ライフサイエンスコーパス: TNF inhibitor

1 ye disease for the first time while taking a TNF inhibitor.

2 for patients with insufficient response to a TNF inhibitor.

3 hout period after primary failure to a first TNF inhibitor.

4 ebo in combination with background MTX and a TNF inhibitor.

5 synovial tissue shortly after initiation of TNF inhibitors.

6 pears to be a class effect among the varying TNF inhibitors.

7 ts could have previously received one or two TNF inhibitors.

8 unity and graft-versus-host disease by using TNF inhibitors.

9 years of followup; 36% took MTX and 16% took TNF inhibitors.

10 nadequate response to tumor necrosis factor (TNF) inhibitors.

11 nadequate response to tumor necrosis factor (TNF) inhibitors.

12 ios for DM were 0.62 (95% CI, 0.42-0.91) for TNF inhibitors, 0.77 (95% CI, 0.53-1.13) for methotrexat

13 nhibitors, 0.94 per 100 000 person-years for TNF inhibitors, 0.80 per 100 000 person-years for IL-12/

14 tients (17%) prompted discontinuation of all TNF inhibitors; 11 patients changed to a non-TNF inhibit

15 -2 (H2) blockers, and tumor necrosis factor (TNF) inhibitors; 2 studies on cancer medications; and 2

16 tarted therapy with a tumor necrosis factor (TNF) inhibitor; 3982 (23.6%), with an interleukin 12 and

17 2; 95% confidence interval [CI], 47.3-53.2); TNF inhibitors (80 cases among 4623 treatment episodes;

18 f these, 4974 (76.2%) started therapy with a TNF inhibitor; 803 (12.3%), with an IL-12/23 inhibitor;

19 he most common indication for treatment with TNF inhibitor (94 patients [91%]).

20 s end, we engineered MYSTI (Myeloid-Specific TNF Inhibitor)--a recombinant bispecific antibody that b

21 mycophenolate mofetil, and azathioprine; the TNF inhibitors adalimumab and infliximab, and cyclospori

22 core [DAS28-ESR] >3.2; rituximab group) or a TNF inhibitor-adalimumab (40 mg subcutaneously every oth

23 and subsequently biologic therapies (such as TNF inhibitors, among others) and oral small molecules h

24 nalysis 4: HR, 0.78 [95% CI, 0.44-1.39]), or TNF inhibitors (analysis 1: HR, 0.93 [95% CI, 0.72-1.20]

25 lone prompted discontinuation of the initial TNF inhibitor and a change to a second-line TNF inhibito

26 y profile of rituximab in combination with a TNF inhibitor and MTX was consistent with the safety pro

27 ts receiving rituximab in combination with a TNF inhibitor and MTX.

28 that it is potentially modified favorably by TNF inhibitors and detrimentally by glucocorticoids.

29 r results thus imply that the combination of TNF inhibitors and ferroptosis inducers may serve as a p

30 Unlike TNF inhibitors and IL-1 inhibitors, established drugs su

31 own to be beneficial for millennia), NSAIDs, TNF inhibitors and IL-17 inhibitors.

32 are the efficacy and safety of two different TNF inhibitors and to assess the efficacy and safety of

33 rved in DBA/2 --> B6D2F1 mice expressing the TNF inhibitor, and colonic sections from these mice had

34 Exposures to methotrexate (MTX), TNF inhibitors, and oral glucocorticoids (GCs) were dete

35 lite therapy (azathioprine or methotrexate), TNF inhibitors, and/or other biologic treatment (anti-in

36 Comparing patients exposed to TNF inhibitors, antimetabolites, calcineurin inhibitors,

37 gic cytokine-targeting agents, particularly, TNF inhibitors, apart from risk of herpes zoster, which

38 TNF inhibitors are commonly used to treat inflammatory d

39 The antiresorptive effects of TNF inhibitors are likely related to their anti-inflamma

40 ence suggests that at least short courses of TNF inhibitors are safe for the treatment of irAEs in pa

41 TNF inhibitors are well tolerated immunosuppressive medi

42 Tumor necrosis factor alpha (TNF) inhibitors are a mainstay of treatment in rheumatoi

43 PURPOSE OF REVIEW: Tumor necrosis factor (TNF) inhibitors are effective for achieving disease cont

44 Although tumor necrosis factor (TNF) inhibitors are widely prescribed globally because o

45 ressed, and mRNA levels of interleukin 10, a TNF inhibitor, are decreased.

