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急性脑梗死患者体内铁储备与早期神经功能恶化

Body iron stores and early neurologic deterioration in acute cerebral infarction.

作者信息

Dávalos A, Castillo J, Marrugat J, Fernandez-Real J M, Armengou A, Cacabelos P, Rama R

机构信息

Sections of Neurology, Hospital Universitari Doctor Josep Trueta, Girona, Spain.

出版信息

Neurology. 2000 Apr 25;54(8):1568-74. doi: 10.1212/wnl.54.8.1568.

Abstract

BACKGROUND

Iron-dependent free radicals formation has been related to greater damage in cerebral ischemia. The authors analyzed whether increased body iron stores were associated with early neurologic worsening and excitatory amino acid release in patients with acute ischemic stroke.

METHODS

Ferritin, total iron, and glutamate concentrations in plasma and CSF were measured on admission in 100 consecutive patients with a cerebral infarction of <24 hours' duration. The authors diagnosed progressing stroke when the Canadian Stroke Scale score decreased one or more points between admission and 48 hours. Cranial CT was performed on admission and repeated on days 4 to 7 of hospitalization.

RESULTS

Ferritin concentrations in plasma (median 391, range 119 to 500 versus 148, 21 to 399 ng/mL) and in CSF (17.4, 6.8 to 82, versus 4.8, 0.6 to 14 ng/mL) were significantly higher in the 45 patients with subsequent progressing stroke than in those with nonprogressing stroke (p < 0.001). There was a positive correlation between ferritin and glutamate concentrations in plasma (r = 0.81, p < 0.001) and CSF (r = 0.64, p < 0.001). Plasma ferritin concentrations >275 ng/mL in plasma (OR, 33.5; 95% CI, 4.7 to 235) and >11 ng/mL in CSF (OR, 11.4; 95% CI, 3. 1 to 41) were independently and significantly related to early neurologic worsening. The effect was reduced by >60% after controlling for glutamate concentrations, but remained significant.

CONCLUSIONS

High plasma and CSF ferritin concentrations within the first 24 hours from the onset of ischemic stroke are associated with early neurologic deterioration. Increased body iron stores may contribute to stroke progression by enhancing the cytotoxic mechanisms in cerebral ischemia.

摘要

背景

铁依赖性自由基的形成与脑缺血中更严重的损伤有关。作者分析了急性缺血性卒中患者体内铁储备增加是否与早期神经功能恶化及兴奋性氨基酸释放有关。

方法

对100例连续入院的病程小于24小时的脑梗死患者入院时测定其血浆和脑脊液中的铁蛋白、总铁及谷氨酸浓度。当加拿大卒中量表评分在入院时和48小时之间下降1分或更多分时,作者诊断为进展性卒中。入院时进行头颅CT检查,并在住院第4至7天复查。

结果

45例随后发生进展性卒中的患者血浆(中位数391,范围119至500,与148,21至399 ng/mL相比)和脑脊液中铁蛋白浓度(17.4,6.8至82,与4.8,0.6至14 ng/mL相比)显著高于未发生进展性卒中的患者(p < 0.001)。血浆中铁蛋白与谷氨酸浓度之间存在正相关(r = 0.81,p < 0.001),脑脊液中也是如此(r = 0.64,p < 0.001)。血浆中铁蛋白浓度>275 ng/mL(比值比,33.5;95%可信区间,4.7至235)和脑脊液中>11 ng/mL(比值比,11.4;95%可信区间,3.1至41)与早期神经功能恶化独立且显著相关。在控制谷氨酸浓度后,这种效应降低了>60%,但仍然显著。

结论

缺血性卒中发病后24小时内血浆和脑脊液中铁蛋白浓度升高与早期神经功能恶化有关。体内铁储备增加可能通过增强脑缺血中的细胞毒性机制促进卒中进展。

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