlled trials (RCTs) have reported that COX-2-selective NSAIDs increase cardiovascular events, although there appear to be gradations of risks among the COX-2-selective NSAIDs. In addition, traditional NSAIDs may increase the risk for cardiovascular events, complicating the interpretation of RCTs that use traditional NSAIDs as comparators. Selective inhibitors of COX-2-selective NSAIDs are effective antiinflammatory and analgesic drugs with improved upper-GI safety compared to traditional NSAIDs. Data on the cost-effectiveness of COX-2-selective NSAIDs indicate that they should be limited to patients at high risk for upper-GI adverse effects. However, they had been increasingly used in patients with lower GI risks until recent events reversed that trend. Circumstances under which COX-2-selective NSAIDs may be appropriate are in patients at high GI risk and in patients who did not respond to multiple traditional NSAIDs. The national spotlight in the United States on NSAID-related adverse events and recent lawsuits against health care providers prescribing COX-2-selective NSAIDs further highlights the need for provider-patient communication and risk disclosure. The relative cardiovascular risks of NSAIDs are similar in magnitude to other currently prescribed therapies. CONCLUSION: Health care providers must consider the efficacy, GI and cardiovascular risks, concomitant medications, and costs when determining the appropriateness of COX-2-selective NSAID therapy

show abstract

“…Second, how can anti-inflammatory processes specifically be targeted toward adipose tissue? Aspirin and COX-2 inhibitors are anti-inflammatory and both lower CRP levels, 130,131 but aspirin dramatically reduces cardiovascular risk, 132 whereas the accumulating data on COX-2 inhibitors suggest an increase in myocardial infarction risk. 133 An explanation for this dichotomy may be their differential effects on platelets.…”

Section: Effects Of Cardioprotective Therapies On Systemic Inflammationmentioning

confidence: 99%

Adipose Tissue, Inflammation, and Cardiovascular Disease

Berg

Scherer

2005

Circulation Research

1,824

1,331

View full text Add to dashboard Cite

Abstract-Mounting evidence highlights the role of adipose tissue in the development of a systemic inflammatory state that contributes to obesity-associated vasculopathy and cardiovascular risk. Circulating mediators of inflammation participate in the mechanisms of vascular insult and atheromatous change, and many of these inflammatory proteins are secreted directly from adipocytes and adipose tissue-derived macrophages. Several factors linking obesity with an increased cardiovascular risk have been identified. The adipocyte-specific secretory protein adiponectin is a particularly promising candidate in this context. Its levels are decreased in obesity. Adiponectin may mediate some of its demonstrated cardioprotective effects through its anti-inflammatory properties. In addition to decreased expression of beneficial adipokines, secretion of a host of inflammatory factors from visceral adipose tissue may contribute to the increased cardiovascular risk associated with obesity. The cardioprotective effects of many of the most popular drug regimens corroborate these conclusions, demonstrating that along with improvements in other therapeutic end points, they mediate improvements in systemic inflammation. In some cases, these improvements are attributable to direct suppression of inflammatory signaling in adipocytes.

show abstract

Rofecoxib, a COX-2 Inhibitor, Lowers C-Reactive Protein and Interleukin-6 Levels in Patients With Acute Coronary Syndromes

Cited by 37 publications

References 51 publications

C-Reactive Protein and Colorectal Cancer Mortality in U.S. Adults

C-Reactive Protein and Colorectal Cancer Mortality in U.S. Adults

Risks versus benefits of cyclooxygenase-2-selective nonsteroidal antiinflammatory drugs

Adipose Tissue, Inflammation, and Cardiovascular Disease

Contact Info

Product

Resources

About