The Role of a Complex of Non-Invasive Laboratory Tests in the Early Detection of Hepatocellular Failure in Viral Etiology Liver Cirrhosis

Abstract

Liver cirrhosis resulting from chronic viral hepatitides (HBV, HCV, HDV) constitutes a severe clinical pathology characterized by the irreversible depletion of hepatocyte mass, fibrotic tissue replacement, and portal hypertension. The early prognosis of the transition from a compensated stage to decompensation (hepatocellular failure) remains one of the most formidable challenges in practical hepatology. This study aims to analyze the prognostic value of a non-invasive laboratory marker complex—albumin, prothrombin time (INR), bilirubin, and blood formed elements—in the integral assessment of hepatic synthetic, excretory, and hemodynamic functions. Utilizing a prospective observational design, the clinico-laboratory parameters of 142 patients diagnosed with viral etiology liver cirrhosis (Child-Pugh Classes A and B) were monitored over an 18-month longitudinal period. Multivariate logistic regression and ROC curve analyses demonstrated that a decline in serum albumin below 34 g/L combined with an INR elevation above 1.3 served as the earliest reliable predictors of failing hepatocyte synthetic function (Sensitivity 88.4%, Specificity 82.1%). Furthermore, severe thrombocytopenia (< 85 x10^9/L) and leukopenia (< 3.0 x10^9/L), reflecting the extent of hypersplenism and intrahepatic shunting, when synchronized with hyperbilirubinemia, independently multiplied the risk of developing ascites and hepatic encephalopathy within 12 months by a factor of 4.2 (p < 0.001). In contrast to isolated laboratory tests, the integral evaluation of these four baseline parameters facilitates the highly accurate diagnosis of hepatocellular failure (AUC = 0.912) approximately 6 to 8 months prior to the manifestation of overt clinical symptoms. This non-invasive, cost-effective laboratory algorithm provides clinical practitioners with an objective substrate for the early stratification of high-risk patient phenotypes, optimizing timely targeted hepatoprotective and antiviral therapeutic interventions.