ライフサイエンスコーパス: DMARD

1 DMARD adjustments were made for 50% of patients in whom

2 DMARD use including prednisone was reported by 1,140 (11

3 DMARD-intolerant patients had better ACR response rates

4 DMARD-recalcitrant disease may become the main indicatio

5 ers that resulted in treatment with > or = 1 DMARD (hydroxychloroquine, sulfasalazine, auranofin, int

6 AQ Disability units (scale 0-3) between 100% DMARD use and 0%.

7 cohorts, respectively, during which time 204 DMARD-treated and 856 anti-TNF-treated patients died.

8 al study of 7,664 anti-TNF-treated and 1,354 DMARD-treated patients with severe RA from the British S

9 Thirty percent of patients filled a DMARD prescription during 12 months of followup.

10 and began with the first prescription for a DMARD after study eligibility was met.

11 Addition of the presence of a DMARD prescription and/or a positive RF to selection cri

12 The addition of a positive RF and/or a DMARD prescription to ICD code 714 dramatically improved

13 rheumatologist were less likely to receive a DMARD and may provide a target for quality improvement i

14 patients diagnosed with RA did not receive a DMARD during the 12 months after cohort entry.

15 least 1 rheumatologist visit, 41% received a DMARD in 1996 compared with 70% in 2003 (P < 0.001).

16 of RA between 2005 and 2008, 63% received a DMARD.

17 rugs, and 166 (19%) of 878 were not taking a DMARD at baseline.

18 A total of 15,597 RA patients in whom a DMARD was initiated between January 1, 1995 and December

19 corticosteroids and 33% received additional DMARDs.

20 ON cases: 3 among anti-TNF users and 3 among DMARD users.

21 Reactivity to ROS-CII among DMARD-naive patients with early RA was significantly hig

22 ximisation of the benefits of biological and DMARD regimens in terms of function, disability, and hea

23 ude ON rates were similar among anti-TNF and DMARD groups: 4.5 (95% CI 1.4-13.8) and 5.4 (95% CI 1.7-

24 ersons with RA disease duration <2 years and DMARD therapy of similar efficacy during followup.

25 ation of their treatment with prednisone and DMARDs was achieved in all 4 patients.

26 e tapering/discontinuation of prednisone and DMARDs, and by measuring the serum concentrations of B l

27 Cotherapy with MTX or another DMARD produced significantly higher rates of remission w

28 interval [95% CI] 1.5-2.7) and with another DMARD (OR 1.2, 95% CI 0.9-1.6) as compared with monother

29 e of SA when compared with not receiving any DMARD.

30 ated permuted blocks; stratified by baseline DMARD and previous TNF inhibitor use) to subcutaneous gu

31 ed prior authorization for > or = 1 biologic DMARD, with wide variation in the specific agents covere

32 The pooled cohort included 1,152 biologic DMARD users and 7,306 MTX users.

33 patients with a prescription for a biologic DMARD as biologic DMARD users, and those with a prescrip

34 ster) with a JAK inhibitor versus a biologic DMARD.

35 rescription for a biologic DMARD as biologic DMARD users, and those with a prescription for methotrex

36 Comparing biologic DMARD users with MTX users, the propensity score-adjuste

37 ption for methotrexate (MTX) but no biologic DMARD as MTX users.

38 We obtained biologic DMARD prior authorization policy information from state

39 tumors during 2,940 person-years of biologic DMARD use, and 88 hematologic malignancies and 558 solid

40 o assess predictors of synthetic or biologic DMARD use in the 12 months after cohort entry.

41 MARD), and treatment alterations to biologic DMARD.

42 e effect of an infrequent exposure (biologic DMARDs) on rare diseases (hematologic malignancies) rema

43 ned the cost-sharing structures for biologic DMARDs in Part D plans or the resulting cost burden for

44 red the cost-sharing provisions for biologic DMARDs in the Medicare Advantage and stand-alone plans.

45 lthough plans assume some costs for biologic DMARDs, the majority of costs are shifted to beneficiari

46 harMetrics database, current use of biologic DMARDs alone was associated with herpes zoster (odds rat

47 After the introduction of biologic DMARDs in 1998, 6% of all patients with RA received a bi

48 gression to estimate the effects of biologic DMARDs on cancer.

49 ndylitis, new data on the effect of biologic DMARDs on structural progression in ankylosing spondylit

50 failure, optimization of the use of biologic DMARDs, the use of drugs for extra-musculoskeletal manif

51 horization policies to limit use of biologic DMARDs.

