Afamin and adropin in patients with alcohol-induced liver cirrhosis
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Department of Internal Medicine, Medical University of Lublin, Lublin, Poland
Department of Experimental Hematooncology, Medical University of Lublin, Lublin, Poland
Department of Medical Chemistry, Medical University of Lublin, Lublin, Poland
Department of Ethics and Human Philosophy, Medical University of Lublin, Lublin, Poland
Independent Public Teaching Hospital No 4 in Lublin, Poland
Students' Scientific Society, Medical University of Lublin, Lublin, Poland
Department of Internal Diseases and Hypertension, Institute of Rural Medicine, Lublin, Poland
Department of Nephrology, Medical University of Lublin, Lublin, Poland
Corresponding author
Andrzej Prystupa   

Department of Internal Medicine, Medical University of Lublin, Lublin, Poland, Staszica, 20-950 Lublin, Poland
Ann Agric Environ Med. 2018;25(3):527-531
The aim of the study was to determine serum concentrations of afamin and adropin in patients with alcoholic liver cirrhosis and to define their correlation with the stage of disease. The study included 99 patients with alcoholic cirrhosis from the region of Lublin, (Eastern Poland). Liver cirrhosis was diagnosed based on clinical features, history of heavy alcohol consumption, laboratory tests and abdominal ultrasonography. The control group consisted of 20 healthy individuals without liver disease who did not abuse alcohol. The serum afamin and adropin concentrations were determined using ELISA kits. The concentration of afamin was found to be significantly lower in patients with compensated alcoholic liver cirrhosis, i.e. P-Ch B (85.1±40.6 μg/ml) and P-Ch C (56.4±32.3 μg/ml) individuals, compared to the control group (135.9±43.6 μg/ml); p-value was <0.01 and <0.001, respectively. As far as adropin is concerned, a reverse relationship was demonstrated: the highest concentration was found in patients with P-Ch C (11.7±5.7 ng/ml) cirrhosis. Furthermore, the above concentration was significantly higher compared to patients with P-Ch A cirrhosis (7.2±2.8 ng/ml; p<0.05) and controls (7.5±2.6 ng/ml; p<0.05). The concentration of afamin decreases with the severity of alcoholic liver cirrhosis, which most likely results from impaired hepatic synthesis. Otherwise, the higher the stage of disease according to the Child-Pugh score, the higher the concentration of adropin.
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