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

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

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

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

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

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

36 We obtained biologic DMARD prior authorization policy information from state

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

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

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

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

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

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

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

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

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

46 horization policies to limit use of biologic DMARDs.

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

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

49 hese are distinct from those of the biologic DMARDs.

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

51 re but serious adverse events for biological DMARDs.

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

53 erapy with either methotrexate or biological DMARDs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 itant disease-modifying antirheumatic drugs (DMARDs).

104 with disease-modifying antirheumatic drugs (DMARDs).

105 eived disease-modifying antirheumatic drugs (DMARDs).

106 ional disease-modifying antirheumatic drugs (DMARDs).

107 ional disease-modifying antirheumatic drugs (DMARDs).

108 hetic disease-modifying antirheumatic drugs (DMARDs).

109 with disease-modifying antirheumatic drugs (DMARDs).

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

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

112 with disease-modifying antirheumatic drugs (DMARDs).

113 logic disease-modifying antirheumatic drugs (DMARDs).

114 ional disease-modifying antirheumatic drugs (DMARDs).

115 oral disease-modifying antirheumatic drugs (DMARDs).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 milar frequency among those with nonbiologic DMARD exposure.

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

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

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

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

153 ompared with initiation of other nonbiologic DMARDs.

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

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

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

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

158 Receipt or nonreceipt of DMARD.

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

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

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

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

163 Rates of DMARD change were sensitive to specifications regarding

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

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

166 Receipt of DMARDs varied based on demographic factors, socioeconomi

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

168 aseline factors associated with the start of DMARDs.

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

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

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

172 re categorized as either DMARD responders or DMARD nonresponders.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 superiority of tocilizumab plus DMARDs over DMARDs alone.

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

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

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

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

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

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

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

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

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

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

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

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

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

202 groups with that for patients not receiving DMARDs.

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

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

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

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

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

208 ts were similar for biological and synthetic DMARDs.

209 nadequate response to conventional synthetic DMARDs.

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

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

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

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

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

215 The DMARD comparison was more powerful in early disease than

216 5 and 50,803 person-years of followup in the DMARD and anti-TNF cohorts, respectively, during which t

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

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

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

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

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

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

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

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

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

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

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

228 .04-2.29), as was current use of traditional DMARDs alone (OR 1.37, 95% CI 1.18-1.59).

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

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

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

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

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

234 compared with those treated with traditional DMARDs.

235 compared with those treated with traditional DMARDs.

236 ed with RA patients treated with traditional DMARDs.

237 iological therapy, compared with traditional DMARDs.

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

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

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

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

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

243 is uncontrolled or toxic effects arise with DMARDs.

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

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

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

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