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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 o placebo, enteric-coated aspirin 81 mg/day, rofecoxib 25 mg combined with aspirin 81 mg/day, or ibup
30 D3582 125 mg, 375 mg, or 750 mg twice a day; rofecoxib 25 mg once a day; naproxen 500 mg twice a day;
31              Smokers and nonsmokers received rofecoxib 25 mg twice daily or placebo for 1 week each i
32 eived either celecoxib 200 mg/day (n = 189), rofecoxib 25 mg/day (n = 190), or placebo (n = 96) for 6
33                     Celecoxib 200 mg/day and rofecoxib 25 mg/day are equally efficacious in treating
34 eoarthritis Index), celecoxib 200 mg/day and rofecoxib 25 mg/day demonstrated similar efficacy.
35 were superior to placebo and as effective as rofecoxib 25 mg/day in treating the signs and symptoms o
36 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);
37  hours before the cyclooxygenase-2 inhibitor rofecoxib (25 mg every morning) and the same medications
38 thesized that COX-2-specific inhibition with rofecoxib (25 mg once daily) in the treatment of patient
39  common (P < 0.001) following treatment with rofecoxib (25 mg or 50 mg) than with ibuprofen after 12
40   Fifty healthy volunteers received placebo, rofecoxib (25 mg), and celecoxib (200 mg), randomized by
41 reatment with a cyclo-oxygenase-2 inhibitor, rofecoxib (25 mg), on recurrence of neoplastic polyps of
42 idence of gastroduodenal ulcers >/=3 mm with rofecoxib (25 or 50 mg once daily) was significantly (P
43  endoscopy were randomly assigned to receive rofecoxib (25 or 50 mg once daily), ibuprofen (800 mg 3
44 e doses of rofecoxib, 12.5 mg/d (P = 0.019); rofecoxib, 25 mg (P = 0.029), and indomethacin (P = 0.08
45 in a randomized, placebo-controlled trial of rofecoxib, 25 mg daily, started after potentially curati
46                                   Once-daily rofecoxib, 25 mg, or twice-daily naproxen sodium, 220 mg
47 ed to receive rofecoxib, 12.5 mg/d (n = 96); rofecoxib, 25 mg/d (n = 95); celecoxib, 200 mg/d (n = 97
48  days of therapy showed greatest response to rofecoxib, 25 mg/d, followed by rofecoxib, 12.5 mg/d, ce
49                                              Rofecoxib, 25 mg/d, or naproxen, 500 mg twice daily.
50                                              Rofecoxib, 25 mg/d, provided efficacy advantages over ac
51                                Over 6 weeks, rofecoxib, 25 mg/d, provided greatest response for night
52 2, - 22.0, - 18.7, and - 18.8 mm; P =.04 for rofecoxib, 25 mg/d, vs both acetaminophen and celecoxib)
53 56%, 46%, and 39%, respectively; P</=.03 for rofecoxib, 25 mg/d, vs celecoxib and acetaminophen; P =.
54 of rofecoxib vs acetaminophen and P =.02 for rofecoxib, 25 mg/d, vs celecoxib), night pain (-25.2, -
55 ts with osteoarthritis treated for 12 weeks, rofecoxib, 25 mg/d, was as effective as naproxen, 500 mg
56          In the first study, single doses of rofecoxib, 250 mg (about 5-fold to 20-fold the recommend
57  reports including 127 trial populations (40 rofecoxib, 37 celecoxib, 29 valdecoxib + parecoxib, 15 e
58 ysis, the 12-week ulcer incidence with 25 mg rofecoxib (4.7%) and with placebo (7.3%) satisfied presp
59 ets: naproxen -5.59+/-0.07 vs. -4.81+/-0.04; rofecoxib -4.93+/-0.04 vs. -3.75+/-0.03; n=7).
