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癫痫患者的生物素状态。

Biotin status of epileptics.

作者信息

Krause K H, Bonjour J P, Berlit P, Kochen W

出版信息

Ann N Y Acad Sci. 1985;447:297-313. doi: 10.1111/j.1749-6632.1985.tb18447.x.

DOI:10.1111/j.1749-6632.1985.tb18447.x
PMID:3925859
Abstract

Microbiologically determined plasma biotin levels in 404 epileptics under long-term treatment with anticonvulsants were markedly lower than in 112 controls (p less than 0.0005). Patients with partial epilepsy had lower biotin levels and higher average daily intake of AC than those with generalized epilepsy. Epileptics treated with valproate sodium in monotherapy showed considerably higher biotin levels than epileptics with monotherapy of primidone (PRM), carbamazepine (CBZ), phenytoin (PHT) or phenobarbital (PB). The group of epileptics with high average daily dose of anticonvulsants had lower biotin levels than the group with low dose. In three patients with newly recognized epilepsy biotin levels were normal before starting anticonvulsant medication, increased during the first week and fell under the starting level in the following weeks. Four epileptics treated with PHT, PB, PRM or CBZ had an increased urinary excretion of organic acids, as found in patients with a deficiency of biotin-dependent carboxylases. In 37 epileptics undergoing long-term treatment plasma lactate concentrations were determined; they had a higher mean concentration than that found in controls. Our results suggest, that the lowering of biotin in epileptics is caused by intake of anticonvulsants and has a biochemical effect in these patients. It is discussed, whether this could be a factor in the mode of action of anticonvulsants.

摘要

404例长期接受抗惊厥药物治疗的癫痫患者经微生物学测定的血浆生物素水平显著低于112例对照者(p<0.0005)。部分性癫痫患者的生物素水平低于全身性癫痫患者,且平均每日抗惊厥药物摄入量更高。接受丙戊酸钠单药治疗的癫痫患者的生物素水平显著高于接受扑米酮(PRM)、卡马西平(CBZ)、苯妥英(PHT)或苯巴比妥(PB)单药治疗的癫痫患者。平均每日抗惊厥药物剂量高的癫痫患者组的生物素水平低于低剂量组。3例新确诊的癫痫患者在开始抗惊厥药物治疗前生物素水平正常,在第一周升高,在接下来的几周内降至起始水平以下。4例接受PHT、PB、PRM或CBZ治疗的癫痫患者的有机酸尿排泄增加,这在生物素依赖性羧化酶缺乏的患者中也有发现。对37例接受长期治疗的癫痫患者测定了血浆乳酸浓度;他们的平均浓度高于对照组。我们的结果表明,癫痫患者生物素水平降低是由抗惊厥药物的摄入引起的,并且在这些患者中具有生化作用。文中讨论了这是否可能是抗惊厥药物作用方式的一个因素。

相似文献

1
Biotin status of epileptics.癫痫患者的生物素状态。
Ann N Y Acad Sci. 1985;447:297-313. doi: 10.1111/j.1749-6632.1985.tb18447.x.
2
Excretion of organic acids associated with biotin deficiency in chronic anticonvulsant therapy.
Int J Vitam Nutr Res. 1984;54(2-3):217-22.
3
Impaired biotin status in anticonvulsant therapy.抗惊厥治疗中生物素状态受损。
Ann Neurol. 1982 Nov;12(5):485-6. doi: 10.1002/ana.410120513.
4
Organic aciduria in late-onset biotin-responsive multiple carboxylase deficiency.
J Inherit Metab Dis. 1985;8 Suppl 2:105-6. doi: 10.1007/BF01811480.
5
Lactic acidosis in biotin-responsive multiple carboxylase deficiency caused by holocarboxylase synthetase deficiency of early and late onset.早发型和晚发型全羧化酶合成酶缺乏所致生物素反应性多种羧化酶缺乏症中的乳酸酸中毒
J Pediatr. 1982 Oct;101(4):546-50. doi: 10.1016/s0022-3476(82)80697-5.
6
Enzyme studies in biotin-responsive disorders.生物素反应性疾病中的酶学研究。
J Inherit Metab Dis. 1985;8 Suppl 1:46-52. doi: 10.1007/BF01800659.
7
Prenatal treatment of biotin responsive multiple carboxylase deficiency.
Lancet. 1982 Jun 26;1(8287):1435-8. doi: 10.1016/s0140-6736(82)92452-7.
8
Biotin-responsive multiple carboxylase deficiency (MCD): deficient biotinidase activity associated with renal loss of biotin.
J Inherit Metab Dis. 1984;7 Suppl 2:123-5. doi: 10.1007/978-94-009-5612-4_36.
9
Multiple carboxylase deficiency: clinical and biochemical improvement following neonatal biotin treatment.多种羧化酶缺乏症:新生儿生物素治疗后的临床及生化改善
Pediatrics. 1981 Jul;68(1):113-8.
10
[Reduction of biotin level as a possible factor in the mode of action of anticonvulsants (author's transl)].生物素水平降低作为抗惊厥药作用方式的一个可能因素(作者译)
Arch Psychiatr Nervenkr (1970). 1982;231(2):141-8. doi: 10.1007/BF00343835.

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