46 r insufficient primary response to the first TNF inhibitor at week 12.

47 lated uveitis glaucoma who were treated with TNF inhibitors at the time of their MMC-augmented primar

48 Fifteen patients were treated with systemic TNF inhibitors at the time of their trabeculectomy to co

49 Those taking tumor necrosis factor (TNF) inhibitors at baseline had a 37% lower adjusted rat

50 ite the evidence that tumor necrosis factor (TNF) inhibitors block TNF and the downstream inflammator

51 nt physiologic levels of TNF may explain why TNF inhibitors cause AA in some individuals, while treat

52 g agents, ocrelizumab and ofatumumab and the TNF-inhibitors certolizumab and golimumab).

53 After adjusting for MI risk factors, the TNF inhibitor cohort had a significantly lower hazard of

54 eived a TNF inhibitor for at least 2 months (TNF inhibitor cohort), 2097 were TNF inhibitor naive and

55 tumor necrosis factor alpha inhibitor," and "TNF inhibitor," combined with the terms "psoriasis," "pu

56 ibitor), tocilizumab (an IL-6 inhibitor), or TNF inhibitors compared with a common comparator abatace

57 ts treated with tofacitinib, tocilizumab, or TNF inhibitors compared with abatacept.

58 oding adenovirus or an adenovirus encoding a TNF inhibitor, composed of the extracellular domain of t

59 ght patients (31%) who started a second-line TNF inhibitor developed a subsequent TNF inhibitor-induc

60 The treatment for JIA, including TNF inhibitors, did not appear to be significantly assoc

61 up-regulation of the host response with IL-1/TNF inhibitors does not cause periodontal damage.

62 12R(-/-) CD4(+) spleen cells that received a TNF inhibitor-encoding adenovirus (5.4 +/- 6.5% weight l

63 y, without a definitive conclusion regarding TNF inhibitors established.

64 Treatment of Nlrp3A350V mice with the TNF inhibitor etanercept resulted in all pups surviving

65 se of MTX (10-25 mg/week) and stable dose of TNF inhibitor (etanercept or adalimumab) for >/= 12 week

66 Here, we compared a specific TNF inhibitor (etanercept) to thalidomide and prednisone

67 sis, treated with the tumor necrosis factor (TNF) inhibitor, etanercept.

68 e children contributed 2,922 person-years of TNF inhibitor exposure.

69 w-onset psoriasiform eruption while taking a TNF inhibitor for a nondermatologic disorder.

70 Of 8845 patients included, 1673 received a TNF inhibitor for at least 2 months (TNF inhibitor cohor

71 ed with higher persistence compared with the TNF inhibitor for PsO (weighted hazard ratio [HR], 0.78

72 associated with higher persistence than the TNF inhibitor for PsO (weighted HR, 0.76 [95% CI, 0.72-0

73 d with higher treatment persistence than the TNF inhibitor for PsO and PsA.

74 eruptions were seen in children treated with TNF inhibitors for any indication, and there appears to

75 Use of TNF inhibitors for psoriasis was associated with a non-s

76 Use of TNF inhibitors for psoriasis was associated with a signi

77 r, tofacitinib was statistically inferior to TNF inhibitors for the occurrence of MACEs and malignanc

78 b group and 143 (95%) of 151 patients in the TNF inhibitor group had adverse events.

79 o the patient's and rheumatologist's choice (TNF inhibitor group).

80 re randomly assigned 1:1 to the rituximab or TNF inhibitor groups with minimisation to account for me

81 atients who were not currently taking MTX or TNF inhibitors had an increased rate of infection (HR(ad

82 Tumor necrosis factor (TNF)inhibitors have been largely unsuccessful in treatin

83 II trial suggest that tumor necrosis factor (TNF) inhibitors hold promise in treating IPS.

84 ar rate of infection as use of MTX without a TNF inhibitor (HR(adj) 1.2 [95% CI 0.8, 1.8]).

85 Compared with TNF inhibitors, IL-23 inhibitors were associated with a

86 ath were observed among those who received a TNF inhibitor in combination with azathioprine/6-mercapt

87 P = .004) but not among those who received a TNF inhibitor in combination with methotrexate therapy (

88 superior to an otherwise analogous systemic TNF inhibitor in protecting mice from lethal LPS/D-Galac

89 ulosis infections and to investigate whether TNF inhibitors in clinical use reduce host immunity.

