Rubin M H, Weston M J, Langley P G, White Y, Williams R
Dig Dis Sci. 1979 Mar;24(3):197-202. doi: 10.1007/BF01308429.
Abnormalities of platelet aggregation in response to adenosine diphosphate in 56 patients with chronic liver disease correlated with impairment of hepatocellular function but not with the etiology of the liver disease. Platelet-poor plasma from some patients appeared to contain an inhibitor since, in cross-over studies, it reduced the degree of aggregation of control subjects. However, platelet-poor plasma from some other patients enhanced aggregation in controls, and this was thought to be due to the presence of fibrin monomer. In the majority of patients with severe liver disease, platelet function still appeared defective, even after exclusion of the effects of plasma, and was independent of the platelet count in peripheral venous blood. Since patient platelet volumes were smaller than those of controls, these findings might be explained by deficiency of the larger hemostatically active type of platelet as a consequence of either bone marrow failure or splenic sequestration.
56例慢性肝病患者对二磷酸腺苷的血小板聚集异常与肝细胞功能损害相关，但与肝病病因无关。一些患者的乏血小板血浆似乎含有一种抑制剂，因为在交叉研究中，它降低了对照受试者的聚集程度。然而，其他一些患者的乏血小板血浆增强了对照中的聚集，这被认为是由于纤维蛋白单体的存在。在大多数严重肝病患者中，即使排除血浆的影响，血小板功能似乎仍有缺陷，并且与外周静脉血中的血小板计数无关。由于患者的血小板体积小于对照组，这些发现可能是由于骨髓衰竭或脾扣押导致较大的具有止血活性的血小板类型缺乏所致。
