scholarly journals Factors Associated with Celecoxib and Rofecoxib Utilization

2005 ◽  
Vol 39 (4) ◽  
pp. 597-602 ◽  
Author(s):  
Nigel SB Rawson ◽  
Parivash Nourjah ◽  
Stella C Grosser ◽  
David J Graham

BACKGROUND: The cyclooxygenase-2 (COX-2) selective nonsteroidal antiinflammatory drugs (NSAIDs) celecoxib and rofecoxib (before its removal) are marketed as having fewer gastrointestinal (GI)-related complications than nonselective NSAIDs. However, adverse reaction data suggest that the use of COX-2 selective NSAIDs is associated with clinically significant GI events. OBJECTIVE: To assess whether patients receiving celecoxib and rofecoxib have a greater underlying disease burden than patients prescribed nonselective NSAIDs. METHODS: The study population consisted of members of 11 health plans, aged >34 years, with a pharmacy claim for celecoxib or rofecoxib or a nonselective NSAID dispensed between February 1, 1999, and July 31, 2001, who had been continuously enrolled for >364 days before the dispensing date. Celecoxib and rofecoxib patients were randomly selected without replacement from a pool of eligible users in each of the 30 months. Nonselective NSAID users were randomly chosen without replacement within each month on a 2:1 ratio to cases; they could be chosen in more than one month. Univariate analyses comparing 9000 cases and 18 000 controls were performed, followed by a multiple logistic regression analysis conditioned on time. RESULTS: Increasing age, treatment by a rheumatologist or an orthopedic specialist, treatment with a high number of different medications in the past year, treatment with oral corticosteroids in the past year, and having had a previous GI bleed increased the likelihood of receiving celecoxib or rofecoxib, whereas treatment with a high number of nonselective NSAID prescriptions in the past year decreased it. Treatment with a high number of different medications was a predictor of increased prevalence of underlying diabetes mellitus and cardiovascular disease. CONCLUSIONS: Patients having a greater underlying disease burden were more likely to receive COX-2 selective NSAIDs than nonselective ones. Paradoxically, patients at higher risk for cardiovascular disease were channeled toward treatment with COX-2 selective NSAIDs, many of which may confer an increased risk of acute myocardial infarction and other adverse cardiovascular outcomes.

2012 ◽  
Vol 39 (11) ◽  
pp. 2163-2169 ◽  
Author(s):  
SHARON DANIEL ◽  
ILAN MATOK ◽  
RAFAEL GORODISCHER ◽  
GIDEON KOREN ◽  
ELIA UZIEL ◽  
...  

Objective.Nonsteroidal antiinflammatory drugs (NSAID) are among the most common medicines used by pregnant women. Published data are controversial regarding fetal safety following intrauterine exposure to NSAID. We investigated exposure to NSAID in the first trimester in a large cohort of infants and fetuses.Methods.A computerized database of medications dispensed from 1998 to 2009 to all women registered in the “Clalit” health maintenance organization in Southern Israel was linked with 2 computerized databases containing maternal and infant hospitalization records. Pregnancy terminations for medical reasons were analyzed. The following confounders were controlled for: parity, maternal age, ethnicity, maternal pregestational diabetes, maternal inflammatory disease, and year of birth or pregnancy termination. First trimester exposure to nonselective cyclooxygenase (COX) inhibitors and to selective COX-2 inhibitors as groups and to individual drugs was analyzed.Results.There were 110,783 pregnancies during the study period: 109,544 singleton births and 1239 pregnancy terminations for medical reasons. In total, 5267 mothers were exposed to NSAID during the first trimester of pregnancy: 5153 to nonselective COX inhibitors and 114 to COX-2 selective inhibitors. Exposure to NSAID in the first trimester, as groups (nonselective COX and selective COX-2 inhibitors) and as individual drugs, was not associated with an increased risk of major congenital malformations in general (adjusted OR 1.07, 95% CI 0.96−1.21 for nonselective; and adjusted OR 1.40, 95% CI 0.70−2.78, for selective COX-2 inhibitors), although an increased risk for musculoskeletal malformations was found following exposure to COX-2 selective inhibitors (adjusted OR 3.39, 95% CI 1.37−8.34).Conclusion.Intrauterine exposure to NSAID was not associated with increased risk for major congenital malformations. Further studies are needed to assess the risk for malformations after exposure to COX-2 selective inhibitors.


2012 ◽  
Vol 39 (5) ◽  
pp. 910-915 ◽  
Author(s):  
CARLO A. MARRA ◽  
LARRY D. LYND ◽  
LINDSEY COLLEY ◽  
STEPHANIE S. HARVARD ◽  
DIANE LACAILLE ◽  
...  