60  to placebo at week 12 (placebo, 9.9%; 25 mg rofecoxib, 4.1%; 50 mg rofecoxib, 7.3%; and ibuprofen, 2
61 costeroid therapy) were randomly assigned to rofecoxib 50 mg daily or naproxen 500 mg twice daily for
62 y assigned to naproxen 500 mg twice daily or rofecoxib 50 mg daily.
63                                              Rofecoxib (50 microM) was without effect in suppressing
64 cipants treated with naproxen (5.8 [8.0]) or rofecoxib (7.6 [7.7]) was not significantly different fr
65 (placebo, 9.9%; 25 mg rofecoxib, 4.1%; 50 mg rofecoxib, 7.3%; and ibuprofen, 27.7%).
66          At 24 weeks, ulcer rates were 25 mg rofecoxib, 9.6%; 50 mg rofecoxib, 14.7%; and ibuprofen,
67 clinB1 since these effects were prevented by rofecoxib (a selective COX-2 inhibitor) and rescued by e
68 -receptor deficient mice treated with either rofecoxib (a selective cyclooxygenase-2 inhibitor) or in
69 ouble-blind study tested the hypothesis that rofecoxib, a drug that specifically inhibits cyclooxygen
70 tic cancer cells were treated with PGE(2) or rofecoxib, a selective COX-2 inhibitor.
71 and BBB integrity, mice were pretreated with rofecoxib, a specific inhibitor of COX-2, prior to Tat t
72 comitant administration of ibuprofen but not rofecoxib, acetaminophen, or diclofenac antagonizes the
73            The concomitant administration of rofecoxib, acetaminophen, or diclofenac did not affect t
74 d that the shortened bleeding time following rofecoxib administration is attributable, in part, to th
75  P4A-like immune reactivity was increased by rofecoxib administration, but 20-HETE production increas
76 usted odds ratios versus celecoxib were: for rofecoxib (all doses), 1.59 (95% CI 1.10-2.32, p=0.015);
77 he cyclooxygenase (COX)-2-specific inhibitor rofecoxib, alone or in combination with the standard ant
78                                              Rofecoxib also conferred a reduction in risk of advanced
79                                              Rofecoxib also decreased growth-enhancing prostaglandin
80                           Celecoxib, but not rofecoxib, also inhibited calcium responses to vasopress
81 GI events per 100 patient-years was 0.41 for rofecoxib and 0.89 for naproxen (relative risk, 0.46; 95
82   At this point, 1,167 patients had received rofecoxib and 1,160 patients had received placebo for me
83 o, the average selectivity attained by 25 mg rofecoxib and 200 mg celecoxib in vivo were not differen
84 e VAS for OA pain, compared with 31.6 mm for rofecoxib and 21.2 mm for placebo.
85                                              Rofecoxib and celecoxib (coxibs) effectively treat chron
86      The renal and cardiovascular effects of rofecoxib and celecoxib have been investigated in relati
87 s-Webster mice were dosed with celecoxib and rofecoxib and challenged with CT in ligated small intest
88 COX-2-selective agents, including celecoxib, rofecoxib and diisopropyl fluorophosphate, demonstrate a
89                                              Rofecoxib and ibuprofen appeared to confer an increased
90       Compared with placebo, single doses of rofecoxib and indomethacin decreased the glomerular filt
91 emonstrated a significant difference between rofecoxib and its NSAID comparator (naproxen) in the ris
92                 Differences observed between rofecoxib and naproxen are likely the result of the anti
93 CHD) in non-users (n=202916) and in users of rofecoxib and other NSAIDs (rofecoxib n=24 132, other n=
94                                      For the rofecoxib and placebo arms, median follow-up times were
95                  The 1167 patients receiving rofecoxib and the 1160 patients receiving placebo were w
96 eduction in adhesion formation compared with rofecoxib and the nonselective COX-2 inhibitors at 10 da
97 omparisons were made between patients taking rofecoxib and those taking either placebo, naproxen (an
98                   Recently, two COX-2 drugs, rofecoxib and valdecoxib, were withdrawn from the United
99  inhibited by the cyclooxygenase-2 inhibitor rofecoxib and was restored by the stable PGI(2) analogue
100 sed cardiovascular event rate among users of rofecoxib, and a decreased rate with naproxen use.
