Submission of the manuscript is online via e-mail
ecgarticle@gmail.com or
cholerez@mail.ru

Tel: +7 903 250 5288

Editorial Correspondence e-mail
gastrossr@gmail.com


Publishing, Subscriptions, Sales and Advertising, Correspondence e-mail
journal@cniig.ru

Tel: +7 917 561 9505

SCImago Journal & Country Rank

    1. Kharkiv National Medical University (Kharkiv, Ukraine)

    Keywords:Non-alcoholic fatty liver disease,obesity,resistin

    Abstract:It were examined 70 patients with non-alcoholic fatty liver disease and its combination with obesity, as well as 20 healthy individuals. The study was carried out using the following methods: clinical, laboratory and instrumental (including liver biopsy). It was found an inverse relationship between the level of resistin and the levels of the indices of lipid metabolism in both groups of patients. There was established the significant increase of plasma level of resistin, and also impairment of lipid metabolism indices in all groups in comparison with the controls, and most pronounced changes in patients with NAFLD and obesity. The established relationships suggests that the increase resistin may represent the presence of dyslipidemia in patients with NAFLD and its combination with obesity. In order to determination the disorder of the lipid metabolism is recommended to determine the level of resistin in patients with NAFLD, especially in presence of obesity. Patients with the level of resistin (>8,06±0,23 ng/ml) should refer to the risk of progression of dyslipidemia.

      1. Kharchenko N.V. Non-alcoholic fatty liver disease: the therapeutic potential of L-carnitine. N.V. Kharchenko. Hepatology, theme number, 2017, p. 28.
      2. Khristich T.N. Significance of the hormones of visceral adipose tissue in the development of comorbidity of chronic pancreatitis and obesity. Bulletin of the club of pacreatologists, 2017, №3 (36), pp. 30-32.
      3. Chalasani N., Younossi Z., Lavine J. E. et al. The diagnosis and management of non-alcoholic fatty liver disease: practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association. Hepatology, 2012, Vol. 55, рр. 2005–2023.
      4. Codoner-Franch P, Alonso-Iglesias E. Resistin: insulin resistance to malignancy. Clin Chim Acta, 2015, Vol. 438, рр. 46–54.
      5. Costandi J, Melone M, Zhao A, Rashid S. Human resistin stimulates hepatic overproduction of atherogenic ApoB-containing lipoprotein particles by enhancing ApoB stability and impairing intracellular insulin signaling. Circ Res., 2011, Vol. 108, рр. 727–742.
      6. Dalamaga M. Resistin as a biomarker linking obesity and inflammation to cancer: potential clinical perspectives. Biomark Med., 2014, Vol. 8, № 1, рр. 107–118
      7. ЕASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol, 2016, http://dx.doi.org/10.1016/j.jhep.2015.11.004
      8. Huang X, Yang Z. Resistin’s, obesity and insulin resistance: the continuing disconnect between rodents and humans. J Endocrinol Invest, 2016, Vol. 39, рр. 607–615.
      9. Sahu A. Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance. Front Neuroendocrinol, 2003, Vol. 24, № 4, рр. 225–253.
      10. Ståi P. Liver fibrosis in non-alcoholic fatty liver disease – diagnostic challenge with prognostic significance. World J Gastroenterol, 2015, Vol.21(39), рр. 11077–110.
     


    Full text is published :
    THE INFLUENCE OF RESISTIN ON LIPID METABOLISM IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE IN PATIENTS WITH NORMAL BODY WEIGHT AND OBESITY. Experimental and Clinical Gastroenterology Journal. 2018;150(02):19-23
    Read & Download full text

    1. FSEBI of HE “The Ulianov Chuvash State University” (Cheboksary, Russian Federation)
    2. BI “City clinical hospital № 1” of the Ministry of Нealthcare of the Chuvash Republic (Cheboksary, Russian Federation)
    3. SAI SVE “The Postgraduaute Doctor' Training Institute” of the Ministry Healthcare of the Chuvash Republic (Cheboksary, Russian Federation)
    4. BI “Chuvash Republic clinical hospital“ of the Ministry of Нealthcare of the Chuvash Republic (Cheboksary, Russian Federation)

    Keywords:elastography,elastometry, shear wave, stiffness, liver, diffuse disease

    Abstract:The results of 128 people’s study (average age - 46,3 ± 2,5 years) was analyzed Non-invasive ultrasound techniques for the study of the liver were used: TE (or single-stage pulse elastometry) on Fibroscan unit (Echo-Sens, France) and ESA on Aixplorer unit (Supersonic Imagine, France) with Elastometry (frequency range of 1.6 MHz). Average value (Emean), the maximum value (Emax) and σ - standard deviation were taken into estimation. Emean according to TE in healthy individuals was 4,8 kP, in patients with chronic viral hepatitis - 7,2 kPa (n1); in patients with steatohepatitis - 9,1 kPa (n2); group with cirrhosis - 43,8 kPa (n3). ESP indicators were slightly higher than the TE and showed the following results for n1 group - 8,3 kPa; n2-9,4 kPa; n3-55,3 kPa (in the group - 4,6 kPa). Efficiency of ESP was more successful, reaching 100% (all the procedures have been completed successfully), compared with TE with 84.6%, which indicated a higher diagnostic value of ESP in the diagnosis of diffuse liver disease.

