Platelet function in chronic liver disease: relationship to disease severity.
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.
D000244:Adenosine Diphosphate / Q000097:blood; D001663:Bilirubin / Q000097:blood; D001792:Blood Platelets / Q000502:physiology*; D002908:Chronic Disease; D006801:Humans; D008107:Liver Diseases / Q000097:blood* / Q000209:etiology; D010974:Platelet Aggregation; D010977:Platelet Factor 3 / Q000032:analysis; D011517:Prothrombin Time; D012709:Serum Albumin / Q000032:analysis; D013997:Time Factors
D012709:Serum Albumin; D010977:Platelet Factor 3; D000244:Adenosine Diphosphate; D001663:Bilirubin