Clinical-Immunogenetic Basis of Early Prediction of Decompensation Phenotypes in Liver Cirrhosis of Various Etiologies
Keywords:
liver cirrhosis, decompensation phenotypes, ascites, variceal bleedingAbstract
Liver cirrhosis remains one of the leading causes of disability and mortality worldwide, including in Uzbekistan. The clinical severity of the disease is often determined not only by the presence of cirrhosis, but also by the development of its decompensation phenotypes, in particular, complications such as ascites, esophageal variceal bleeding, spontaneous bacterial peritonitis, and hepatic encephalopathy. In recent years, scientific views on the Th17/IL-23/IL-17 inflammatory pathway and the IL-6 cascade in the pathogenesis of liver cirrhosis have been expanding, with the deepening of liver fibrosis, portal hypertension, disruption of the gut-hepatic immune axis, and infectious complications. This article systematically analyzes the role of clinical, immunological, and genetic factors in the early prediction of decompensation phenotypes in liver cirrhosis of various etiologies. The relationship of IL-23R, IL-17A, IL-17F, and IL-6 gene polymorphisms with the course of the disease, decompensation phenotypes, and clinical and biochemical indicators was highlighted. The scientific and practical prospects for the introduction of clinical and genetic risk stratification, along with traditional criteria such as Child–Pugh, are also shown.
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