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1 er for 6 months, in addition to at least one disease-modifying antirheumatic drug.
2 of 13.7 years, and almost all were taking a disease-modifying antirheumatic drug.
3 nosuppression and use of glucocorticoids and disease modifying antirheumatic drugs.
4 going examination of the efficacy of several disease-modifying antirheumatic drugs.
5 ared with 58.7% (43.3%-79.7%; P=0.0025) with disease-modifying antirheumatic drugs.
6 s had been treated unsuccessfully with other disease-modifying antirheumatic drugs.
7 l manifestations of SpA that is resistant to disease-modifying antirheumatic drugs.
8 d arthritis, and thus these are the original disease-modifying antirheumatic drugs.
9 es of nonsteroidal antiinflammatory drugs or disease-modifying antirheumatic drugs.
10 risk of serious infections compared to other disease-modifying antirheumatic drugs.
11 Both groups were naive to all disease-modifying antirheumatic drugs.
12 nts who inadequately respond to conventional disease-modifying antirheumatic drugs.
13 ntional, biological, and newz non-biological disease-modifying antirheumatic drugs.
14 ents had active disease and had not received disease-modifying antirheumatic drugs.
15 us 36 mm/hr), and a lower number of lifetime disease-modifying antirheumatic drugs (1.9 versus 2.5).
16 fewer Treg cells had suboptimal responses to disease-modifying antirheumatic drugs and a longer durat
18 d evidence that supports the use of selected disease-modifying antirheumatic drugs and novel biologic
21 tic diseases frequently require therapy with disease-modifying antirheumatic drugs and/or biologic ag
22 scular risks/benefits associated with use of disease-modifying antirheumatic drugs and/or biologics r
23 i-tumor necrosis factor-alpha therapy, other disease modifying antirheumatic drugs, and nonsteroidal
24 ozygous carriers of this variant needed more disease-modifying antirheumatic drugs, and more patients
25 ith rheumatic disease have been reported for disease modifying antirheumatic drugs, antimetabolites a
26 nts, as is usually the case, combinations of disease-modifying antirheumatic drugs appear to be a rea
29 ervational studies show that nonmethotrexate disease-modifying antirheumatic drugs are widely prescri
30 monotherapies or stepping-up to combination disease-modifying antirheumatic drugs are, however, unre
31 ti-inflammatory drugs but had to stop taking disease-modifying antirheumatic drugs at least 28 days b
32 l corticosteriods (< or =10 mg per day), and disease-modifying antirheumatic drugs at stable doses du
35 ed version would preclude a trial of another disease-modifying antirheumatic drug before use of a BRM
36 gs (NSAIDs), glucocorticoids and traditional disease-modifying antirheumatic drugs before and during
37 gies for rheumatoid arthritis include use of disease-modifying antirheumatic drugs, but a minority of
38 the use of biologic agents after failure of disease-modifying antirheumatic drugs, but differed or d
39 sease in which early aggressive therapy with disease-modifying antirheumatic drugs can improve outcom
40 mized controlled trials of intensive initial disease-modifying antirheumatic drug combinations showed
41 tients who failed monotherapy benefited from disease-modifying antirheumatic drug combinations withou
43 atment algorithm, and argue that traditional disease-modifying antirheumatic drugs continue to play a
45 exate would set a standard against which new disease-modifying antirheumatic drugs could be compared.
47 ospective cohort study of rates of change in disease-modifying antirheumatic drug (DMARD) and/or syst
48 an College of Rheumatology criteria) without disease-modifying antirheumatic drug (DMARD) or steroid
49 ic JIA receiving anakinra as part of initial disease-modifying antirheumatic drug (DMARD) therapy wer
50 ously demonstrated that an intensive step-up disease-modifying antirheumatic drug (DMARD) treatment s
51 nse to treatment included any prior use of a disease-modifying antirheumatic drug (DMARD), higher dis
52 rdation of radiographic progression by a new disease-modifying antirheumatic drug (DMARD), LEF, as we
57 thout methotrexate (a conventional synthetic disease-modifying antirheumatic drug [DMARD]), versus in
58 ents with early RA, following treatment with disease-modifying antirheumatic drugs (DMARDs) (either m
59 =33,324) and patients initiating nonbiologic disease-modifying antirheumatic drugs (DMARDs) (n=25,742
60 d a quality measure to assess the receipt of disease-modifying antirheumatic drugs (DMARDs) among pat
61 th RA who have failed to respond to standard disease-modifying antirheumatic drugs (DMARDs) and antit
62 association between treatment with biologic disease-modifying antirheumatic drugs (DMARDs) and devel
63 obtained summary data from trials comparing disease-modifying antirheumatic drugs (DMARDs) and from
64 hose disease activity persists despite prior disease-modifying antirheumatic drugs (DMARDs) and ongoi
66 at the use of specialty tiering for biologic disease-modifying antirheumatic drugs (DMARDs) by Medica
67 t, infliximab, or adalimumab) or nonbiologic disease-modifying antirheumatic drugs (DMARDs) during 20
68 ents with active RA who had discontinued all disease-modifying antirheumatic drugs (DMARDs) for an ap
70 ther herpes zoster is associated with use of disease-modifying antirheumatic drugs (DMARDs) in patien
