Mechanism-oriented Bioregulatory Therapy in Compensated

Chronic hepatitis C virus (HCV) infection remains one of the leading causes of progressive hepaticfibrosis and cirrhosis, despite the high efficacy of direct-acting antiviral (DAA) agents. However, inclinical practice, certain patients are compelled to discontinue antiviral therapy due to severe drugintolerance. In such circumstances, persistent viral replication continues to drive the inflammatory,mitochondrial, and metabolic mechanisms underlying fibrogenesis.A 12-month prospective clinical observation is presented of a 46-year-old patient with chronic hepatitisC (genotype 1a) and compensated liver cirrhosis (Child–Pugh class A) who discontinued DAA therapyafter 7 days due to pronounced systemic adverse reactions. The objective of the observation was toevaluate the longitudinal dynamics of biochemical, structural, and metabolic parameters in the contextof persistent viremia during the administration of structured mechanism-oriented bioregulatory therapy.After 12 months, liver stiffness decreased from 12.4 to 8.6 kPa (–30.6%). Alanine aminotransferase(ALT) levels declined by 50.6%, C-reactive protein decreased by 96.6%, and serum albumin increasedby 36.6%. Total bilirubin levels were reduced by 60.4%, and the APRI index decreased by 51.6%.Regression of hepatic steatosis from stage S2 to S1 was also observed. HCV RNA remained detectablethroughout the entire observation period.The concordant dynamics of inflammatory, metabolic, synthetic, and noninvasive structural parametersin the presence of persistent viremia suggest that mechanism-oriented bioregulatory therapy may beconsidered a potential supportive pathogenetic approach in patients in whom antiviral treatment is notfeasible.