Thrombocytopenia in patients with hepatitis B virus-related chronic hepatitis: Evaluation of the immature platelet fraction

Abstract

The immature platelet fraction (IPF) measures the number of reticulated platelets in peripheral blood, and can be used to help determine if thrombocytopenia is secondary to low-platelet production or increased platelet turnover. The aim of this study was to determine whether abnormalities in the IPF were associated with thrombocytopenia in patients with hepatitis B virus-related chronic hepatitis (CHB). One hundred fifty-six patients with chronic hepatitis B, including 80 thrombocytopenia, 76 without thrombocytopenia, and 48 healthy controls were enrolled in the study. The IPF percentages (IPF%) were measured using a XE-2100 multiparameter automatic hematology analyzer. We demonstrated that in the thrombocytopenic group, the IPF% was significantly increased compared with that in healthy controls and the non-thrombocytopenic group (both p < 0.001). Multivariate analysis demonstrated that IPF%, splenomegaly, and the model for end-stage liver disease score were independent predictors for thrombocytopenia (both p < 0.001). High IPF% during the course of thrombocytopenia suggests that platelet destruction/sequestration due to hypersplenism is a major factor contributing to thrombocytopenia in patients with CHB.

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“…The immature platelet fraction (IPF) is routinely reported as percentage of the total platelet count (%IPF) or for research purpose also as absolute numbers (a‐IPF), indicating the degree of destruction and production of platelets, respectively . Alterations in %IPF or a‐IPF have been reported in bacterial and viral infections . In contrast, increments in IG have only been reported in bacterial infections and, to the best of our knowledge, have not been studied in viral infections, and as such also not in studies comparing viral and bacterial infections.…”

Clinical applicability of reticulated platelets

“…Interferon therapy for hepatitis may also induce thrombocytopenia and finding which can justify suspension of antiviral therapy. Mechanisms of thrombocytopenia vary and some have multiple causes [34]. A new thrombopoietin receptor agonist has recently been reported to increase platelet counts in hepatitis C virus related cirrhosis, thereby allowing a subset of untreatable patients to receive antiviral therapy.…”

Platelet interactions with viruses and parasites

“…Adenovirus Type 3 enhanced ADPinduced platelet activation [58]. Enhanced platelet activation and sequestration was found with Hepatitis B infection [59]. Co-infection of influenza H1N1 and Staphylococcus aureus greatly increased the chances of developing DIC [60].…”