ライフサイエンスコーパス: rofecoxib

1 ly inhibit only COX-2 (such as celecoxib and rofecoxib).

2 45.8% (P < 0.001, ibuprofen vs. 25 and 50 mg rofecoxib).

3 the cyclooxygenase inhibitors diclofenac and rofecoxib.

4 d adenomas to receive daily placebo or 25 mg rofecoxib.

5 mokers and nonsmokers and were unaffected by rofecoxib.

6 celecoxib was the most common alternative to rofecoxib.

7 ge 34 to 125 pg/mg creatinine (P=0.001) with rofecoxib.

8 n cyclooxygenase-2 inhibitors, in particular rofecoxib.

9 early because of the worldwide withdrawal of rofecoxib.

10 ctive COX-2 inhibitors NS-398, celecoxib, or rofecoxib.

11 other COX-2 inhibitors such as celecoxib and rofecoxib.

12 taking naproxen and 42.7% among those taking rofecoxib.

13 ith the use of the selective COX-2 inhibitor rofecoxib.

14 dverse cardiovascular events associated with rofecoxib.

15 vascular disease following the withdrawal of rofecoxib.

16 prematurely owing to worldwide withdrawal of rofecoxib.

17 ition in humans in response to celecoxib and rofecoxib.

18 tively, whereas no such effect was seen with rofecoxib.

19 inophen, 4000 mg/d, celecoxib, 200 mg/d, and rofecoxib, 12.5 mg, for symptomatic knee OA.

20 Patients were randomly assigned to receive rofecoxib, 12.5 mg/d (n = 96); rofecoxib, 25 mg/d (n = 9

21 0 mL/s were observed after multiple doses of rofecoxib, 12.5 mg/d (P = 0.019); rofecoxib, 25 mg (P =

22 b and P =.006 vs acetaminophen and P =.02 vs rofecoxib, 12.5 mg/d), composite pain subscale (P</=.03

23 response to rofecoxib, 25 mg/d, followed by rofecoxib, 12.5 mg/d, celecoxib, and acetaminophen, resp

24 , vs celecoxib and acetaminophen; P =.02 for rofecoxib, 12.5 mg/d, vs acetaminophen).

25 In the second study, multiple doses of rofecoxib, 12.5 or 25 mg/d; indomethacin, 50 mg three ti

26 lcer rates were 25 mg rofecoxib, 9.6%; 50 mg rofecoxib, 14.7%; and ibuprofen, 45.8% (P < 0.001, ibupr

27 0.001, respectively) and were noninferior to rofecoxib (-2 mm [-8, 4], P < 0.001 and -3 mm [-9, 3], P

28 nd III CRC were randomly assigned to receive rofecoxib (20 mg daily) or placebo.

29 150 mg/day, etoricoxib 60 and 90 mg/day, and rofecoxib 25 and 50 mg/day) had 99% probability of more

30 o placebo, enteric-coated aspirin 81 mg/day, rofecoxib 25 mg combined with aspirin 81 mg/day, or ibup

31 D3582 125 mg, 375 mg, or 750 mg twice a day; rofecoxib 25 mg once a day; naproxen 500 mg twice a day;

32 Smokers and nonsmokers received rofecoxib 25 mg twice daily or placebo for 1 week each i

33 eived either celecoxib 200 mg/day (n = 189), rofecoxib 25 mg/day (n = 190), or placebo (n = 96) for 6

34 Celecoxib 200 mg/day and rofecoxib 25 mg/day are equally efficacious in treating

35 eoarthritis Index), celecoxib 200 mg/day and rofecoxib 25 mg/day demonstrated similar efficacy.

36 were superior to placebo and as effective as rofecoxib 25 mg/day in treating the signs and symptoms o

37 oses), 1.59 (95% CI 1.10-2.32, p=0.015); for rofecoxib 25 mg/day or less, 1.47 (0.99-2.17, p=0.054);

38 hours before the cyclooxygenase-2 inhibitor rofecoxib (25 mg every morning) and the same medications

39 thesized that COX-2-specific inhibition with rofecoxib (25 mg once daily) in the treatment of patient

40 common (P < 0.001) following treatment with rofecoxib (25 mg or 50 mg) than with ibuprofen after 12

41 Fifty healthy volunteers received placebo, rofecoxib (25 mg), and celecoxib (200 mg), randomized by

42 reatment with a cyclo-oxygenase-2 inhibitor, rofecoxib (25 mg), on recurrence of neoplastic polyps of

