ライフサイエンスコーパス: antirheumatic drug

1 n addition to at least one disease-modifying antirheumatic drug.

2 week 24, either compared with placebo or an antirheumatic drug.

3 nce conventional synthetic disease-modifying antirheumatic drug.

4 d almost all were taking a disease-modifying antirheumatic drug.

5 sease and had not received disease-modifying antirheumatic drugs.

6 of the efficacy of several disease-modifying antirheumatic drugs.

7 unsuccessfully with other disease-modifying antirheumatic drugs.

8 f SpA that is resistant to disease-modifying antirheumatic drugs.

9 hus these are the original disease-modifying antirheumatic drugs.

10 antiinflammatory drugs or disease-modifying antirheumatic drugs.

11 use of corticosteroids or disease-modifying antirheumatic drugs.

12 logical/targeted synthetic disease-modifying antirheumatic drugs.

13 nt with corticosteroids or disease-modifying antirheumatic drugs.

14 l, and newz non-biological disease-modifying antirheumatic drugs.

15 3.3%-79.7%; P=0.0025) with disease-modifying antirheumatic drugs.

16 fections compared to other disease-modifying antirheumatic drugs.

17 h groups were naive to all disease-modifying antirheumatic drugs.

18 ly respond to conventional disease-modifying antirheumatic drugs.

19 use of glucocorticoids and disease modifying antirheumatic drugs.

20 a lower number of lifetime disease-modifying antirheumatic drugs (1.9 versus 2.5).

21 nflammation with conventional and biological antirheumatic drugs affects cardiovascular risk.

22 ad suboptimal responses to disease-modifying antirheumatic drugs and a longer duration of arthritis a

23 Together, use of disease-modifying antirheumatic drugs and anti-CCP2 positivity increased P

24 ple conventional synthetic disease-modifying antirheumatic drugs and glucocorticoid.

25 pports the use of selected disease-modifying antirheumatic drugs and novel biologic agents in childre

26 vity for the initiation of disease-modifying antirheumatic drugs and persistent disease is increased,

27 The subsequent sequence of disease-modifying antirheumatic drugs and the value of changing disease-mo

28 ently require therapy with disease-modifying antirheumatic drugs and/or biologic agents.

29 its associated with use of disease-modifying antirheumatic drugs and/or biologics remain controversia

30 rategy, advent of targeted disease-modifying antirheumatic drugs, and combination therapy).

31 untreated with biological disease-modifying antirheumatic drugs, and had inadequate response to at l

32 f this variant needed more disease-modifying antirheumatic drugs, and more patients with this genotyp

33 actor-alpha therapy, other disease modifying antirheumatic drugs, and nonsteroidal anti-inflammatory

34 ase have been reported for disease modifying antirheumatic drugs, antimetabolites and biologic drugs.

35 the case, combinations of disease-modifying antirheumatic drugs appear to be a reasonable considerat

36 Synthetic and biological disease-modifying antirheumatic drugs are a cornerstone for the treatment

37 Nonmethotrexate disease-modifying antirheumatic drugs are effective, relatively well toler

38 ior noninfectious uveitis, disease-modifying antirheumatic drugs are first-line therapy; biologics su

39 tations of nonmethotrexate disease-modifying antirheumatic drugs are reduced impact on comorbidities

40 show that nonmethotrexate disease-modifying antirheumatic drugs are widely prescribed; their usage h

41 stepping-up to combination disease-modifying antirheumatic drugs are, however, unresolved.

42 ranofin, an orally bioavailable FDA-approved antirheumatic drug, as having potent bactericidal activi

43 ugs but had to stop taking disease-modifying antirheumatic drugs at least 28 days before randomizatio

44 (< or =10 mg per day), and disease-modifying antirheumatic drugs at stable doses during the trial.

45 exate (MTX), an equivalent disease-modifying antirheumatic drug, at 24 months.

46 gic and targeted synthetic disease-modifying antirheumatic drug (b/tsDMARD) use on the development of

47 Although biological disease-modifying antirheumatic drugs (bDMARDs) are effective, they are co

48 cDNA induced by biological disease-modifying antirheumatic drugs (bDMARDs) in RA patients with an emp

49 with response to biologic disease-modifying antirheumatic drugs (bDMARDs) in rheumatoid arthritis (R

50 were receiving biological disease-modifying antirheumatic drugs (bDMARDs).

51 reclude a trial of another disease-modifying antirheumatic drug before use of a BRM).

52 corticoids and traditional disease-modifying antirheumatic drugs before and during pregnancy.

