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1 n addition to at least one disease-modifying antirheumatic drug.
2 d almost all were taking a disease-modifying antirheumatic drug.
3 of the efficacy of several disease-modifying antirheumatic drugs.
4 3.3%-79.7%; P=0.0025) with disease-modifying antirheumatic drugs.
5 unsuccessfully with other disease-modifying antirheumatic drugs.
6 f SpA that is resistant to disease-modifying antirheumatic drugs.
7 hus these are the original disease-modifying antirheumatic drugs.
8 antiinflammatory drugs or disease-modifying antirheumatic drugs.
9 fections compared to other disease-modifying antirheumatic drugs.
10 h groups were naive to all disease-modifying antirheumatic drugs.
11 ly respond to conventional disease-modifying antirheumatic drugs.
12 use of glucocorticoids and disease modifying antirheumatic drugs.
13 l, and newz non-biological disease-modifying antirheumatic drugs.
14 sease and had not received disease-modifying antirheumatic drugs.
17 ad suboptimal responses to disease-modifying antirheumatic drugs and a longer duration of arthritis a
19 pports the use of selected disease-modifying antirheumatic drugs and novel biologic agents in childre
20 vity for the initiation of disease-modifying antirheumatic drugs and persistent disease is increased,
21 The subsequent sequence of disease-modifying antirheumatic drugs and the value of changing disease-mo
23 its associated with use of disease-modifying antirheumatic drugs and/or biologics remain controversia
24 f this variant needed more disease-modifying antirheumatic drugs, and more patients with this genotyp
25 actor-alpha therapy, other disease modifying antirheumatic drugs, and nonsteroidal anti-inflammatory
26 ase have been reported for disease modifying antirheumatic drugs, antimetabolites and biologic drugs.
27 the case, combinations of disease-modifying antirheumatic drugs appear to be a reasonable considerat
29 tations of nonmethotrexate disease-modifying antirheumatic drugs are reduced impact on comorbidities
30 show that nonmethotrexate disease-modifying antirheumatic drugs are widely prescribed; their usage h
32 ranofin, an orally bioavailable FDA-approved antirheumatic drug, as having potent bactericidal activi
33 ugs but had to stop taking disease-modifying antirheumatic drugs at least 28 days before randomizatio
34 (< or =10 mg per day), and disease-modifying antirheumatic drugs at stable doses during the trial.
39 erative management of the most commonly used antirheumatic drugs being used to treat patients with rh
40 d arthritis include use of disease-modifying antirheumatic drugs, but a minority of patients achieve
41 ic agents after failure of disease-modifying antirheumatic drugs, but differed or did not provide spe
43 ly aggressive therapy with disease-modifying antirheumatic drugs can improve outcome and prevent join
44 rials of intensive initial disease-modifying antirheumatic drug combinations showed they reduce synov
45 monotherapy benefited from disease-modifying antirheumatic drug combinations without excess toxicity.
47 and argue that traditional disease-modifying antirheumatic drugs continue to play a pivotal role.
48 round medications included disease-modifying antirheumatic drugs, corticosteroids, and nonsteroidal a
51 tudy of rates of change in disease-modifying antirheumatic drug (DMARD) and/or systemic corticosteroi
52 matology criteria) without disease-modifying antirheumatic drug (DMARD) or steroid therapy in 8 of th
53 nakinra as part of initial disease-modifying antirheumatic drug (DMARD) therapy were identified from
54 that an intensive step-up disease-modifying antirheumatic drug (DMARD) treatment strategy targeting
55 ncluded any prior use of a disease-modifying antirheumatic drug (DMARD), higher disease functional cl
56 aphic progression by a new disease-modifying antirheumatic drug (DMARD), LEF, as well as 2 commonly u
61 (a conventional synthetic disease-modifying antirheumatic drug [DMARD]), versus initiation of methot
62 , following treatment with disease-modifying antirheumatic drugs (DMARDs) (either methotrexate or lef
63 nts initiating nonbiologic disease-modifying antirheumatic drugs (DMARDs) (n=25,742) within each infl
64 e to assess the receipt of disease-modifying antirheumatic drugs (DMARDs) among patients with rheumat
65 led to respond to standard disease-modifying antirheumatic drugs (DMARDs) and antitumour necrosis fac
66 en treatment with biologic disease-modifying antirheumatic drugs (DMARDs) and development of cancer i
67 data from trials comparing disease-modifying antirheumatic drugs (DMARDs) and from comparative coxib-
68 ity persists despite prior disease-modifying antirheumatic drugs (DMARDs) and ongoing MTX monotherapy
70 ialty tiering for biologic disease-modifying antirheumatic drugs (DMARDs) by Medicare Part D plans im
71 adalimumab) or nonbiologic disease-modifying antirheumatic drugs (DMARDs) during 2000-2007 from the f
72 A who had discontinued all disease-modifying antirheumatic drugs (DMARDs) for an appropriate washout
73 he past 2 years, three new disease-modifying antirheumatic drugs (DMARDs) have been approved: lefluno
75 n the role of conventional disease-modifying antirheumatic drugs (DMARDs) in the current management o
76 though early initiation of disease-modifying antirheumatic drugs (DMARDs) is effective in controlling
77 To evaluate the effect of disease-modifying antirheumatic drugs (DMARDs) on the likelihood of patien