43 idence of gastroduodenal ulcers >/=3 mm with rofecoxib (25 or 50 mg once daily) was significantly (P

44 endoscopy were randomly assigned to receive rofecoxib (25 or 50 mg once daily), ibuprofen (800 mg 3

45 e doses of rofecoxib, 12.5 mg/d (P = 0.019); rofecoxib, 25 mg (P = 0.029), and indomethacin (P = 0.08

46 in a randomized, placebo-controlled trial of rofecoxib, 25 mg daily, started after potentially curati

47 Once-daily rofecoxib, 25 mg, or twice-daily naproxen sodium, 220 mg

48 ed to receive rofecoxib, 12.5 mg/d (n = 96); rofecoxib, 25 mg/d (n = 95); celecoxib, 200 mg/d (n = 97

49 days of therapy showed greatest response to rofecoxib, 25 mg/d, followed by rofecoxib, 12.5 mg/d, ce

50 Rofecoxib, 25 mg/d, or naproxen, 500 mg twice daily.

51 Rofecoxib, 25 mg/d, provided efficacy advantages over ac

52 Over 6 weeks, rofecoxib, 25 mg/d, provided greatest response for night

53 2, - 22.0, - 18.7, and - 18.8 mm; P =.04 for rofecoxib, 25 mg/d, vs both acetaminophen and celecoxib)

54 56%, 46%, and 39%, respectively; P</=.03 for rofecoxib, 25 mg/d, vs celecoxib and acetaminophen; P =.

55 of rofecoxib vs acetaminophen and P =.02 for rofecoxib, 25 mg/d, vs celecoxib), night pain (-25.2, -

56 ts with osteoarthritis treated for 12 weeks, rofecoxib, 25 mg/d, was as effective as naproxen, 500 mg

57 In the first study, single doses of rofecoxib, 250 mg (about 5-fold to 20-fold the recommend

58 reports including 127 trial populations (40 rofecoxib, 37 celecoxib, 29 valdecoxib + parecoxib, 15 e

59 ysis, the 12-week ulcer incidence with 25 mg rofecoxib (4.7%) and with placebo (7.3%) satisfied presp

60 ets: naproxen -5.59+/-0.07 vs. -4.81+/-0.04; rofecoxib -4.93+/-0.04 vs. -3.75+/-0.03; n=7).

61 to placebo at week 12 (placebo, 9.9%; 25 mg rofecoxib, 4.1%; 50 mg rofecoxib, 7.3%; and ibuprofen, 2

62 costeroid therapy) were randomly assigned to rofecoxib 50 mg daily or naproxen 500 mg twice daily for

63 y assigned to naproxen 500 mg twice daily or rofecoxib 50 mg daily.

64 Rofecoxib (50 microM) was without effect in suppressing

65 cipants treated with naproxen (5.8 [8.0]) or rofecoxib (7.6 [7.7]) was not significantly different fr

66 (placebo, 9.9%; 25 mg rofecoxib, 4.1%; 50 mg rofecoxib, 7.3%; and ibuprofen, 27.7%).

67 At 24 weeks, ulcer rates were 25 mg rofecoxib, 9.6%; 50 mg rofecoxib, 14.7%; and ibuprofen,

68 clinB1 since these effects were prevented by rofecoxib (a selective COX-2 inhibitor) and rescued by e

69 -receptor deficient mice treated with either rofecoxib (a selective cyclooxygenase-2 inhibitor) or in

70 ouble-blind study tested the hypothesis that rofecoxib, a drug that specifically inhibits cyclooxygen

71 tic cancer cells were treated with PGE(2) or rofecoxib, a selective COX-2 inhibitor.