52 r necrosis factor inhibitors, other biologic DMARDs, or both, we randomly assigned the patients in a

53 DMARDs are much less expensive than biologic DMARDs, and in many cases can be successful in achieving

54 hese are distinct from those of the biologic DMARDs.

55 idelines, the FDA approval of three biologic DMARDs to treat non-radiographic axSpA, the FDA and EMA

56 ritis and an inadequate response to biologic DMARDs, baricitinib at a daily dose of 4 mg was associat

57 rheumatoid arthritis refractory to biologic DMARDs, upadacitinib was superior to abatacept in the ch

58 oriatic arthritis who were naive to biologic DMARDs.

59 sease that could be associated with biologic DMARDs and with the occurrence of MAS.

60 re but serious adverse events for biological DMARDs.

61 Various combinations of biological DMARDs plus methotrexate improved clinical response rate

62 erapy with either methotrexate or biological DMARDs.

63 or (SPM) concentrations are linked with both DMARD responsiveness and disease pathotype.

64 The ultimate value of combination DMARD therapy with methotrexate will be determined by lo

65 (infliximab or etanercept) plus concomitant DMARDs was more effective than treatment with etanercept

66 drugs (DMARDs), etanercept with concomitant DMARDs, and etanercept alone.

67 An association between consistent DMARD use and improvement in long-term functional outcom

68 ectly assess associations between consistent DMARD use and long-term functional outcomes.

69 tion in long term disability with consistent DMARD use, are most likely conservative.

70 Conventional DMARDs have proven efficacy in the management of RA and

71 In addition, conventional DMARDs are much less expensive than biologic DMARDs, and

72 Although conventional DMARDs have associated toxicities, these are distinct fr

73 en with JIA who are resitant to conventional DMARDs or biologics.

74 w to effectively and safely use conventional DMARDs, either as monotherapy or in combinations.

75 activity can be achieved using conventional DMARDs as part of an intensive disease management strate

76 erienced at least 1 adverse event in the CTC-DMARD and CTC groups, respectively.

77 95% CI, 0.55-0.72), respectively, in the CTC-DMARD and CTC groups.

78 the TFFS was significantly higher in the CTC-DMARD group compared with the CTC group (hazard ratio, 2

79 and 6 months was noted (P < 0.05) in the CTC-DMARD group compared with the CTC group.

80 rior sarcoidosis-associated uveitis, the CTC-DMARD seemed to be more efficient than CTC, with an acce

81 ients had better ACR response rates than did DMARD-resistant patients.

82 nterferon (IFN) gene signature distinguished DMARD-naive patients who will subsequently develop persi

83 nge in disease-modifying antirheumatic drug (DMARD) and/or systemic corticosteroid drug or dose for 5

84 ithout disease-modifying antirheumatic drug (DMARD) or steroid therapy in 8 of the patients originall

85 ion of disease-modifying antirheumatic drug (DMARD) therapy (18 548 [3.2%]).

86 nitial disease-modifying antirheumatic drug (DMARD) therapy were identified from 11 centers in 4 coun

87 tep-up disease-modifying antirheumatic drug (DMARD) treatment strategy targeting persistent disease a

88 e of a disease-modifying antirheumatic drug (DMARD), higher disease functional class (according to th

89 a new disease-modifying antirheumatic drug (DMARD), LEF, as well as 2 commonly used DMARDs, MTX and

90 cluded disease-modifying antirheumatic drug (DMARD)-naive patients with early RA (n = 85 serum sample

91 prised disease-modifying antirheumatic drug (DMARD)-naive patients with early seropositive active RA

92 n of a disease-modifying antirheumatic drug (DMARD).

93 for a disease-modifying antirheumatic drug (DMARD).

94 used disease-modifying anti-rheumatic drug (DMARD) for rheumatoid arthritis (RA).

95 after disease-modifying anti-rheumatic drug (DMARD) treatment in the inflammatory arthritis groups (i

96 ms of disease-modifying anti-rheumatic drug (DMARD); conventional synthetic (cs), biologic (b) or tar

97 thetic disease-modifying antirheumatic drug [DMARD]), versus initiation of methotrexate monotherapy i

98 etic disease-modifying anti-rheumatic drugs (DMARD; 90%), or 45% biologicals.

99 with disease-modifying antirheumatic drugs (DMARDs) (either methotrexate or leflunomide).