      1. Sherlock Sch, Dooley J. Diseases of the liver and biliary tract: A practical guide. Moscow: GEOTAR-MED, 2002. 864 p.
      2. Yakovenko E. P. Cirrhosis of the liver, clinical and pathogenetic aspects. / Yakovenko E. P., Yakovenko A. V. // Pharmateka. 201. – No. 13. – P. 32–36.
      3. Bataller R., Brenner D. A. Liver fibrosis. J. Clin. Invest. 2005; 115(2):209–218.
      4. Iredale J. P. Models of liver fi brosis: exploring the dynamic nature of inflammation and repair in a solid organ. J. Clin. Invest. 2007; 117(3):539–548.
      5. Parsons C. J, Takashima M., Rippe RA. Molecular mechanisms of hepatic fi brogenesis. J Gastroenterol Hepatol. 2007; 22(1):79–84.
      6. Bataller R., Brenner D. A. Liver fi brosis. J. Clin. Invest. 2005; 115(2):209–218.
      7. Pavlov Ch. S., Zolotarevsky VB, Tomkevich MS. Possibilities of reversibility of liver cirrhosis // Ross. Journal of Gastroenterology, Hepatology and Coloproctology. 2006. – No. 1. – P. 20–29.
      8. Severov MV. Reversibility of liver fibrosis and cirrhosis in HCV infection, Geopathologic Forum. 2008. – No. 1. – P. 2–6.
      9. Serum fibrosis markers predict future clinical decompensation in primary billiary cirrhosis better than liver biopsy, bilirubin or Mayo risk score / M. Mayo, J. Parks, B. Huet [et al.] // Hepatology. – 2006. – № 44. – P. 630.
      10. Ghany M. Assessment of liver fi brosis: palpate, poke or pulse? / M. Ghany, E. Doo // Hepatology. – 2005. – Vol. 42, № 4. – P. 759–761.
      11. Сhronic hepatitis C and liver fi brosis/ Giada Sebastiani, Konstantinos Gkouvatsos, Kostas Pantopoulos// World J Gastroenterol. 2014Aug 28; 20(32).
      12. Pavlov Ch. S., Glushenkov DV, Ivashkin VT. Modern possibilities of elastometry, fibro- and acti-test in the diagnosis of liver fibrosis. Ross. Journal of Gastroenterology, Hepatology and Coloproctology. 2008. – No. 4. – P. 43–52.
      13. Comparison of ELF, FibroTest and FibroScan for the non-invasive assessment of liver fi brosis (Сравнение ELF, FibroTest и FibroScan для неинвазивной оценки фиброза печени) / Mireen Friedrich-Rust, WilliamRosenberg, Julie Parkes et al. // BMC Gastroenterology 2010 10:103
      14. Diagnostic value of biochemical markers (FibroTest-FibroSURE) for the prediction of liver fi brosis in patients with non-alcoholic fatty liver disease / Vlad Ratziu, Julien Massard, Frederic Charlotte et al. // BMC Gastroenterology 2006 6:6.
      15. Sheptulina AF. Noninvasive diagnostics of liver fibrosis: the role of serum markers / Sheptulina AF, Shirokova Ye. N., Ivashkin VT // Roskine gastroenterol hepatol coloproctol 2015; 2: 28–40.
      16. Peregudov IV. Possibilities of ultrasound elastography and morphological study of blood serum in the diagnosis and prognosis of the clinical course of steatohepatitis of mixed nature: author’s abstract. Diss. … candidate of medical sciences. Smolensk, 2010.
      17. Ponnekanti H., Ophir J., Cespedes I. Axial stress distributions between coaxial compressors in elastography: an analytical model // Ultrasound Med. Biol. 1992. V.
      18. No. 8. P. 667–73. 18. Huako, SA, Elastography of a Shear Wave in the Diagnosis of Diffuse and Nodal Pathology in Myometrium. Diss. … candidate of medical sciences. 2012, Moscow.
      19. Mitkov VV, Vasilieva AK, Mitkova MD. Possibilities of Ultrasonic Elastography in the Diagnosis of Prostate Cancer, Ultrasonic and Functional Diagnostics. 2012. – No. 3. – p. 13–21.
      20. Diomidova VN, Petrova OV. Comparative analysis of the results of shear wave elastography and transient elastography in the diagnosis of diffuse liver diseases // Ultrasonic and functional diagnostics. 2013. № 5. p. 17–24.
      21. Eiler J, Kleinholdermann U, Albers D et al. Standard value of ultrasound elastography using acoustic radiation force impulse imaging (ARFI) in healthy liver tissue of children and adolescents // Ultraschall Med. 2012 Oct; 33(5):474–9.
      22. Marginean CO, Marginean C. Elastographic assessment of liver fi brosis in children: A prospective single center experience // Eur J Radiol. 2012 Aug;81(8): 870–4.
     