72 and BBB integrity, mice were pretreated with rofecoxib, a specific inhibitor of COX-2, prior to Tat t

73 comitant administration of ibuprofen but not rofecoxib, acetaminophen, or diclofenac antagonizes the

74 The concomitant administration of rofecoxib, acetaminophen, or diclofenac did not affect t

75 d that the shortened bleeding time following rofecoxib administration is attributable, in part, to th

76 P4A-like immune reactivity was increased by rofecoxib administration, but 20-HETE production increas

77 usted odds ratios versus celecoxib were: for rofecoxib (all doses), 1.59 (95% CI 1.10-2.32, p=0.015);

78 he cyclooxygenase (COX)-2-specific inhibitor rofecoxib, alone or in combination with the standard ant

79 Rofecoxib also conferred a reduction in risk of advanced

80 Rofecoxib also decreased growth-enhancing prostaglandin

81 Celecoxib, but not rofecoxib, also inhibited calcium responses to vasopress

82 GI events per 100 patient-years was 0.41 for rofecoxib and 0.89 for naproxen (relative risk, 0.46; 95

83 At this point, 1,167 patients had received rofecoxib and 1,160 patients had received placebo for me

84 o, the average selectivity attained by 25 mg rofecoxib and 200 mg celecoxib in vivo were not differen

85 e VAS for OA pain, compared with 31.6 mm for rofecoxib and 21.2 mm for placebo.

86 Rofecoxib and celecoxib (coxibs) effectively treat chron

87 The renal and cardiovascular effects of rofecoxib and celecoxib have been investigated in relati

88 s-Webster mice were dosed with celecoxib and rofecoxib and challenged with CT in ligated small intest

89 COX-2-selective agents, including celecoxib, rofecoxib and diisopropyl fluorophosphate, demonstrate a

90 Rofecoxib and ibuprofen appeared to confer an increased

91 Compared with placebo, single doses of rofecoxib and indomethacin decreased the glomerular filt

92 emonstrated a significant difference between rofecoxib and its NSAID comparator (naproxen) in the ris

93 Differences observed between rofecoxib and naproxen are likely the result of the anti

94 CHD) in non-users (n=202916) and in users of rofecoxib and other NSAIDs (rofecoxib n=24 132, other n=

95 For the rofecoxib and placebo arms, median follow-up times were

96 The 1167 patients receiving rofecoxib and the 1160 patients receiving placebo were w

97 eduction in adhesion formation compared with rofecoxib and the nonselective COX-2 inhibitors at 10 da

98 omparisons were made between patients taking rofecoxib and those taking either placebo, naproxen (an

99 Recently, two COX-2 drugs, rofecoxib and valdecoxib, were withdrawn from the United

100 inhibited by the cyclooxygenase-2 inhibitor rofecoxib and was restored by the stable PGI(2) analogue

101 sed cardiovascular event rate among users of rofecoxib, and a decreased rate with naproxen use.

102 observed with amitriptyline, carbamazepine, rofecoxib, and diazepam.

103 Celecoxib, rofecoxib, and diclofenac are clinically used cyclooxyge

104 We investigated the effects of celecoxib, rofecoxib, and diclofenac on ionic currents and calcium

105 l infarction (AMI) among users of celecoxib, rofecoxib, and NSAIDs in Medicare beneficiaries with a c

106 The potencies of diclofenac, naproxen, rofecoxib, and salicylate, but not aspirin, celecoxib, i

107 ith the selective COX-2 agents, celecoxib or rofecoxib, and the nonspecific COX inhibitors, aspirin,

108 such as celecoxib, etoricoxib, lumiracoxib, rofecoxib, and valdecoxib have been developed and the gr

109 n the US during the study period (celecoxib, rofecoxib, and valdecoxib), as well as oral formulations

110 Rofecoxib appeared to augment CD8 T cell infiltration in

111 ffects of a withdrawn anti-inflammatory drug rofecoxib are also reviewed here.

112 To study rofecoxib as adjuvant therapy, large established tumors

113 A second group (celecoxib, rofecoxib, aspirin) was treated for 10 days and observed

114 e randomly assigned to receive 50 mg of oral rofecoxib at 24 hours and at 1 to 2 hours before TKA, 50

115 prominent apoptosis in these cells, whereas rofecoxib at 50 microM was without effect in either supp

116 th osteoarthritis were randomized to receive rofecoxib at a dosage of 25 mg or 50 mg once daily, ibup

117 Rofecoxib at a dose of 25 mg (the highest dose recommend

118 Rofecoxib at dosages of 12.5 and 25 mg demonstrated effi

119 Rofecoxib at dosages of 12.5 mg/day and 25 mg/day and et

120 vidence of raised risk of CHD among users of rofecoxib at doses of 25 mg or less or among users of ot

121 ought to establish if risk was enhanced with rofecoxib at either high or standard doses compared with

