The purpose of this study was to assess the platelet aggregation and releasable platelet ATP in patients with alcoholic cirrhosis (n = 10) and primary biliary cirrhosis (n = 10). In patients with liver disease a significant decrease was found in both adenosine diphosphate-induced aggregation (P less than 0.01) and collagen-induced aggregation (P less than 0.001) compared with that of controls, but there was no significant difference between the two groups of patients. Patients with primary biliary cirrhosis release smaller amounts of ATP than patients with alcoholic cirrhosis, and compared with the controls there was a significant (P less than 0.001) decrease in the releasable ATP in the patient groups. These results suggest that platelets are damaged during an intravascular activation (loss of granules), which gives rise to their subsequent hypo-function when tested in vitro.
Mean platelet volume (MPV) and count (PLT) were assessed in patients with moderately affected liver function. PLT was significantly decreased in patients with liver disease (197 X 10(9)l-1 +/- 87 (SD), no. = 79) compared with that of controls (273 X 10(9)l-1 +/- 53 (SD), no. = 37, P less than 0.001). MPV in patients with liver disease (9.25 +/- 1.14 fl) was significantly lower than that of controls (10.52 +/-0.74 fl, P less than 0.001). In control subjects MPV and PLT were inversely correlated (r = -0.48, P less than 0.01), but statistical significance was not found in patients with liver disease (r = -0.2, 0.05 less than P less than 0.1). It is concluded that the low MPV and PLT are compatible with an intravascular activation (loss of granules) and increased consumption of platelets, which may take place in the diseased liver even in patients with a relatively well preserved liver function.
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