71 eview will focus on the role of conventional disease-modifying antirheumatic drugs (DMARDs) in the cu
74 t in 2,170 patients treated with traditional disease-modifying antirheumatic drugs (DMARDs) recruited
75 an outcome measure with interest moving from disease-modifying antirheumatic drugs (DMARDs) to biolog
76 and 3,522 biologic-naive patients receiving disease-modifying antirheumatic drugs (DMARDs) until eit
77 h rheumatoid arthritis (RA) in whom specific disease-modifying antirheumatic drugs (DMARDs) were init
78 strategies were infliximab with concomitant disease-modifying antirheumatic drugs (DMARDs), etanerce
79 rd one based upon early and sustained use of disease-modifying antirheumatic drugs (DMARDs), in the h
80 lesion (TL) >/=2 cm who had previously taken disease-modifying antirheumatic drugs (DMARDs), includin
81 rthritis (RA) in remission who are receiving disease-modifying antirheumatic drugs (DMARDs), radiogra
96 d had received at least 1 prescription for a disease-modifying antirheumatic drug during the study pe
97 factor-alpha inhibitors in combination with disease-modifying antirheumatic drugs early after the di
98 as monotherapy is recommended as the initial disease-modifying antirheumatic drug for rheumatoid arth
99 >3 years from symptom onset) RA treated with disease-modifying antirheumatic drugs, from patients wit
101 compared with traditional immunosuppressant disease-modifying antirheumatic drugs have been shown to
102 als with combinations of biologics and other disease-modifying antirheumatic drugs have reported sign
103 necrosis factor-alpha agents to traditional disease-modifying antirheumatic drugs in early rheumatoi
104 ecent research findings with nonmethotrexate disease-modifying antirheumatic drugs in rheumatoid arth
105 sk of heart failure associated with biologic disease-modifying antirheumatic drugs in rheumatoid arth
106 ethotrexate is one of the most commonly used disease-modifying antirheumatic drugs in the management
107 tant than drug-related risks, though several disease-modifying antirheumatic drugs increase both type
108 ing in which early aggressive treatment with disease-modifying antirheumatic drugs is used, seeking t
109 ered, 217 (65%) rheumatologists included new disease-modifying antirheumatic drugs (leflunomide, etan
110 ients with established RA who were naive for disease-modifying antirheumatic drugs, matched healthy c
112 -43% rheumatoid factor positive; no previous disease-modifying antirheumatic drugs; mean swollen join
113 methotrexate therapy to a triple regimen of disease-modifying antirheumatic drugs (methotrexate, sul
114 ntirheumatic drugs and the value of changing disease-modifying antirheumatic drug monotherapies or st
116 trials will more clearly define the role of disease-modifying antirheumatic drugs, novel therapeutic
118 56 patients after 6 months of treatment with disease-modifying antirheumatic drugs or biologics.
119 information suggesting that combinations of disease-modifying antirheumatic drugs or newer biologic
120 eased risk of malignancy compared with other disease-modifying antirheumatic drugs or with placebo.
121 Kinase inhibitors have shown promising oral disease-modifying antirheumatic drug potential with effi
122 as having RA if they had an appropriate GPRD disease-modifying antirheumatic drug prescription or 3 o
123 th supportive therapy and discontinuation of disease-modifying antirheumatic drugs, resulting in stab
124 id in combination with bDMARDs and synthetic disease-modifying antirheumatic drugs (sDMARDs) had the
125 these drugs in combination with conventional disease-modifying antirheumatic drugs seems to produce t
126 ntiinflammatory drugs and traditionally used disease-modifying antirheumatic drugs, such as methotrex
127 omide and sulfasalazine monotherapies; early disease-modifying antirheumatic drug therapy reduces ero
131 ts, respectively) required corticosteroid or disease-modifying antirheumatic drug treatment because o
132 m onset) who had active disease, no previous disease-modifying antirheumatic drug treatment, and >or=
134 rticoid dosage and duration, duration of RA, disease-modifying antirheumatic drug use, and the propor
135 The percentage met was high for QI-2 (RA disease-modifying antirheumatic drug use; 94%), QI-3 (in
136 Reduction of concomitant corticosteroid and disease-modifying antirheumatic drug was also assessed.
137 The proportion of patients not taking any disease-modifying antirheumatic drugs was 66% in 1985 ve
139 ion who had not been previously treated with disease-modifying antirheumatic drugs were randomized to
140 tivity, and a lack of current treatment with disease-modifying antirheumatic drugs were significantly
141 ed by a physician or by self-reported use of disease modifying antirheumatic drugs, were compared wit
142 med by physicians or by self-reported use of disease-modifying antirheumatic drugs, were compared wit
143 omising results for combination therapy with disease-modifying antirheumatic drugs, whereas results o
145 patients with placebo and/or any traditional disease-modifying antirheumatic drugs with a minimum of
146 ional therapy consisting of a combination of disease-modifying antirheumatic drugs with biologic agen
147 paring the efficacy and safety of biological disease-modifying antirheumatic drugs within the same cl
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