101  observed with amitriptyline, carbamazepine, rofecoxib, and diazepam.
102                                   Celecoxib, rofecoxib, and diclofenac are clinically used cyclooxyge
103    We investigated the effects of celecoxib, rofecoxib, and diclofenac on ionic currents and calcium
104 l infarction (AMI) among users of celecoxib, rofecoxib, and NSAIDs in Medicare beneficiaries with a c
105       The potencies of diclofenac, naproxen, rofecoxib, and salicylate, but not aspirin, celecoxib, i
106 ith the selective COX-2 agents, celecoxib or rofecoxib, and the nonspecific COX inhibitors, aspirin,
107  such as celecoxib, etoricoxib, lumiracoxib, rofecoxib, and valdecoxib have been developed and the gr
108 n the US during the study period (celecoxib, rofecoxib, and valdecoxib), as well as oral formulations
109                                              Rofecoxib appeared to augment CD8 T cell infiltration in
110 ffects of a withdrawn anti-inflammatory drug rofecoxib are also reviewed here.
111                                     To study rofecoxib as adjuvant therapy, large established tumors
112                   A second group (celecoxib, rofecoxib, aspirin) was treated for 10 days and observed
113 e randomly assigned to receive 50 mg of oral rofecoxib at 24 hours and at 1 to 2 hours before TKA, 50
114  prominent apoptosis in these cells, whereas rofecoxib at 50 microM was without effect in either supp
115 th osteoarthritis were randomized to receive rofecoxib at a dosage of 25 mg or 50 mg once daily, ibup
116                                              Rofecoxib at a dose of 25 mg (the highest dose recommend
117                                              Rofecoxib at dosages of 12.5 and 25 mg demonstrated effi
118                                              Rofecoxib at dosages of 12.5 mg/day and 25 mg/day and et
119 vidence of raised risk of CHD among users of rofecoxib at doses of 25 mg or less or among users of ot
120 ought to establish if risk was enhanced with rofecoxib at either high or standard doses compared with
121        Characteristics of patients receiving rofecoxib at our institution, details of their prescript
122       Celecoxib and another COX-2 inhibitor, rofecoxib, at 5 microM were almost equally effective in
123                                              Rofecoxib, at clinical anti-inflammatory plasma concentr
124                                              Rofecoxib, at doses 2-4 times the dose demonstrated to r
125     When mice were fed chow containing 0.01% rofecoxib beginning on day 0 after tumor cell implantati
126                 After 25 days, celecoxib and rofecoxib, but not aspirin, had fewer adhesions than con
127                                              Rofecoxib, but perhaps not all cyclooxygenase-2 inhibito
128 -4 times the therapeutically effective dose, rofecoxib caused fewer endoscopically detected ulcers th
129 ies highlight the cardiovascular toxicity of rofecoxib, celecoxib, parecoxib, valdecoxib and naproxen
130 isk of cardiovascular events when given with rofecoxib, celecoxib, sulindac, meloxicam, and indometac
131  orally with low doses of a COX-2 inhibitor (rofecoxib chow, 0.0075%).
132 etary groups: control chow, low-dose (0.01%) rofecoxib chow, and high-dose (0.025%) rofecoxib chow.
133 .01%) rofecoxib chow, and high-dose (0.025%) rofecoxib chow.
134 cebo (N = 381) 5.8%, aspirin (N = 387) 7.3%, rofecoxib combined with aspirin (N = 377) 16.1%, and ibu
135  0.17, aspirin 0.85 (P = 0.002 vs. placebo), rofecoxib combined with aspirin 1.67, and ibuprofen 1.91
136 and ibuprofen (N = 374) 17.1% (P < 0.001 for rofecoxib combined with aspirin and for ibuprofen vs. ea
137 he relative risk of AMI in patients who used rofecoxib compared with persons taking no NSAID, taking
138 consumption were less in the group receiving rofecoxib compared with the group receiving placebo (P<.
