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.
Role of Liver Transplantation in Tolvaptan-Associated Acute Liver Failure
