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血小板、酒精摄入与脑梗死的发病

Platelets, alcohol consumption, and onset of brain infarction.

作者信息

Numminen H, Hillbom M, Juvela S

机构信息

Department of Neurology, Oulu University Hospital, Finland.

出版信息

J Neurol Neurosurg Psychiatry. 1996 Oct;61(4):376-80. doi: 10.1136/jnnp.61.4.376.

DOI:10.1136/jnnp.61.4.376
PMID:8890776
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC486578/
Abstract

OBJECTIVES

Previous investigations have suggested that recurrent rebound thrombocytosis after alcohol misuse may be a factor in the pathogenesis of thromboembolic disease. Alcohol consumption, platelet count, and platelet function were examined among patients of working age with brain infarction.

METHODS

Platelet count and risk factors for stroke were studied in 426 stroke patients and 157 control patients in hospital. The measures were platelet count obtained within four days after the stroke onset, in vitro adenosine diphosphate induced platelet aggregation, associated thromboxane B2 formation, and urinary excretion of 11-dehydrothromboxane B2.

RESULTS

After adjustment for sex, age, cardiac disease, diabetes, and alcohol intake, hypertension (OR 3.4, 95% confidence interval (95% CI) 2.0-6.0) and current smoking (OR 2.1, 95% CI 1.4-3.3) were associated with an increased risk for brain infarction. Platelet count shortly after the onset of disease was higher in the stroke patients than in the controls (OR 1.05/10(10)/1 platelets; 95% CI 1.02-1.09). The patients with brain infarction who were heavy alcohol drinkers (n = 144) showed both thrombocytosis (OR 2.30, 95% CI 0.82-6.44) and thrombocytopenia (OR 3.20, 95% CI 1.19 to 8.59) more often at the onset of the stroke than the other patients with brain infarction. The thromboxane variables showed inconsistent associations with the onset of stroke. There was no consistent platelet abnormality among alcohol misusers at the onset of ischaemic brain infarction.

CONCLUSIONS

Alcohol induced thrombocytopenia and rebound thrombocytosis were both often seen at the onset of brain infarction in patients who were heavy alcohol drinkers. Therefore, other mechanisms which could contribute to the high frequency of recurrences of ischaemic stroke among heavy drinkers should be investigated.

摘要

目的

先前的研究表明,酒精滥用后反复出现的反应性血小板增多可能是血栓栓塞性疾病发病机制中的一个因素。对工作年龄段的脑梗死患者进行了酒精摄入量、血小板计数和血小板功能的检查。

方法

对426例中风患者和157例住院对照患者的血小板计数和中风危险因素进行了研究。测量指标为中风发病后4天内的血小板计数、体外二磷酸腺苷诱导的血小板聚集、相关血栓素B2的形成以及11-脱氢血栓素B2的尿排泄量。

结果

在对性别、年龄、心脏病、糖尿病和酒精摄入量进行调整后,高血压(比值比3.4,95%置信区间[95%CI]2.0-6.0)和当前吸烟(比值比2.1,95%CI 1.4-3.3)与脑梗死风险增加相关。疾病发作后不久,中风患者的血小板计数高于对照组(比值比1.05/10¹⁰/升血小板;95%CI 1.02-1.09)。与其他脑梗死患者相比,重度饮酒的脑梗死患者(n = 144)在中风发作时更常出现血小板增多(比值比2.30,95%CI 0.82-6.44)和血小板减少(比值比3.20,95%CI 1.19至8.59)。血栓素变量与中风发作的关联不一致。在缺血性脑梗死发作时,酒精滥用者中没有一致的血小板异常。

结论

在重度饮酒的脑梗死患者中,酒精诱导的血小板减少和反应性血小板增多在中风发作时都很常见。因此,应研究其他可能导致重度饮酒者缺血性中风复发频率高的机制。

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