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

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

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

9 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

10 2; 95% confidence interval [CI], 47.3-53.2); TNF inhibitors (80 cases among 4623 treatment episodes;

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

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

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

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

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

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

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

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

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

20 TNF inhibitors are well tolerated immunosuppressive medi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

37 12R(-/-) CD4(+) spleen cells that received a TNF inhibitor-encoding adenovirus (5.4 +/- 6.5% weight l

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 In TNF inhibitor recipients, mucosal permeability to sucral

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

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

78 Anti-TNF inhibitors successfully improve the quality of life

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

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

81 2.9, 5.5 years), and the median duration of TNF inhibitor therapy was 685 days (interquartile range,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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