Evaluation via telephone was carried out at 3-, 9-, and 15-month intervals. UDCA and placebo were shipped to the participating medical centers and were handed to randomized patients upon entry into the study after 6 and 12 months. Regular

drug intake was determined by phone calls. Unused drugs were returned to the medical centers during visits, and this made calculation of patient compliance possible. Duplex ultrasonography was performed at entrance into the study and after 6, 12, and 18 MAPK inhibitor months. Primary Criterion for Evaluation: The primary criterion for efficacy was an overall improvement of liver histology after 18 months. Pre-post differences of the sum scores were compared in each

group, and this was followed by a comparison of the UDCA and placebo groups. Secondary Criteria for Evaluation: The pre-post differences of each of four histological criteria were compared and this was followed by comparison of the UDCA and placebo groups. Further pre-post differences for the liver function tests and for the other clinical parameters were evaluated. Subgroup analyses comparing the secondary variables of the UDCA group with those of the placebo group included age (<50 years and ≥50 years), inflammation (sum score >7 points), improvement of alanine aminotransferase (ALT; by ≥50%), Doxacurium chloride body mass index (BMI; ≤30 kg/m2 and >30 kg/m2), and blood pressure (<130/85 mm Hg and ≥130/85 mm Hg). Because in the UDCA group only 10 patients

LY2109761 supplier and in the placebo group only 11 patients presented with type 2 diabetes, diabetes was not used for subgroup analysis. Symptoms such as fatigue, malaise, pruritis, right upper quadrant abdominal discomfort, right upper quadrant abdominal pain, and tenderness were assessed by the investigator on each visit. The sum scores of symptoms were determined according to a scale ranging from 0 to 3 (none, mild, moderate, and severe). The assessment of the safety and tolerability profile of UDCA included adverse events, laboratory data, liver biopsy, and ultrasonography. Adverse events were registered throughout the study and were coded according to MedDRA version 10.1, and the number of patients was compared between the treatment groups. Although our study was started 3 years before publication of the NAS,2 a second evaluation was performed according to the NAS, a score in which steatosis, lobular inflammation, and hepatocellular ballooning are used as variables. The definition of NASH according to the NAS was applied to all randomized patients, and the response to therapy was assessed with the NAS. Liver biopsy samples were obtained from 137 patients; 107 (78%) underwent biopsy a second time.

Patients

were staged according to the TNM 6th edition (2006) and Barcelona Clinic Liver Cancer staging system.19 Tumor size was based on the largest dimension of the tumor specimen. Tumor grade was scored using the modified nuclear grading scheme outlined by Edmondson and Steiner.20 Grades 1 and 2 were defined as well-differentiated and grades 3 and 4 as moderately/poorly differentiated. The majority of patients in the three cohorts had not received anti-HBV treatment after surgery. The Eastern Cooperative Oncology Group (ECOG) performance score of all patients was 0 or 1. The presence of cirrhosis was also confirmed on the surgical specimen. OS was defined as the EPZ-6438 cell line time from surgery to death and censored when a patient was alive at last contact. Table 1 shows the pathologic and clinical characteristics of the patients in all five cohorts. All patients had undergone surgical resection as their primary treatment. Patient data were retrospectively collected from medical records. BCLC staging is based on preoperation data, and vasculature

invasion is pathologically defined as the presence of endolymphatic or lymphovascular tumor emboli within tumors. Survival data are not publicly available for the MSH and INSERM cohorts; thus, these patients were not used for survival analyses. For generation of gene expression data from the Korean cohort, total RNA was isolated from tissue samples using a mirVana RNA Isolation labeling kit (Ambion, Austin, TX). Five hundred nanograms PI3K activation of total RNA were used for labeling and hybridization, in accordance with the manufacturer’s protocols (Illumina).

After the bead chips were scanned with an Illumina BeadArray Reader (Illumina), the microarray data were normalized using the quantile normalization method in the Linear Models for Microarray Data package in the R language environment (http://www.r-project.org).21 The expression level of each gene was transformed into a log-2 base for further analysis. Primary microarray data are available from the NCBI GEO public database Cytidine deaminase (accession number GSE16757). BRB-ArrayTools were primarily used for statistical analysis of gene expression data22 and all other statistical analyses were performed in the R language environment. We estimated patient prognoses using Kaplan-Meier plots and the log-rank test. Stratification of patients in the NCI cohort according to Seoul National University (SNU) recurrence signature was done as described.18 Receiver-operating characteristic (ROC) curve analyses were carried out to estimate discriminatory power of the prognostic gene expression signatures and clinical variables. We calculated the area under the curve (AUC), which ranges from 0.5 (for a noninformative predictive marker) to 1 (for a perfect predictive marker) and a bootstrap method (1,000 resampling) was used to calculate the 95% confidence internal (CI) for AUC.