139 V thrombotic events in patients treated with rofecoxib compared with those treated with placebo or no
140 tudy was to test whether the COX-2 inhibitor rofecoxib could reduce recurrence and improve survival w
141 tion: 1287 were assigned to receive 25 mg of rofecoxib daily, and 1299 to receive placebo.
142                                              Rofecoxib decreased GI complications by 1.1 per 100 user
143               These studies demonstrate that rofecoxib decreases the growth and metastatic potential
144                                 Three drugs (rofecoxib, diclofenac, etoricoxib) ranked consistently h
145 I within 180 days after initiation of NSAID (rofecoxib, diclofenac, ibuprofen, and naproxen compared
146 ated therapy in the adjuvant setting of CRC, rofecoxib did not improve OS or protect from recurrence
147 non-steroidal anti-inflammatory drug (NSAID) rofecoxib, especially at doses greater than 25 mg.
148 ed larger effect sizes versus placebo in the rofecoxib/etoricoxib trials than in the celecoxib/valdec
149 ersus placebo, as determined using data from rofecoxib/etoricoxib trials, were consistently higher th
150    These data suggest 20-HETE as a marker of rofecoxib exposure and that inhibition of 20-HETE's degr
151 20%, and 10% in control, low-, and high-dose rofecoxib fed groups, respectively.
152 , we demonstrate that oral administration of rofecoxib for 3 mo results in a greater than 120-fold hi
153 ZD3582 with placebo for superiority and with rofecoxib for noninferiority using a predefined margin o
154                                Celecoxib and rofecoxib given at 160 micro g per mouse inhibited CT-in
155 ically relevant doses of the COX-2 inhibitor rofecoxib given orally were effective in inhibiting the
156  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.
157 There was less postoperative vomiting in the rofecoxib group (6%) compared with the placebo group (26
158 , 59 individuals had an APTC endpoint in the rofecoxib group and 34 in the placebo group (hazard rati
159 ing the follow-up period, one patient in the rofecoxib group and five patients in the placebo group d
160                         Four patients in the rofecoxib group and two in the placebo group died from t
161            Knee flexion was increased in the rofecoxib group compared with the placebo group at disch
162 0-10) achieved for the knee was lower in the rofecoxib group compared with the placebo group during h
163 scular thrombotic events, 16 occurred in the rofecoxib group during or within 14 days after the treat
164                A total of 46 patients in the rofecoxib group had a confirmed thrombotic event during
165 ere statistically significantly lower in the rofecoxib group than in the naproxen group (5.9% vs. 8.1
166                                          The rofecoxib group was more satisfied with analgesia and an
167 lure (hazard ratio for the comparison of the rofecoxib group with the placebo group, 4.61; 95 percent
168 cardiovascular thrombotic events, six in the rofecoxib group, were reported within the 2 years after
169 s and ischemic cerebrovascular events in the rofecoxib group.
170 OR, 1.21; 95% CI, 1.01 to 1.44; P=0.036) and rofecoxib &gt;25 mg versus celecoxib >200 mg (OR, 1.70; 95%
171                                   Dosages of rofecoxib &gt;25 mg were associated with a higher risk than
172 0%, whereas only one mouse (5%) treated with rofecoxib had died after 30 days.
173 strumental variable analysis, diclofenac and rofecoxib had the least favorable benefit-risk balance a
174               Since that time, celecoxib and rofecoxib have become two of the most commonly prescribe
175 tion, publicly available articles related to rofecoxib identified via MEDLINE.
