ライフサイエンスコーパス: vigabatrin

1 herapy alone and 17 on hormonal therapy with vigabatrin).

2 amiloride, and not at all by dipyridamole or vigabatrin.

3 ions were measured in 11 patients started on vigabatrin.

4 in; 4 (6%) were caregivers of patients using vigabatrin.

5 tional developmental outcomes, and safety of vigabatrin.

6 iguat, 15 (24%) sodium oxybate, and 10 (16%) vigabatrin.

7 , alternatively, due to the weak efficacy of vigabatrin.

8 avorable toxicity profile when compared with vigabatrin.

9 umbens at (1)/(300) to (1)/(600) the dose of vigabatrin.

10 place preference at a dose (1)/(300) that of vigabatrin.

11 ject receiving placebo and in none receiving vigabatrin.

12 d hormone treatments than in those allocated vigabatrin.

13 rapy alone and four on hormonal therapy with vigabatrin.

14 nal treatments and 28 (54%) of 52 infants on vigabatrin.

15 s given hormonal treatments than those given vigabatrin.

16 se with the anticonvulsant gamma-vinyl GABA (vigabatrin; 0.05-100 microm) resulted in a large leak cu

17 ally rigid analogue (2) of the epilepsy drug vigabatrin (1) did not inactivate gamma-aminobutyric aci

18 The antiepilepsy drug vigabatrin (1, 4-aminohex-5-enoic acid, gamma-vinylGABA)

19 Minimum doses were vigabatrin 100 mg/kg per day, oral prednisolone 40 mg pe

20 mg (40 IU) on alternate days with or without vigabatrin 100 mg/kg per day.

21 e randomly assigned to hormonal therapy with vigabatrin (186) or hormonal therapy alone (191).

22 plication of the GABA transaminase inhibitor vigabatrin (194 nmol).

23 d them carbamazepine 600 mg daily (n=230) or vigabatrin 2 g daily (n=229).

24 Cocaine addicts were randomized to receive vigabatrin 3000 mg/day, cumulative dose 218 g (n = 92),

25 clinical assessment (hormone 41/55 [75%] vs vigabatrin 39/51 [76%]) was similar in each treatment gr

26 Larger doses of vigabatrin (4 g) further increased homocarnosine but cha

27 e participant had taken both natalizumab and vigabatrin; 4 (6%) were caregivers of patients using vig

28 fer significantly (hormone 78.6 [SD 16.8] vs vigabatrin 77.5 [SD 12.7]; difference 1.0, 95% CI -4.9 t

29 ed hormone treatment than in those allocated vigabatrin (88.2 [17.3] vs 78.9 [14.3]; difference 9.3,

30 or larger k(inact)/K(I) values than that of vigabatrin, a clinically used antiepilepsy drug, and the

31 Vigabatrin, a GABA aminotransferase (GABA-AT) inactivato

32 howed 187 times greater potency than that of vigabatrin, a known inactivator of GABA-AT and approved

33 (prednisolone, adrenocorticotropic hormone, vigabatrin), adjusting for demographic and clinical vari

34 rmation with the GABA transaminase inhibitor vigabatrin also failed to influence glucagon secretion a

35 ients with this disorder has been limited to vigabatrin, an anticonvulsant that blocks GABA transamin

36 gues of the epilepsy and drug addiction drug vigabatrin and as potential mechanism-based inactivators

37 ng slices in the GABA transaminase inhibitor vigabatrin and blocking uptake with tiagabine reduced th

38 ed to be high for all these drugs except for vigabatrin and lovastatin/simvastatin.

39 Moreover, in contrast to treatment with vigabatrin and rapamycin, TrkB inhibition rescued brain

40 ionally rigid analogues of the epilepsy drug vigabatrin and tested as inhibitors and substrates of ga

41 reen failures, 4 went straight to open label vigabatrin, and 12 were not randomized (normal EEG throu

42 red to 39% for oral corticosteroids, 36% for vigabatrin, and 9% for other (p < 0.001).

43 s or caregivers of adult patients prescribed vigabatrin, and adult female patients of reproductive ag

44 ce GABA neurotransmission, such as diazepam, vigabatrin, and baclofen, provide mild to modest relief

45 sion are gabapentin, lamotrigine, felbamate, vigabatrin, and topiramate.

46 igine, levetiracetam, tiagabine, topiramate, vigabatrin, and zonisamide do not induce the metabolism

47 Hormonal therapies or vigabatrin are the most commonly used treatments.

48 Two others, tiagabine and vigabatrin, are likely to be approved in the near future

49 The retention rate was 62.0% in the vigabatrin arm versus 41.5% in the placebo arm.

50 nd placebo-controlled trial was conducted of vigabatrin at first epileptiform electroencephalogram (E

51 ileptiform electroencephalogram (EEG) versus vigabatrin at seizure onset in infants with TSC.