90 rs in combination with methotrexate therapy, TNF inhibitors in combination with azathioprine/6-mercap

91 inhibitor monotherapy (reference treatment), TNF inhibitors in combination with methotrexate therapy,

92 es, this strategy is not more effective than TNF inhibitors in improving musculoskeletal symptoms in

93 s mechanism may contribute to the effects of TNF inhibitors in inflammatory diseases and indicates po

94 tis, strategy trials on tapering or stopping TNF inhibitors in patients in remission, trials of treat

95 Treatment with TNF inhibitors in RA patients reverses the expression ch

96 Given the success of TNF inhibitors in the treatment of human Crohn's disease

97 matic drugs within the same class, including TNF inhibitors, in patients with active rheumatoid arthr

98 nd-line TNF inhibitor developed a subsequent TNF inhibitor-induced psoriasiform eruption at a median

99 In this case series, paradoxical TNF inhibitor-induced psoriasiform eruptions were seen i

100 Tumor necrosis factor alpha (TNF) inhibitor-induced psoriasiform eruption is well rec

101 Several studies using the TNF inhibitors infliximab and etanercept suggest that th

102 dian of 14.5 months (IQR, 9-24 months) after TNF inhibitor initiation.

103 ration of exposure to tumor necrosis factor (TNF) inhibitors, interleukin (IL) 17 inhibitors, IL-12/2

104 inical remission of psoriasis in response to TNF inhibitors is the inhibition of the CCR7/CCL19 axis

105 ate; or (4) other nonbiologic DMARDs without TNF inhibitors, methotrexate, or hydroxychloroquine (ref

106 Treatment exposure categories included TNF inhibitor monotherapy (reference treatment), TNF inh

107 In this cohort study, TNF inhibitor monotherapy was associated with a lower ri

108 nalysis, compared with patients who received TNF inhibitor monotherapy, higher odds of hospitalizatio

109 Tumor necrosis factor (TNF) inhibitors (mostly infliximab, adalimumab, and etan

110 signed and given either rituximab (n=144) or TNF inhibitor (n=151) treatment.

111 t 2 months (TNF inhibitor cohort), 2097 were TNF inhibitor naive and received other systemic agents o

112 Following any use of TNF inhibitors, no probable or highly probable malignanc

113 ximab compared with 26 in patients receiving TNF inhibitors, of which 27 were deemed to be possibly,

114 GS: There are many studies of the effects of TNF inhibitors on markers of bone turnover; however, few

115 k of DM was lower for individuals starting a TNF inhibitor or hydroxychloroquine compared with initia

116 thout other DMARDs; (2) methotrexate without TNF inhibitors or hydroxychloroquine; (3) hydroxychloroq

117 ychloroquine; (3) hydroxychloroquine without TNF inhibitors or methotrexate; or (4) other nonbiologic

118 The incidence of MI in the TNF inhibitor, oral/phototherapy, and topical cohorts we

119 rapy cohort), and 5075 were not treated with TNF inhibitors, other systemic therapies, or phototherap

120 date have not demonstrated any advantages of TNF inhibitors over traditional nonbiologic therapies in

121 46] years; 10 105 [79.4%] women), and 11 976 TNF inhibitor pairs (mean [SD] age 72.67 [5.91] years; 1

122 fter 7 days, and rats were then treated with TNF inhibitor (pegsunercept) or vehicle alone and euthan

123 e development of AA in patients treated with TNF inhibitors.Pharmacogenetics and the inherent physiol

124 Peripheral administration of a soluble TNF inhibitor prevented abnormal turnover of dendritic s

125 enteropathy, an adenoviral vector encoding a TNF inhibitor protein was administered.

126 The success of TNF inhibitors raised unrealistic expectations for targe

127 In TNF inhibitor recipients, mucosal permeability to sucral

128 ort (1846 patients enrolled at initiation of TNF inhibitor; recruitment: 2006-2010; 2011 as final fol

129 ong individuals with IMIDs who are receiving TNF inhibitors remains insufficiently understood.

130 h the rituximab strategy were lower than the TNF inhibitor strategy ( pound9,405 vs pound11,523 per p

131 Anti-TNF inhibitors successfully improve the quality of life

132 TNF inhibitors; 11 patients changed to a non-TNF inhibitor systemic therapy, and 7 discontinued all s

133 per year) and with better EULAR response to TNF inhibitor therapy (OR, 1.14 [95% CI, 1.01-1.30], P =

134 be significantly associated with response to TNF inhibitor therapy (P < 0.01 by Fisher's exact test).

