The significance of platelet consumption in the development of thrombocytopenia in patients with cirrhosis.

Introduction: Thrombocytopenia in cirrhosis is mainly explained by accelerated platelet destruction/sequestration because of hypersplenism or by decreased thrombopoietin levels. Excessive platelet consumption because of cirrhosis-related hypercoagulability has also been assumed to be an etiopathologic factor in thrombocytopenia. To clarify whether excessive platelet consumption (eg, venous thrombosis and disseminated intravascular coagulation) contributes to thrombocytopenia in cirrhosis, the following autopsy-based study was performed.

Methods: Ninety-nine autopsies of chronic liver disease (80 cirrhosis and 19 noncirrhosis) were examined retrospectively. Platelet count, weight of spleen and thrombotic complications were checked in autopsy protocols. Megakaryocytes in bone marrow were counted under high-power microscopic view. Univariate and multivariate analyses were performed to evaluate significances of these factors in thrombocytopenia.

Results: The platelet count was significantly lower in the cirrhosis cases (88 ± 51 × 10/L) than in the noncirrhosis cases (150 ± 120 × 10/L). The megakaryocyte count was also lower in the cirrhosis cases (1.5 ± 0.6 per high-power field) than in the noncirrhosis cases (1.9 ± 0.5 per high-power field). The weight of the spleen was greater in the cirrhosis cases (264 ± 179 g) than in the noncirrhosis cases (142 ± 82 g). Thrombotic complications had been recorded in 29 cases, whose platelet count (70 ± 41 × 10/L) was lower than that of those without these complications (113 ± 80 × 10/L). Multivariate analysis revealed that these 3 factors (megakaryocyte count, weight of spleen, and thrombotic complications) were independently correlated with the platelet count.

Conclusions: These results suggest that the imbalance of platelet production-destruction/sequestration-consumption contributes to thrombocytopenia in cirrhosis. Excessive platelet consumption cannot be ignored to explain this complex condition, especially in patients with major thrombotic events.