122 Characteristics of patients receiving rofecoxib at our institution, details of their prescript

123 Celecoxib and another COX-2 inhibitor, rofecoxib, at 5 microM were almost equally effective in

124 Rofecoxib, at clinical anti-inflammatory plasma concentr

125 Rofecoxib, at doses 2-4 times the dose demonstrated to r

126 When mice were fed chow containing 0.01% rofecoxib beginning on day 0 after tumor cell implantati

127 After 25 days, celecoxib and rofecoxib, but not aspirin, had fewer adhesions than con

128 Rofecoxib, but perhaps not all cyclooxygenase-2 inhibito

129 -4 times the therapeutically effective dose, rofecoxib caused fewer endoscopically detected ulcers th

130 ies highlight the cardiovascular toxicity of rofecoxib, celecoxib, parecoxib, valdecoxib and naproxen

131 isk of cardiovascular events when given with rofecoxib, celecoxib, sulindac, meloxicam, and indometac

132 orally with low doses of a COX-2 inhibitor (rofecoxib chow, 0.0075%).

133 etary groups: control chow, low-dose (0.01%) rofecoxib chow, and high-dose (0.025%) rofecoxib chow.

134 .01%) rofecoxib chow, and high-dose (0.025%) rofecoxib chow.

135 cebo (N = 381) 5.8%, aspirin (N = 387) 7.3%, rofecoxib combined with aspirin (N = 377) 16.1%, and ibu

136 0.17, aspirin 0.85 (P = 0.002 vs. placebo), rofecoxib combined with aspirin 1.67, and ibuprofen 1.91

137 and ibuprofen (N = 374) 17.1% (P < 0.001 for rofecoxib combined with aspirin and for ibuprofen vs. ea

138 he relative risk of AMI in patients who used rofecoxib compared with persons taking no NSAID, taking

139 consumption were less in the group receiving rofecoxib compared with the group receiving placebo (P<.

140 V thrombotic events in patients treated with rofecoxib compared with those treated with placebo or no

141 tudy was to test whether the COX-2 inhibitor rofecoxib could reduce recurrence and improve survival w

142 tion: 1287 were assigned to receive 25 mg of rofecoxib daily, and 1299 to receive placebo.

143 Rofecoxib decreased GI complications by 1.1 per 100 user

144 These studies demonstrate that rofecoxib decreases the growth and metastatic potential

145 Three drugs (rofecoxib, diclofenac, etoricoxib) ranked consistently h

146 I within 180 days after initiation of NSAID (rofecoxib, diclofenac, ibuprofen, and naproxen compared

147 ated therapy in the adjuvant setting of CRC, rofecoxib did not improve OS or protect from recurrence

148 non-steroidal anti-inflammatory drug (NSAID) rofecoxib, especially at doses greater than 25 mg.

149 ed larger effect sizes versus placebo in the rofecoxib/etoricoxib trials than in the celecoxib/valdec

150 ersus placebo, as determined using data from rofecoxib/etoricoxib trials, were consistently higher th

151 These data suggest 20-HETE as a marker of rofecoxib exposure and that inhibition of 20-HETE's degr

152 20%, and 10% in control, low-, and high-dose rofecoxib fed groups, respectively.

153 , we demonstrate that oral administration of rofecoxib for 3 mo results in a greater than 120-fold hi

154 ZD3582 with placebo for superiority and with rofecoxib for noninferiority using a predefined margin o

155 Celecoxib and rofecoxib given at 160 micro g per mouse inhibited CT-in

156 ically relevant doses of the COX-2 inhibitor rofecoxib given orally were effective in inhibiting the

157 or less, 1.47 (0.99-2.17, p=0.054); and for rofecoxib greater than 25 mg/day, 3.58 (1.27-10.11, p=0.

158 There was less postoperative vomiting in the rofecoxib group (6%) compared with the placebo group (26

159 , 59 individuals had an APTC endpoint in the rofecoxib group and 34 in the placebo group (hazard rati

160 ing the follow-up period, one patient in the rofecoxib group and five patients in the placebo group d

161 Four patients in the rofecoxib group and two in the placebo group died from t

162 Knee flexion was increased in the rofecoxib group compared with the placebo group at disch

163 0-10) achieved for the knee was lower in the rofecoxib group compared with the placebo group during h

164 scular thrombotic events, 16 occurred in the rofecoxib group during or within 14 days after the treat

165 A total of 46 patients in the rofecoxib group had a confirmed thrombotic event during

166 ere statistically significantly lower in the rofecoxib group than in the naproxen group (5.9% vs. 8.1

167 The rofecoxib group was more satisfied with analgesia and an

168 lure (hazard ratio for the comparison of the rofecoxib group with the placebo group, 4.61; 95 percent

169 cardiovascular thrombotic events, six in the rofecoxib group, were reported within the 2 years after

170 s and ischemic cerebrovascular events in the rofecoxib group.