100 logic disease-modifying antirheumatic drugs (DMARDs) (n=25,742) within each inflammatory disease coho

101 pt of disease-modifying antirheumatic drugs (DMARDs) among patients with rheumatoid arthritis (RA).

102 ndard disease-modifying antirheumatic drugs (DMARDs) and antitumour necrosis factor-alpha biologic ag

103 logic disease-modifying antirheumatic drugs (DMARDs) and development of cancer in patients with RA.

104 aring disease-modifying antirheumatic drugs (DMARDs) and from comparative coxib-placebo trials to tes

105 prior disease-modifying antirheumatic drugs (DMARDs) and ongoing MTX monotherapy.

106 ce to disease-modifying antirheumatic drugs (DMARDs) and prednisone was determined as the percentage

107 logic disease-modifying antirheumatic drugs (DMARDs) are unclear.

108 logic disease-modifying antirheumatic drugs (DMARDs) by Medicare Part D plans imposes a heavy financi

109 logic disease-modifying antirheumatic drugs (DMARDs) during 2000-2007 from the following data sources

110 d all disease-modifying antirheumatic drugs (DMARDs) for an appropriate washout period (at least 1 mo

111 e new disease-modifying antirheumatic drugs (DMARDs) have been approved: leflunomide, etanercept, and

112 se of disease-modifying antirheumatic drugs (DMARDs) in patients with RA.

113 ional disease-modifying antirheumatic drugs (DMARDs) in the current management of rheumatoid arthriti

114 on of disease-modifying antirheumatic drugs (DMARDs) is effective in controlling short-term joint dam

115 ct of disease-modifying antirheumatic drugs (DMARDs) on the likelihood of patients with rheumatoid ar

116 hetic disease-modifying antirheumatic drugs (DMARDs) or to biologic or targeted synthetic DMARDs to r

117 ional disease-modifying antirheumatic drugs (DMARDs) recruited to the British Society for Rheumatolog

118 from disease-modifying antirheumatic drugs (DMARDs) to biological therapies and a more technical foc

119 iving disease-modifying antirheumatic drugs (DMARDs) until either July 31, 2008, or death, whichever

120 cific disease-modifying antirheumatic drugs (DMARDs) were initiated.

121 itant disease-modifying antirheumatic drugs (DMARDs), etanercept with concomitant DMARDs, and etanerc

122 se of disease-modifying antirheumatic drugs (DMARDs), in the hope of improving long-term health outco

123 taken disease-modifying antirheumatic drugs (DMARDs), including anti-tumor necrosis factor (anti-TNF)

124 logic disease-modifying antirheumatic drugs (DMARDs), or at least 4 weeks of non-steroidal anti-infla

125 iving disease-modifying antirheumatic drugs (DMARDs), radiographic progression correlates with imagin

126 Disease-modifying antirheumatic drugs (DMARDs), the key therapeutic agents, reduce synovitis an

127 oral disease-modifying antirheumatic drugs (DMARDs).

128 with disease-modifying antirheumatic drugs (DMARDs).

129 eived disease-modifying antirheumatic drugs (DMARDs).

130 ional disease-modifying antirheumatic drugs (DMARDs).

131 itant disease-modifying antirheumatic drugs (DMARDs).

132 hetic disease-modifying antirheumatic drugs (DMARDs).

133 with disease-modifying antirheumatic drugs (DMARDs).

134 es of disease-modifying antirheumatic drugs (DMARDs).

135 logic disease-modifying antirheumatic drugs (DMARDs).

136 hetic disease-modifying antirheumatic drugs (DMARDs).

137 ional disease-modifying antirheumatic drugs (DMARDs).

138 ss of disease modifying antirheumatic drugs (DMARDs).

139 se of disease-modifying antirheumatic drugs (DMARDs).

140 with disease-modifying antirheumatic drugs (DMARDs).

141 ional disease-modifying antirheumatic drugs (DMARDs).

142 etic disease modifying anti-rheumatic drugs (DMARDs) from 35 rheumatology departments in the UK.

143 etic disease modifying anti-rheumatic drugs (DMARDs) has also transformed clinical outcomes.

144 ogic disease-modifying anti-rheumatic drugs (DMARDs), such as tumour necrosis factor (TNF) antagonist

145 dard disease-modifying anti-rheumatic drugs (DMARDs).

146 ve disease seemed to benefit most from early DMARD initiation (P = 0.04).