135 2.9, 5.5 years), and the median duration of TNF inhibitor therapy was 685 days (interquartile range,

136 rity of these children were able to continue TNF inhibitor therapy with adequate skin-directed and ot

137 Among JIA patients not receiving TNF inhibitor therapy, MTX users had a similar rate of i

138 cination, particularly in those treated with TNF inhibitor therapy.

139 table or active disease and before and after TNF inhibitor therapy.

140 bjects with active RA prior to initiation of TNF inhibitor therapy.

141 een patients and predict ultimate success of TNF inhibitor therapy.

142 g the hypothesis that tumor necrosis factor (TNF) inhibitor therapy of psoriasis may also reduce card

143 inhibitor, IL-1 receptor antagonist, and the TNF inhibitor, TNF binding protein.

144 ediated inflammatory diseases treated with a TNF inhibitor (TNFi) and/or methotrexate (MTX), dupiluma

145 Despite TNF inhibitor (TNFi) being foundational in managing acti

146 Here we demonstrate that TNF inhibitor (TNFi) drugs induce the anti-inflammatory

147 hough literature suggests that resistance to TNF inhibitor (TNFi) therapy in patients with ulcerative

148 role of alternative tumour necrosis factor (TNF) inhibitors (TNFi), rituximab, abatacept and tociliz

149 Non-responders to the first TNF inhibitor to which they were randomised were switche

150 res to the randomised therapies: etanercept (TNF-inhibitor), tocilizumab (interleukin-6 receptor inhi

151 hritis who had had an inadequate response to TNF inhibitors, tofacitinib was more effective than plac

152 soriasiform eruptions were identified in 103 TNF inhibitor-treated patients (median age, 13.8 years [

153 cally non-inferior and cheaper compared with TNF inhibitor treatment in biological-treatment naive pa

154 nt with rituximab is non-inferior to initial TNF inhibitor treatment in patients seropositive for rhe

155 and mortality, but inversely correlated with TNF inhibitor treatment response.

156 with no GC use, after adjustment for MTX and TNF inhibitor use (HR(adj) 3.1 [95% CI 2.0, 4.7]).

157 TNF inhibitor use (irrespective of MTX) resulted in a si

158 y distinct pathophysiologic contributions of TNF inhibitor use to kidney and nonkidney outcomes in pa

159 s; stratified by baseline DMARD and previous TNF inhibitor use) to subcutaneous guselkumab 100 mg eve

160 e of infection was not increased with MTX or TNF inhibitor use, but was significantly increased with

161 For those taking MTX without TNF inhibitor use, the SIR was 3.9 (95% CI 0.4-14).

162 re was a potentially lower risk of ADRD with TNF inhibitors vs abatacept, but only in analyses 2 and

163 assigned to rituximab was -2.6 (SD 1.4) and TNF inhibitor was -2.4 (SD 1.5), with a difference withi

164 culectomy for patients who were treated with TNF inhibitors was 73% (95% CI, 44%-89%) at 1, 5, and 10

165 th incident IBD, incident use (vs nonuse) of TNF inhibitors was independently associated with higher

166 ble adjustments, incident use (vs nonuse) of TNF inhibitors was significantly associated with higher

167 ethotrexate (MTX) and tumor necrosis factor (TNF) inhibitors was categorized as ever exposed or never

168 ctomy for patients who were not treated with TNF inhibitors were 57%, 16%, and 0% at 1, 5, and 10 yea

169 tomies of patients who were not treated with TNF inhibitors were successful for a median of 1.2 years

170 ulectomies of patients who were treated with TNF inhibitors were successful for a median of 3.2 years

171 g recommendations for tumor necrosis factor (TNF) inhibitors were consistently included, recommendati

172 ged in diabetic rats and was reversed by the TNF inhibitor, which reduced cytokine mRNA levels, leuko

173 TNF inhibitor and a change to a second-line TNF inhibitor with cutaneous improvement in 23 patients

174 y were randomised were switched to the other TNF inhibitor with no washout period.

175 exclusive groups: (1) tumor necrosis factor (TNF) inhibitors with or without other DMARDs; (2) methot

176 nation with MTX in other RA trials without a TNF inhibitor, with no new safety signals observed.

177 fficacy and safety of switching to the other TNF inhibitor without a washout period after insufficien

178 benefit and safety of switching to a second TNF inhibitor without a washout period after primary fai