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儿童糖尿病第一年期间的血小板聚集

Platelet aggregation during the first year of diabetes in childhood.

作者信息

Kobbah M, Ewald U, Tuvemo T

出版信息

Acta Paediatr Scand Suppl. 1985;320:50-5. doi: 10.1111/j.1651-2227.1985.tb10138.x.

Abstract

Platelet aggregability in 24 newly diagnosed diabetic children was investigated on five occasions from onset of the disease until one year after diagnosis. Twenty healthy children of similar age and sex served as controls. The magnitude of the platelet shape change after adenosine diphosphate (ADP) stimulation was decreased in diabetic children on admission (p less than 0.05) in comparison with controls, but normalized during the year of the study. Maximal aggregation and initial rate of aggregation after ADP stimulation did not change significantly during the study year, and did not differ from those in controls. Aggregation by low dose collagen (0.5 and 1.0 mg/l) increased significantly (maximal aggregation, p less than 0.01; aggregation velocity, p less than 0.001) in the diabetics during the first year after admission from seemingly normal to clearly supranormal. Aggregation induced by high-dose collagen (5.5 mg/l) remained unchanged during the observation period and did not differ from that in the control group. No correlations were found between the indicators of platelet aggregation and those of carbohydrate control at any time after diagnosis. Platelet dysfunction is thus present already during the first year of diabetes. The different time course of the ADP-induced platelet shape change and collagen-induced aggregation imply that the mechanisms underlying the abnormalities of these two platelet functions differ.

摘要

对24名新诊断的糖尿病儿童从发病直至诊断后一年的血小板聚集性进行了五次研究。20名年龄和性别相仿的健康儿童作为对照。与对照组相比,糖尿病儿童入院时经二磷酸腺苷(ADP)刺激后血小板形状变化的幅度降低(p<0.05),但在研究的一年中恢复正常。在研究年度内,ADP刺激后的最大聚集率和初始聚集率无显著变化,且与对照组无差异。入院后第一年,低剂量胶原蛋白(0.5和1.0mg/l)诱导的聚集显著增加(最大聚集率,p<0.01;聚集速度,p<0.001),从看似正常增加到明显高于正常水平。高剂量胶原蛋白(5.5mg/l)诱导的聚集在观察期内保持不变,与对照组无差异。诊断后任何时间,血小板聚集指标与碳水化合物控制指标之间均未发现相关性。因此,糖尿病第一年就已存在血小板功能障碍。ADP诱导的血小板形状变化和胶原蛋白诱导的聚集的不同时间进程表明,这两种血小板功能异常的潜在机制不同。

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