147 We examined the long-term benefit of early DMARD initiation on radiographic progression in early RA

148 standing of the critical importance of early DMARD treatment with a goal of remission or low disease

149 Minocycline is an effective DMARD in patients with early seropositive RA.

150 SF samples), who were categorized as either DMARD responders or DMARD nonresponders.

151 Other established DMARDs, such as sulfasalazine and hydroxychloroquine, ha

152 meaningfully improved when new and existing DMARDs are added to methotrexate.

153 n at the SPP compared with the CPJ following DMARD therapy in the RA patients (mean reduction 35% at

154 emissions are more frequent and the need for DMARD therapy is less in those treated early in the dise

155 the percentage of correct doses was 64% for DMARDs and 70% for prednisone.

156 A change in DMARD drug or dose was observed for 21%, 23%, and 34% of

157 Over 12 months, a change in DMARD drug or dose was observed for 44%, 50%, and 68% of

158 and 3-month time blocks who had a change in DMARD drug or dose were 36%, 57%, and 74%, respectively.

159 nts with established RA, serum reactivity in DMARD nonresponders was significantly higher than that i

160 pressed as a multiple of the Larsen score in DMARD-treated patients compared with untreated patients,

161 onders was significantly higher than that in DMARD responders (P < 0.01); 58.3% of serum samples from

162 Increased DMARD use was strongly associated with better long-term

163 Infliximab and other infused DMARDs were not included because of substantial missing

164 The leading DMARD is methotrexate, which can be combined with other

165 sus 11.8 years; P = 0.016) and received more DMARDs prior to TLI (mean 2.1 versus 1.3; P = 0.0001).

166 minority of patients are exposed to multiple DMARDs without necessarily benefitting from them; a grou

167 o only 5.5% for women with anti-CCP-negative DMARD-positive RA and 6.6% for anti-CCP-negative, RF-neg

168 and 6.6% for anti-CCP-negative, RF-negative DMARD nonusers).

169 ng-term safety and efficacy data for the new DMARD agents and combination regimens will also further

170 lso become apparent that combinations of new DMARDs and methotrexate virtually halt radiographic prog

171 Patients on MTX, ETA, and no DMARD treatment were comparable in JIA-associated uveiti

172 istically significant differences between no DMARD treatment, methotrexate (MTX), and etanercept (ETA

173 RDs was stratified to represent 4 groups: no DMARD use, <6 months, 6-12 months, and >12 months.

174 receiving DMARDs compared with receiving no DMARDs were different for different medications.

175 ere similar between anti-TNF and nonbiologic DMARD initiators (adjusted HR, 1.00 [95% CI, 0.77-1.29])

176 cidence between new anti-TNF and nonbiologic DMARD users while controlling for baseline corticosteroi

177 notherapy users, and 2) multiple nonbiologic DMARD users.

178 with either new anti-TNF or new nonbiologic DMARD use.

179 milar frequency among those with nonbiologic DMARD exposure.

180 dose escalation of biologic and nonbiologic DMARDs in response to active disease was assessed cross-

181 the patients receiving multiple nonbiologic DMARDs, 31-47% of those with moderate or high disease ac

182 er 1000 person-years were: other nonbiologic DMARDs (55 cases among 3993 treatment episodes; rate, 50

183 rs or methotrexate; or (4) other nonbiologic DMARDs without TNF inhibitors, methotrexate, or hydroxyc

184 ompared with initiation of other nonbiologic DMARDs.

185 active RA despite treatment with nonbiologic DMARDs, primarily methotrexate.

186 f plasma SPM concentrations as biomarkers of DMARD responsiveness in RA.

187 ent episodes starting 1 of the categories of DMARD regimens between January 1996 and June 2008.

188 als with RA was calculated and the effect of DMARD use determined.

189 Frequency of DMARD use increased steadily over time: 24% received DMA

190 Receipt or nonreceipt of DMARD.

191 ntaenoic-derived Maresin 1 are predictive of DMARD responsiveness at 6 months.

192 was to determine the rate and predictors of DMARD use in a cohort of elderly patients with RA.

193 Addition of presence of DMARD prescription to ICD-9 codes of AS and PsA decrease

194 ending data, we calculated the proportion of DMARD prescriptions and spending attributed to adalimuma

195 lder had a 30 percentage point lower rate of DMARD receipt (95% confidence interval [CI], -29 to -32

196 Rates of DMARD change were sensitive to specifications regarding

197 joints (DAS28) was > or =3.2, the dosage of DMARDs was increased according to protocol, and swollen

198 Patients remained on stable doses of DMARDs and received tocilizumab 8 mg/kg or placebo (cont

199 Receipt of DMARDs varied based on demographic factors, socioeconomi

200 aseline factors associated with the start of DMARDs and/or steroids within 12 months of baseline.