However, effects of PDRN on gastric ulcer (GU) healing are still unknown. Methods: 60 Adult male Mongolian gerbils were used in this

experiment. They were randomly divided into six groups (n = 10 each group): sham-operation group, GU-induced group, GU-induced and 2, 4, 8, and 16 mg/kg PDRN-treated group. GU was induced by injection of acetic acid into subserosal surface of stomach. After convalescent period of 2 days, gerbils in PDRN-treated groups underwent intraperitoneal injection of 100 μl distilled water, which included PDRN of each concentration, once a day for 14 consecutive days. We investigated effects of PDRN on the size of ulcer and VEGF expression in GU-induced Mongolian gerbils. In addition, we evaluated the effects of PDRN on apoptosis in GU. Results: PDRN of 8 and 16 mg/kg significantly decreased the size of GU. Compared with GU-induced group, 8 and 16 mg/kg PDRN-treated Z-VAD-FMK datasheet group showed significant overexpression of VEGF protein. In terms of anti-apoptosis, 8 and 16 mg/kg PDRN-treated group significantly decreased number of TUNEL-positive cells in stomach. In addition, 8 mg/kg PDRN-treated group significantly suppressed caspase-3 expression.

ABT-263 cell line Induction of GU significantly enhanced the ratio of Bax to Bcl-2. The suppressing effect of PDRN on Bax to Bcl-2 ratio appeared most potent at 8 mg/kg dose. Conclusion: PDRN overexpressed VEGF protein on acetic acid-induced GU in Mongolian gerbils. This alteration is considered to promote GU healing. In addition, VEGF overexpressed by PDRN inhibited apoptosis,

and this effect is considered to prevent gastric ulcer. Key Word(s): 1. Gastric ulcer; 2. polydeoxyribonucleotide; 3-mercaptopyruvate sulfurtransferase 3. apoptosis; 4. vascular endothelial growth factor Presenting Author: HWONG-RUEY LEOW Additional Authors: YEN YIN LIM, WEI CHEE LIEW, KHEAN LEE GOH Corresponding Author: HWONG RUEY LEOW Affiliations: University of Malaya, University of Malaya, University of Malaya Objective: To report on prevalence of upper gastrointestinal diseases between 2009–2010 in a multi-ethnic Asian population. Methods: Endoscopy records of patient that presented for first time gastroscopy between 2009–2010 in the University of Malaya Medical Centre, Kuala Lumpur, Malaysia were reviewed. Results: 4745 patients undergone first time endoscopy examinations between 2009–2010. Prevalence of peptic ulcer disease (PUD) was reported to be 2.5% and 3.4% respectively for duodenal ulcer (DU) and gastric ulcer (GU). Helicobacter pylori (H.pylori) infection was reported in 11.1% of patients. However only 6.7% of DU and 0.6% of GU were associated with H.pylori infection. Although Prevalence of gastric cancer (GCA) was only noted in 0.8% of patients, Chinese remains the highest at risk at 67.5%. Erosive oesophagitis (EO) was noted in 9.4% of patents. Higher proportion of Malay male (24.4%) and Chinese male (49.

The hand and its tactile receptors can function to locate objects and stimuli with respect to both the compound screening assay bodily

location on which the stimulus impinges and the external locations (see Martin, 1995). It is possible that varying the kinds of information available concerning the body and external space might bias the brain towards or away from encoding touch with respect to one or another of these frames of reference. The richer and more reliable cues to the body which we receive when we look at it might bias processing of, or attract attention towards, the intrinsic spatial reference frames which play a role in representing location on the body surface. Thus, when the hands are visible, as well as felt through proprioception, their location, and the locations of the tactile stimuli upon them, may

be more likely to be encoded with respect to anatomical coordinates. In line with this suggestion, recent research shows that vision of the hand modulates somatosensory processing (Forster & Eimer, 2005; Sambo et al., 2009; Longo et al., 2011) and also improves tactile acuity with respect to the body surface (Kennett et al., 2001; Fiorio & Haggard, 2005; Cardini et al., 2011). Thus, we suggest that in our study, hand position (posture) effects were observed ipsilaterally in Experiment 2 (no sight of hands), because there were fewer cues to the anatomical location of AZD4547 cell line the hands and to the tactile stimuli applied to them in this condition (i.e. buy 5-FU just proprioceptive cues). When visual and proprioceptive cues were provided, this may have given more

