English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

With the global growth of obesity, fatty liver, which is characteristic to alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD), becomes one of the most common among hepatic pathological changes throughout the world. Both ALD and NAFLD are associated with a lipid metabolism disorder. There are three main sources of excessive accumulation of lipids in the liver: increased lipolysis of visceral adipose tissue, accompanied by excessive intake of free fatty acids (FFA) from adipose tissue (59%), activation of de novo liver lipogenesis (26%) and high calorie and/or fat content in the diet (15%). Excessive input of FFA in adipose tissue leads to “overloading” of fat cells that are no longer able to contain such an amount of FFA and the accumulation of fat in other tissues of the body that is not adapted for such function – in the liver, pancreas, muscles, etc. Such ectopia and large amount of FFA in the body result in a decrease in insulin sensitivity and the development of lipotoxicity. The consequence of these processes is a disorder of the synthesis of adipokines. The purpose of the research was to study the changes of lipids in patients with alcoholic 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 ALC with NAFLD. Patients were subgrouped according to compensation classes by the Child-Pugh score (A, B, C). Diagnosis was verified using clinical and laboratory-instrumental methods in accordance with the order of the Ministry of Health of Ukraine No. 826 dated November 6, 2014, adapted clinical guidelines "Non-Alcoholic Fatty Liver Disease", 2014, adapted clinical guidelines "Alcoholic Liver Disease", 2014, adapted clinical guidelines " Liver Cirrhosis, 2017 (State Expert Centre of the Ministry of Health of Ukraine, Ukrainian Gastroenterology Association, Kyiv), recommendations of the European Association for the Study of Liver, Diabetes and Obesity (EASL-EASD-EASO, 2016). Higher levels of total cholesterol, lipoprotein cholesterol of low and very low density, atherogenic coefficient and triacylglycerides were in patients of classes A and B. Patients of group II had higher rates than those in group I (p<0.05). The content of lipoprotein cholesterol of high density in patients of group II was significantly lower in comparison with patients in group I (p<0.05). With the progression of the liver cirrhosis the level of leptin decreased, while the levels of adiponectin increased. The higher content of leptin in patients of classes A and B is accompanied not only by the impaired liver function, but also by its increased release from adipose tissue. In patients of class C fat depot is exhausted, therefore the level of leptin decreases. Moreover, this decrease correlates with the severity of the disease and the prognostic MELD score. The level of adiponectin was lowered in class A patients and increased in patients with more severe course and correlated with severity of the disease and MELD score. The revealed correlation between the levels of leptin and adiponectin with the degree of severity of the liver cirrhosis and the prognostic MELD score allows considering their changes for assessment of the severity of the liver cirrhosis and predicting the course of the disease.

CHANGES IN LIPIDS IN PATIENTS WITH ALCOHOLIC CIRRHOSIS OF THE LIVER ASSOCIATED WITH NON-ALCOHOLIC FATTY LIVER DISEASE DEPENDING ON THE STAGE OF DECOMPENSATION