ライフサイエンスコーパス: disease-modifying antirheumatic drug

1 er for 6 months, in addition to at least one disease-modifying antirheumatic drug.

2 the primary reference conventional synthetic disease-modifying antirheumatic drug.

3 of 13.7 years, and almost all were taking a disease-modifying antirheumatic drug.

4 nosuppression and use of glucocorticoids and disease modifying antirheumatic drugs.

5 ents had active disease and had not received disease-modifying antirheumatic drugs.

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

7 s had been treated unsuccessfully with other disease-modifying antirheumatic drugs.

8 l manifestations of SpA that is resistant to disease-modifying antirheumatic drugs.

9 d arthritis, and thus these are the original disease-modifying antirheumatic drugs.

10 es of nonsteroidal antiinflammatory drugs or disease-modifying antirheumatic drugs.

11 vitis and previous use of corticosteroids or disease-modifying antirheumatic drugs.

12 intolerance to biological/targeted synthetic disease-modifying antirheumatic drugs.

13 defined by treatment with corticosteroids or disease-modifying antirheumatic drugs.

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

15 ared with 58.7% (43.3%-79.7%; P=0.0025) with disease-modifying antirheumatic drugs.

16 risk of serious infections compared to other disease-modifying antirheumatic drugs.

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

18 nts who inadequately respond to conventional disease-modifying antirheumatic drugs.

19 us 36 mm/hr), and a lower number of lifetime disease-modifying antirheumatic drugs (1.9 versus 2.5).

20 fewer Treg cells had suboptimal responses to disease-modifying antirheumatic drugs and a longer durat

21 Together, use of disease-modifying antirheumatic drugs and anti-CCP2 posi

22 ociated with multiple conventional synthetic disease-modifying antirheumatic drugs and glucocorticoid

23 d evidence that supports the use of selected disease-modifying antirheumatic drugs and novel biologic

24 Sensitivity for the initiation of disease-modifying antirheumatic drugs and persistent dis

25 The subsequent sequence of disease-modifying antirheumatic drugs and the value of c

26 tic diseases frequently require therapy with disease-modifying antirheumatic drugs and/or biologic ag

27 scular risks/benefits associated with use of disease-modifying antirheumatic drugs and/or biologics r

28 i-tumor necrosis factor-alpha therapy, other disease modifying antirheumatic drugs, and nonsteroidal

29 treat-to-target strategy, advent of targeted disease-modifying antirheumatic drugs, and combination t

30 a, were previously untreated with biological disease-modifying antirheumatic drugs, and had inadequat

31 ozygous carriers of this variant needed more disease-modifying antirheumatic drugs, and more patients

32 ith rheumatic disease have been reported for disease modifying antirheumatic drugs, antimetabolites a

33 nts, as is usually the case, combinations of disease-modifying antirheumatic drugs appear to be a rea

34 Synthetic and biological disease-modifying antirheumatic drugs are a cornerstone

35 Nonmethotrexate disease-modifying antirheumatic drugs are effective, rel

36 For posterior noninfectious uveitis, disease-modifying antirheumatic drugs are first-line the

37 Two limitations of nonmethotrexate disease-modifying antirheumatic drugs are reduced impact

38 ervational studies show that nonmethotrexate disease-modifying antirheumatic drugs are widely prescri

39 monotherapies or stepping-up to combination disease-modifying antirheumatic drugs are, however, unre

40 ti-inflammatory drugs but had to stop taking disease-modifying antirheumatic drugs at least 28 days b

41 l corticosteriods (< or =10 mg per day), and disease-modifying antirheumatic drugs at stable doses du

42 safety of methotrexate (MTX), an equivalent disease-modifying antirheumatic drug, at 24 months.

43 the risk of biologic and targeted synthetic disease-modifying antirheumatic drug (b/tsDMARD) use on

44 Although biological disease-modifying antirheumatic drugs (bDMARDs) are effe

45 e the changes of ecDNA induced by biological disease-modifying antirheumatic drugs (bDMARDs) in RA pa

46 ntidrug antibodies with response to biologic disease-modifying antirheumatic drugs (bDMARDs) in rheum

47 , including 36 who were receiving biological disease-modifying antirheumatic drugs (bDMARDs).