52 the reductions observed in rats treated with vigabatrin at the same dose needed to treat addiction in

53 slowly over 4 d of treatment with 100 microm vigabatrin, at which time it reached an equivalent condu

54 Preventative treatment with vigabatrin based on EEG epileptiform activity prior to s

55 3-6 and molecular dynamics simulations with vigabatrin bound provide rationalizations for the inhibi

56 ABA-AT recently reported a computer model of vigabatrin bound to the PLP was constructed and energy m

57 iting VAVFL; Group II, 8 patients exposed to vigabatrin but with normal fields; Group III, 14 patient

58 creased the leak current that was induced by vigabatrin by 47%.

59 Vigabatrin cannot therefore be recommended as a first-li

60 The GABAergic anti-seizure medication (ASM) vigabatrin caused life-threatening side-effects in two i

61 A conformationally rigid analogue of vigabatrin, cis-3-aminocyclohex-4-ene-1-carboxylic acid

62 2%) of 186 patients on hormonal therapy with vigabatrin compared with 108 (57%) of 191 patients on ho

63 y contrast, specific inhibition of GABA-T by vigabatrin did not affect carnosine and anserine levels

64 Short-term use of vigabatrin did not cause a decrease in visual acuity or

65 5 [76%]) and 28 (54%) of 52 infants assigned vigabatrin (difference 19%, 95% CI 1%-36%, p=0.043).

66 g semi-automated kinetic perimetry (SKP) and Vigabatrin dosage in epilepsy patients with pretreatment

67 adherence may have obscured any evidence of vigabatrin efficacy.

68 o electroencephalography (EEG), and received vigabatrin either as conventional antiepileptic treatmen

69 Vigabatrin enhanced this depolarization-evoked nonvesicu

70 The ppRNFL was significantly thinner in vigabatrin-exposed compared with nonexposed individuals

71 years, 129 with vigabatrin-treated epilepsy (vigabatrin-exposed group) and 87 individuals with epilep

72 Eighty-four vigabatrin-exposed individuals underwent Goldmann kineti

73 with nonexposed individuals (P<0.05) and in vigabatrin-exposed individuals with normal visual fields

74 In 91 vigabatrin-exposed individuals, the cumulative vigabatri

75 gabatrin-exposed individuals, the cumulative vigabatrin exposure could be ascertained: 41 subjects re

76 After vigabatrin exposure in individuals receiving cumulative

77 With higher cumulative doses of vigabatrin exposure, additional ppRNFL thinning was obse

78 ur in people with epilepsy, independently of vigabatrin exposure, and be related to clinical characte

79 g ppRNFL thinning with increasing cumulative vigabatrin exposure.

80 d, even in individuals with large cumulative vigabatrin exposures and moderate or severe VAVFL.

81 ve clinical trial of early intervention with vigabatrin for pre-symptomatic epilepsy treatment in Tub

82 clinicians to evaluate patients treated with vigabatrin for refractory epilepsy.

83 present study was to assess the efficacy of vigabatrin for short-term cocaine abstinence in cocaine-

84 d their enzyme activity in liver (GABA-T for vigabatrin; GABA-T and AGXT2 for AOA).

85 The atypical antiepileptic vigabatrin (gamma-vinyl gamma-aminobutyric acid [GABA])

86 detected in 2 of 54 subjects (3.7%) from the vigabatrin group and in 1 of 49 subjects (2%) from the p

87 ficant differences were observed between the vigabatrin group and the placebo group on the primary ou

88 Twelve subjects in the vigabatrin group and two subjects in the placebo group m

89 han 66% of all participants (and >63% of the vigabatrin group) took more than 70% of their medication

90 spasms after randomization was later in the vigabatrin group.

91 eizure control improved with the addition of vigabatrin had higher mean homocarnosine, but the same m

92 Vigabatrin had profound effects on many metabolites, inc

93 Vigabatrin has been recorded to have a beneficial effect

94 Although vigabatrin has been used for many years in Europe, this

95 mma-aminobutyric acid (GABA)ergic medication vigabatrin has previously been shown to be effective in

96 e with epilepsy with no previous exposure to vigabatrin have a significantly thinner RNFL than health

97 d risk of adverse effects of SCBs in LoF and vigabatrin in GoF variants.

98 Daily low-dose (2 g) vigabatrin increased both homocarnosine and GABA.

99 The antiepileptic drug vigabatrin increases human cerebrospinal fluid homocarno

100 OCT of the RNFL can efficiently identify vigabatrin-induced damage and will be useful for adults

101 have demonstrated light exposure exacerbates vigabatrin-induced retinal toxicity.

