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热性惊厥中的低锌血症。

Hypozincaemia in febrile convulsion.

作者信息

Burhanoğlu M, Tütüncüoğlu S, Coker C, Tekgül H, Ozgür T

机构信息

Paediatrics Department, Ege University Hospital, Bornova Izmir, Turkey.

出版信息

Eur J Pediatr. 1996 Jun;155(6):498-501. doi: 10.1007/BF01955189.

DOI:10.1007/BF01955189
PMID:8789769
Abstract

UNLABELLED

To understand further the role role of trace elements in pathogenesis of febrile convulsions, serum zinc (Zn), copper (Cu), magnesium (Mg) and CSF An, Cu, Mg and protein levels were measured by spectrometry in patients with febrile convulsion (n = 19), bacterial meningitis (n = 9), viral CNS infection (n = 16) and in the control group (n = 10) which consisted of children with signs of meningeal irritation due to upper respiratory tract infection but normal CSF findings. Samples were obtained within 6 h after admission to hospital. Mean serum and CSF Zn levels in the febrile convulsion group were significantly lower than in the other groups (for serum Zn: 0.66 +/- 0.03 mg/1 vs 0.98 +/- 0.07 mg/1, 1.06 +/- 0.08 mg/1, 1.05 +/- 0.09 mg/1 P < 0.05; for CSF Zn: 22.96 +/- 1.62 micrograms/1 vs 75.47 +/- 6.9 micrograms/1, 50.32 +/- 5.235 micrograms/1, 39.85 +/- 2.81 micrograms/1 P < 0.05). A linear relationship was established between serum Zn and CSF Zn levels (P < 0.001). Mean CSF Zn, Cu and protein levels in the bacterial meningitis group were significantly higher than in the other groups (for CSF Cu 63.94 +/- 6.33 micrograms/1 vs 38.77 +/- 2.70 micrograms/1, 35.84 +/- 3.48 micrograms/1, 33.86 +/- 2.88 micrograms/1 P < 0.05; for CSF protein 0.80 +/- 0.12 g/1 vs 0.22 +/- 0.02 g/1, 0.53 +/- 0.08 g/1, 0.19 +/- 0.01 g/1 P < 0.05). In children with meningitis, the elevation of the mean CSF Zn and Cu levels may result from the breakdown of the blood-brain barrier and subsequent leakage of trace elements and protein from serum to CSF. There was no significant difference between the four groups in terms of mean serum Mg and mean CSF Mg levels.

CONCLUSION

Serum and CSF Zn levels are decreased in children with febrile seizures. Zinc deprivation may play a role in the pathogenesis of febrile seizures.

摘要

未标记

为进一步了解微量元素在热性惊厥发病机制中的作用,采用光谱法测定了热性惊厥患者(n = 19)、细菌性脑膜炎患者(n = 9)、病毒性中枢神经系统感染患者(n = 16)以及对照组(n = 10,由因上呼吸道感染出现脑膜刺激征但脑脊液检查结果正常的儿童组成)的血清锌(Zn)、铜(Cu)、镁(Mg)以及脑脊液锌、铜、镁和蛋白质水平。样本在入院后6小时内采集。热性惊厥组的血清和脑脊液锌平均水平显著低于其他组(血清锌:0.66±0.03mg/1 对比 0.98±0.07mg/1、1.06±0.08mg/1、1.05±0.09mg/1,P < 0.05;脑脊液锌:22.96±1.62μg/1 对比 75.47±6.9μg/1、50.32±5.235μg/1、39.85±2.81μg/1,P < 0.05)。血清锌和脑脊液锌水平之间建立了线性关系(P < 0.001)。细菌性脑膜炎组的脑脊液锌、铜和蛋白质平均水平显著高于其他组(脑脊液铜:63.94±6.33μg/1 对比 38.77±2.70μg/1、35.84±3.48μg/1、33.86±2.88μg/1,P < 0.05;脑脊液蛋白质:0.80±0.12g/1 对比 0.22±0.02g/1、0.53±0.08g/1、0.19±0.01g/1,P < 0.05)。在患有脑膜炎的儿童中,脑脊液锌和铜平均水平的升高可能是由于血脑屏障破坏以及随后微量元素和蛋白质从血清渗漏到脑脊液所致。四组之间的血清镁平均水平和脑脊液镁平均水平无显著差异。

结论

热性惊厥患儿的血清和脑脊液锌水平降低。锌缺乏可能在热性惊厥的发病机制中起作用。

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本文引用的文献

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