The Relationship Between Iron Metabolism and Erythrocytic Indices in Chronic Hepatitis B

Abstract

Chronic hepatitis B (CHB) viral infection is a severe pathological process that, alongside initiating a cascade of cholestasis and necrosis within hepatic parenchymal cells, precipitates a systemic dysbalance in iron metabolism. The release of excess iron into the bloodstream consequent to hepatocellular destruction and the impairment of hepcidin regulation exert a direct influence on the erythropoietic system, specifically on the morphometric parameters of erythrocytes. This study aims to quantitatively evaluate the pathogenetic correlation between markers of iron homeostasis (ferritin, serum iron, transferrin, hepcidin) and erythrocytic indices (MCV, MCH, RDW) across varying clinical phases and fibrosis stages of CHB. Utilizing a prospective clinico-laboratory design, the blood parameters of 175 patients diagnosed with CHB were subjected to in-depth analysis over a 12-month period. Dispersion and multivariate regression models confirmed that high viral replication activity (HBV DNA > 2000 IU/mL) and advanced hepatic fibrosis (F3-F4) provoke a pathological, nearly 3.5-fold elevation in serum ferritin levels (reaching 542.4 ± 86.5 ng/mL). Against the backdrop of this hepatocellular iron overload, the red blood cell distribution width (RDW) expanded precipitously from a baseline of 12.5% to 17.8 ± 1.2% (anisocytosis). The decline in serum hepcidin attributable to progressive liver failure (< 10.5 ng/mL) creates a substrate for the proliferation of circulating free iron radicals and the oxidative degradation of erythrocyte membranes. The integral monitoring of ferritin and RDW indices within a unified diagnostic panel (AUC = 0.885) equips clinical practitioners with a highly sensitive modality to predict hepatic inflammatory activity, tissue hypoxia, and fibrotic risk without resorting to invasive biopsy procedures.