Objective.To examine the incidence of gastrointestinal (GI) events in patients with rheumatoid arthritis (RA) after the removal of rofecoxib from the market.Methods.Residents of British Columbia with a diagnosis of RA who were chronic users of cyclooxygenase 2 (COX-2) inhibitors or nonselective nonsteroidal antiinflammatory drugs (nsNSAID) as of September 30, 2004, were included. We studied the risk of GI events using incidence rates and adjusted HR from Cox proportional hazards regression using time-dependent covariates.Results.The cohort comprised 4266 patients with a mean age of 60 years and over 72% women, of which 2034 (48%) were classified as COX-2 inhibitor users and 2232 (52%) as chronic nsNSAID users as of September 30, 2004. The 2 groups were well balanced on baseline covariates except for comorbid conditions. In the year following rofecoxib withdrawal, 174 patients (5.5%) experienced 1 or more GI events, defined as a GI-related physician visit or hospitalization. There was no statistically significant increase in the risk of a GI event between those classified as a COX-2 inhibitor or nsNSAID user at the time of withdrawal (HR 1.03, 95% CI 0.69–1.54). Considering the drug exposure at the time of the event, there was no increased risk of GI events associated with the use of either COX-2 inhibitors or nsNSAID, or with the use of oral corticosteroids, low-dose aspirin, or clopidogrel, after adjustment for potential confounders.Conclusion.In this cohort, withdrawal of rofecoxib did not result in a significant increase in GI events among patients with RA.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Hong Seok Lee ◽  
Yong-Moon Park ◽  
Kyungdo Han

Background: It has been reported that people with teeth loss have an increased risk of cardiovascular disease. However, there is limited evidence for the specific relationship between remained teeth and cardiovascular disease (CVD). Method: Among subjects who participated in Korea National Health and Nutrition Examination Survey conducted in 2008-2013, a total of 12,612 adults with mean age of 60.2±1.2 years old were analyzed. Number of teeth was classified as number less than 20, from 20 to 27 and more than 27. Multiple logistic regression analysis was performed to determine the relationship between cardiovascular disease and remained teeth number after adjusting for potential confounders. Result: The prevalence of cardiovascular disease was 6.5%, 3.3% and 1.4% respectively in groups having number less than 20, 20 to 27 and more than 27 ( P < 0.001). Total number of cardiovascular disease was 666. Diabetes, hypertension, total cholesterol level, waist circumference, metabolic syndrome had large proportion in a group having less than 20 teeth ( P < 0.001). People having less than 20 remained teeth had statistically significant cardiovascular disease after adjusting for age, sex, body mass index, smoking, drinking alcohol, exercise, education, income status, stress, diabetes, and hypertension. A group having less 20 teeth was likely to have statistically significant relationship with cardiovascular disease. (Odds ratio [OR]: 1.41, 95 % confidence interval [CI]: 1.06-1.89) and stroke (OR:1.90, CI:1.03-3.48). Conclusion: Our findings suggest that the number of remained teeth could be a useful additional indicator for assessing cardiovascular disease and stroke


2005 ◽  
Vol 39 (5) ◽  
pp. 944-948 ◽  
Author(s):  
Leisa L Marshall

OBJECTIVE: To report the probable association of angioedema with aspirin therapy and the selective cyclooxygenase-2 (COX-2) inhibitor rofecoxib. CASE SUMMARY: A 44-year-old white woman, previously tolerant to aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs), developed angioedema of the lips after ingesting two 325-mg aspirin tablets during one day. The reaction occurred 3 hours after taking the second aspirin and resolved within 3 hours. Two weeks later, the patient took a 25-mg rofecoxib tablet for a sore throat, and she developed angioedema 51/2 hours later. Although the woman took 50 mg of diphenhydramine, the swelling did not subside. She repeated the diphenhydramine dose in the evening and, by noon the next day, 261/2 hours after the angioedema began, it was resolved. The patient's internist prescribed an epinephrine auto-injector and advised her to consult an allergist. With skin testing and oral rechallenge with aspirin, but not rofecoxib, the allergist determined the cause of the reactions to be aspirin-induced angioedema and selective COX-2 inhibitor intolerance. The Naranjo probability scale indicated that aspirin was a highly probable cause and rofecoxib was a probable cause of this patient's angioedema. DISCUSSION: Aspirin-induced angioedema and NSAID intolerance have been well documented. There are reports of both tolerance and intolerance to selective COX-2 inhibitors in patients with documented allergy-like reactions to aspirin and NSAIDs. CONCLUSIONS: Patients with aspirin and NSAID intolerance may develop intolerance to COX-2 inhibitors, especially with repeated exposure.


1997 ◽  
Vol 40 (6) ◽  
pp. 980-989 ◽  
Author(s):  
Edward S. Lazer ◽  
Clara K. Miao ◽  
Charles L. Cywin ◽  
Ronald Sorcek ◽  
Hin-Chor Wong ◽  
...  

