State of endogenous intoxication and immune-inflammatory response in patients with alcoholic liver cirrhosis associated with non-alcoholic fatty liver disease

N.R. Matkovska, N.H. Virstiuk, U.V. Balan


Background. The purpose was to evaluate the state of endogenous intoxication and immune-inflammatory response in patients with alcoholic liver cirrhosis (ALC) associated with non-alcoholic fatty liver disease (NAFLD), depending on the stage of decompensation. Materials and methods. The study included 204 patients. Among them, 78 patients were diagnosed with alcoholic liver disease at the stage of liver cirrhosis (group I) and 126 patients had a combination of ALC and NAFLD (group II). General-clinical and instrumental examinations were performed. The leukocyte index of intoxication (LII), sorption capacity of erythrocytes (SCE), levels of resistin, highly sensitive C-reactive protein (hs-CRP) and tumor necrosis factor α (TNFα) in the blood were determined. Results. Patients with a combination of ALC and NAFLD had a more severe clinical picture with the development of astheno-vegetative, pain, dyspeptic, hepatorenal, hepatopulmonary syndromes, jaundice, portal hypertension, liver encephalopathy. Among severe infectious complications, pneumonia and spontaneous bacterial peritonitis were more common in persons with subcompensation and decompensation. In all patients, SCE, LII, TNFα, hs-CRP and resistin levels increased with increasing decompensation of the disease. Higher SCE, LII, TNFα, hs-CRP and resistin levels were observed in patients with ALC associated with NAFLD due to a more severe course of the pathological condition. Positive correlations were found between resistin level and TNFα, hs-CRP, SCE, and LII. Conclusions. Analyzing the results of the study, it was found that with an increase in ALC decompensation, the degree of endogenous intoxication, which is accompanied by the development of immune-inflammatory response, is increasing, as evidenced by elevated SCE, LII, TNFα, hs-CRP, and resistin levels. Significantly higher SCE, LII, TNFα, hs-CRP, and resistin levels were detected in patients with a combination of ALCs and NAFLD accompanied by a more severe course of the disease. In patients with ALC associated with NAFLD, correlation between the resistin level and SCE, LII, TNFα, hs-CRP was found.


alcoholic liver disease; non-alcoholic fatty liver disease; liver cirrhosis; endogenous intoxication; immune-inflammatory response

Full Text:



Allen AM, Kim WR. Epidemiology and Healthcare Burden of Acute-on-Chronic Liver Failure. Semin Liver Dis. 2016 May;36(2):123-6. doi: 10.1055/s-0036-1583201.

Bekaert M, Verhelst X, Geerts A, Lapauw B, Calders P. Association of recently described adipokines with liver histology in biopsy-proven non-alcoholic fatty liver disease: a systematic review. Obes Rev. 2016 Jan;17(1):68-80. doi: 10.1111/obr.12333.

Aller R, Burgueño Gomez B, Sigüenza R, et al. Comparative study of overweight and obese patients with nonalcoholic fatty liver disease. Rev Esp Enferm Dig. 2019 Apr;111(4):256-263. doi: 10.17235/reed.2019.5926/2018.

Fazel Y, Koenig AB, Sayiner M, et al. Epidemiology and natural history of non-alcoholic fatty liver disease. Metabolism. 2016 Aug;65(8):1017-25. doi: 10.1016/j.metabol.2016.01.012.

Kim D, Kim WR. Nonobese fatty liver disease. Clin Gastroenterol Hepatol. 2017 Apr;15(4):474-485. doi: 10.1016/j.cgh.2016.08.028.

Coelho M, Oliveira T, Fernandes R. Biochemistry of adipose tissue: an endocrine organ. Arch Med Sci. 2013 Apr 20;9(2):191-200. doi: 10.5114/aoms.2013.33181.

Panera N, Della Corte C, Crudele A, Stronati L, Nobili V, Alisi A. Recent advances in understanding the role of adipocytokines during non-alcoholic fatty liver disease pathogenesis and their link with hepatokines. Expert Rev Gastroenterol Hepatol. 2016;10(3):393-403. doi: 10.1586/17474124.2016.1110485.

Zhang Q, Wang Y, Liu Y,  et al. Effects of telmisartan on resistin expression in a rat model of nonalcoholic steatohepatitis and insulin resistance. Zhonghua Gan Zang Bing Za Zhi. 2015 Apr;23(4):281-5. doi: 10.3760/cma.j.issn.1007-3418.2015.04.010.

