We have aimed at generating liver cirrhosis in experimental animal and further in performing splenoportogramm. The team has performed splenoportogramm in the pathologic model of toxin induced liver cirrhosis first time in Mongolia. After liver cirrhosis was developed (50% CCI4 /greasy sQltiiiofl/) H W3S proved by hematology, biochemistry and coagulogramm examinations. Video appearance of spleen vein and its branch was taken. The pathogenic model of liver cirrhosis was developed at 35th day of experiment. Symptoms of liver cell cytolyses revealed in hematology, biochemistry and coagulogramm examinations. Liver vascularization image proved emptiness in peripheral blood supply and damaged small caliber vessels.

BACKGROUND. HCV-infected and obesity related liver diseases are leading to increases in the prevalence of advanced liver disease. So, studying liver disease, especially liver fibrosis is crucial issue of today. In Mongolia digestive system disease is second causation of non-communicable disease. Therefrom in last years hepatocellular carcinoma is most common malignancy, first of all cancers in Mongolia. In response to acute or chronic liver injury, hepatic fibrosis is the accumulation of extracellular matrix and ultimately leads to cirrhosis. Cirrhosis is the end-stage of fibrosis, resulting in nodule formation that may lead to altered hepatic function and blood flow. Defining the phase of liver fibrosis is crucial for therapeutic choice prognosis, important role in monitoring treatment. At the present time, use of direct and undirect biomarkers methods could be recommended for liver fibrosis stage. The aim of this study is to determine liver fibrosis stage and to compare undirect biomarkers in chronic viral hepatitis, cirrhosis. METHODS: 630 cases by chronic viral hepatitis and cirrhosis at third central hospital in Mongolia from retrospectively reviewed and analysed. The clinical data including AST, ALT, platelet count and INR were recorded. APRI, FIB-4, AAR and FibroQ were calculated. RESULT: From all, males 42.06% and females 57.94%, with mean age of 55.35±24.0, in 130 cases with chronic viral hepatitis and 500 cases with cirrhosis. In cases of cirrhosis, mean value of platelet count, ALT, AST, INR was 120.54±73.53, 104.55±500.22, 111.68±279.97, 2.19±10.45, respectively. And in cases of chronic viral hepatitis platelet count mean value was 211.18±6.42. APRI was detected <0.5 cutoff value (F0-F1) 11.7% non-fibrosis, 0.5-1.5 score (F2-F3) 27.5% fibrosis, >1.5 cutoff value (F4) 60.8% cirrhosis. FIB-4 was determined <1.45 cutoff value (F0-F1) 14.8% non-fibrosis, 1.45-3.25 score (F2-F3) 15.7% fibrosis, >3.25 cutoff value (F4) 69.5%, AAR was showed <0.4 cutoff value (F0-F1) 2.3% non-fibrosis, 0.4-1 score (F2-F3) 30.2% fibrosis, >1 cutoff value (F4) 67.5%. And FibroQ was detected <0.6 cutoff value (F0- F1) 0.5% non-fibrosis, 0.6-2.6 score (F2-F3) 6% fibrosis, cutoff value 2.6< (F4) 93.5 cirrhosis. In study liver fibrosis staging by APRI, AAR, FIB-4 and FibroQ score system, AAR was determined fibrosis in 190 cases. CONCLUSION: Recorded data ALT, AST, INR in cases of cirrhosis were detected 104.55±500.22, 111.68±279.97, 2.19±10.45, respectively. And in cases of chronic hepatitis platelet count mean value was 211.18±6.42. APRI, AAR, FIB-4, FibroQ was determined fibrosis 27.5%,30.16%,15.71% and 6.03%, respectively.