weight to an anatomical frame of reference, leading to hand position being encoded anatomically (i.e. via contralateral pathways). The current experiments are the first to demonstrate the electrophysiological time course of somatosensory spatial remapping in the absence of manipulations of voluntary attention. The data reported here suggest that the process of remapping tactile locations according to the current posture of the limbs occurs from around 128 to 150 ms after stimulus onset (affecting primarily the somatosensory N140 component). Vision of the limbs plays an important role in the way that the brain processes posture. Sight of the limbs modulated the hemispheric distribution of activity associated with processing changes in the posture of the limbs. When there was no vision of the limbs, somatosensory remapping processes (postural effects on the N140) were observed over ipsilateral sites, but when participants could see their hands these processes appeared over contralateral sites.

The rationale of selecting one reference surface only was based on the evidence that the diffuse establishment of osteochondral damage in haemophilic arthropathy may allow one surface to be considered as representative of the overall status of the joint without significantly reducing the sensitivity

of the method. This also keeps the HEAD-US method reliable, easy and quick to perform. The protocol can be accomplished with portable ultrasound machines without any need for high-end or proprietary technology. An additive scoring scale has also been implemented as part of the HEAD-US method [47]. Generally speaking, MRI scoring scales have been widely used and approved as reference standards in haemophilia arthropathy trials, although rarely applied in clinical practice for diagnosis and outcome because of their complexity and extensive time requirements. In MLN0128 order addition, it is difficult to harness the large Ferroptosis assay amount of information generated by MRI into effective information to influence a patient’s management. Similarly,

the existing ultrasound protocols are somewhat complex, with only trained readers potentially able to get an acceptable level of reproducibility. These existing protocols include the evaluation of poorly relevant structures or give an incomplete estimation of osteochondral damage compared with the potential offered by the HEAD-US technique. The HEAD-US scoring method has been specifically designed to be relatively simple and quick to complete in a busy practice allowing, at the same time, a reliable quantification of the two domains of disease: activity and damage. In contrast to other ultrasound scoring scales available, Doppler imaging has not been included due to the high inter- and intra-observer variability of results expected from inexperienced examiners, the need for high-end machines to get better performance and the lack of any evidence that hyperaemia detection

in chronic synovitis may impact the management of patients with haemophilia. We would expect the use of ultrasound as part of routine clinical examination by haemophilia specialists to optimize the diagnostic workflow, avoiding additional costs and long waiting lists for patients referred to imaging departments. Preliminary clinical experience with the integrated use of ultrasound in routine clinical assessment has made it feasible to screen Idoxuridine six joints in a single examination, and has enabled detection of subclinical bleeds and initial asymptomatic damage in an unexpectedly high percentage of cases. Especially in children, who have hyperlax joints and an immature skeleton, ultrasound has proved able to disclose severe joint involvement with high-grade synovitis and chondral abnormalities, despite a normal physical examination. The information on early joint involvement provided by ultrasound could guide the clinical management of haemophilia by influencing prophylaxis regimen decisions on a personalized basis in the future.

It was shown that HSCs could act as a regulatory bystander, enhancing differentiation and accumulation of Tregs.[9] Activated HSCs can also induce NK cell activation, which results in suppression of liver fibrosis and HCV infection.[5-7, 11] Furthermore, TLR-3 or RIG-I-activated HSCs could produce both type I and type III IFNs that could inhibit HCV replication in hepatocytes.[8, 12, 15] These novel observations, although require further ex vivo and in vivo studies

to confirm, highlight the importance of HSCs in liver immunity against HCV infection. This work was supported by grants (DA12815, DA22177, and DA27550) from the National Institutes of Health. The authors declare that there is no conflict of interest. “
“Wilson disease is a copper metabolism disorder caused by mutations in ATP7B, a copper-transporting adenosine triphosphatase. A molecular diagnosis was performed on 135 Alectinib in vivo patients with Wilson disease in Taiwan. We identified 36 different mutations, eight of which were novel: five missense mutations (Ser986Phe, Ile1348Asn, Gly1355Asp, Met1392Lys,

and Ala1445Pro), one deletion (2810delT) in the coding region, and two nucleotide substitutions (−133AC and −215AT) in the promoter region. These mutations were MI-503 purchase not observed in 100 control subjects and reduced the activity of the mutated protein by at least 50% when compared with wild-type ATP7B. In addition to exon 8, our data indicate another mutation hotspot in exon 12 where 9.62% of all mutations occurred. An alternative splice variant of ATP7B lacking exon 12 was observed in one patient who had a homozygous 2810delT mutation and very mild clinical symptoms. Clinical examination and functional characterization of alternative splice variants Sunitinib clinical trial of ATP7B lacking exon 12 showed that they retained 80% of their biological activity. The 2810delT mutation increased the expression of these variants, which may have explained the mild symptoms in the patient with the 2810delT mutation. We also discovered that treating liver cancer cells with a Na+/H+ exchanger inhibitor,