176 ith the use of the selective COX-2 inhibitor rofecoxib in a long-term, multicenter, randomized, place
177 presented mortality findings associated with rofecoxib in clinical trials of patients with Alzheimer
178 eraction by revacept was more effective than rofecoxib in preventing platelet-induced mRNA changes of
179                                  Benefits of rofecoxib in subgroup analyses were consistent with find
180      Despite the higher COX-2 selectivity of rofecoxib in vitro, the average selectivity attained by
181 rounded the question about whether high-dose rofecoxib increases or naproxen decreases the risk of se
182 , but not COX-2 selective inhibitors such as rofecoxib, induce bronchoconstriction and asthma in sens
183              The number needed to treat with rofecoxib instead of naproxen to avert 1 GI event was 10
184 ecame available during litigation related to rofecoxib involving Merck & Co, including internal compa
185  2 articles concluded that regarding safety, rofecoxib is "well tolerated." In contrast, in April 200
186  that inhibition of 20-HETE's degradation by rofecoxib is a partial explanation for its dramatic incr
187                                       Use of rofecoxib is associated with increased rates of APTC eve
188 loped synthesis of a NO-releasing prodrug of rofecoxib is described.
189                           Celecoxib, but not rofecoxib, is shown to act as an "opener" of voltage-gat
190 ial that compared placebo, low-dose aspirin, rofecoxib + low-dose aspirin, and ibuprofen.
191  also elevated in dose-specific comparisons: rofecoxib &lt; or =25 mg versus celecoxib < or =200 mg (OR,
192 omparisons of efficacy between celecoxib and rofecoxib met the predefined criteria for noninferiority
193  and in users of rofecoxib and other NSAIDs (rofecoxib n=24 132, other n=151 728).
194  the effect of three years of treatment with rofecoxib on the risk of recurrent neoplastic polyps of
195 mized to 1 of 3 treatment groups: 12.5 mg of rofecoxib once daily, 25 mg of rofecoxib once daily, and
196 s: 12.5 mg of rofecoxib once daily, 25 mg of rofecoxib once daily, and 50 mg of diclofenac 3 times da
197  to inform our patients of the withdrawal of rofecoxib, one of the largest drug withdrawals in United
198 , controlled trials with the COX-2 inhibitor rofecoxib, one study demonstrated a significant differen
199 any other drug, as well as in those who took rofecoxib or acetaminophen before taking aspirin.
200                           Celecoxib, but not rofecoxib or diclofenac, dramatically enhanced KCNQ (K(v
201  male LDLR-/- mice fed the Western diet with rofecoxib or indomethacin for 6 weeks resulted in signif
202          After 14 days, mice that were given rofecoxib or irinotecan, but not 5-fluoruracil, had sign
203      The results of this study indicate that rofecoxib or low-dose naproxen does not slow cognitive d
204 of the cyclo-oxygenase-2 selective inhibitor rofecoxib or the mixed cyclo-oxygenase-1/cyclo-oxygenase
205 ransgenic mice in the absence or presence of rofecoxib oral administration.
206 oduced cyclo-oxygenase-2 selective inhibitor rofecoxib, owe part of their inhibitory actions to effec
207 factors, ischemic stroke was associated with rofecoxib (P = 0.060, OR 2.27 [95% CI 0.97-5.28]), and p
208 rimary prevention trials (0.52%): 0.74% with rofecoxib (P =.04 compared with the placebo group of the
209 an 206, range 154 to 383 pg/mg creatinine by rofecoxib (P=0.04) but was not changed in nonsmokers.
210 th overall mortality of 34 deaths among 1069 rofecoxib patients and 12 deaths among 1078 placebo pati
211 ithin 14 days of the last dose (24 among 725 rofecoxib patients and 15 among 732 placebo patients) an
212 ods and reported 29 deaths (2.7%) among 1067 rofecoxib patients and 17 deaths (1.6%) among 1075 place
213 ed deaths" were reported (9 deaths among 346 rofecoxib patients and 2 deaths among 346 placebo patien
214 onal 22 deaths in the off-drug period (17 in rofecoxib patients and 5 in placebo patients).
215                   The 11,699 patients with a rofecoxib prescription in our practice were sent notific
216  of patients and providers and to deactivate rofecoxib prescriptions in the EMR.
