ライフサイエンスコーパス: coxib

1 ts intolerant of naproxen were switched to a coxib.

2 tion increased in vitro with the addition of coxib.

3 rction nor stroke predicted utilization of a coxib.

4 dentified 47 gene products to be affected by coxibs.

5 efits of coxibs and for development of safer coxibs.

6 ere significantly less with NSAIDs than with coxibs.

7 ugs at the recommended doses and 6% received coxibs.

8 rentially blocked by COX-2 inhibitors called coxibs.

9 irin on COX-1 may be blunted when taken with coxibs.

10 ncurrent users of proton pump inhibitors and coxibs.

11 persons not currently using either NSAIDs or coxibs.

12 ective COX-2 inhibitors, collectively called coxibs.

13 ar events in patients requiring therapy with coxibs.

14 (GPA) cotherapy, and 1,207 (65.8%) received coxibs.

15 cardiovascular side effects associated with coxibs.

16 y drugs and COX-2-specific inhibitors called coxibs.

17 ed the selection of nonselective NSAIDs over coxibs.

18 fined daily doses of NSAIDs accounted for by coxibs.

19 nce-based recommendations for prescribing of coxibs.

20 alternate end-game strategies to prepare NO-COXIB 1 from this intermediate were explored and develop

21 ry cohort, we identified 76,082 new users of coxibs, 53,014 new users of nonselective NSAIDs, and 46,

22 By 2001, coxibs accounted for half of all NSAID doses covered by

23 d 3) a cyclooxygenase 2-selective inhibitor (coxib) alone.

24 y greater, but perhaps less selective use of coxibs among specialists, even after accounting for impo

25 significantly more likely to selectively use coxibs among their patients with a history of gastrointe

26 ent of the inhibition of COX-2 because a non-coxib analogue of this drug, 2,5-dimethyl-celecoxib (DMC

27 The effect size for coxibs and common active internal controls (nonsteroidal

28 Coxibs and common active internal controls showed larger

29 cal for evaluating the risks and benefits of coxibs and for development of safer coxibs.

30 cardiovascular adverse effects of selective coxibs and nonselective NSAIDs, but many patients with a

31 Other coxibs and NSAIDs did not appear to be associated with a

32 to examine, in a large group of new users of coxibs and NSAIDs, the rate of cardiovascular events, th

33 The use of coxibs and spending on NSAIDs varies widely by state and

34 ngs demonstrate overlap of genes affected by coxibs and those mediating CAD risk and points to furthe

35 Both coxibs and traditional NSAIDs may contribute to a dose-d

36 with selective cyclooxygenase 2 inhibitors (coxibs) and nonselective nonsteroidal antiinflammatory d

37 We identified 74,838 users of NSAIDs or coxibs, and 23,532 comparable users of other drugs compr

38 Many nonselective NSAIDs and coxibs are not associated with an increased risk of CVD

39 Newer agents termed "coxibs" are selective inhibitors of COX-2.

40 Cyclooxygenase-2 inhibitors (coxibs) are characterized by multiple molecular off-targ

41 Although cyclooxygenase (COX)-2 inhibitors (coxibs) are effective in controlling inflammation, pain,

42 were significantly more likely to receive a coxib, as well as patients with a history of osteoarthri

43 nisms, which are potentially responsible for coxib-associated CAD risk.

44 Predefined exposure groups included the 3 coxibs available in the US during the study period (cele

45 prising observation that celecoxib and other coxibs bind tightly to a subunit of COX-1.

46 group of patients who did not use NSAIDs or coxibs, but started other medications unrelated to cardi

47 ced the proportion of NSAID doses made up by coxibs by 15.0 percent (95 percent confidence interval,

48 ed the effect of such programs on the use of coxibs by Medicaid beneficiaries.

49 ti-inflammatory cyclooxygenase 2 inhibitors (coxibs) by targeting the prostaglandin pathway downstrea

50 nted prior-authorization requirements before coxibs can be prescribed.