53 erative management of the most commonly used antirheumatic drugs being used to treat patients with rh

54 d arthritis include use of disease-modifying antirheumatic drugs, but a minority of patients achieve

55 ic agents after failure of disease-modifying antirheumatic drugs, but differed or did not provide spe

56 osteroid plus conventional disease-modifying antirheumatic drugs (C-DMARDs) as first-line therapy in

57 east milk of nursing mothers may limit which antirheumatic drugs can be safely used.

58 ly aggressive therapy with disease-modifying antirheumatic drugs can improve outcome and prevent join

59 , addition of conventional disease-modifying antirheumatic drugs (cDMARD), and treatment alterations

60 rials of intensive initial disease-modifying antirheumatic drug combinations showed they reduce synov

61 monotherapy benefited from disease-modifying antirheumatic drug combinations without excess toxicity.

62 nd optimal clinical use of disease-modifying antirheumatic drug combinations.

63 and argue that traditional disease-modifying antirheumatic drugs continue to play a pivotal role.

64 round medications included disease-modifying antirheumatic drugs, corticosteroids, and nonsteroidal a

65 standard against which new disease-modifying antirheumatic drugs could be compared.

66 und conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) in patients with rheumato

67 ing conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), but how to best treat pa

68 Other conventional disease-modifying antirheumatic drugs did not have a significant effect on

69 tudy of rates of change in disease-modifying antirheumatic drug (DMARD) and/or systemic corticosteroi

70 matology criteria) without disease-modifying antirheumatic drug (DMARD) or steroid therapy in 8 of th

71 ing prior to initiation of disease-modifying antirheumatic drug (DMARD) therapy (18 548 [3.2%]).

72 nakinra as part of initial disease-modifying antirheumatic drug (DMARD) therapy were identified from

73 that an intensive step-up disease-modifying antirheumatic drug (DMARD) treatment strategy targeting

74 ncluded any prior use of a disease-modifying antirheumatic drug (DMARD), higher disease functional cl

75 aphic progression by a new disease-modifying antirheumatic drug (DMARD), LEF, as well as 2 commonly u

76 This group included disease-modifying antirheumatic drug (DMARD)-naive patients with early RA

77 The cohort comprised disease-modifying antirheumatic drug (DMARD)-naive patients with early ser

78 F), and prescription for a disease-modifying antirheumatic drug (DMARD).

79 odes and prescription of a disease-modifying antirheumatic drug (DMARD).

80 (a conventional synthetic disease-modifying antirheumatic drug [DMARD]), versus initiation of methot

81 , following treatment with disease-modifying antirheumatic drugs (DMARDs) (either methotrexate or lef

82 nts initiating nonbiologic disease-modifying antirheumatic drugs (DMARDs) (n=25,742) within each infl

83 e to assess the receipt of disease-modifying antirheumatic drugs (DMARDs) among patients with rheumat

84 led to respond to standard disease-modifying antirheumatic drugs (DMARDs) and antitumour necrosis fac

85 en treatment with biologic disease-modifying antirheumatic drugs (DMARDs) and development of cancer i

86 data from trials comparing disease-modifying antirheumatic drugs (DMARDs) and from comparative coxib-

87 ity persists despite prior disease-modifying antirheumatic drugs (DMARDs) and ongoing MTX monotherapy

88 Adherence to disease-modifying antirheumatic drugs (DMARDs) and prednisone was determin

89 tis refractory to biologic disease-modifying antirheumatic drugs (DMARDs) are unclear.

90 ialty tiering for biologic disease-modifying antirheumatic drugs (DMARDs) by Medicare Part D plans im

91 adalimumab) or nonbiologic disease-modifying antirheumatic drugs (DMARDs) during 2000-2007 from the f

92 A who had discontinued all disease-modifying antirheumatic drugs (DMARDs) for an appropriate washout

93 he past 2 years, three new disease-modifying antirheumatic drugs (DMARDs) have been approved: lefluno

94 is associated with use of disease-modifying antirheumatic drugs (DMARDs) in patients with RA.

95 n the role of conventional disease-modifying antirheumatic drugs (DMARDs) in the current management o

96 though early initiation of disease-modifying antirheumatic drugs (DMARDs) is effective in controlling

97 To evaluate the effect of disease-modifying antirheumatic drugs (DMARDs) on the likelihood of patien

98 ith conventional synthetic disease-modifying antirheumatic drugs (DMARDs) or to biologic or targeted

99 s treated with traditional disease-modifying antirheumatic drugs (DMARDs) recruited to the British So

100 with interest moving from disease-modifying antirheumatic drugs (DMARDs) to biological therapies and

101 c-naive patients receiving disease-modifying antirheumatic drugs (DMARDs) until either July 31, 2008,

102 itis (RA) in whom specific disease-modifying antirheumatic drugs (DMARDs) were initiated.