217                 Recent litigation related to rofecoxib provided a unique opportunity to examine guest
218                                   Except for rofecoxib, RA treatment does not appear to be associated
219 cohort receiving aspirin, both celecoxib and rofecoxib reduced risk of admission for gastrointestinal
220 s no evidence for an excess of CV events for rofecoxib relative to either placebo or the non-naproxen
221 posure showed an increase in the MI risk for rofecoxib (risk difference [RD] 1.40, 95% confidence int
222  significant elevation in the event rate for rofecoxib (RR 1.15, 95% confidence interval [95% CI] 1.0
223 ts for new users of each agent increased for rofecoxib (RR 1.22, 95% confidence interval [95% CI] 1.1
224 e prices of three commonly prescribed drugs: rofecoxib, sertraline, and atorvastatin.
225                 Furthermore, 20-HETE but not rofecoxib significantly increases rat platelet aggregati
226                                              Rofecoxib significantly reduced the recurrence rate afte
227                    In this randomized trial, rofecoxib significantly reduced the risk of colorectal a
228 nhibition of COX-2 by oral administration of Rofecoxib significantly slowed but did not cure the grow
229                                              Rofecoxib significantly slowed the growth of small (0-12
230 omethacin, lumiracoxib, meloxicam, naproxen, rofecoxib, sodium salicylate, and SC560 as inhibitors of
231 cally debulked and animals were treated with rofecoxib starting 3 days before surgery.
232 vents were assessed across 23 phase IIb to V rofecoxib studies.
233     Adenoma recurrence was less frequent for rofecoxib subjects than for those randomized to placebo
234 en but also by the COX-2 selective inhibitor rofecoxib, suggesting that the majority of PGE2 formed i
235                                              Rofecoxib suppressed MMP-2 expression and activity, Ets-
236                               Unlike NSAIDs, rofecoxib targets only the COX-2 isoform.
237  Time-cumulative analyses indicated that for rofecoxib the adverse risks for peripheral edema and hyp
238 ad reduced microvessel density compared with rofecoxib, the nonselective COX inhibitors, and control
239 e-free survival and overall survival between rofecoxib therapy and placebo and between the use and no
240                                              Rofecoxib therapy was associated with an increased frequ
241 e 85 to 390 pg/mg creatinine) was reduced by rofecoxib to 78+/-27, median 71.5, range 50 to 135 pg/mg
242 ascular adverse events in patients receiving rofecoxib to reduce rates of recurrence of colorectal ca
243 as the selective cyclooxygenase 2 inhibitor, rofecoxib, to avert a clinical GI event.
244 cal analyses of the primary splenic tumor in rofecoxib-treated mice showed no alteration in COX-1 exp
245 stroke, and transient ischemic attacks) with rofecoxib treatment compared with naproxen was 2.38 (95%
246  found no evidence of a greater benefit from rofecoxib treatment compared with placebo in patients wh
247                                              Rofecoxib treatment did not inhibit platelet thromboxane
248 IK3CA mutation does not predict benefit from rofecoxib treatment, it merits further evaluation as a p
249 xib, with correspondingly lower levels after rofecoxib treatment.
250                                              Rofecoxib use increases the risk of serious coronary hea
251 justed relative risks of AMI associated with rofecoxib use of 1 to 30 days (OR, 1.40; 95% CI, 1.12 to
252                       In this study, current rofecoxib use was associated with an elevated relative r
253                                              Rofecoxib use was not documented in any country.
254 aration of the event curves) among long-term rofecoxib users at low or high baseline cardiovascular r
255  compared with 1.16 (CI, 0.70 to 1.93) among rofecoxib users.
256 cal trials of coxibs (etoricoxib, celecoxib, rofecoxib, valdecoxib) in patients with hip and/or knee
257 tive COX-2 inhibitors (coxibs), particularly rofecoxib, valdecoxib, and parecoxib, increases risk for
258 ascular variables did not predict the use of rofecoxib versus celecoxib.