51 The evidence that coxibs cause thrombotic heart disease is weak.

52 ate that rheumatologists broadly adopted the coxib class of NSAIDs in a nonselective manner with resp

53 tential GI-related cost savings suggested in coxib clinical trials may not be fully realized in "real

54 ning the cardiovascular risk associated with coxibs comes from three main sources: basic research dem

55 CI: -$139, $55), although after adding NSAID/coxib costs, the total cost in the coxib period was sign

56 yclooxygenase 2 (COX-2)-specific inhibitors (coxibs) decrease gastrointestinal (GI) events in control

57 Cyclooxygenase-2 inhibitors, or coxibs, designed to provide comparable pain relief to tr

58 The risk reduction seen with coxibs does not offset their increased costs compared wi

59 When NSAID/coxib drug costs were included, costs were significantly

60 implemented prior-authorization programs for coxibs during the study period.

61 Rofecoxib and celecoxib (coxibs) effectively treat chronic arthritis pain and red

62 mized, placebo-controlled clinical trials of coxibs (etoricoxib, celecoxib, rofecoxib, valdecoxib) in

63 Because coxibs exhibit cardiovascular side effects, they are oft

64 or with an NSAID is as effective as use of a coxib for reducing the risk of NSAID-induced gastropathy

65 s of genes representing molecular targets of coxibs for association with CAD.

66 The effect size for all coxib groups combined (0.44) indicated greater efficacy

67 Based on this rationale, some coxibs have been used in clinical trials for AD patients

68 ears, selective cyclooxygenase-2 inhibitors (coxibs) have accounted for a growing proportion of presc

69 with NSAIDs and COX-2 selective inhibitors (coxibs) have provoked more scrutiny of the precise role

70 traditional NSAID with gastroprotection or a coxib in high-risk NSAID users.

71 and it is reported to be the most selective COXIB in vivo.

72 dministration schedule, and toxicity for the coxibs in adenoma recurrence prevention trials.

73 in evaluating relative benefits and risk of COXIBs in appropriately selected patients for cancer pre

74 ists may be used therapeutically to suppress coxib-induced cardiovascular side effects.

75 Importantly, PPARdelta agonists suppress coxib-induced TF expression and decrease circulating TF

76 NSAIDs and coxibs inhibit PG biosynthesis.

77 Multivariable adjusted associations between coxib initiation and discontinuation and patient and pro

78 Using a coxib instead of a nonselective NSAID in average-risk pa

79 Coxibs may be a safer alternative in that setting.

80 Newer coxibs may have safety and advantages over existing comp

81 However, coxibs may provide an acceptable incremental cost-effect

82 e not significantly lower after switching to coxibs (mean difference, -$19; 95% CI: -$139, $55), alth

83 received gastroprotection, defined as either coxib monotherapy and/or gastroprotective agent (GPA) co

84 ded 860 (46.9%) patients who were prescribed coxib monotherapy, 347 (18.9%) prescribed dual coxib plu

85 "New NSAID" (n = 25,989) and "new coxib" (n = 2125) groups were assessed for the 12-month

86 COX inhibitors, including coxibs, nonselective nonsteroidal antiinflammatory drugs

87 ugs (NSAIDs) and selective COX-2 inhibitors (COXIBs) on CRC.

88 Naproxen, 500 mg twice daily, and coxib, once daily.

89 re more likely than generalists to prescribe coxibs, only family or general practitioners were signif

90 nti-inflammatory drugs (NSAIDs) are use of a coxib or concurrent use of a proton pump inhibitor or do

91 All study patients started use of a coxib or NSAID after January 1, 1999.

92 No other coxib or NSAID was associated with a significant increas

93 re, and cardiovascular death) among users of coxibs or nonselective NSAIDs in the prior 6 months comp

94 ection of a nonselective NSAID rather than a coxib (OR 0.73, 95% CI 0.55-0.98).