48 ed version would preclude a trial of another disease-modifying antirheumatic drug before use of a BRM

49 gs (NSAIDs), glucocorticoids and traditional disease-modifying antirheumatic drugs before and during

50 gies for rheumatoid arthritis include use of disease-modifying antirheumatic drugs, but a minority of

51 the use of biologic agents after failure of disease-modifying antirheumatic drugs, but differed or d

52 lone versus corticosteroid plus conventional disease-modifying antirheumatic drugs (C-DMARDs) as firs

53 sease in which early aggressive therapy with disease-modifying antirheumatic drugs can improve outcom

54 njection intervals, addition of conventional disease-modifying antirheumatic drugs (cDMARD), and trea

55 mized controlled trials of intensive initial disease-modifying antirheumatic drug combinations showed

56 tients who failed monotherapy benefited from disease-modifying antirheumatic drug combinations withou

57 ess, toxicities, and optimal clinical use of disease-modifying antirheumatic drug combinations.

58 atment algorithm, and argue that traditional disease-modifying antirheumatic drugs continue to play a

59 Background medications included disease-modifying antirheumatic drugs, corticosteroids,

60 exate would set a standard against which new disease-modifying antirheumatic drugs could be compared.

61 ith stable background conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) in pati

62 hritis (RA) receiving conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), but ho

63 Other conventional disease-modifying antirheumatic drugs did not have a sig

64 ospective cohort study of rates of change in disease-modifying antirheumatic drug (DMARD) and/or syst

65 an College of Rheumatology criteria) without disease-modifying antirheumatic drug (DMARD) or steroid

66 hepatitis B screening prior to initiation of disease-modifying antirheumatic drug (DMARD) therapy (18

67 ic JIA receiving anakinra as part of initial disease-modifying antirheumatic drug (DMARD) therapy wer

68 ously demonstrated that an intensive step-up disease-modifying antirheumatic drug (DMARD) treatment s

69 nse to treatment included any prior use of a disease-modifying antirheumatic drug (DMARD), higher dis

70 rdation of radiographic progression by a new disease-modifying antirheumatic drug (DMARD), LEF, as we

71 This group included disease-modifying antirheumatic drug (DMARD)-naive patie

72 The cohort comprised disease-modifying antirheumatic drug (DMARD)-naive patie

73 eumatoid factor (RF), and prescription for a disease-modifying antirheumatic drug (DMARD).

74 4) > or =2 ICD-9 codes and prescription of a disease-modifying antirheumatic drug (DMARD).

75 thout methotrexate (a conventional synthetic disease-modifying antirheumatic drug [DMARD]), versus in

76 e needed for predicting the effectiveness of disease modifying antirheumatic drugs (DMARDs).

77 ents with early RA, following treatment with disease-modifying antirheumatic drugs (DMARDs) (either m

78 =33,324) and patients initiating nonbiologic disease-modifying antirheumatic drugs (DMARDs) (n=25,742

79 d a quality measure to assess the receipt of disease-modifying antirheumatic drugs (DMARDs) among pat

80 th RA who have failed to respond to standard disease-modifying antirheumatic drugs (DMARDs) and antit

81 association between treatment with biologic disease-modifying antirheumatic drugs (DMARDs) and devel

82 obtained summary data from trials comparing disease-modifying antirheumatic drugs (DMARDs) and from

83 hose disease activity persists despite prior disease-modifying antirheumatic drugs (DMARDs) and ongoi

84 Adherence to disease-modifying antirheumatic drugs (DMARDs) and predn

85 rheumatoid arthritis refractory to biologic disease-modifying antirheumatic drugs (DMARDs) are uncle

86 at the use of specialty tiering for biologic disease-modifying antirheumatic drugs (DMARDs) by Medica

87 t, infliximab, or adalimumab) or nonbiologic disease-modifying antirheumatic drugs (DMARDs) during 20

88 ents with active RA who had discontinued all disease-modifying antirheumatic drugs (DMARDs) for an ap

89 In the past 2 years, three new disease-modifying antirheumatic drugs (DMARDs) have been

90 ther herpes zoster is associated with use of disease-modifying antirheumatic drugs (DMARDs) in patien

91 eview will focus on the role of conventional disease-modifying antirheumatic drugs (DMARDs) in the cu

92 Although early initiation of disease-modifying antirheumatic drugs (DMARDs) is effect

93 To evaluate the effect of disease-modifying antirheumatic drugs (DMARDs) on the li

94 ble side effects with conventional synthetic disease-modifying antirheumatic drugs (DMARDs) or to bio