102 These results indicate that vigabatrin induces spontaneous GABA efflux from neighbor

103 e treatment controls spasms better than does vigabatrin initially, but not at 12-14 months of age.

104 Vigabatrin is a newly licensed drug for use in patients

105 INTERPRETATION: Hormonal therapy with vigabatrin is significantly more effective at stopping i

106 Hormonal therapy with vigabatrin is significantly more effective at stopping i

107 approximately 40% to 60% of patients taking vigabatrin may not have been adherent.

108 Fifty-six were randomized to early vigabatrin (n = 29) or placebo (n = 27).

109 re randomly assigned to a fixed titration of vigabatrin (N=50) or placebo (N=53) in a 9-week double-b

110 andomly assigned hormone treatment (n=55) or vigabatrin (n=52) and were followed up until clinical as

111 and assessed, 107 were randomly assigned to vigabatrin (n=52) or hormonal treatments (prednisolone n

112 individuals with epilepsy never treated with vigabatrin (nonexposed group).

113 ure website to receive hormonal therapy with vigabatrin or hormonal therapy alone.

114 were similar for participants randomized to vigabatrin or placebo.

115 ytoin ineffective, whereas intervention with vigabatrin or the GABAB receptor antagonist CGP 35348 pr

116 pine to be significantly more effective than vigabatrin (p=0.0001).

117 s allocated tetracosactide and one allocated vigabatrin received prednisolone.

118 subjects who reported prestudy alcohol use, vigabatrin, relative to placebo, was associated with sup

119 ic cidofovir (Vistide), sildenafil (Viagra), vigabatrin (Sabril), tamoxifen (Nolvadex), hydroxychloro

120 Vigabatrin seems less effective but better tolerated tha

121 anges comparable to or greater than previous vigabatrin spectroscopy studies in healthy epilepsy-naiv

122 loyed in a synthesis of gamma-amino acid (S)-vigabatrin, the bioactive enantiomer of Sabril.

123 ore efficient an inactivator of GABA-AT than vigabatrin, the only FDA-approved inactivator of GABA-AT

124 Participants received twice-daily doses of vigabatrin (total dosage, 3.0 g/d) or matched placebo, p

125 s confirm light is a significant enhancer of vigabatrin toxicity and that a portion of this is mediat

126 proximately 65% of the decrease in V(GAD) in vigabatrin-treated animals suggesting that inhibition of

127 Subjects were older than 18 years, 129 with vigabatrin-treated epilepsy (vigabatrin-exposed group) a

128 V(GAD) was significantly lower in vigabatrin-treated rats (0.030-0.05 micromol/min per g,

129 we compared V(GAD) in cortex of control and vigabatrin-treated rats under alpha-chloralose/70% nitro

130 l end-of-trial abstinence was achieved in 14 vigabatrin-treated subjects (28.0%) versus four subjects

131 ocol-defined differences in efficacy between vigabatrin treatment and placebo were detected for any o

132 undertaken to test the hypothesis that early vigabatrin treatment in tuberous sclerosis complex (TSC)

133 pports the safety and efficacy of short-term vigabatrin treatment of cocaine dependence.

134 his relationship by examining the effects of vigabatrin treatment on the retinal structures of mice w

135 r basal conditions and the entire flux after vigabatrin treatment.

136 more than 70% of their medication, post hoc vigabatrin urine concentration levels suggested that app

137 Vigabatrin (VGB) is a commonly prescribed antiepileptic

138 Vigabatrin (VGB) is an anti-epileptic medication which h

139 The current therapy, vigabatrin (VGB), is not uniformly successful.

140 current literature about the pathogenesis of vigabatrin visual toxicity is reviewed in order to devel

141 Preventative vigabatrin was associated with later time to onset and l

142 Vigabatrin was better tolerated than carbamazepine with

143 Preventive treatment with vigabatrin was safe and modified the natural history of

144 ic hormone (ACTH), oral corticosteroids, and vigabatrin were considered individually, and all other n

145 GABA aminotransferase (GABA-AT) inactivator vigabatrin were not inactivators of GABA-AT.

146 reaction catalysed by GABA-T is inhibited by vigabatrin, whereas both GABA-T and AGXT2 activity is in

147 ministered at significantly lower doses than vigabatrin, which suggests a potential new treatment for

148 We aimed to compare the effects of vigabatrin with those of prednisolone and tetracosactide

149 n the placebo arm transitioned to open label vigabatrin, with a median delay of 44 days after randomi