Bedossa P. Pathology of non-alcoholic fatty liver disease. Liver Int. 2017;37 Suppl 1:85-89. doi: 10.1111/liv.13301.

Garbuzenko D, Arefyev N, Kazachkov E. Antiangiogenic therapy for portal hypertension in liver cirrhosis: Current progress and perspectives. World J Gastroenterol. 2018 Sep 7;24(33):3738-3748. doi: 10.3748/wjg.v24.i33.3738.

Kasztelan-Szczerbinska B, Surdacka A, Slomka M, et al. Association of Serum Adiponectin, Leptin, and Resistin Concentrations with the Severity of Liver Dysfunction and the Disease Complications in Alcoholic Liver Disease. Mediators Inflamm. 2013;2013:148526. doi: 10.1155/2013/148526.

Ayeser T, Basak M, Arslan K, Sayan I. Investigating the correlation of the number of diagnostic criteria to serum adiponectin, leptin, resistin, TNF-alpha, EGFR levels and abdominal adipose tissue. Diabetes Metab Syndr. 2016 Apr-Jun;10(2 Suppl 1): 165-9. doi: 10.1016/j.dsx.2016.03.010.

Fukui H, Saito H, Ueno Y, et al. Evidence-based clinical practice guidelines for liver cirrhosis 2015. J Gastroenterol. 2016 Jul;51(7):629-50. doi: 10.1007/s00535-016-1216-y.

Hadizadeh F, Faghihimani E, Adibi P. Nonalcoholic fatty liver disease: diagnostic biomarkers. World J Gastrointest Pathophysiol. 2017;8(2):11-26. doi: 10.4291/wjgp.v8.i2.11.

European Association for the Study of the Liver (EASL); European Association for the Study of Diabetes (EASD); European Association for the Study of Obesity (EASO). EASL–EASD–EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol. 2016 Jun;64(6):1388-402. doi: 10.1016/j.jhep.2015.11.004.

Kakizaki S, Sohara N, Yamazaki Y, et al. Elevated plasma resistin concentrations in patients with liver cirrhosis. J Gastroenterol Hepatol. 2008 Jan;23(1):73-7. doi: 10.1111/j.1440-1746.2006.04757.x.

Boutari C,  Perakakis N,  Mantzoros CS. Association of Adipokines with Development and Progression of Nonalcoholic Fatty Liver Disease. Endocrinol Metab (Seoul). 2018 Mar;33(1):33-43. doi: 10.3803/EnM.2018.33.1.33.

Trzeciak-Ryczek A, Tokarz-Deptuła B, Deptuła W. Adipocytokines affecting the immune system – selected data. Centr Eur J Immunol. 2011;36(2):92-94.

Musso G, Cassader M, De Michieli F, Paschetta E, Pinach S, Gambino R. et al. MERTK rs4374383 variant predicts incident nonalcoholic fatty liver disease and diabetes: role of mononuclear cell activation and adipokine response to dietary fat. Hum Mol Genet. 2017 May 1;26(9):1747-1758. doi: 10.1093/hmg/ddw400.

Kemmotsu Y, Saji T, Kusunoki N, et al. Serum adipokine profiles in Kawasaki disease. Mod Rheumatol. 2012 Feb;22(1):66-72. doi: 10.1007/s10165-011-0468-x.

Tanaka N, Masuoka S, Kusunoki N, Nanki T, Kawai S. Serum Resistin Level and Progression of Atherosclerosis during Glucocorticoid Therapy for Systemic Autoimmune Diseases. Metabolites. 2016 Sep 16;6(3). pii: E28. doi: 10.3390/metabo6030028.

Yoshino T, Kusunoki N, Tanaka N, Kaneko K, Kusunoki Y, Endo H. Elevated serum levels of resistin, leptin, and adiponectin are associated with C-reactive protein and also other clinical conditions in rheumatoid arthritis. Intern Med. 2011;50(4):269-75.

Su CM, Huang CY, Tang CH. Characteristics of resistin in rheumatoid arthritis angiogenesis. Biomark Med. 2016 Jun;10(6):651-60. doi: 10.2217/bmm.15.125.

Shen Ch, Zhao CY, Wang W, et al. The relationship between hepatic resistin overexpression and inflammation in patients with nonalcoholic steatohepatitis. BMC Gastroenterol. 2014 Feb 23;14:39. doi: 10.1186/1471-230X-14-39.

Copyright (c) 2019 GASTROENTEROLOGY

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.


© Publishing House Zaslavsky, 1997-2020


   Seo анализ сайта