95 t in 2,170 patients treated with traditional disease-modifying antirheumatic drugs (DMARDs) recruited

96 an outcome measure with interest moving from disease-modifying antirheumatic drugs (DMARDs) to biolog

97 and 3,522 biologic-naive patients receiving disease-modifying antirheumatic drugs (DMARDs) until eit

98 h rheumatoid arthritis (RA) in whom specific disease-modifying antirheumatic drugs (DMARDs) were init

99 strategies were infliximab with concomitant disease-modifying antirheumatic drugs (DMARDs), etanerce

100 rd one based upon early and sustained use of disease-modifying antirheumatic drugs (DMARDs), in the h

101 lesion (TL) >/=2 cm who had previously taken disease-modifying antirheumatic drugs (DMARDs), includin

102 premilast, at least 3 months of non-biologic disease-modifying antirheumatic drugs (DMARDs), or at le

103 rthritis (RA) in remission who are receiving disease-modifying antirheumatic drugs (DMARDs), radiogra

104 Disease-modifying antirheumatic drugs (DMARDs), the key

105 rticipants to continue using any concomitant disease-modifying antirheumatic drugs (DMARDs).

106 nadequate response to conventional synthetic disease-modifying antirheumatic drugs (DMARDs).

107 outcomes with those in patients treated with disease-modifying antirheumatic drugs (DMARDs).

108 ods to identify candidates for subclasses of disease-modifying antirheumatic drugs (DMARDs).

109 initiation of biologic or targeted synthetic disease-modifying antirheumatic drugs (DMARDs).

110 previously received treatment with biologic disease-modifying antirheumatic drugs (DMARDs).

111 oriatic arthritis who were naive to biologic disease-modifying antirheumatic drugs (DMARDs).

112 e or more conventional synthetic or biologic disease-modifying antirheumatic drugs (DMARDs).

113 serious infection compared with traditional disease-modifying antirheumatic drugs (DMARDs).

114 positivity or self-reported validated use of disease-modifying antirheumatic drugs (DMARDs).

115 not achieve adequate and safe responses with disease-modifying antirheumatic drugs (DMARDs).

116 eatment with glucocorticoids and traditional disease-modifying antirheumatic drugs (DMARDs).

117 eumatoid arthritis (RA) patients taking oral disease-modifying antirheumatic drugs (DMARDs).

118 matoid arthritis (RA) should be treated with disease-modifying antirheumatic drugs (DMARDs).

119 A total of 85% of patients received disease-modifying antirheumatic drugs (DMARDs).

120 ents with active RA treated with traditional disease-modifying antirheumatic drugs (DMARDs).

121 d had received at least 1 prescription for a disease-modifying antirheumatic drug during the study pe

122 factor-alpha inhibitors in combination with disease-modifying antirheumatic drugs early after the di

123 ther alone or in combination with a biologic disease-modifying antirheumatic drug, etanercept, ESMA04

124 as monotherapy is recommended as the initial disease-modifying antirheumatic drug for rheumatoid arth

125 >3 years from symptom onset) RA treated with disease-modifying antirheumatic drugs, from patients wit

126 The adverse risks of nonmethotrexate disease-modifying antirheumatic drugs have been evaluate

127 compared with traditional immunosuppressant disease-modifying antirheumatic drugs have been shown to

128 eatment, and expanded therapeutic options of disease-modifying antirheumatic drugs have markedly impr

129 als with combinations of biologics and other disease-modifying antirheumatic drugs have reported sign

130 pective cohort studies showed that synthetic disease-modifying antirheumatic drugs improved periodont

131 necrosis factor-alpha agents to traditional disease-modifying antirheumatic drugs in early rheumatoi

132 ecent research findings with nonmethotrexate disease-modifying antirheumatic drugs in rheumatoid arth

133 sk of heart failure associated with biologic disease-modifying antirheumatic drugs in rheumatoid arth

134 ethotrexate is one of the most commonly used disease-modifying antirheumatic drugs in the management

135 tant than drug-related risks, though several disease-modifying antirheumatic drugs increase both type

136 ing in which early aggressive treatment with disease-modifying antirheumatic drugs is used, seeking t

137 ered, 217 (65%) rheumatologists included new disease-modifying antirheumatic drugs (leflunomide, etan