78 s treated with traditional disease-modifying antirheumatic drugs (DMARDs) recruited to the British So
79 with interest moving from disease-modifying antirheumatic drugs (DMARDs) to biological therapies and
80 c-naive patients receiving disease-modifying antirheumatic drugs (DMARDs) until either July 31, 2008,
82 nfliximab with concomitant disease-modifying antirheumatic drugs (DMARDs), etanercept with concomitan
83 early and sustained use of disease-modifying antirheumatic drugs (DMARDs), in the hope of improving l
84 m who had previously taken disease-modifying antirheumatic drugs (DMARDs), including anti-tumor necro
85 emission who are receiving disease-modifying antirheumatic drugs (DMARDs), radiographic progression c
101 bitors in combination with disease-modifying antirheumatic drugs early after the diagnosis of aggress
103 tom onset) RA treated with disease-modifying antirheumatic drugs, from patients with osteoarthritis (
104 e risks of nonmethotrexate disease-modifying antirheumatic drugs have been evaluated, including infec
105 ditional immunosuppressant disease-modifying antirheumatic drugs have been shown to be highly effecti
106 ons of biologics and other disease-modifying antirheumatic drugs have reported significant improvemen
107 nable guidelines; however, for the remaining antirheumatic drugs in current use, the available data c
108 lpha agents to traditional disease-modifying antirheumatic drugs in early rheumatoid arthritis is a n
109 dings with nonmethotrexate disease-modifying antirheumatic drugs in rheumatoid arthritis and seronega
111 of the most commonly used disease-modifying antirheumatic drugs in the management of psoriatic arthr
113 ated risks, though several disease-modifying antirheumatic drugs increase both types of adverse react
114 aggressive treatment with disease-modifying antirheumatic drugs is used, seeking to minimize long-te
115 eumatologists included new disease-modifying antirheumatic drugs (leflunomide, etanercept, and inflix
116 shed RA who were naive for disease-modifying antirheumatic drugs, matched healthy controls, and 2 gro
118 ctor positive; no previous disease-modifying antirheumatic drugs; mean swollen joint count 8.6-10.4).
119 apy to a triple regimen of disease-modifying antirheumatic drugs (methotrexate, sulfasalazine, and hy
120 and the value of changing disease-modifying antirheumatic drug monotherapies or stepping-up to combi
121 from healthy children and disease-modifying antirheumatic drug-naive patients with JIA were characte
122 clearly define the role of disease-modifying antirheumatic drugs, novel therapeutic agents, and antib
125 sting that combinations of disease-modifying antirheumatic drugs or newer biologic therapy is more ef
127 have shown promising oral disease-modifying antirheumatic drug potential with efficacy similar to an
128 ey had an appropriate GPRD disease-modifying antirheumatic drug prescription or 3 other GPRD characte
129 apy and discontinuation of disease-modifying antirheumatic drugs, resulting in stabilization of the d
130 with bDMARDs and synthetic disease-modifying antirheumatic drugs (sDMARDs) had the highest risk of HB
131 bination with conventional disease-modifying antirheumatic drugs seems to produce the best outcomes.
133 ugs and traditionally used disease-modifying antirheumatic drugs, such as methotrexate, often fails i
134 rexate (MTX) is a widely used anticancer and antirheumatic drug that has been postulated to protect a
135 azine monotherapies; early disease-modifying antirheumatic drug therapy reduces erosive progression.
136 107 RA patients receiving disease-modifying antirheumatic drug therapy who were judged by their cons
139 required corticosteroid or disease-modifying antirheumatic drug treatment because of active disease b
140 ctive disease, no previous disease-modifying antirheumatic drug treatment, and >or=2 sets of scored r
142 rs while seeking to avoid use of second-line antirheumatic drugs until evidence of joint damage was s
143 duration, duration of RA, disease-modifying antirheumatic drug use, and the proportion with comorbid
144 met was high for QI-2 (RA disease-modifying antirheumatic drug use; 94%), QI-3 (intervention if RA w
146 of patients not taking any disease-modifying antirheumatic drugs was 66% in 1985 versus 13% in 2000.
148 en previously treated with disease-modifying antirheumatic drugs were randomized to receive 100 mg of
149 of current treatment with disease-modifying antirheumatic drugs were significantly associated with a
150 or by self-reported use of disease modifying antirheumatic drugs, were compared with noncases (n = 24
151 or by self-reported use of disease-modifying antirheumatic drugs, were compared with noncases (n=26,1
152 r combination therapy with disease-modifying antirheumatic drugs, whereas results of studies with mon
153 andard single therapy with disease-modifying antirheumatic drugs, which was previously the final step
154 ous nodules and greater use of slowly acting antirheumatic drugs, while female RA patients had earlie
155 ebo and/or any traditional disease-modifying antirheumatic drugs with a minimum of 24 weeks of follow
156 isting of a combination of disease-modifying antirheumatic drugs with biologic agents in patients wit
157 y and safety of biological disease-modifying antirheumatic drugs within the same class, including TNF
158 rescriptions for LEF and 9 disease-modifying antirheumatic drugs written between October 1998 and Jun
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