Springer Online Journal Archives 1860-2000
Summary Besides decreased platelet production and an increased platelet sequestration in the spleen chronic DIC is thought to cause thrombocytopenia in chronic liver diseases. To investigate if this mechanism could play a role in patients with severe, but stable hepatic cirrhosis, we studied 32 pts. Twenty-eight of them had portal hypertension, 22 had bleeding episodes from oesophageal varices. To evaluate platelet activity, thrombin generation and fibrinolytic activity in vivo, plasma and platelet levels ofβ-thromboglobulin (β-TG) and platelet factor 4 (PF4) as well as fibrinopeptide A (FPA) and the fibrinogen degradation product FCB-3, generated by the action of plasmin, were determined radioimmunologically. Plasma levels and platelet content of serotonin (5-HT) were measured fluorometrically. The mean platelet count/µl was reduced in pts. (109.000±67.000) compared to a control group (n=25, 264,000±52,000,p〈0.001). Factor VII (45±20%), prothrombin time (63±16%) AT-III activity (65±19%) and AT-III concentration (67±23%) were decreased in the pts'. group (p〈0.01). In contrast, plasma levels ofβ-TG (17±7 ng/ml) and of PF4 (4±2 ng/ml) as well as platelet content (µg/109 platelets) ofβ-TG (59±18), PF4 (21±6) and 5-HT (400±210) were found to be in the normal range. Neither mean FPA plasma concentration (3±2 ng/ml) nor mean FCB-3 scrum level (11±5 pmol/ml) differed significantly from controls. Our results demonstrate that pts. with thrombocytopenia and stable hepatic cirrhosis do not have evidence of chronic DIC, primary fibrinolysis or increased platelet activity in vivo. However, our results are compatible with increased platelet sequestration in the spleen and/or decreased platelet survival due to faster extravascular platelet clearance, or decreased platelet production within the bone marrow.
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