Stages of Anemia Development in Viral Hepatitis C

Abstract

In the pathogenesis of chronic viral hepatitis C (CVHC), the impairment of the hematopoietic system, particularly the formation of anemic syndrome, constitutes one of the most prevalent and severe extrahepatic complications. Throughout the progression of the disease, the disruption of erythropoiesis does not occur stochastically but evolves through systemic stages governed by strict molecular and hemodynamic principles. This study aims to evaluate the pathophysiological transformation of the erythroid lineage in patients with CVHC and to classify the stages of anemia development using precise clinico-laboratory criteria. Within a prospective clinico-laboratory monitoring framework, the hematological, biochemical, and immunochemical parameters of 210 patients diagnosed with viral hepatitis C (encompassing fibrosis stages F1 to F4) were comprehensively analyzed over an 18-month period. Multivariate dispersion and correlational modeling outcomes demonstrated that the pathogenetic progression of anemia encompasses three interrelated stages. In the initial stage (F1-F2), an "iron blockade" predominates, driven by a profound elevation in serum hepcidin levels (54.6 ± 11.2 ng/mL), thereby inducing functional iron deficiency. The second stage (F3) is characterized by hypersplenic activation and erythrocyte sequestration secondary to portal hypertension, presenting synchronously with thrombocytopenia and reticulocytosis (3.1 ± 0.5%). The third terminal stage (F4, cirrhosis) is defined by the cessation of endogenous erythropoietin (EPO) synthesis (14.2 ± 3.8 mIU/mL) resulting from hepatorenal axis degradation, and the absolute suppression of bone marrow erythroid reserves (soluble transferrin receptors – sTfR > 4.5 mg/L). The integral dynamic profiling of molecular markers such as serum hepcidin, sTfR, and EPO (AUC = 0.914) serves as a highly accurate objective laboratory substrate for early differentiation of anemia etiology, anticipation of complications, and correct personalization of antianemic interventions (transfusions, EPO stimulating agents, or iron chelators).