COX-2 selective non-steroidal anti-inflammatory drugs and risk of serious coronary heart disease

Ray, Wayne A.; Stein, C.M.; Daugherty, James R.; Hall, Kathryn T.; Arbogast, Patrick G.; Griffin, Marie R.

doi:10.1016/s1062-1458(02)00991-1

Cited by 130 publications

(182 citation statements)

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“…8 An observational study conducted in the Tennessee Medicaid population found that rofecoxib at dosages Ͼ25 mg/d was associated with a nearly 2-fold increased risk of AMI compared with nonuse of any NSAID. 9 Our findings differ from the pooled analyses of rofecoxib randomized controlled trials, which showed no significant increase in cardiovascular events compared with non-naproxen NSAIDs. 6,7 In addition, a recently published observational analysis from Ontario also found no increased risk of AMI associated with any dosage of rofecoxib.…”

Section: Discussioncontrasting

confidence: 99%

“…On the basis of previous findings that first-time users may be at the highest risk for cardiovascular events associated with coxibs, 9 we constructed conditional regression models that considered persons exposed only if their use on the index date was their first time using a coxib. We examined the relationship between AMI and the duration of exposure to coxibs in this group of users.…”

Section: Solomon Et Al Cox-2 Inhibitors and Acute Myocardial Infarctimentioning

confidence: 99%

“…8 A large observational study suggested that rofecoxib at dosages Ͼ25 mg was associated with an approximately 2-fold increased risk of AMI compared with celecoxib or no NSAID, whereas rofecoxib Յ25 mg was not associated with an elevated risk. 9 A smaller observational study found no increased risk of AMI with either coxib, but dosage was not addressed. 10 In 2002, more than 41 million prescriptions were filled in the United States for coxibs, 11 making any potential relationship between coxibs and AMI a substantial clinical and public health issue.…”

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confidence: 98%

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Relationship Between Selective Cyclooxygenase-2 Inhibitors and Acute Myocardial Infarction in Older Adults

et al. 2004

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Background-Although cyclooxygenase-2 inhibitors (coxibs) were developed to cause less gastrointestinal hemorrhage than nonselective nonsteroidal antiinflammatory drugs (NSAIDs), there has been concern about their cardiovascular safety. We studied the relative risk of acute myocardial infarction (AMI) among users of celecoxib, rofecoxib, and NSAIDs in Medicare beneficiaries with a comprehensive drug benefit. Celecoxib was not associated with an increased relative risk of AMI in these comparisons. Conclusions-In this study, current rofecoxib use was associated with an elevated relative risk of AMI compared with celecoxib use and no NSAID use. Dosages of rofecoxib Ͼ25 mg were associated with a higher risk than dosages Յ25 mg. The risk was elevated in the first 90 days of use but not thereafter.

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Section: Discussioncontrasting

confidence: 99%

Section: Solomon Et Al Cox-2 Inhibitors and Acute Myocardial Infarctimentioning

confidence: 99%

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confidence: 98%

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Relationship Between Selective Cyclooxygenase-2 Inhibitors and Acute Myocardial Infarction in Older Adults

et al. 2004

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“…In fact, we observed a significant resistance of HUVE cells to the pSUPER.retro viral infection in comparison with different types of human cancer cells, either CRC cells (HT29 and HCA7) and cervix carcinoma cells (HeLa). This observation indicates that endothelial cells are refractory to retroviral infection and suggests that this kind of virus-based approach might not affect the physiological prostaglandins production in vascular tissues, avoiding some of the well-known side effects coming from therapies based on selective COX-2 inhibitors (coxibs) (Ray et al, 2002;Fitzegerald, 2004;Horton, 2004;Mamdani et al, 2004;Oberholzer and Inamdar, 2004;Mitchell and Warner, 2005).…”