    Full text is published :
    MODERN POSSIBILITIES OF THE SEVERITY OF LIVER FIBROSIS. Experimental and Clinical Gastroenterology Journal. 2018;150(02):24-30
    Read & Download full text

    1. Institute of Biology of Karelian Research Centre Russian Academy of Sciences (Petrozavodsk, Russian Federation)
    2. Petrozavodsk State University, the Department of Internal Medicine Propaedeutics and hygiene (Petrozavodsk, Russian Federation)

    Keywords:nonalcoholic steatohepatitis (NASH),interleukin-6polymorphism,ursodeoxycholic acid (UDCA)

    Abstract:The aim was a comparative analysis of clinical and laboratory parameters in carriers of different genotypes for the -174G>C IL6 gene polymorphic marker (rs1800795) in healthy donors and patients with NASH in the absence of hepatoprotective therapy and after therapy with UDCA. There were examined 50 patients with the diagnosis of NASH. NASH patients were treated with UDCA at a dose of 10-15 mg/kg for 8-10 weeks. The control group consisted of 50 donors without the clinical manifestations of NAFLD. Genotyping was carried out using the PCR-RFLP method. Functional liver tests, the level of cytokines IL6 and TNFα in the blood, the level of expression of the IL6 and TNF genes, the activity of caspases in peripheral leukocytes were estimated before the treatment and after UDCA monotherapy. In NASH patients with different alleles for the -174G>C IL6 gene polymorphic marker, there are significant differences in the level of the indicator of hepatic cell damage - AST, and the mRNA level of the TNF gene in PBL. In carriers of C allele, the effect of UDCA therapy on the level of AST and the TNF gene transcripts in PBL is less pronounced than in carriers of the GG genotype. This indicates a lower sensitivity to UDCA therapy in carriers of the mutant allele. The medians of decrease in the AST level and in the level of mRNA relative expression of the TNF gene in carriers of C allele are significantly lower than in carriers of the GG genotype, p<0.05. Significant differences in the effect of UDCA therapy on the level of other studied parameters depending on the genotype were not found. The presence of the -174G>C single nucleotide substitution in the IL6 gene (rs1800795), which is associated with the development of NASH, can determine not only the genetic predisposition to the development of this disease, but also the different sensitivity of patients with NAFLD to UDCA-based drugs.

      1. Drapkina O. M., Deeva T. A., Volkova N. P., Ivashkin V. T. Current approaches to diagnosing and treating nonalcoholic fatty liver disease // Ter. Arkh. – 2014. – Vol. 86, № 10. – P. 116–123.
      2. Braunersreuther V., Viviani G. L., Mach F., Montecucco F. Role of cytokines and chemokines in non-alcoholic fatty liver disease // World J. Gastroenterol. – 2012. – Vol. 18, № 8. – P. 727–735.
      3. Cheng Y., An B., Jiang M. et al. Association of tumor necrosis factor-alpha polymorphisms and risk of coronary artery disease in patients with non-alcoholic fatty liver disease // Hepat. Mon. – 2015. – Vol. 15, № 3. – e26818.
      4. Cengiz M., Yasar D. G., Ergun M. A. et al. The role of interleukin-6 and interleukin-8 gene polymorphisms in non-alcoholic steatohepatitis // Hepat. Mon. – 2014. – Vol. 14, № 12. – e24635.
      5. Kurbatova I. V., Topchieva L. V., Dudanova O. P. Expression rates of the caspase 3, 6, 8 and 9 genes in peripheral blood leukocytes and the concentration of IL6 and TNFα in blood plasma of donors with different genotypes for the –174G>C IL6 gene polymorphic marker, associated with a risk of non-alcoholic steatohepatitis development // Bull. Exp. Biol. Med. – 2017. – Т. 162, № 3. – С. 370–374.
      6. Xiang Z., Chen Y. P., Ma K. F. et al. The role of ursodeoxycholic acid in non-alcoholic steatohepatitis: a systematic review // BMC Gastroenterol – 2013. – Vol. 13, № 140. – Online: http://www.biomedcentral.com/1471–230X/13/140.
      7. Brunt E. M., Janney C. G., Di Bisceglie A. M. et al. Nonalcoholic steatohepatitis: a proposal for grading and staging the histological lesions // Am. J. Gastroenterol. – 1999. – Vol. 94, № 9. – P. 2467–2474.
      8. Fernández-Real J. M., Broch M., Vendrell J. et al. Interleukin-6 gene polymorphism and lipid abnormalities in healthy subjects // J. Clin. Endocrinol. Metab. – 2000. – Vol. 85, № 3. – P. 1334–1339.
      9. Lindor K. D., Kowdley K. V., Heathcote E. J. et al. Ursodeoxycholic acid for treatment of nonalcoholic steatohepatitis: Results of a randomized trial // Hepatology. – 2004. – Vol. 39, № 3. – P. 770–778.
      10. Fishman D., Faulds G., Jeffery R. et al. The effect of novel polymorphisms in the interleukin-6 (IL-6) gene on IL-6 transcription and plasma IL-6 levels, and an association with systemic-onset juvenile chronic arthritis // J. Clin. Invest. – 1998. – Vol. 102, № 7. – P. 1369–1376.
      11. Giannitrapani L., Soresi M., Balasus D. et al. Genetic association of interleukin-6 polymorphism (–174 G/C) with chronic liver diseases and hepatocellular carcinoma // World J. Gastroenterol. – 2013. – Vol. 19, № 16. – P. 2449–2455.
      12. Noss E. H., Nguyen H. N., Chang S. K. et al. Genetic polymorphism directs IL-6 expression in fibroblasts but not selected other cell types // Proc. Natl. Acad. Sci. USA. – 2015. – Vol. 112, № 48. – P. 14948–14953.
      13. Ishizaki K., Iwaki T., Kinoshita S. et al. Ursodeoxycholic acid protects concanavalin A-induced mouse liver injury through inhibition of intrahepatic tumor necrosis factor-alpha and macrophage inflammatory protein-2 production // Eur. J. Pharmacol. – 2008. – Vol. 578, № 1. – P. 57–64.
      14. Xiang X., Vakkilainen J., Backman J. T. et al. No significant effect of the SLCO1B1 polymorphism on the pharmacokinetics of ursodeoxycholic acid // Eur. J. Clin. Pharmacol. – 2011. – Vol. 67, № 11. – P. 1159–1167.
      15. Chen R. R., Li Y. J., Zhou X. M. et al. The association between bile salt export pump single-nucleotide polymorphisms and primary biliary cirrhosis susceptibility and ursodeoxycholic acid response // Dis. Markers. – 2014. – ID350690. – Online: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4216684/
      16. Hu M., Fok B. S., Wo S. K. et al. Effect of common polymorphisms of the farnesoid X receptor and bile acid transporters on the pharmacokinetics of ursodeoxycholic acid // Clin. Exp. Pharmacol.Physiol. – 2016. – Vol. 43, № 1. – P. 34–40.
     


