Ⅱ型糖尿病病人血小板聚集、第Ⅷ因子相关抗原的临床研究

Clinical Studies on Platelet Aggregation, Factor Ⅷ-Related Antigen in Patients with Non-Insulin-Dependent Diabetes Mellitus

本文对23例初发Ⅱ型糖尿病病人口服降糖药吡磺环已脲(Glipizide)治疗前后的血小板聚集、第Ⅷ僵因子相关抗原(ⅧR:Ag)和纤维蛋白原进行动态研究。结果表明:Ⅱ型糖尿病病人在临床未发现微血管病变时已有血小板聚集率升高,血小板聚集率与空腹血糖、糖化血红蛋白A1(GHbA1)无相关性,与ⅧR:Ag呈正相关(P<0.001)。吡磺环己脲治疗后血小板聚集率明显下降。提示血小板功能异常可能参与Ⅱ型糖尿病微血管病变的发生;内皮损害会加剧血小板聚集功能;吡磺环已脲对抑制血小板聚集功能有一定作用。

Platelet aggregation, plasma factor Ⅷ related antigen (Ⅷ R:Ag) and fibrinogen were measured on 23 newly diagnosed non-insulin-dependent diabetic patients (male 11, female 12) after two weeks of dietary treatment, and then at the 2nd, 4th and 6th month of gilpizide therapy. Their mean age was 49± 9 years. Nine patients had evidences of complicating with microangiopathy and the other 14 without. The platelet maximal aggregation rate induced by either ADP or adrenaline was significantly increased in the diabetic patients as compared with that in normal controls, but there was no significant difference between the patients with and without microangiopathy. Although the platelet aggregation rate exhibited a positive linear correlation with plasma levels of factor Ⅷ R:Ag in diabetic patients, it did not correlate with fasting blood glucose or glycosylated hemoglobin. After two months of glipizide therapy there were a significant reduction of platelet aggregability and plasma , levels of fibrinogen along with improvement of glycemic control, and they all maintained throughout the 6-month period of glipizide therapy. These results suggested that platelet hyperaggregability in diabetic patients might be induced by high plasma Ⅷ R:Ag resulting from endothelial damage and this abnormal platelet function may play a role in the pathogenesis of diabetic microangiopathy.; It is possible that glipizide might have a direct effect in reducing the platelet function of aggregation.