ライフサイエンスコーパス: vigabatrin

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

2 avorable toxicity profile when compared with vigabatrin.

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

4 ions were measured in 11 patients started on vigabatrin.

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

6 rapy alone and four on hormonal therapy with vigabatrin.

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

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

9 ject receiving placebo and in none receiving vigabatrin.

10 d hormone treatments than in those allocated vigabatrin.

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

12 s given hormonal treatments than those given vigabatrin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 3-6 and molecular dynamics simulations with vigabatrin bound provide rationalizations for the inhibi

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

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

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

47 Vigabatrin cannot therefore be recommended as a first-li

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

49 2%) of 186 patients on hormonal therapy with vigabatrin compared with 108 (57%) of 191 patients on ho

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

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

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

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

54 adherence may have obscured any evidence of vigabatrin efficacy.

55 Vigabatrin enhanced this depolarization-evoked nonvesicu

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

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

58 Eighty-four vigabatrin-exposed individuals underwent Goldmann kineti

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

60 In 91 vigabatrin-exposed individuals, the cumulative vigabatri

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

62 After vigabatrin exposure in individuals receiving cumulative

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

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

65 g ppRNFL thinning with increasing cumulative vigabatrin exposure.

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

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

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

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

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

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

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

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

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

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

76 Vigabatrin has been recorded to have a beneficial effect

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

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

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

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

81 The antiepileptic drug vigabatrin increases human cerebrospinal fluid homocarno

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

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

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

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

86 Vigabatrin is a newly licensed drug for use in patients

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

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

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

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

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

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

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

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

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

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

97 s allocated tetracosactide and one allocated vigabatrin received prednisolone.

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

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

100 Vigabatrin seems less effective but better tolerated tha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 Vigabatrin (VGB) is a commonly prescribed antiepileptic

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

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

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

120 Vigabatrin was better tolerated than carbamazepine with

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

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

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

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

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