    Full text is published :
    -174g>c polymorphism (rs1800795) of il6 gene and its impact on the effectiveness of treatment with ursodeoxycholic acid in patients with nonalcoholic steatohepatitis. Experimental and Clinical Gastroenterology Journal. 2018;150(02):31-36
    Read & Download full text

    1. Kharkov Medical Academy of Postgraduate Education (Kharkiv, Ukraine)

    Keywords:non-alcoholic fatty liver disease,non-alcoholic steatohepatitis,L-carnitine,homocysteine,hyperhomocysteinemia

    Abstract:Examined 65 patients with verified NASH. The age of the patients ranged from 23 to 67 years. Among them were 36 (55.4%) women and 29 (44.6%) men. The control group consisted of 20 healthy individuals. The effectiveness of complex therapy with the inclusion of the drug L-carnitine, deproteinized hemoderivat of calves and folic acid was studied. The presence of carnitine insufficiency, hyperhomocysteinemia, increase in the level of proinflammatory cytokines in all patients with NASH. After a month of treatment with complex therapy, the level of L-carnitine increased from 14.5 (13.1, 15.7) μmol/l to 31.1 (28.8, 34.1) μmol/l (p<0.001), homocysteine decreased to subnormal figures - 11.8 (11.0, 12.8) μmol/l (p<0.001). When studying the cytokine profile in the group after treatment, a significant decrease in the level of proinflammatory cytokines was revealed. The use of complex therapy with the inclusion of drugs L-carnitine, deproteinized hemoderevate blood of calves as an antihypoxant and folic acid has a positive effect on the clinical course of the disease, contributes to the elimination of L-carnitine deficiency, hyperhomocysteinemia, a decrease in the level of pro-inflammatory cytokines.

      1. Kleiner D., Brunt E. Non-alcoholic fatty liver disease: pathologic patterns and biopsy evaluation in clinical research. Semin Liver Dis 2012; 32: 003–13.
      2. Musso G., Gambino R., Cassader M. Non-alcoholic fatty liver disease from pathogenesis to management: an update. Obesity Reviews 2010; 11: 6: 430-45.
      3. Lopaschuk G.D., Ussher J. R., Folmes C. D.L. et al. Myocardial fatty acid metabolism in health and disease. Physiol Rev 2010; 90: 1: 207-58.
      4. Noland R.C., Koves T. R., Seiler S. E. et al. Carnitine insufficiency caused by aging and overnutrition compromises mitochondrial performance and metabolic control. J Biol Chem 2009; 284: 34: 22840-52.
      5. Sharma Sh., Black St. M. Carnitine homeostasis, mitochondrial function, and cardiovascular disease. Drug Disc Today Dis Mech 2009; 6: 1-4: e31-e39.
      6. Indiveri C., Iacobazzi V., Tonazzi A. et al. The mitochondrial carnitine/acylcarnitine carrier: Function, structure and physiopathology. Mol Aspects Med 2011; 32: 4-6: 223-33.
      7. Lee K., Kerner J., Hoppel Ch. L. Mitochondrial camitinepalmitoyl-transferase 1a (CPT1a) is part of an outer membrane fatty acid transfer complex. J Biol Chem 2011; 286: 29: 25655-62.
      8. Li H., Ying H., Hu A. et al. Therapeutic Effect of Gypenosides on Nonalcoholic Steatohepatitis via Regulating Hepatic Lipogenesis and Fatty Acid Oxidation. Biol Pharm Bull. 2017; 40 (5): 650-57.
      9. Tonazzi A., Giangregorio N., Console L. et al. Nitric oxide inhibits the mitochondrial carnitine/acylcarnitine carrier through reversible S-nitrosylation of cysteine 136. Biochim Biophys Acta 2017; 1858 (7): 475-82.
      10. Tiniakos D.G., Vos M. B., Brunt E. M. Nonalcoholic fatty liver disease: pathology and pathogenesis. Annu Rev Pathol 2010; 5: 145-71.
      11. Polyzos S.A., Kountouras J., Zavos C. Curr Nonalcoholic fatty liver disease: the pathogenetic roles of insulin resistance and adipocytokines. Мol Med 2009; 9: 3: 299-314.
      12. Furuno T., Kanno T., Arita K. et al. Roles of long chain fatty acids and carnitine in mitochondrial membrane permeability transition. Biochem Pharmacol 2001; 62: 8: 1037-46.
      13. Oyanagi E., Yano H., Kato Y. et al. L-Carnitine suppresses oleic acid-induced membrane permeability transition of mitochondria. Cell Biochem Funct 2008; 26: 7: 778-86.
      14. Pillich R.T., Scarsella G., Risuleo G. Reduction of apoptosis through the mitochondrial pathway by the administration of acetyl-L-carnitine to mouse fibroblasts in culture. Exp Cell Res 2005; 306: 1: 1-8.
      15. Mel’nik A.V., Voloshchouk N. I., Pentyuk N. O. et al. Role of Hydrogen Sulfide and Sulfur-Containing Amino Acids in Regulation of Tone of Smooth Muscles of the Vascular Wall in Rats. Neurophysiol 2010; 2: 126-31.
      16. Grattagliano I., Bari O., Bernardo T. C. et al. Role of mitochondria in nonalcoholic fatty liver disease-from origin to propagation. Clin Biochem 2012; 45: 610-18.
      17. Ivanov I., Heydeck D., Hofheinz K. et al. Molecular enzymology of lipoxygenases. Archives of Biochemistry and Biophysics 2010; 503: 2: 161-74.
      18. Maron A.B., Loscalzo J. The Treatment of Hyperhomocysteinemia. Annu Rev Med 2009; 60: 39-54.
      19. Naik A., Belic A., Zander U. M., Rozman D. Molecular interactions between NAFLD and xenobiotic metabolism. Frontiers sn genetics 2013; 4: 2: 75-88.
      20. Newton J. L. Systemic Symptoms in Non-Alcoholic Fatty Liver Disease. Dig Dis 2010; 28: 1: 214-19.
      21. Farrell G.C., McCullough A.J., Day C. P. et al. Non-Alcoholic Fatty Liver Disease: A Practical Guide. 2013, Wiley-Blackwell - 324p.
      22. Powel E.E., Jonsson J. R., Clouston A. D. Metabolic Factors and Non-Alcoholic Fatty Liver Disease as Co-Factors in Other Liver Diseases. Dig Dis 2010; 28: 1: 186-91.
     


