Colwell J A, Halushka P V, Sarji K, Levine J, Sagel J, Nair R M
Diabetes. 1976;25(2 SUPPL):826-31.
An increased sensitivity of platelets to aggregation from ADP and epinephrine is described in diabetics with or without vascular disease. This sensitivity correlates with elevated levels on von Willebrand factor (vWF), which, in turn appears to be influenced by growth hormone. VWF activity correlates with previously described "plasma factor" activity. Platelets from diabetic subjects are more sensitive than platelets from normal subjects to arachidonic acid-induced aggregation. This sensitivity is abolished by aspirin, which is a prostaglandin synthetase (cyclo-oxygenase) inhibitor. Platelets from diabetc subjects synthesize increased amounts of PGE2-like material (iPGE) in response to ADP, epinephrine, collagen, and arachidonic acid. The latter finding suggests that a fundamental mechanism for increased platelet aggregation in diabetes is increased prostaglandin synthetase activity. Therapeutic endeavors that would lower growth hormone levels, vWF activity, and/or prostaglandin synthetase activity may be of benefit in the prophylaxis of diabetic vascular disease. Prospective studies are needed to explore these hypothesis, as are more studies on the precise mechanisms and platelet aggregation in diabetes mellitus.
患有或未患有血管疾病的糖尿病患者体内的血小板对二磷酸腺苷（ADP）和肾上腺素诱导的聚集表现出更高的敏感性。这种敏感性与血管性血友病因子（vWF）水平升高相关，而vWF水平升高反过来似乎又受生长激素的影响。vWF活性与先前描述的“血浆因子”活性相关。糖尿病患者的血小板比正常受试者的血小板对花生四烯酸诱导的聚集更敏感。这种敏感性可被阿司匹林消除，阿司匹林是一种前列腺素合成酶（环氧化酶）抑制剂。糖尿病患者的血小板在受到ADP、肾上腺素、胶原蛋白和花生四烯酸刺激后，合成的PGE2样物质（iPGE）量增加。后一项发现表明，糖尿病中血小板聚集增加的一个基本机制是前列腺素合成酶活性增加。降低生长激素水平、vWF活性和/或前列腺素合成酶活性的治疗措施可能有助于预防糖尿病血管疾病。需要进行前瞻性研究来探索这些假设，同时也需要对糖尿病中血小板聚集的确切机制进行更多研究。