171 OR, 1.21; 95% CI, 1.01 to 1.44; P=0.036) and rofecoxib >25 mg versus celecoxib >200 mg (OR, 1.70; 95%

172 Dosages of rofecoxib >25 mg were associated with a higher risk than

173 0%, whereas only one mouse (5%) treated with rofecoxib had died after 30 days.

174 strumental variable analysis, diclofenac and rofecoxib had the least favorable benefit-risk balance a

175 Since that time, celecoxib and rofecoxib have become two of the most commonly prescribe

176 tion, publicly available articles related to rofecoxib identified via MEDLINE.

177 ith the use of the selective COX-2 inhibitor rofecoxib in a long-term, multicenter, randomized, place

178 presented mortality findings associated with rofecoxib in clinical trials of patients with Alzheimer

179 eraction by revacept was more effective than rofecoxib in preventing platelet-induced mRNA changes of

180 Benefits of rofecoxib in subgroup analyses were consistent with find

181 Despite the higher COX-2 selectivity of rofecoxib in vitro, the average selectivity attained by

182 rounded the question about whether high-dose rofecoxib increases or naproxen decreases the risk of se

183 , but not COX-2 selective inhibitors such as rofecoxib, induce bronchoconstriction and asthma in sens

184 The number needed to treat with rofecoxib instead of naproxen to avert 1 GI event was 10

185 ecame available during litigation related to rofecoxib involving Merck & Co, including internal compa

186 2 articles concluded that regarding safety, rofecoxib is "well tolerated." In contrast, in April 200

187 that inhibition of 20-HETE's degradation by rofecoxib is a partial explanation for its dramatic incr

188 Use of rofecoxib is associated with increased rates of APTC eve

189 loped synthesis of a NO-releasing prodrug of rofecoxib is described.

190 Celecoxib, but not rofecoxib, is shown to act as an "opener" of voltage-gat

191 ial that compared placebo, low-dose aspirin, rofecoxib + low-dose aspirin, and ibuprofen.

192 also elevated in dose-specific comparisons: rofecoxib < or =25 mg versus celecoxib < or =200 mg (OR,

193 omparisons of efficacy between celecoxib and rofecoxib met the predefined criteria for noninferiority

194 and in users of rofecoxib and other NSAIDs (rofecoxib n=24 132, other n=151 728).

195 the effect of three years of treatment with rofecoxib on the risk of recurrent neoplastic polyps of

196 mized to 1 of 3 treatment groups: 12.5 mg of rofecoxib once daily, 25 mg of rofecoxib once daily, and

197 s: 12.5 mg of rofecoxib once daily, 25 mg of rofecoxib once daily, and 50 mg of diclofenac 3 times da

198 to inform our patients of the withdrawal of rofecoxib, one of the largest drug withdrawals in United

199 , controlled trials with the COX-2 inhibitor rofecoxib, one study demonstrated a significant differen

200 any other drug, as well as in those who took rofecoxib or acetaminophen before taking aspirin.

201 Celecoxib, but not rofecoxib or diclofenac, dramatically enhanced KCNQ (K(v

202 male LDLR-/- mice fed the Western diet with rofecoxib or indomethacin for 6 weeks resulted in signif

203 After 14 days, mice that were given rofecoxib or irinotecan, but not 5-fluoruracil, had sign

204 The results of this study indicate that rofecoxib or low-dose naproxen does not slow cognitive d

205 of the cyclo-oxygenase-2 selective inhibitor rofecoxib or the mixed cyclo-oxygenase-1/cyclo-oxygenase

206 ransgenic mice in the absence or presence of rofecoxib oral administration.

207 oduced cyclo-oxygenase-2 selective inhibitor rofecoxib, owe part of their inhibitory actions to effec

208 factors, ischemic stroke was associated with rofecoxib (P = 0.060, OR 2.27 [95% CI 0.97-5.28]), and p

209 rimary prevention trials (0.52%): 0.74% with rofecoxib (P =.04 compared with the placebo group of the

210 an 206, range 154 to 383 pg/mg creatinine by rofecoxib (P=0.04) but was not changed in nonsmokers.