    Full text is published :
    THE ROLE OF MITOCHONDRIAL DYSFUNCTION IN THE DEVELOPMENT OF NON-ALCOHOLIC FATTY LIVER DISEASE. Experimental and Clinical Gastroenterology Journal. 2018;150(02):37-43
    Read & Download full text

    1. North-Western State Medical University named after I. I. Mechnikov (St. Petersburg, Russian Federation)

    Keywords:non-alcoholic fatty liver disease,cholelithiasis,cholecystectomy,Ursofalk,prophylaxis

    Abstract:We examined 60 patients aged 38 ± 10.3 years who underwent cholecystectomy for cholelithiasis. According to ultrasonography, all patients did not have signs of non-alcoholic fatty liver disease. The observation period was 1 year. The patients were divided into 2 groups of 30 people each. Group 1 included patients assigned to: Ursofalk, Mukofalk and Hofitol. Group 2 included patients who received symptomatic therapy. All patients were examined: a biochemical blood test and ultrasonography of the abdominal organs, before surgery and 6 and 12 months after cholecystectomy. Of the 60 patients enrolled in the study, 21.6% by the end of the first year after cholecystectomy, ultrasonography from the liver showed signs of non-alcoholic fatty liver disease. In the first group of patients, by the end of the first year after cholecystectomy, signs of non-alcoholic fatty liver disease were found to be 6.6%. In the second group, the signs of non-alcoholic fatty liver disease appeared in 36.6% of patients. Against the backdrop of using the prophylaxis scheme developed by Ursofalk, Mukofalk and Hofitol, the incidence of non-alcoholic fatty liver disease in patients with cholelithiasis is lower by the end of the first year after cholecystectomy than in patients who did not use this scheme 6-fold.