259 with nonselective NSAIDs were the following: rofecoxib versus naproxen (odds ratio, 3.39 [CI, 1.37 to
260 genase-2 inhibition led to the withdrawal of rofecoxib (Vioxx) and valdecoxib (Bextra), but the mecha
261 ibitors of cyclooxygenase-2 (COX-2), such as rofecoxib (Vioxx), celecoxib (Celebrex), and valdecoxib
262 hibitors, including celecoxib (Celebrex) and rofecoxib (Vioxx), produced two unanticipated findings.
263 l anti-inflammatory drugs until one of them, rofecoxib (Vioxx), was found to be associated with incre
264 een under intense scrutiny because long-term rofecoxib (Vioxx; Merck, Whitehouse Station, NJ) treatme
265 idal anti-inflammatory drugs (NSAIDs) (e.g., rofecoxib [Vioxx]) increase the risk of heart attack and
266 5, and - 12.5 mm; P</=.02 for either dose of rofecoxib vs acetaminophen and P =.02 for rofecoxib, 25
267 7, and - 20.9 mm; P</=.02 for either dose of rofecoxib vs acetaminophen).
268 ll others vs acetaminophen; P =.05 for 25-mg rofecoxib vs celecoxib), rest pain (-21.8, - 18.6, - 15.
269 he use of celecoxib (adjusted odds ratio for rofecoxib vs. celecoxib, 2.72 [CI, 1.24 to 5.95]; P = 0.
270         The difference between celecoxib and rofecoxib was -2.5 mm, with an upper limit of the 95% co
271                                   The use of rofecoxib was associated with a statistically significan
272                               Current use of rofecoxib was associated with an elevated relative risk
273 a history of colorectal adenomas, the use of rofecoxib was associated with an increased cardiovascula
274 randomized trials with 116,094 participants, rofecoxib was associated with increased renal and arrhyt
275                      Compared with controls, rofecoxib was associated with increased risk of arrhythm
276         For all individual renal end points, rofecoxib was associated with increased risk of peripher
277                      As reported previously, rofecoxib was associated with increased risks of signifi
278 pared with remote exposure to any NSAID, and rofecoxib was compared with celecoxib.
279                                     However, rofecoxib was ineffective in preventing downregulation o
280           The increased rate associated with rofecoxib was seen in the first 60 days of use (adjusted
281         The increase in rate associated with rofecoxib was seen within the first 60 days and persiste
282                 The reduction in events with rofecoxib was similar in high- and low-risk subgroups (R
283                                              Rofecoxib was voluntarily withdrawn by the manufacturer.
284                                              Rofecoxib was well tolerated and provided efficacy that
285                           Users of high-dose rofecoxib were 1.70 (95% CI 0.98-2.95, p=0.058) times mo
286                                Celecoxib and rofecoxib were associated with different odds of MI.
287 s that clinical trial manuscripts related to rofecoxib were authored by sponsor employees but often a
288 g division to promote prescription of Vioxx (rofecoxib) when it became available on the market in 199
289 , which blocks COX-1 selectively, but not by rofecoxib, which is a selective inhibitor of COX-2.
290        Diclofenac has a risk very similar to rofecoxib, which was withdrawn from worldwide markets ow
291 and 1.69 (95% CI: 1.07, 2.69) when comparing rofecoxib with naproxen.
292 bo; 0.79 (95% CI: 0.40, 1.55) when comparing rofecoxib with non-naproxen NSAIDs; and 1.69 (95% CI: 1.
293 R) trial, a large randomized trial comparing rofecoxib with placebo after primary CRC resection.
294 was 0.84 (95% CI: 0.51, 1.38) when comparing rofecoxib with placebo; 0.79 (95% CI: 0.40, 1.55) when c
295 ed that COX-2 inhibitor drugs, celecoxib and rofecoxib, with similar COX-2-selectivity and clinical e
296 whether use of the selective COX-2 inhibitor rofecoxib would reduce the risk of colorectal adenomas.

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