138 ients with established RA who were naive for disease-modifying antirheumatic drugs, matched healthy c

139 Disease-modifying antirheumatic drugs may confer greater

140 -43% rheumatoid factor positive; no previous disease-modifying antirheumatic drugs; mean swollen join

141 methotrexate therapy to a triple regimen of disease-modifying antirheumatic drugs (methotrexate, sul

142 ntirheumatic drugs and the value of changing disease-modifying antirheumatic drug monotherapies or st

143 The odds were similar for RA treated with disease-modifying antirheumatic drugs (n = 80) (odds rat

144 le of protein citrullination, and serum from disease-modifying antirheumatic drug-naive early arthrit

145 IgG glycans from healthy children and disease-modifying antirheumatic drug-naive patients with

146 cterized clinical cohort of newly diagnosed, disease-modifying antirheumatic drugs-naive rheumatoid a

147 trials will more clearly define the role of disease-modifying antirheumatic drugs, novel therapeutic

148 Among patients with MDA, 82% received disease-modifying antirheumatic drugs or biologic agents

149 56 patients after 6 months of treatment with disease-modifying antirheumatic drugs or biologics.

150 information suggesting that combinations of disease-modifying antirheumatic drugs or newer biologic

151 eased risk of malignancy compared with other disease-modifying antirheumatic drugs or with placebo.

152 Kinase inhibitors have shown promising oral disease-modifying antirheumatic drug potential with effi

153 as having RA if they had an appropriate GPRD disease-modifying antirheumatic drug prescription or 3 o

154 th supportive therapy and discontinuation of disease-modifying antirheumatic drugs, resulting in stab

155 id in combination with bDMARDs and synthetic disease-modifying antirheumatic drugs (sDMARDs) had the

156 these drugs in combination with conventional disease-modifying antirheumatic drugs seems to produce t

157 r posterior uveitis, first-line therapy with disease-modifying antirheumatic drugs such as methotrexa

158 ntiinflammatory drugs and traditionally used disease-modifying antirheumatic drugs, such as methotrex

159 omide and sulfasalazine monotherapies; early disease-modifying antirheumatic drug therapy reduces ero

160 We studied 107 RA patients receiving disease-modifying antirheumatic drug therapy who were ju

161 astatin or placebo as an adjunct to existing disease-modifying antirheumatic drug therapy.

162 randomized, prospective, open-label study of disease-modifying antirheumatic drug therapy.

163 ts, respectively) required corticosteroid or disease-modifying antirheumatic drug treatment because o

164 m onset) who had active disease, no previous disease-modifying antirheumatic drug treatment, and >or=

165 in SERENE who had an inadequate response to disease-modifying antirheumatic drug treatment.

166 ated permuted blocks; stratified by baseline disease-modifying antirheumatic drug use and C-reactive

167 rticoid dosage and duration, duration of RA, disease-modifying antirheumatic drug use, and the propor

168 The percentage met was high for QI-2 (RA disease-modifying antirheumatic drug use; 94%), QI-3 (in

169 Reduction of concomitant corticosteroid and disease-modifying antirheumatic drug was also assessed.

170 The proportion of patients not taking any disease-modifying antirheumatic drugs was 66% in 1985 ve

171 All other disease-modifying antirheumatic drugs were discontinued;

172 Biological, disease-modifying antirheumatic drugs were prescribed mo

173 ion who had not been previously treated with disease-modifying antirheumatic drugs were randomized to

174 tivity, and a lack of current treatment with disease-modifying antirheumatic drugs were significantly

175 ed by a physician or by self-reported use of disease modifying antirheumatic drugs, were compared wit

176 med by physicians or by self-reported use of disease-modifying antirheumatic drugs, were compared wit

177 omising results for combination therapy with disease-modifying antirheumatic drugs, whereas results o

178 Standard single therapy with disease-modifying antirheumatic drugs, which was previou

179 patients with placebo and/or any traditional disease-modifying antirheumatic drugs with a minimum of

180 ional therapy consisting of a combination of disease-modifying antirheumatic drugs with biologic agen

181 paring the efficacy and safety of biological disease-modifying antirheumatic drugs within the same cl

182 Prescriptions for LEF and 9 disease-modifying antirheumatic drugs written between Oc

183 -positive) and previous exposure to biologic disease-modifying antirheumatic drugs (yes vs no).