RESEARCH PAPER
Factors influencing serum chemerin and kallistatin concentrations in patients with alcohol-induced liver cirrhosis
 
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1
Department of Internal Medicine, Medical University, Lublin, Poland
2
Department of Experimental Haematooncology, Medical University, Lublin, Poland
3
Department of Medical Chemistry, Medical University, Lublin, Poland
4
Department of Ethics and Human Philosophy, Medical University, Lublin, Poland
5
Independent Public Teaching Hospital No. 4, Lublin, Poland
6
Students’ Scientic Society, Medical University, Lublin, Poland
7
Department of Internal Diseases and Hypertension, Institute of Rural Health, Lublin, Poland
8
Department of Nephrology, Medical University, Lublin, Poland
 
KEYWORDS:
TOPICS:
ABSTRACT:
Introduction:
In Poland, an increasing number of patients are hospitalized due to liver diseases. One of the common liver diseases is cirrhosis, which can be caused by alcohol, viral hepatitis, autoimmune processes and metabolic diseases.

Material and methods:
The study included 99 patients with alcoholic cirrhosis from the Lublin region of Eastern Poland. The control group consisted of 20 healthy individuals without liver disease who did not abuse alcohol. The concentrations of serum kallistatin and chemerin were determined using ELISA kits.

Objective:
The aim of the study is to evaluate serum levels of kallistatin and chemerin in patients with different stages of alcoholic liver cirrhosis.

Results:
The highest chemerin level was found in the control group – 182.6±80.4 ng/ml. In other stages of liver cirrhosis, the following levels were observed: 175.7±62.7 ng/ml in Child-Pugh stage A (Ch-P A), 150.2±59.7 ng/ml in Ch-P B and 110.3±73.6 ng/ml in Ch-P C. Significant differences in chemerin levels between controls and Ch-P C patients (p=0.01), as well as between the Ch-P A patients and Ch-P C patients (p=0.02), were demonstrated. The highest kallistatin level was demonstrated in the control group – 8.2±3.5 μg/ml. In other stages of liver cirrhosis, the following concentrations were found: 7.2±27 μg/ml in Ch-P A, 4.4±2.2 μg/ml in Ch-P B and 3.5±1.9 μg/ml in Ch-P C. Statistically significant differences were observed between controls and Ch-P B patients (p<0.001), controls and Ch-P C patients (p<0.001), Ch-P A and Ch-P B patients (p=0.01), as well as Ch-P A and Ch-P C patients (<0.001).

Conclusions:
The levels of chemerin and kallistatin decrease with progression of liver damage during alcoholic liver cirrhosis. The impairment of its synthetic function leads to reductions in levels of the adipokines studied.

CORRESPONDING AUTHOR:
Andrzej Prystupa   
Department of Internal Medicine, Medical University, Lublin, Poland
 
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