      1. Harchenko, N.V., Babak, O. Y. Gastroenterologiya. – К., 2007. – 720 p.
      2. Degtyareva, I. I. Klinicheskaya gastroenterologiya: Rukovodstvo dlya vrachey. – М.: Medicinskoe informacionnoe agentstvo, 2004. – 640 p.
      3. Cimmerman, Y. S. Klinicheskaya gastroenterologiya: izbrannie razdeli. – М.: GEOTAR-Media, 2009. – 416 p.
      4. Bellentani, S., Scaglioli, F., Marino, M., Bedogni, G. Epidemiology of non–alcoholic fatty liver disease. Dig Dis 2010; 28: 155–161.
      5. Drapkin O. M., Smirnov V. I., Ivashkin V. T. Patogenez, lechenie I epidemiologiya NAJBP- chto novogo? Epidemiologiya NAJBP v Rossii. RMJ, 2011, № 28, p. 1717–1721.
      6. Minushkin O. N. Nealkogolniy steatoz pecheni, diagnostika, lechebnie podhodi. Lechaschiy Vrach, 2012, № 2, p. 45–49.
      7. Chernogorova, M. V. Postholecistektomicheskiy sindrom: uchebnoe posobie / M. V. Chernogorova, E. A. Belousova, M. B. Dolgova. – Moskva: Forte print, 2013. – 40 p.
      8. Bistrovskaya, E. V. Postholecistektomicheskiy sindrom: patogeneticheskie I terapevticheskie aspekti problemi / E. V. Bistrovskaya // Medicinskiy sovet. – 2012. – № 2. – p. 83–87.
      9. Dlya thego, u kogo udalen jelchniy puzir I kak ego sohranit: uchebnoe posobie / A. V. Shabrov [i dr.]; pod red. A. V. Shabrova. – Sankt-Peterburg: ООО «Tipografiya “Bresta”», 2009. – 204 p.
      10. Maniakov А. V., Ledencova S. S., Seliverstov P. V., Radchenko V. G. Chastota vozniknoveniya steatoza pecheni u pacientov posle holecistektomii na fone jelchnokamennoy bolezni v otdalennom posleoperacionnom periode. Gastroenterologiya Sankt-Peterburga, 2016, № 1–2, p. М20-М21.
      11. MEDI.RU podrobno o lekarstvah [electronic resource]. – Access mode: https://medi.ru – Урсофальк – официальная инструкция по применению. – (date of the application: 30.06.2017).
      12. PILULI Medicina ot A do Ya [electronic resource]. – Access mode: http://www.piluli.kharkov.ua – Урсофальк. – (date of the application: 30.06.2017).
      13. Agafonova, N. A. Postholecistektomicheskiy sindrom: voprosi diagnostiki I lecheniya / N. A. Agafonova. – М.: Prima Print, 2015. – 68 p.
      14. Mucofalk® Unikalniy preparat pischevih volokon [electronic resource]. – Access mode: http://www.mucofalk.ru. – Неалкогольная жировая болезнь печени. – (date of the application: 30.06.2017).
      15. Mucofalk® Unikalniy preparat pischevih volokon [electronic resource]. – Access mode: http://www.mucofalk.ru. – Способ применения Мукофалька. – (date of the application: 30.06.2017).
      16. Minushkin, O. N. Primenenie preparata “Odeston” (Hymecromone) v klinicheskoy praktike: posobie dlya vrachey obschey praktiki – terapevtov, gastroenterologov, studentov medicinskih institutov / O. N. Minushkin. – М.: ООО Izdatelstvo “Adamant”, 2014. – 80 p.
      17. Radchenko V. G., Seliverstov P. V., Ledencova S. S., Maniakov А. V. Nealkogolniy steatogepatit i biliarniy sladj u lic s metabolicheskim sindromom. Terapevticheskiy arhiv, 2016, volume 88, № 9, p. 78–83.
     


    Full text is published :
    PREVENTION OF NON-ALCOHOLIC FATTY LIVER DISEASE IN PATIENTS WITH CHOLELITHIASIS AFTER CHOLECYSTECTOMY. Experimental and Clinical Gastroenterology Journal. 2018;150(02):44-50
    Read & Download full text

    1. Moscow Clinical Scientific and Practical Center of the Moscow City Health Department (Moscow, Russian Federation)

    Abstract:Six patients with right-sided hemihepatectomy were observed. In the preoperative period, along with clinical and laboratory, CT, ultrasound, gastroscopy, the functional reserve of the liver was assessed before and after the operative increase in the volume of the left lobe of the liver. We estimated not only the increase in volume, but also the functional preservation of liver functions. The criterion of nutritional consistency was the well-known alimentary-vollemic diagnosis. Given the high nutritional risk, a nutritional correction included a mixed nutrition (sparing diet + sipping with a mixture of hepatoprotective composition, enzyme therapy and parenteral correction with electrolyte solutions, vitamins and albumin). Against the background of the correction, the patient’s state was satisfactory with positive dynamics.

      1. Shumakov V. I. (ed.) Transplantology. Ed. MIA, 2006. – 544 p.
      2. Efanov MG, Melekhina OV, Alikhanov RB, Tsvirkun VV, Kulezneva Yu. V. et al. Surgical methods of preventing hepatic insufficiency after extensive liver resection. Ann chir hepatology. 2016.3: 47.
      3. Kostyuchenko L. N. Clinical nutriciology in gastroenterology. – M., 2013. – 412 p.
      4. Kostyuchenko LN, Kuzmina TN, Smirnova OA Peculiarities of nutricional support for the consequences of extensive reactions of the thin intestine. Exper clin gastroenterol. 2014, 4: 32–36.
      5. V. A. Vishnevsky – Manual for Surgeons, 2009. – 516 p.
      6. Schnitzbauer A.A., Lang S. A., Goessmann H., Nadalin S., Baumgart J., Farkas S. A., Fichtner-Feigl S., Lorf T., Goralcyk A., Hörbelt R., Kroemer A., Loss M., Rümmele P., Scherer M. N., Padberg W., Königsrainer A., Lang H., Obed A., Schlitt H. J. Right portal vein ligation combined with in situ splitting induces rapid left lateral liver lobe hypertrophy enabling 2-staged extended right hepatic resection in smallfor-size settings. Ann. Surg. 2012; 255 (3): 405–414. doi: 10.1097/SLA.0b013e31824856f5.
      7. Schadde E., Schnitzbauer A. A., Tschuor C., Raptis D. A., Bechstein W. O., Clavien P. A. Systematic review and metaanalysis of feasibility, safety, and efficacy of a novel procedure: associating liver partition and portal vein ligation for staged hepatectomy. Ann. Surg. Oncol. 2015; 22 (9): 3109–3120. doi: 10.1245/s10434–014–4213–5.
      8. Lam V. W., Laurence J. M., Johnston E., Hollands M. J., Pleass H. C., Richardson A. J. A systematic review of two-stage hepatectomy in patients with initially unresectable colorectal liver metastases. HPB (Oxford). 2013; 15 (7): 483–491. doi: 10.1111/j.1477–2574.2012.00607.
      9. Shindoh J., Vauthey J. N., Zimmitti G., Curley S. A., Huang S. Y., Mahvash A., Gupta S., Wallace M. J., Aloia T. A. Analysis of the efficacy of portal vein embolization for patients with extensive liver malignancy and very low future liver remnant volume, including a comparison with the associating liver partition with portal vein ligation for staged hepatectomy approach. J. Am. Coll. Surg. 2013; 217 (1): 126–133. doi: 10.1016/j.jamcollsurg.2013.03.004.
     