201 aseline factors associated with the start of DMARDs.

202 The time from symptom onset to first use of DMARDs was stratified to represent 4 groups: no DMARD us

203 d to both the disease process and the use of DMARDs.

204 stratified according to DMARD intolerance or DMARD resistance, and randomized to receive a single dai

205 re categorized as either DMARD responders or DMARD nonresponders.

206 ysis considering current or past anti-TNF or DMARD use, we identified a total of 6 ON cases: 3 among

207 ing either combination treatment (n = 50) or DMARDs (n = 50) were matched for clinical variables.

208 patients receiving combination treatment or DMARDs (median DAS28 1.65 versus 1.78, median disease du

209 phase 3 studies, we may soon have new, oral DMARD therapies available.

210 options for RA patients beyond existing oral DMARDs and parenteral biologics.

211 LY2439821 added to oral DMARDs improved signs and symptoms of RA, with no strong

212 similar remission rates in the MTX and other DMARD cotherapy groups (8% and 5%, respectively) as in t

213 d to model the response in the MTX and other DMARD cotherapy groups relative to the monotherapy group

214 he use of MTX and, to a lesser extent, other DMARDs as cotherapy with etanercept was associated with

215 ) for MTX and 1.3 (95% CI 0.8-2.1) for other DMARDs versus monotherapy.

216 ients received MTX (10-25 mg/week); no other DMARDs were permitted.

217 The use of other DMARDs including methotrexate showed no such effect.

218 (prednisolone) enhance the effects of other DMARDs, including anti-TNF agents.

219 a therapy (RR 1.0 [95% CI 0.6-1.7]) or other DMARDs as compared with initiators of MTX.

220 actor (TNF) inhibitors with or without other DMARDs; (2) methotrexate without TNF inhibitors or hydro

221 superiority of tocilizumab plus DMARDs over DMARDs alone.

222 ignificantly greater in the tocilizumab plus DMARD group than in the control group (61% versus 25%; P

223 anercept alone (P = 0.04) or etanercept plus DMARDs (P = 0.02).

224 The combination of infliximab plus DMARDs was also more effective at controlling progressiv

225 The combination of infliximab plus DMARDs was significantly more effective than etanercept

226 evels showed superiority of tocilizumab plus DMARDs over DMARDs alone.

227 Less than two-thirds of the prescribed DMARD doses were correctly taken.

228 on > or =1 occasion and had been prescribed DMARDs was identified.

229 mpared with MTX use, independent of previous DMARD use (rate ratio [RR] 2.1 [95% CI 1.5-3.1]), with a

230 ts with early disease, and female sex, prior DMARD use, disease functional class, and disease activit

231 Among patients with RA, DMARDs and/or use of oral corticosteroids appeared to be

232 s ages 75-84 were 52% less likely to receive DMARDs (95% confidence interval [95% CI] 46-58%) and pat

233 e increased steadily over time: 24% received DMARDs in 1996 compared with 43% in 2003 (P for trend <0

234 nti-TNFalpha therapy with patients receiving DMARD therapy was 1.22 (95% confidence interval [95% CI]

235 s with rheumatologist referral and receiving DMARDs and varied associations between meeting quality c

236 groups with that for patients not receiving DMARDs.

237 ios (IRRs) for developing SA while receiving DMARDs compared with receiving no DMARDs were different

238 the original placebo group currently require DMARD therapy (P = 0.02).

239 After 6 months of stable DMARD use, 47.1% of Medicare patients and 39.5% of Optum

240 In patients with RA receiving stable DMARD therapy, glucocorticoids were associated with a do

241 esults indicate that, compared with standard DMARD therapy, treatment with anti-TNF therapies was not

242 In this observational study, DMARD treatment was a marker not only of worse disease a

243 at least one biologic or targeted synthetic DMARD (b/tsDMARD), extending beyond biological non-respo

244 th RA and new biologic or targeted synthetic DMARD exposures, individuals initiating rituximab, abata

245 tant differences in efficacy among synthetic DMARDs (limited to methotrexate, leflunomide, and sulfas

246 ts were similar for biological and synthetic DMARDs.

