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癫痫患者甲状腺激素水平的变化。

Changes of thyroid hormone levels in epileptic patients.

作者信息

Zhu S Q, Liu X M, Ruan X Z, Cai Z

机构信息

Department of Neurology, Tongji Hospital, Tongji Medical University, Wuhan.

出版信息

J Tongji Med Univ. 1994;14(2):119-23.

PMID:7966515
Abstract

We measured serum T3, T4, FT3, FT4 and thyrotropin (TSH) by radioimmunoassay in 150 patients with epilepsy. Of the 150 epileptic patients, 120 cases received single antiepileptic drug, including Sod valproate (VPA), carbamazepine (CBZ), phenytoin (PHT), or MixtBrodsky (MB). Each subgroup consisted of 30 cases. The other 30 were untreated epileptics. The results suggested that there was no significant difference in serum thyroid hormone levels among healthy control group, untreated group, and hepatic non-enzyme-inducing anticonvulsant group (P < 0.05). As compared with the three groups mentioned above, the serum T3, T4, FT3, FT4 concentrations of the enzyme inducer groups were decreased, however, significant decrease was found in PHT group and CBZ group (P < 0.05, P < 0.005). All 12 patients with circulating thyroid hormone concentrations below normal reference values were given enzyme inducer. None of them revealed any clinical manifestation of hypothyroidism. There was no significant difference in serum TSH level among the above 6 groups (P < 0.05), and the serum TSH level of all patients was within normal reference limits. Our study showed that the changes of thyroid hormone in epileptics were due to the effect of some AEDs and not the disease itself. The disparity between the effect of enzyme inducer and that of non-enzyme-inducing anticonvulsants indicated that the hepatic microsomal enzyme system metabolizing thyroid hormone to be induced was the main mechanism for decreased serum thyroid hormone concentrations. Though the serum thyroid hormone levels of the enzyme inducer groups were decreased, no significant increase of the mean serum TSH concentration was found. This implies that AEDs may interfere the HPA function in some way.

摘要

我们采用放射免疫分析法对150例癫痫患者的血清三碘甲状腺原氨酸(T3)、甲状腺素(T4)、游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)和促甲状腺激素(TSH)进行了检测。在这150例癫痫患者中,120例接受单一抗癫痫药物治疗,包括丙戊酸钠(VPA)、卡马西平(CBZ)、苯妥英(PHT)或米克斯布罗茨基(MB)。每个亚组由30例患者组成。另外30例为未治疗的癫痫患者。结果表明,健康对照组、未治疗组和非肝酶诱导性抗惊厥药物组之间血清甲状腺激素水平无显著差异(P<0.05)。与上述三组相比,肝酶诱导剂组的血清T3、T4、FT3、FT4浓度降低,然而,PHT组和CBZ组有显著降低(P<0.05,P<0.005)。12例循环甲状腺激素浓度低于正常参考值的患者均给予了肝酶诱导剂。他们均未出现任何甲状腺功能减退的临床表现。上述6组之间血清TSH水平无显著差异(P<0.05),所有患者的血清TSH水平均在正常参考范围内。我们的研究表明,癫痫患者甲状腺激素的变化是由于某些抗癫痫药物的作用,而非疾病本身。肝酶诱导剂与非肝酶诱导性抗惊厥药物作用的差异表明,代谢甲状腺激素的肝微粒体酶系统被诱导是血清甲状腺激素浓度降低的主要机制。虽然肝酶诱导剂组的血清甲状腺激素水平降低,但平均血清TSH浓度未显著升高。这意味着抗癫痫药物可能以某种方式干扰下丘脑-垂体-肾上腺(HPA)功能。

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