Section: Discussionmentioning

confidence: 99%

RNA interference as a key to knockdown overexpressed cyclooxygenase-2 gene in tumour cells

et al. 2006

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Silencing those genes that are overexpressed in cancer and contribute to the survival and progression of tumour cells is the aim of several researches. Cyclooxygenase-2 (COX-2) is one of the most intensively studied genes since it is overexpressed in most tumours, mainly in colon cancer. The use of specific COX-2 inhibitors to treat colon cancer has generated great enthusiasm. Yet, the side effects of some inhibitors emerging during long-term treatment have caused much concern. Genes silencing by RNA interference (RNAi) has led to new directions in the field of experimental oncology. In this study, we detected sequences directed against COX-2 mRNA, that potently downregulate COX-2 gene expression and inhibit phorbol 12-myristate 13-acetate-induced angiogenesis in vitro in a specific, nontoxic manner. Moreover, we found that the insertion of a specific cassette carrying anti-COX-2 short hairpin RNA sequence into a viral vector (pSUPER.retro) greatly increased silencing potency in a colon cancer cell line (HT29) without activating any interferon response. Phenotypically, COX-2 deficient HT29 cells showed a significant impairment of their in vitro malignant behaviour. Thus, the retroviral approach enhancing COX-2 knockdown, mediated by RNAi, proved to be an useful tool to better understand the role of COX-2 in colon cancer. Furthermore, the higher infection efficiency we observed in tumour cells, if compared to normal endothelial cells, may disclose the possibility to specifically treat tumour cells without impairing endothelial COX-2 activity.

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“…These side effects appear to be related to the drugs' inhibition of COX-1 because constitutive expression of COX-2 in normal gastric mucosal tissue is low or absent [9] . However, COX-2 inhibitors may increase the risk of cardiovascular complications, such as heart attack or stroke, especially if they are used for a prolonged time [10] . In this study, we focused on finding NSAIDs that target the nuclear factor-kappa B (NF-κB) signaling pathway, but not COXs.…”

Section: Introductionmentioning

confidence: 99%

Lobolide, a diterpene, blockades the NF-κB pathway and p38 and ERK MAPK activity in macrophages in vitro

Chen

et al. 2012

Acta Pharmacol Sin

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Aim: Recent studies have shown that constitutive activation of the nuclear factor κB (NF-κB) plays a key role in chronic inflammation and cancers. The aim of this study was to characterize lobolide, a cembrane diterpene, as a drug candidate targeting the NF-κB signaling pathway. Methods: A HEK 293/NF-κB-Luc stable cell line was constructed to evaluate the effect of lobolide on NF-κB activation. THP-1 human monocytes and peripheral blood mononuclear cells (PBMCs) from healthy volunteers were tested. Lipopolysaccharide (LPS)-induced TNFα and IL-1β production and activation of the TAK1-IKK-NF-κB pathway were studied using ELISA and Western blot analysis. Results: In HEK 293/NF-κB-Luc stable cells, lobolide (0.19-50 μmol/L) inhibited NF-κB activation in a concentration-dependent manner with an IC 50 value of 4.2±0.3 μmol/L. Treatment with lobolide (2.5-10 μmol/L) significantly suppressed LPS-induced production of TNFα and IL-1β in both THP-1 cells and PBMCs. In THP-1 cells, the suppression was partially caused by blockade of the translocation of NF-κB from the cytoplasm to the nucleus via affecting the TAK1-IKK-NF-κB pathway and p38 and ERK MAPK activity. Conclusion: Lobolide is a potential inhibitor of the NF-κB pathway, which blocks the translocation of NF-κB from the cytoplasm to the nucleus. Lobolide inhibits LPS-stimulated TNFα and IL-1β release, suggesting that the compound might be an anti-inflammatory compound.

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COX-2 selective non-steroidal anti-inflammatory drugs and risk of serious coronary heart disease

Cited by 130 publications

References 0 publications

Relationship Between Selective Cyclooxygenase-2 Inhibitors and Acute Myocardial Infarction in Older Adults

Relationship Between Selective Cyclooxygenase-2 Inhibitors and Acute Myocardial Infarction in Older Adults

RNA interference as a key to knockdown overexpressed cyclooxygenase-2 gene in tumour cells

Lobolide, a diterpene, blockades the NF-κB pathway and p38 and ERK MAPK activity in macrophages in vitro

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