The circulating platelet count is not dictated by the liver, but may be determined in part by the bone marrow: analyses from human liver and stem cell transplantations

Abstract

Summary. Background: The platelet count varies considerably between individuals, but within an individual the platelet count is remarkably stable over time. Mechanisms controlling the platelet count are not yet established. Objective: In the present study, we tested the hypothesis that the liver is important in controlling the circulating platelet count, as the liver is the main producer of thrombopoietin. Methods: We compared the platelet count prior to and after liver transplantation in > 250 patients transplanted for familial amyloidotic polyneuropathy (FAP). In contrast to most patients undergoing liver transplantation, patients with FAP have normal liver function before transplantation. Furthermore, we compared platelet counts in 89 living liver donors with the platelet count in the recipients of these grafts. Finally we compared platelet counts in donor-recipient pairs of hematopoietic stem cells. Results and conclusions: The platelet count prior to transplantation correlated with the platelet count at 3 or 12 months after transplantation in patients with FAP (r = 0.48, P < 0.0001 at 3 months, r = 0.39, P < 0.0001 at 12 months), whereas the platelet count in a living liver donor did not correlate with the platelet count in the recipient at 3 or 12 months after transplantation (r = 0.16, P = 0.26 at 3 months, r = 0.11, P = 0.30 at 12 months). The platelet count of related donors of hematopoietic stem cells correlated with the platelet count in the recipient after transplantation (r = 0.25, P = 0.011). Conclusions: These results suggest that the liver, in spite of being the prime producer of thrombopoietin, does not dictate the circulating platelet count, whereas the bone marrow does appear to play a role.

The evolving knowledge on primary hemostasis in patients with cirrhosis: A comprehensive review

“…[83] The pathogenesis of cirrhosis-driven thrombocytopenia is multifactorial and includes both decreased platelet production and increased sequestration/destruction. [1,84] Reduced hepatic synthesis of TPO, [85,86] increased catabolism of TPO by platelets sequestered in the spleen, [87] bone marrow suppression by alcohol and/or viral infections, [88,89] and altered bone marrow function [90] may synergistically contribute to impaired platelet production. In addition, hypersplenism, [91] antiplatelet antibodies, [92] and platelet consumption due to the activation of coagulation lead to increased platelet clearance, [93] which contributes to an additional decrease in platelet count.…”

Relationship Between Platelets and the Clinical Efficacy of Umbilical Cord Mesenchymal Stem Cells for HBV-Related Acute-on-Chronic Liver Failure and Liver Cirrhosis: A Preliminary Clinical Study

“…Data from human liver and stem cell transplantations showed that the liver is not involved in determining the circulating platelet count and that the bone marrow is partly involved in determining the circulating platelet count. 20 As such, there were differences in platelet count after MSC treatment between patients of different ages. Of course, increasing the number of stem cells transfused may promote the restoration of bone marrow function.…”