European Journal of Molecular & Clinical Medicine

Background:Kallistatin is a glycoprotein found in human plasma. Kallistatin is mostly generated by the liver, with minor quantities made by the kidney, pancreas, heart, lung, and colon. In the tissue kallikrein – kinin system, kallistatin acts as a balancing agent. Kinins, kininogens, and kallikrein, kallistatin, and bradykinin receptors are all part of this system. When compensated disease sets in, kallistatin can be employed as a critical biomarker in detecting alcoholic liver disease early. In the early stages of liver disease, it is normally quiet and asymptomatic, but as it progresses to the symptomatic decompensated stage, it can cause serious consequences. The patient's prognosis is dismal, with portosystemic encephalopathy, variceael haemorrhage, and hepatocellular cancer. The  current study was done  to evaluate the use of Kallistatin  as a non-invasive marker in the diagnosis of alcoholic liver disease (ALD), and to compare serum Kallistatin  levels in alcoholic liver disease patients and healthy controls.
Materials and Methods: This study includes sixty patients with alcoholic liver disease (divided into two groups based on compensated and decompensated features) and thirty healthy controls. Total and direct bilirubin, AST, ALT, ALP, GGT, albumin, and serum Kallistatin concentrations were determined using a regular automated analyzer and Kallistatin  levels were analyzed using an Enzyme Linked Immunosorbent Assay. The t-test, Pearson Spearman rank correlation, Anova, and Receiver operating characteristic (ROC) Curve have been used to examine the data (SPSS version 16.0 software).
Results: ThemeanserumKallistatin levelswere(25.22 ±3.62µg/mL   ),(15.2 ±3.8 µg/mL )and(13± 3.3µg/mL  ) in Control group,compensatedgroup and decompensatedgroup .A statistically significant p value (p value 0.001) was obtained. As liver damage progresses, Kallistatin  levels decrease. In alcoholic liver disease patients, serum levels of AST, ALT, ALP, and GGT were increased, while albumin levels decreased, which was statistically significant. SerumKallistatin and albumin levels have a significant positive correlation (p= 0.05), while Serum Kallistatin and GGT levels have a significant negative correlation (p= 0.05). For Kallistatin , ANOVA revealed a statistically significant p value of 0.001 and a ROC with optimal cut off value of 0.922.
Conclusion: SerumKallistatin levelscanplay avitalandprotectivevariableinpreventingalcoholicliverdisease. This study leads a pathway for therapeuticinterventionto be started earlieron the basisofserumKalli statinlevels.Estimationofserum Kallistatin levelscanbeaddedinroutineinvestigationsforliverfunctiontestsin patientswithalcoholicliverdisease