Vallés J, Santos M T, Aznar J, Velert M, Barberá G, Carmena R
Research Center and Department of Clinical Pathology, University Hospital La Fe, Valencia, Spain.
Diabetes. 1997 Jun;46(6):1047-53. doi: 10.2337/diab.46.6.1047.
Platelets participate in the atherothrombotic complications of diabetes. Recent data demonstrate that platelet reactivity can be modulated via cell-cell interactions with erythrocytes and neutrophils. In this study, platelet reactivity was evaluated in 30 IDDM patients. We used an analytical procedure that permits an independent evaluation of platelet activation (granule release, eicosanoid formation) and platelet recruitment (pro-aggregatory activity of cell-free releasates) after platelet stimulation with collagen in the presence or absence of other blood cells. The interaction between platelets and erythrocytes (hematocrit 40%) resulted in a marked enhancement of platelet activation (5HT, betaTG, TXA2 release) and recruitment in both patients and control subjects. The erythrocyte enhancement of platelet TXA2 synthesis and recruitment was significantly higher in the patients, while no differences were detected in platelet granule release. The elevated platelet recruitment in the IDDM patients was found to be due to 1) increased susceptibility of diabetic platelets to the prothrombotic effect of erythrocytes and 2) the greater response of diabetic platelets to their own cell-free releasate. Patients with poor metabolic control (elevated HbA1c) or longer evolution time had an even greater platelet recruitment. The presence of microalbuminuria is not related to the platelet recruitment. Since platelet recruitment is an essential step in thrombus growth, its enhancement may favor thrombotic complications in IDDM.
血小板参与糖尿病的动脉粥样硬化血栓形成并发症。最近的数据表明,血小板反应性可通过与红细胞和中性粒细胞的细胞间相互作用进行调节。在本研究中,对30例胰岛素依赖型糖尿病(IDDM)患者的血小板反应性进行了评估。我们采用了一种分析方法,该方法能够在有或无其他血细胞存在的情况下,在血小板受到胶原刺激后,独立评估血小板活化(颗粒释放、类花生酸形成)和血小板募集(无细胞释放物的促聚集活性)。血小板与红细胞(血细胞比容40%)之间的相互作用导致患者和对照受试者的血小板活化(5-羟色胺、β-血小板球蛋白、血栓素A2释放)和募集均显著增强。红细胞对血小板血栓素A2合成和募集的增强作用在患者中明显更高,而在血小板颗粒释放方面未检测到差异。发现IDDM患者中血小板募集增加是由于1)糖尿病血小板对红细胞促血栓形成作用的敏感性增加,以及2)糖尿病血小板对其自身无细胞释放物的反应更大。代谢控制不佳(糖化血红蛋白升高)或病程较长的患者血小板募集甚至更高。微量白蛋白尿的存在与血小板募集无关。由于血小板募集是血栓形成过程中的一个关键步骤,其增强可能会增加IDDM患者发生血栓并发症的风险。