CLINICAL AND IMMUNOGENETIC FOUNDATIONS FOR EARLY PREDICTION OF DECOMPENSATION PHENOTYPES IN LIVER CIRRHOSIS OF DIFFERENT ETIOLOGIES

Boburjon Abduqoxxorovich Rasulov

Assistant, Department of Pharmacology, Clinical Pharmacology and Medical Biotechnologies, Andijan State Medical Institute, Andijan, Uzbekistan

Jasurbek Ravzatov

PhD, Associate Professor, Department of Family Physician Training, Andijan State Medical Institute, Andijan, Uzbekistan

Keywords: liver cirrhosis, decompensation phenotypes, ascites, variceal bleeding, spontaneous bacterial peritonitis, hepatic encephalopathy, IL-23R, IL-17A, IL-17F, IL-6, clinical-genetic prognosis.


Abstract

Liver cirrhosis remains one of the leading causes of disability and mortality worldwide, including in Uzbekistan. The clinical severity of cirrhosis is determined not merely by the presence of cirrhotic transformation itself, but also by the development of decompensation phenotypes, including ascites, bleeding from esophageal varices, spontaneous bacterial peritonitis, and hepatic encephalopathy. In recent years, increasing attention has been paid to the role of the Th17/IL-23/IL-17 inflammatory axis and the IL-6 cascade in the pathogenesis of cirrhosis, particularly in relation to fibrosis progression, portal hypertension, disruption of the gut-liver immune axis, and infectious complications. This review systematically analyzes the role of clinical, immunological, and genetic factors in the early prediction of decompensation phenotypes in liver cirrhosis of different etiologies. Particular attention is given to the association of IL-23R, IL-17A, IL-17F, and IL-6 gene polymorphisms with disease course, decompensation phenotypes, and clinical-biochemical parameters. In addition, the scientific and practical prospects of integrating clinical-genetic risk stratification alongside conventional tools such as the Child-Pugh score are discussed.


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