Role of tissue molecular pathogens in development of acute chronic liver failure in alcoholic liver cirrhosis

Abstract

The aim of the study was to assess the pathogenetic, diagnostic and clinical role of tissue molecular pathogens – fragments of cytokeratin-18 in the development of acute chronic liver failure (ACLF) in decompensated alcoholic liver cirrhosis (ALC).Materials and methods. 80 patients with ALC were examined: 30 without signs of ACLF and 50 with signs of ACLF and 36 healthy individuals. Hepatic functional tests were determined, a marker of hepatocyte apoptosis – fragments of cytokeratin-18 (FCK-18) (Biotech, Sweden) by the enzyme immunoassay, ACLF scores were calculated using an on-line calculator at www.efclif.com/scientific-activity/score-calculators/ clif-c-aclf.Results. With ACLF, a high level of FCK-18 was detected – 1505.4 ± 446.9 U/L, more than 20 times higher than that in healthy individuals – 71.5 ± 19.6 U/L (p < 0.05) and three times higher than the level of FCK-18 in patients with ALC without ACLF – 489.4 ± 490.2 U/L. The levels of aminotransferases, bilirubin, creatinine, INR were significantly higher in patients with ACLF compared with patients without ACLF, and the level of albumin was lower. FCK-18 level directly correlated with ALT – r = 0.61 (p < 0.05), AST – r = 0.68 (p < 0.05), with bilirubin level – r = 0.41 (p < 0, 05) and the ACLF score – r = 0.48 (p < 0.05) and inversely correlated with the albumin level r = –0.51 (p < 0.05).Conclusion. Apoptosis of hepatocytes and tissue molecular pathogens released during it – fragments of cytokeratin-18 – play a role in the development of acute chronic liver failure in decompensated alcoholic liver cirrhosis.