103 nfliximab with concomitant disease-modifying antirheumatic drugs (DMARDs), etanercept with concomitan

104 early and sustained use of disease-modifying antirheumatic drugs (DMARDs), in the hope of improving l

105 m who had previously taken disease-modifying antirheumatic drugs (DMARDs), including anti-tumor necro

106 t 3 months of non-biologic disease-modifying antirheumatic drugs (DMARDs), or at least 4 weeks of non

107 emission who are receiving disease-modifying antirheumatic drugs (DMARDs), radiographic progression c

108 Disease-modifying antirheumatic drugs (DMARDs), the key therapeutic agents

109 cting the effectiveness of disease modifying antirheumatic drugs (DMARDs).

110 A treated with traditional disease-modifying antirheumatic drugs (DMARDs).

111 inue using any concomitant disease-modifying antirheumatic drugs (DMARDs).

112 to conventional synthetic disease-modifying antirheumatic drugs (DMARDs).

113 e in patients treated with disease-modifying antirheumatic drugs (DMARDs).

114 ndidates for subclasses of disease-modifying antirheumatic drugs (DMARDs).

115 ogic or targeted synthetic disease-modifying antirheumatic drugs (DMARDs).

116 ed treatment with biologic disease-modifying antirheumatic drugs (DMARDs).

117 who were naive to biologic disease-modifying antirheumatic drugs (DMARDs).

118 onal synthetic or biologic disease-modifying antirheumatic drugs (DMARDs).

119 compared with traditional disease-modifying antirheumatic drugs (DMARDs).

120 -reported validated use of disease-modifying antirheumatic drugs (DMARDs).

121 te and safe responses with disease-modifying antirheumatic drugs (DMARDs).

122 corticoids and traditional disease-modifying antirheumatic drugs (DMARDs).

123 (RA) patients taking oral disease-modifying antirheumatic drugs (DMARDs).

124 RA) should be treated with disease-modifying antirheumatic drugs (DMARDs).

125 f 85% of patients received disease-modifying antirheumatic drugs (DMARDs).

126 least 1 prescription for a disease-modifying antirheumatic drug during the study period.

127 bitors in combination with disease-modifying antirheumatic drugs early after the diagnosis of aggress

128 ombination with a biologic disease-modifying antirheumatic drug, etanercept, ESMA04 demonstrated ther

129 recommended as the initial disease-modifying antirheumatic drug for rheumatoid arthritis (RA).

130 tom onset) RA treated with disease-modifying antirheumatic drugs, from patients with osteoarthritis (

131 e risks of nonmethotrexate disease-modifying antirheumatic drugs have been evaluated, including infec

132 ditional immunosuppressant disease-modifying antirheumatic drugs have been shown to be highly effecti

133 ded therapeutic options of disease-modifying antirheumatic drugs have markedly improved both the mana

134 ons of biologics and other disease-modifying antirheumatic drugs have reported significant improvemen

135 dies showed that synthetic disease-modifying antirheumatic drugs improved periodontal clinical parame

136 nable guidelines; however, for the remaining antirheumatic drugs in current use, the available data c

137 lpha agents to traditional disease-modifying antirheumatic drugs in early rheumatoid arthritis is a n

138 dings with nonmethotrexate disease-modifying antirheumatic drugs in rheumatoid arthritis and seronega

139 e associated with biologic disease-modifying antirheumatic drugs in rheumatoid arthritis.

140 of the most commonly used disease-modifying antirheumatic drugs in the management of psoriatic arthr

141 stablished for a majority of the traditional antirheumatic drugs in use today.

142 ated risks, though several disease-modifying antirheumatic drugs increase both types of adverse react

143 aggressive treatment with disease-modifying antirheumatic drugs is used, seeking to minimize long-te

144 eumatologists included new disease-modifying antirheumatic drugs (leflunomide, etanercept, and inflix

145 shed RA who were naive for disease-modifying antirheumatic drugs, matched healthy controls, and 2 gro

146 Disease-modifying antirheumatic drugs may confer greater benefits when com

147 ctor positive; no previous disease-modifying antirheumatic drugs; mean swollen joint count 8.6-10.4).