211 th overall mortality of 34 deaths among 1069 rofecoxib patients and 12 deaths among 1078 placebo pati

212 ithin 14 days of the last dose (24 among 725 rofecoxib patients and 15 among 732 placebo patients) an

213 ods and reported 29 deaths (2.7%) among 1067 rofecoxib patients and 17 deaths (1.6%) among 1075 place

214 ed deaths" were reported (9 deaths among 346 rofecoxib patients and 2 deaths among 346 placebo patien

215 onal 22 deaths in the off-drug period (17 in rofecoxib patients and 5 in placebo patients).

216 The 11,699 patients with a rofecoxib prescription in our practice were sent notific

217 of patients and providers and to deactivate rofecoxib prescriptions in the EMR.

218 Recent litigation related to rofecoxib provided a unique opportunity to examine guest

219 Except for rofecoxib, RA treatment does not appear to be associated

220 cohort receiving aspirin, both celecoxib and rofecoxib reduced risk of admission for gastrointestinal

221 s no evidence for an excess of CV events for rofecoxib relative to either placebo or the non-naproxen

222 posure showed an increase in the MI risk for rofecoxib (risk difference [RD] 1.40, 95% confidence int

223 significant elevation in the event rate for rofecoxib (RR 1.15, 95% confidence interval [95% CI] 1.0

224 ts for new users of each agent increased for rofecoxib (RR 1.22, 95% confidence interval [95% CI] 1.1

225 e prices of three commonly prescribed drugs: rofecoxib, sertraline, and atorvastatin.

226 Furthermore, 20-HETE but not rofecoxib significantly increases rat platelet aggregati

227 Rofecoxib significantly reduced the recurrence rate afte

228 In this randomized trial, rofecoxib significantly reduced the risk of colorectal a

229 nhibition of COX-2 by oral administration of Rofecoxib significantly slowed but did not cure the grow

230 Rofecoxib significantly slowed the growth of small (0-12

231 omethacin, lumiracoxib, meloxicam, naproxen, rofecoxib, sodium salicylate, and SC560 as inhibitors of

232 cally debulked and animals were treated with rofecoxib starting 3 days before surgery.

233 vents were assessed across 23 phase IIb to V rofecoxib studies.

234 Adenoma recurrence was less frequent for rofecoxib subjects than for those randomized to placebo

235 en but also by the COX-2 selective inhibitor rofecoxib, suggesting that the majority of PGE2 formed i

236 Rofecoxib suppressed MMP-2 expression and activity, Ets-

237 Unlike NSAIDs, rofecoxib targets only the COX-2 isoform.

238 Time-cumulative analyses indicated that for rofecoxib the adverse risks for peripheral edema and hyp

239 ad reduced microvessel density compared with rofecoxib, the nonselective COX inhibitors, and control

240 e-free survival and overall survival between rofecoxib therapy and placebo and between the use and no

241 Rofecoxib therapy was associated with an increased frequ

242 e 85 to 390 pg/mg creatinine) was reduced by rofecoxib to 78+/-27, median 71.5, range 50 to 135 pg/mg

243 ascular adverse events in patients receiving rofecoxib to reduce rates of recurrence of colorectal ca

244 as the selective cyclooxygenase 2 inhibitor, rofecoxib, to avert a clinical GI event.

245 cal analyses of the primary splenic tumor in rofecoxib-treated mice showed no alteration in COX-1 exp

246 stroke, and transient ischemic attacks) with rofecoxib treatment compared with naproxen was 2.38 (95%

247 found no evidence of a greater benefit from rofecoxib treatment compared with placebo in patients wh

248 Rofecoxib treatment did not inhibit platelet thromboxane

249 IK3CA mutation does not predict benefit from rofecoxib treatment, it merits further evaluation as a p

250 xib, with correspondingly lower levels after rofecoxib treatment.

251 Rofecoxib use increases the risk of serious coronary hea

252 justed relative risks of AMI associated with rofecoxib use of 1 to 30 days (OR, 1.40; 95% CI, 1.12 to

253 In this study, current rofecoxib use was associated with an elevated relative r

254 Rofecoxib use was not documented in any country.

255 aration of the event curves) among long-term rofecoxib users at low or high baseline cardiovascular r

256 compared with 1.16 (CI, 0.70 to 1.93) among rofecoxib users.