247 f biologic therapies, conventional synthetic DMARDs (csDMARDs) provided effective disease control for

248 nadequate response to conventional synthetic DMARDs.

249 kinetics than that of conventional synthetic DMARDs.

250 trials (n = 23), mostly examining synthetic DMARDs, showed no clinically important differences in ef

251 t, each in combination with stable synthetic DMARDs.

252 DMARDs) or to biologic or targeted synthetic DMARDs to receive 700 mg of peresolimab, 300 mg of peres

253 ing at least two biologic/targeted synthetic DMARDs), persistent symptoms considered problematic by b

254 l synthetic, biologic and targeted synthetic DMARDs), therapeutic failure, optimization of the use of

255 s, including biologic and targeted synthetic DMARDs, have enabled substantial improvements in the con

256 initiation of biologic or targeted synthetic DMARDs.

257 initiation of biologic or targeted synthetic DMARDs.

258 y failed, combination therapy with synthetic DMARDs improved response rates.

259 Abatacept in combination with synthetic DMARDs was well tolerated and improved physical function

260 ortion of time in which patients were taking DMARDs (P < 0.0001), with a model R2 of 0.54.

261 of R0A pathogenesis and developing targeted DMARD-biologic therapies.

262 als of newer biologic and synthetic targeted DMARDs.

263 The DMARD comparison was more powerful in early disease than

264 5 and 50,803 person-years of followup in the DMARD and anti-TNF cohorts, respectively, during which t

265 years of followup and 17 MIs occurred in the DMARD cohort during 2,893 person-years of followup, equi

266 Patients in the DMARD cohort were more likely to have a history of myoca

267 n the anti-TNFalpha cohort compared with the DMARD cohort (incidence rate ratio 1.44 [95% confidence

268 When compared with the DMARD cohort, the anti-TNF cohort was younger (median ag

269 P = 0.229) in any joint as compared with the DMARD group.

270 Tocilizumab combined with any of the DMARDs evaluated was safe and effective in reducing arti

271 swollen joints) were stratified according to DMARD intolerance or DMARD resistance, and randomized to

272 SPM concentrations in patients resistant to DMARD therapy.

273 e patients (21%) had an average adherence to DMARDs >/=80%.

274 h of RA patients had an overall adherence to DMARDs of at least 80%.

275 arthritis who had an inadequate response to DMARDs.

276 (Tocilizumab in Combination With Traditional DMARD Therapy) study.

277 methotrexate naive compared with traditional DMARD-experienced or anti-tumour necrosis factor biologi

278 .04-2.29), as was current use of traditional DMARDs alone (OR 1.37, 95% CI 1.18-1.59).

279 In the GPRD, current use of traditional DMARDs was associated with herpes zoster (OR 1.27, 95% C

280 active RA (n = 200) treated with traditional DMARDs in the prebiologic era.

281 eumatoid arthritis compared with traditional DMARDs, although low-dose biological drugs are not.

282 When combined with traditional DMARDs, both etanercept and infliximab appear to offer s

283 Compared with traditional DMARDs, standard-dose biological drugs (OR 1.31, 95% cre

284 ed with RA patients treated with traditional DMARDs.

285 compared with those treated with traditional DMARDs.

286 compared with those treated with traditional DMARDs.

287 iological therapy, compared with traditional DMARDs.

288 iological drugs (with or without traditional DMARDs) are associated with an increase in serious infec

289 cs), biologic (b) or targeted synthetic (ts) DMARD with more than 6 months of follow-up from 01-Jan-2

290 rug (DMARD), LEF, as well as 2 commonly used DMARDs, MTX and SSZ.

291 thritis within 1 year before inclusion, were DMARD-naive, aged 18 years or older, met current rheumat

292 re used to determine factors associated with DMARD receipt and logistic regression was used to adjust

293 k of overall serious infection compared with DMARD treatment, after adjustment for baseline risk.

294 n that their uveitis is well controlled with DMARD therapy and the surgical technique is appropriate.

295 is uncontrolled or toxic effects arise with DMARDs.

296 atacept's safety profile in combination with DMARDs also seems to be favourable but should be avoided

297 ractice, both monotherapy and cotherapy with DMARDs other than MTX are used.

298 ion who had not been previously treated with DMARDs were randomized to receive minocycline, 100 mg tw

299 f NSAIDs and glucocorticoids, treatment with DMARDs (including conventional synthetic, biologic and t

300 this study showed that early treatment with DMARDs/steroids (within 6 months of symptom onset) reduc