148 Previous small studies suggest that the antirheumatic drug methotrexate may be a potential treat

149 apy to a triple regimen of disease-modifying antirheumatic drugs (methotrexate, sulfasalazine, and hy

150 and the value of changing disease-modifying antirheumatic drug monotherapies or stepping-up to combi

151 imilar for RA treated with disease-modifying antirheumatic drugs (n = 80) (odds ratio, 3.30 [95% CI,

152 ullination, and serum from disease-modifying antirheumatic drug-naive early arthritis patients, we as

153 from healthy children and disease-modifying antirheumatic drug-naive patients with JIA were characte

154 cohort of newly diagnosed, disease-modifying antirheumatic drugs-naive rheumatoid arthritis patients

155 nsification, auranofin (an apoptotic-inducer antirheumatic drug), nicotinamide (vitamin B3), and a pe

156 clearly define the role of disease-modifying antirheumatic drugs, novel therapeutic agents, and antib

157 nts with MDA, 82% received disease-modifying antirheumatic drugs or biologic agents.

158 6 months of treatment with disease-modifying antirheumatic drugs or biologics.

159 sting that combinations of disease-modifying antirheumatic drugs or newer biologic therapy is more ef

160 gnancy compared with other disease-modifying antirheumatic drugs or with placebo.

161 have shown promising oral disease-modifying antirheumatic drug potential with efficacy similar to an

162 ey had an appropriate GPRD disease-modifying antirheumatic drug prescription or 3 other GPRD characte

163 apy and discontinuation of disease-modifying antirheumatic drugs, resulting in stabilization of the d

164 with bDMARDs and synthetic disease-modifying antirheumatic drugs (sDMARDs) had the highest risk of HB

165 bination with conventional disease-modifying antirheumatic drugs seems to produce the best outcomes.

166 s, first-line therapy with disease-modifying antirheumatic drugs such as methotrexate achieved remiss

167 or early monitoring of treatment response to antirheumatic drugs such as MTX.

168 ugs and traditionally used disease-modifying antirheumatic drugs, such as methotrexate, often fails i

169 rexate (MTX) is a widely used anticancer and antirheumatic drug that has been postulated to protect a

170 azine monotherapies; early disease-modifying antirheumatic drug therapy reduces erosive progression.

171 107 RA patients receiving disease-modifying antirheumatic drug therapy who were judged by their cons

172 as an adjunct to existing disease-modifying antirheumatic drug therapy.

173 ctive, open-label study of disease-modifying antirheumatic drug therapy.

174 LA) NPs were loaded with auranofin (ARN), an antirheumatic drug, to induce mitogen-activated protein

175 required corticosteroid or disease-modifying antirheumatic drug treatment because of active disease b

176 ctive disease, no previous disease-modifying antirheumatic drug treatment, and >or=2 sets of scored r

177 an inadequate response to disease-modifying antirheumatic drug treatment.

178 rs while seeking to avoid use of second-line antirheumatic drugs until evidence of joint damage was s

179 ks; stratified by baseline disease-modifying antirheumatic drug use and C-reactive protein concentrat

180 duration, duration of RA, disease-modifying antirheumatic drug use, and the proportion with comorbid

181 met was high for QI-2 (RA disease-modifying antirheumatic drug use; 94%), QI-3 (intervention if RA w

182 omitant corticosteroid and disease-modifying antirheumatic drug was also assessed.

183 of patients not taking any disease-modifying antirheumatic drugs was 66% in 1985 versus 13% in 2000.

184 All other disease-modifying antirheumatic drugs were discontinued; stable dosage of

185 Biological, disease-modifying antirheumatic drugs were prescribed more frequently in n

186 en previously treated with disease-modifying antirheumatic drugs were randomized to receive 100 mg of

187 of current treatment with disease-modifying antirheumatic drugs were significantly associated with a

188 or by self-reported use of disease modifying antirheumatic drugs, were compared with noncases (n = 24

189 or by self-reported use of disease-modifying antirheumatic drugs, were compared with noncases (n=26,1

190 r combination therapy with disease-modifying antirheumatic drugs, whereas results of studies with mon

191 andard single therapy with disease-modifying antirheumatic drugs, which was previously the final step

192 ous nodules and greater use of slowly acting antirheumatic drugs, while female RA patients had earlie

193 ebo and/or any traditional disease-modifying antirheumatic drugs with a minimum of 24 weeks of follow

194 isting of a combination of disease-modifying antirheumatic drugs with biologic agents in patients wit

195 y and safety of biological disease-modifying antirheumatic drugs within the same class, including TNF

196 rescriptions for LEF and 9 disease-modifying antirheumatic drugs written between October 1998 and Jun

197 vious exposure to biologic disease-modifying antirheumatic drugs (yes vs no).