THE CONTENT OF SERUM CYTOTOXINS UNDER LIVER CIRRHOSIS OF VIRAL ETIOLOGY AT VARIOUS STAGES OF COMPENSATION

Abstract

The study was implemented concerning the level of interleukins 2 and 6 (IL-2 and IL-6), tumor necrosis factor alpha (TNF-α) under hepatic cirrhosis (HC) of viral etiology classes А, В, С according Child-Pugh. The purpose was to evaluate level of serum cytokinemies and their relationship under HC of viral etiology depending on class of severity according Child-Pugh and level of portal pressure. The cytokines concentration was determined using technique of solid-phase enzyme-linked immunosorbent assay. It is established that against the background of decreasing of compensation of HC occurs increasing of serum level of IL-2, IL-6 and TNF-α within the limits of reference values at the exception of level of IL-6 under HC class C. In the given category of patients, level of IL-6 exceeds reference values and is within the limits of 9,94-25,21 pg ̸ml with average concentration 14,89±4,96 pg ̸ml. It is demonstrated that quantitative ratios and degrees of relationships between cytokines are determined by compensation of cirrhosis. The correlation relationships are mostly expressed in the form of feedback between TNF-α and IL-6 (r = 0,499) in case of HC class A. and in the form of direct relation between TNF-α and IL-2 (r = 0,421) in case of HC class B. It is proved that against the background of decreasing of compensation of HC increasing is occurring of serum levels of IL-2, IL-6 and TNF-α within the limits of reference values with the exception of level of IL-6 in case of HC class C. In the given category of patients’ level of IL-6 exceeds reference values and is within limits of 9,94-25,21 pg/ml with average concentration 14,89 4,96 pg/ml.

Keywords

interleukin-2 / interleukin-6 / tumor necrosis factor alpha / hepatic cirrhosis

References

[1] Назыров Ф.Г., Девятов А.В., Бабаджанов А.Х., Раимов С.А. Особенности развития и течения осложнений цирроза печени в зависимости от этиологического фактора. Новости хирургии. 2013; 21(4): 45-50.

[2] Голованова Е.В. Механизмы фиброзообразования при хронических заболеваниях печени и возможности антифибротической терапии. Consilium medicum. 2014; 16(8): 52-9.

[3] Ивашкин В.Т. Резистентный асцит у больных циррозами печени. М.: Медицина; 2013.

[4] Iwakir Y., Groszmann R.J. The hyperdynamic circulation of chronic liver diseases: from the patient to the molecule. Hepatology. 2006; 43(2 Suppl. 1): S121-31.

[5] Giannitrapani L., Soresi М., Balasus D., Licata A., Montalto G. Genetic association of interleukin-6 polymorphism (-174 G/C) with chronic liver diseases and hepatocellular carcinoma. World J. Gastroenterol. 2013; 19(16): 2449-55.

[6] Osawa Y., Hoshi M., Yasuda I. Tumor necrosis factor-α promotes cholestasis-induced liver fibrosis in the mouse through tissue inhibitor of metalloproteinase-1 production in hepatic stellate cells. PloS One. 2013; 8(6): 65251-62.

[7] Handa P., Kowdley K.V. Chemokines: potent mediators of hepatic inflammation and fibrosis in chronic liver diseases. Ann. Hepatol. 2014; 13(1): 152-4.

[8] Филиппова Л.П., Белобородова Э.И., Белобородова Е.В., Алексеева А.С. Качество жизни больных циррозом печени в зависимости от тонуса вегетативной нервной системы. Бюллетень сибирской медицины. 2012; 11(4): 152-7.

[9] Яковенко Э.П., Яковенко А.В., Каграманова А.В. Современные подходы к терапии больных цирроз печени. Фарматека. 2012; (13): 88-93.

[10] Chen T.A., Sao C., Chen К., Lo G.H., Lin C.K., Yu H.C. et al. Effect of intravenous albumin on endotoxin removal, cytokines, and nitric oxide production in patients with cirrhosis and spontaneous bacterial peritonitis. Scand. J. Gastroenterol. 2009; 44(5): 619-25.

[11] Fuster D., Tsui J.I., Cheng D.M., Quinn E.K., Armah K.A., Nunes D. et al. Interleukin-6 is associated with noninvasive markers of liver fibrosis in HIV-infected patients with alcohol problems. AIDS Res. Hum. Retroviruses. 2013; 29(8): 1110-6.

[12] Мироджанов Г.К., Авезов С.А., Гиясов М.М., Абдуллаева З.М. Интерлейкин-6 и оксид азота в патогенезе портальной гипертензии и декомпенсации цирроза печени. Клиническая медицина. 2012; 90(1): 47-53.

[13] Li S., Huang X., Zhong H., Chen Z., Peng Q., Deng Y. et al. Tumour necrosis factor alpha (TNF-α) genetic polymorphisms and the risk of autoimmune liver disease: a meta-analysis. J. Genet. 2013; 92(3): 617-28.

[14] Lisman T., Porte R.J. Rebalanced hemostasis in patients with liver disease: evidence and clinical consequences. Blood. 2010; 116(6): 878-85.

RIGHTS & PERMISSIONS

Eco-Vector