257 cal trials of coxibs (etoricoxib, celecoxib, rofecoxib, valdecoxib) in patients with hip and/or knee

258 tive COX-2 inhibitors (coxibs), particularly rofecoxib, valdecoxib, and parecoxib, increases risk for

259 ascular variables did not predict the use of rofecoxib versus celecoxib.

260 with nonselective NSAIDs were the following: rofecoxib versus naproxen (odds ratio, 3.39 [CI, 1.37 to

261 genase-2 inhibition led to the withdrawal of rofecoxib (Vioxx) and valdecoxib (Bextra), but the mecha

262 ibitors of cyclooxygenase-2 (COX-2), such as rofecoxib (Vioxx), celecoxib (Celebrex), and valdecoxib

263 hibitors, including celecoxib (Celebrex) and rofecoxib (Vioxx), produced two unanticipated findings.

264 l anti-inflammatory drugs until one of them, rofecoxib (Vioxx), was found to be associated with incre

265 een under intense scrutiny because long-term rofecoxib (Vioxx; Merck, Whitehouse Station, NJ) treatme

266 idal anti-inflammatory drugs (NSAIDs) (e.g., rofecoxib [Vioxx]) increase the risk of heart attack and

267 5, and - 12.5 mm; P</=.02 for either dose of rofecoxib vs acetaminophen and P =.02 for rofecoxib, 25

268 7, and - 20.9 mm; P</=.02 for either dose of rofecoxib vs acetaminophen).

269 ll others vs acetaminophen; P =.05 for 25-mg rofecoxib vs celecoxib), rest pain (-21.8, - 18.6, - 15.

270 he use of celecoxib (adjusted odds ratio for rofecoxib vs. celecoxib, 2.72 [CI, 1.24 to 5.95]; P = 0.

271 The difference between celecoxib and rofecoxib was -2.5 mm, with an upper limit of the 95% co

272 The use of rofecoxib was associated with a statistically significan

273 Current use of rofecoxib was associated with an elevated relative risk

274 a history of colorectal adenomas, the use of rofecoxib was associated with an increased cardiovascula

275 randomized trials with 116,094 participants, rofecoxib was associated with increased renal and arrhyt

276 Compared with controls, rofecoxib was associated with increased risk of arrhythm

277 For all individual renal end points, rofecoxib was associated with increased risk of peripher

278 As reported previously, rofecoxib was associated with increased risks of signifi

279 pared with remote exposure to any NSAID, and rofecoxib was compared with celecoxib.

280 However, rofecoxib was ineffective in preventing downregulation o

281 The increased rate associated with rofecoxib was seen in the first 60 days of use (adjusted

282 The increase in rate associated with rofecoxib was seen within the first 60 days and persiste

283 The reduction in events with rofecoxib was similar in high- and low-risk subgroups (R

284 Rofecoxib was voluntarily withdrawn by the manufacturer.

285 Rofecoxib was well tolerated and provided efficacy that

286 Users of high-dose rofecoxib were 1.70 (95% CI 0.98-2.95, p=0.058) times mo

287 Celecoxib and rofecoxib were associated with different odds of MI.

288 s that clinical trial manuscripts related to rofecoxib were authored by sponsor employees but often a

289 g division to promote prescription of Vioxx (rofecoxib) when it became available on the market in 199

290 , which blocks COX-1 selectively, but not by rofecoxib, which is a selective inhibitor of COX-2.

291 Diclofenac has a risk very similar to rofecoxib, which was withdrawn from worldwide markets ow

292 and 1.69 (95% CI: 1.07, 2.69) when comparing rofecoxib with naproxen.

293 bo; 0.79 (95% CI: 0.40, 1.55) when comparing rofecoxib with non-naproxen NSAIDs; and 1.69 (95% CI: 1.

294 R) trial, a large randomized trial comparing rofecoxib with placebo after primary CRC resection.

295 was 0.84 (95% CI: 0.51, 1.38) when comparing rofecoxib with placebo; 0.79 (95% CI: 0.40, 1.55) when c

296 ed that COX-2 inhibitor drugs, celecoxib and rofecoxib, with similar COX-2-selectivity and clinical e

297 whether use of the selective COX-2 inhibitor rofecoxib would reduce the risk of colorectal adenomas.