    Full text is published :
    NUTRITIOUS ACCOMPANIMENT OF EXTENSIVE LIVER RESECTIONS. Experimental and Clinical Gastroenterology Journal. 2018;150(02):51-54
    Read & Download full text

    1. State Higher Educational Institution “Uzhhorod national university” (Uzhgorod, Ukraine)

    Keywords:liver cirrhosis,ascites,hepatorenal syndrome,prostaglandines,treatment

    Abstract:The group under study consisted of 387 patients with LC. The levels of prostaglandins (Pg) I2 and F, their dynamics in patients with LC were studied depending on the differentiated method of correction of ascites and (HRS) in these patients. In all patients with LC a statistically significant increase in serum levels of Pg I2 and F was observed. Our studies indicate the presence of regularity in the dynamics of serum Pg I2 levels in patients with ascites and HRS with LC, namely: in patients with LC and ascites class B, an increase in the level of Pg I2 was observed, which tends to normalize in class C in these patients, whereas in patients LC and HRS class B level of Pg I2 in the blood serum is within normal range, and in class C in these patients, is decreased in 2-2.5 times than normal. 1. In patients with LC, ascites and HRS there is a violation of serum prostaglandins levels, namely, an increase in Pg F, and decrease in Pg I2, which indicates the formation of refractory ascites and HRS in these patients. 2. An effective method of correction prostaglandins levels in patients with LC is the use of symbiotic and combined drugs “Gepadif” in the early stages of ascites formation, which contributes to the prevention of resistance to treatment of ascites and HRS.

      1. Kon’kova MV Dopplerographic predictors of hepatorenal syndrome. Scientific herald of Uzhgorod University. 2009; 36: 23–25.
      2. Hennenberg M, Trebicka J, Kohistani AZ et al. Vascular hyporesponsiveness to angiotensin II in rats with CCl (4)-induced liver cirrhosis. Eur. J. Clin. Invest. 2009; 39 (10): 906–913.
      3. Lugo-Baruqui A, Munoz-Valle JF, Arevalo-Gallegos S et al. Role of angiotensin II in liver fibrosisinduced portal hypertension and therapeutic implications. Hepatol. Res. 2010; 40 (1): 95–104.
      4. Fadejenko GD, Gridnev AE. Hepatorenal syndrome Acute and urgent states in the practice of a doctor. 2009; 5: 21.
     


    Full text is published :
    DYNAMICS OF INDICATORS OF PROSTAGLANDINS IN PATIENTS WITH LIVER CIRRHOSIS WITH ASCITES AND HEPATORENAL SYNDROME. Experimental and Clinical Gastroenterology Journal. 2018;150(02):55-60
    Read & Download full text

    1. Belarusian stat medical university, Department of Infectious Diseases (Minsk, Belarus)
    2. Belarusian research center for pediatric oncology, hematology and immunology (Minsk, Belarus)
    3. Grodno stat medical university, Department of Infectious Diseases (Grodno, Belarus)
    4. Grodno stat medical university, Research Laboratory (Grodno, Belarus)

    Keywords:Cirrhosis,hepatitis C virus,liver damage,mesenchymal bone marrow stem cells

    Abstract:The importance of the HCV-infection is determined by the wide spread, progressive course, the formation of liver cirrhosis (LC) and hepatocellular carcinoma. The mechanisms of the effect of the virus on hepatic cells and regeneration of hepatocytes, the processes of fibrogenesis and fibrolysis, mechanisms of the reverse development of the LC remain unexplored. There is no effective pathogenetic therapy, which contributes to the regress of the formed fibrosis in the liver tissue. A patient with HCV-LC who has a secondary hemorrhagic vaculities who underwent autologous MSC transplantation into the liver tissue. The liver biopsy specimens were studied in dynamics by light and electronic microscopy and by immunohistochemistry. The procedure of transplantation and posttransplantation period proceeded without complications. After the introduction of MSC from the data of the morphological study, the features of the formed micronodular LC remained. In some parts of the samples, the septa looked thin, sometimes perforated, indicating a resorption in this place of fibrous tissue. There was a decrease in the degree of transdifferentiation of stellate cells into myofibroblasts, a decrease in the number of fibroblasts and fibroblasts, there were no immune reactions in the form of deposition of amorphous and fibrous masses of moderate electron density along the sinusoidal capillaries that were significantly expressed in the primary biopsy. These changes were combined with the appearance of hepatocyte heterogeneity in the density of the cytoplasmic matrix, the state and quantity of organelles and inclusions, and the structural improvement of intracellular organelles Autologous transplantation of mesenchymal bone marrow stem cells reduces the degree of destructive changes in hepatocytes, the severity of fibrosis and contributes to the improvement of the morpho-functional state of the liver, and therefore, it can be recommended as an important component of medical interventions.

