Abstract

According to the literature, alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) aretwo hepatic diseases with similar pathogenetic mechanisms of the development, progression and histologicalcharacteristics. Both ALD and NAFLD are associated with a lipid metabolism disorder and a disorder of thesynthesis of adipokines. Adiponectin, leptin and resistin are the most described adipokines whose role in thedevelopment and progression of diseases accompanied by lipid disorders is ambiguous and is still the subjectof scientific research. The purpose of the research was to study the changes in adipocytokines in patients withalcoholic liver cirrhosis (ALC) associated with NAFLD depending on the stage of decompensation. The study included 204 patients. Among them, 78 patients (Gr. I) had ALC and 126 patients (Gr. II) had a combination of ALCwith NAFLD. Patients were subgrouped according to compensation classes by the Child-Pugh score (A, B, C).With the progression of the liver cirrhosis the level of leptin decreased, while the levels of adiponectin andresistin increased. The higher content of leptin in patients of classes A and B is accompanied not only by theimpaired liver function, but also by its increased release from adipose tissue. In patients of class C fat depot isexhausted, therefore the level of leptin decreases. Moreover, this decrease correlates with the severity of thedisease and the prognostic MELD score. The level of adiponectin was lowered in class A patients and increasedin patients with more severe course and correlated with severity of the disease and MELD score. The level ofresistin was increased in proportion to the deterioration of the liver function and correlated with the Child-Pughscore and the MELD score. The revealed correlation between the levels of resistin, leptin and adiponectin withthe degree of severity of the liver cirrhosis and the prognostic MELD score allows considering their changes forassessment of the severity of the liver cirrhosis and predicting the course of the disease.

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