95 espite cardiovascular concerns regarding the coxibs, our data suggest that aspirin use, but not cardi

96 n a broad spectrum of pleiotropic effects of coxibs, our intention was to narrow potential mechanisms

97 f high levels of selective COX-2 inhibitors (coxibs), particularly rofecoxib, valdecoxib, and parecox

98 ing NSAID/coxib costs, the total cost in the coxib period was significantly higher (mean increase, $3

99 heumatic drugs (DMARDs) and from comparative coxib-placebo trials to test the power of 2 a priori out

100 xib monotherapy, 347 (18.9%) prescribed dual coxib plus GPA cotherapy, 173 (9.4%) prescribed a nonsel

101 tifiable gastrointestinal (GI) risk factors, coxib prescribing rates as a proportion of NSAID agents

102 espectively; among dual aspirin/NSAID users, coxib prescribing rates were 66.2%, 78.3%, and 68.5% of

103 vity for inhibition of COX-2 achieved by the coxibs relates both to chemical properties of the drug a

104 le several questions regarding the safety of coxibs remain, especially the role of dose in the increa

105 gencies to determine whether prescription of coxibs required prior authorization and, if so, the crit

106 nti-inflammatory drugs, the newer generation coxibs (selective inhibitors of cyclooxygenase-2), and l

107 earch suggests that some clinical effects of coxibs, selective inhibitors of cyclooxygenase-2 (COX-2)

108 The coxib strategy became dominant when the cost of coxibs w

109 The coxib strategy was less effective and more expensive tha

110 Coxibs suppress PPARdelta activity and induce TF express

111 NSAIDs provide analgesic efficacy similar to coxibs, their use has been limited in the perioperative

112 inflammatory drug (NSAID) therapy to chronic coxib therapy and in patients starting chronic NSAID the

113 tching from chronic NSAID therapy to chronic coxib therapy had a slight decrease in the proportion us

114 s starting chronic NSAID therapy vs. chronic coxib therapy in a U.S. administrative claims database o

115 fter switching from chronic NSAID therapy to coxib therapy.

116 ggest systematic differences among published coxib trials and emphasize the need for direct-compariso

117 .04) groups based on data available from all coxib trials.

118 ded only new episodes of prescribed NSAID or coxib use and controlled for multiple baseline risk fact

119 Multivariate adjusted associations between coxib use and specific cardiovascular variables, includi

120 ivariate analyses, independent predictors of coxib use versus nonselective NSAID use included diagnos

121 234,010 and 48,710 new episodes of NSAID and coxib use, respectively, with 363,037 person-years of fo

122 Coxib utilization rates were consistently high across al

123 otective strategy, primarily attributable to coxib utilization.

124 sease versus 100 for later disease), but the coxib-versus-placebo comparison was less powerful in ear

125 Adjusted OR for GI resource use for new-coxib vs. new-NSAID was 1.04 (0.92-1.16), but GI costs w

126 The adjusted OR for any GI resource use (coxib vs. NSAID period) among switchers was 0.86 (0.74-0

127 The initiation and discontinuation of coxibs was influenced by physician specialty and by pati

128 ib strategy became dominant when the cost of coxibs was reduced by 90% of the current average wholesa

129 selective cyclooxygenase 2-inhibiting drug (coxib), was measured and categorized by risk for ulcer c

130 f NSAID prescriptions were discontinued, and coxibs were significantly less likely to be discontinued

131 Although cyclooxygenase-2 inhibitors (coxibs) were developed to cause less gastrointestinal he

132 attenuation of TF expression is abrogated by coxibs, which may explain the prothrombotic side-effects

133 looxygenase (COX)-2 inhibitors, known as the coxibs, with second-generation compounds already approve

134 tion drug plan that fully covered NSAIDs and coxibs without restriction.

135 erapy and 40% (23%-54%) for current users of coxibs without such cotherapy.