      1. Jacobson I.M., Cacoub P., Dal Maso L. et al. Manifestations of chronic hepatitis C virus infection beyond the liver // Clin. Gastroenterol. Hepatol. - 2010. - Vol. 12. - P. 1017-1029.
      2. Matignon M., Cacoub P., Colombat M. et al. Clinical and morphologic spectrum of renal involvement in patients with mixed cryoglobulinaemia without evidence of hepatitis C virus infection // Medicine (Baltimore). - 2009. - Vol. 6. - P. 341-348.
      3. Ramos-Casals M., Stone J. H., Cid M. C., Bosch X. The cryoglobulinaemias. Lancet. 2012; 9813: 348-360.
      4. Almpanisa Z., Demonakoua M., Tiniakos D. Evaluation of liver fibrosis: “Something old, something new…” // Annals of Gastroenterology. - 2016. Vol. 29. P. 1-9.
      5. Mityushin V.М., Kozyreva E. V. Some types of ultrastructure of mitochondria of animal cells and their relationship to energy production // Cytology. - 1978. Vol.4. - P. 371-379.
      6. Wanless I.R., Nakashima E., Sherman M. Regression of Human Cirrhosis Morphologic Features and the Genesis of Incomplete Septal Cirrhosis // Arch Pathol Lab Med. - 2000. - Vol. 124. - P. 1599-1607.
      7. Garcia-Tsao G., Friedman S., Iredale J. et al. Now there are many (stages) where before there was one: In search of a pathophysiological classification of cirrhosis // Hepatology. - 2010. - Vol. 51. P. 445-9.
      8. Mederacke I., Hsu C. C., Troeger J. S. et al. Fate tracing reveals hepatic stellate cells as dominant contributors to liver fibrosis independent of its aetiology. Nat Commun. 2013; 4: 2823.
      9. Pradere J.P., Kluwe J., De Minicis S. et al. Hepatic macrophages but not dendritic cells contribute to liver fibrosis by promoting the survival of activated hepatic stellate cells in mice. Hepatology. 2013; 58: 1461-1473.
      10. Radaeva S., Sun R., Jaruga B. et al. Natural killer cells ameliorate liver fibrosis by killing activated stellate cells in NKG2D-dependent and tumor necrosis factor-related apoptosis-inducing ligand-dependent manners // Gastroenterology. - 2006. - Vol. 130. - P. 435-452.
      11. Syal G., Fausther M., Dranoff J. A. Advances in cholangiocyte immunobiology // Am J Physiol Gastrointest Liver Physiol. - 2012. Vol. 303. - P. G1077-G1086.
      12. Luedde T., Kaplowitz N., Schwabe R. F. Cell death and cell death responses in liver disease: mechanisms and clinical relevance // Gastroenterology. - 2014. Vol. 4. - P. 765-783.
      13. Knodell R.G., Ishak K. G., Black W. C. et al. Formulation and application of a numerical scoring system for assessing histological activity in asymptomatic chronic active hepatitis // Hepatology. - 1981. - Vol. 1. P. 431-435.
      14. Scheuer P. J. Classification of chronic viral hepatitis: a need for reassessment// J Hepatol. - 1991. Vol. 13. - P. 372-374.
      15. Ding B.S., Cao Z., Lis R. et al. Divergent angiocrine signals from vascular niche balance liver regeneration and fibrosis. Nature. 2014; 505: 97-102.
      16. Biswas S, Sharma S Hepatic Fibrosis and its Regression: The Pursuit of Treatment // J Liver Res Disord Ther. - 2016. -Vol. 2. - P. 1-4.
      17. Luetkemeyer A. F., Wyles D. L. CROI 2016: Viral Hepatitis and Liver Fibrosis. - 2016. - Vol. 24. - P. 47-58.
      18. Pradhan A.M., Bhave S. A., Joshi V. V. et al. Reversal of Indian childhood cirrhosis by D-penicillamine therapy // J Pediatr Gastroenterol Nutr. - 1995. - Vol. 20. P. 28-35.
      19. Stueck A.E., Wanless I. R. Hepatocyte Buds Derived From Progenitor Cells Repopulate Regions of Parenchymal Extinction in Human Cirrhosis // Hepatology. - 2015. Vol. 5. P. 1696-1707.
      20. Deleve L.D., Wang X., Guo Y. Sinusoidal endothelial cells prevent rat stellate cell activation and promote reversion to quiescence. Hepatology. 2008; 48: 920-930.
      21. Taguchi K, Asano G. Neovascularization of pericellular fibrosis in alcoholic liver disease // Acta Pathol Jpn. - 1988. - Vol. 38. P. 615-626.
     


    Full text is published :
    EFFECTS OF AUTOLOGICAL MESENCHIMAL STEM CELLS, TRANSPLANTED IN LIVER WITH VIRUS CYRROSIS. Experimental and Clinical Gastroenterology Journal. 2018;150(02):61-67
    Read & Download full text