1999 ◽  
Vol 190 (4) ◽  
pp. 451-460 ◽  
Author(s):  
Xinping Zhang ◽  
Scott G. Morham ◽  
Robert Langenbach ◽  
Donald A. Young

In this study, we use primary embryonic fibroblasts derived from cyclooxygenase-deficient transgenic embryos to further investigate the role of the two cyclooxygenases, cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2), in the process of neoplastic transformation. Cells with either, neither, or both of the cyclooxygenases were transformed by Ha-ras and/or SV40. Our results show that when a cyclooxygenase enzyme is present, the transformed cells have marked increases in COX-2 and/or COX-1 expression. Nevertheless, each type of cell, deficient in either or both cyclooxygenases, can be readily transformed at almost equal efficiency. Different nonsteroidal antiinflammatory drugs (NSAIDs) were used to examine their possible antineoplastic effects on the transformed cells, which have various levels of expression of COX-1 or COX-2. Our results show that NSAIDs suppress the colony formation in soft agar in a dosage-dependent manner in the absence of the cyclooxygenase(s). Thymidine incorporation and apoptosis analyses further demonstrate that the NSAIDs are effective in the cyclooxygenase-null cells. Our findings with cyclooxygenase knockout cells confirm recent reports that some of the antiproliferative and antineoplastic effects of NSAIDs are independent of the inhibition of either COX-1 or COX-2. They also show that transformation is independent of the status of cyclooxygenase expression, suggesting that the involvement of the cyclooxygenases in tumorigenesis may occur at later steps.


2001 ◽  
Vol 29 (6) ◽  
pp. 801-805 ◽  
Author(s):  
Christopher L. Elder ◽  
Laurence E. Dahners ◽  
Paul S. Weinhold

Celecoxib was the first of a new class of nonsteroidal antiinflammatory drugs, the cyclooxygenase-2 (COX-2) specific inhibitors, marketed as having the same antiinflammatory efficacy as other nonsteroidal antiinflammatory drugs without their increased risk of gastrointestinal ulceration. Among the widest uses of nonsteroidal antiinflammatory drugs is in the treatment of acute soft tissue injuries. Although the benefits of celecoxib have been shown when used for rheumatoid arthritis and osteoarthritis, we are unaware of any studies concerning its effect on soft tissues. We used the surgically incised medial collateral ligament of male Sprague-Dawley rats as an experimental model for acute ligament injuries to investigate the effects of celecoxib on ligament healing. Fifty rats underwent surgical transection of the right medial collateral ligament. Postoperatively, half were given celecoxib for the first 6 days of recovery, the other half were not. The animals were sacrificed 14 days after the operation, and both the injured and uninjured medial collateral ligaments were mechanically tested to failure in tension. Celecoxib-treated/injured ligaments were found to have a 32% lower load to failure than untreated/ injured ligaments. The results of this study do not support use of cyclooxygenase-2 specific inhibitors in the treatment of ligament injuries.


2005 ◽  
Vol 39 (5) ◽  
pp. 797-802 ◽  
Author(s):  
Jefferson Fredy ◽  
Daniel A Diggins ◽  
Gregory B Morrill

BACKGROUND: Nonsteroidal antiinflammatory drugs have been associated with exacerbation of hypertension. Differing effects on blood pressure (BP) have been reported in studies comparing celecoxib and rofecoxib. Concern regarding the cardiovascular safety of the cyclooxygenase-2 (COX-2) inhibitor class has intensified since the removal of rofecoxib from the market. OBJECTIVE: To evaluate the effect of a formulary change from celecoxib to rofecoxib on the BP of Native American patients at an Indian Health Service medical center. METHODS: Medical records of patients switched from celecoxib to rofecoxib were retrospectively reviewed. BP during the respective treatments was compared as follows: measurements recorded while taking celecoxib within 6 months before the index date and while taking rofecoxib from 1 week after the index date through 6 months of treatment were averaged. Differences in systolic and diastolic BP before and after the therapy change were evaluated using a paired Student's t-test. Subgroup analysis was performed for patients with preexisting hypertension. RESULTS: During rofecoxib therapy, the mean systolic BP was 2.9 mm Hg higher (p = 0.015) and the mean diastolic BP was 1.5 mm Hg higher (p = 0.042) than during celecoxib therapy. Among hypertensive patients, the respective mean systolic and diastolic BPs were 4.8 mm Hg (p = 0.009) and 2.0 mm Hg (p = 0.063) higher while taking rofecoxib. CONCLUSIONS: Switching patients from celecoxib to rofecoxib resulted in an increase in BP, with a larger difference observed in patients with hypertension. Future studies assessing the cardiovascular safety of currently marketed and investigational COX-2 inhibitors should evaluate the possible contribution of BP effects of these agents to overall risk.


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