EVIDENCE FOR A STORAGE POOL DEFECT IN PLATELETS FROM CIRRHOTIC-PATIENTS WITH DEFECTIVE AGGREGATION

The mechanisms underlying the defective platelet function in cirrhotic patients were investigated. Eleven cirrhotic patients with mild disease (group 1), 20 patients with severe cirrhosis (group 2), and 31 controls were studied. Platelet aggregation was significantly reduced in cirrhotics compared with controls. Compared with controls, cirrhotic patients in group 2 showed a significant reduction in the total content of adenosine triphosphate (57.8 ± 7.8 vs. 26.1 ± 6.3 μmol/1011 platelets; P < 0.05), 5-hydroxytryptamine (285 ± 26 vs. 104 ± 38 nmol/1011 platelets; P < 0.05), β-thromboglobulin (2129 ± 120 vs. 1223 ± 161 ng/108 platelets; P < 0.01), and platelet factor 4 (1389 ± 108 vs. 805 ± 176 ng/108 platelets; P < 0.05). In patients with severe disease, an increase in plasma β-thromboglobulin-platelet factor 4 ratio, an index of in vivo platelet activation, was observed (controls, 3.50 ± 0.50; group 1, 4.02 ± 0.80; and group 2, 6.59 ± 1.15). Our data indicate the existence of a platelet storage pool defect, which may favor the bleeding tendency of cirrhotic patients. © 1992.