5-(N-ethyl-N-isopropyl)-amiloride, significantly enhanced the expression of the alternative splice variant of ATP7B lacking exon 12. Conclusion: This study suggests a novel therapeutic strategy for patients with mutations in exon 12. (Hepatology 2010;52:1662-1670) Wilson disease (WD) is an autosomal recessive copper metabolism disorder with a prevalence of 1 in 35,000 to 100,000 live births.1-3 It is characterized by impaired biliary excretion and deficient incorporation of copper into ceruloplasmin, leading to toxic accumulation of copper in the liver, brain, cornea, and kidney. The resulting liver cirrhosis and neurological damage are fatal if not treated with copper-chelating agents such as penicillamine. Prompt and appropriate treatment depends on correctly diagnosing WD in the patient and any affected siblings.

It was shown that HSCs could act as a regulatory bystander, enhancing differentiation and accumulation of Tregs.[9] Activated HSCs can also induce NK cell activation, which results in suppression of liver fibrosis and HCV infection.[5-7, 11] Furthermore, TLR-3 or RIG-I-activated HSCs could produce both type I and type III IFNs that could inhibit HCV replication in hepatocytes.[8, 12, 15] These novel observations, although require further ex vivo and in vivo studies

to confirm, highlight the importance of HSCs in liver immunity against HCV infection. This work was supported by grants (DA12815, DA22177, and DA27550) from the National Institutes of Health. The authors declare that there is no conflict of interest. “
“Wilson disease is a copper metabolism disorder caused by mutations in ATP7B, a copper-transporting adenosine triphosphatase. A molecular diagnosis was performed on 135 Tofacitinib cost patients with Wilson disease in Taiwan. We identified 36 different mutations, eight of which were novel: five missense mutations (Ser986Phe, Ile1348Asn, Gly1355Asp, Met1392Lys,

and Ala1445Pro), one deletion (2810delT) in the coding region, and two nucleotide substitutions (−133AC and −215AT) in the promoter region. These mutations were Small molecule library ic50 not observed in 100 control subjects and reduced the activity of the mutated protein by at least 50% when compared with wild-type ATP7B. In addition to exon 8, our data indicate another mutation hotspot in exon 12 where 9.62% of all mutations occurred. An alternative splice variant of ATP7B lacking exon 12 was observed in one patient who had a homozygous 2810delT mutation and very mild clinical symptoms. Clinical examination and functional characterization of alternative splice variants 2-hydroxyphytanoyl-CoA lyase of ATP7B lacking exon 12 showed that they retained 80% of their biological activity. The 2810delT mutation increased the expression of these variants, which may have explained the mild symptoms in the patient with the 2810delT mutation. We also discovered that treating liver cancer cells with a Na+/H+ exchanger inhibitor,

5-(N-ethyl-N-isopropyl)-amiloride, significantly enhanced the expression of the alternative splice variant of ATP7B lacking exon 12. Conclusion: This study suggests a novel therapeutic strategy for patients with mutations in exon 12. (Hepatology 2010;52:1662-1670) Wilson disease (WD) is an autosomal recessive copper metabolism disorder with a prevalence of 1 in 35,000 to 100,000 live births.1-3 It is characterized by impaired biliary excretion and deficient incorporation of copper into ceruloplasmin, leading to toxic accumulation of copper in the liver, brain, cornea, and kidney. The resulting liver cirrhosis and neurological damage are fatal if not treated with copper-chelating agents such as penicillamine. Prompt and appropriate treatment depends on correctly diagnosing WD in the patient and any affected siblings.

8%), C=9 (9.2%), hepatocellular carcinoma (HCC): 14 (14.3%), portal vein thrombosis (PVT): 6 (6.1%), follow-up: median 45 (1-140) months. Median L4-L5 total psoas area (TPA): 2022 (777-3806) mm2, L4-L5 average total psoas density (ATPD): 42.52 (21.26-59.8) HU. ATPD was significantly correlated with creatinine (r=−0.41, p<0.001), albumin (r=0.224, p=0.035), MELD score (r=−0.218, p=0.034), TPA (r=0.415, p<0.001) and TPA/h2 (r=0.372, p=0.002). Fifty-four patients (55.1%) died during follow-up. In the univariate analysis, factors associated with survival were HCC (hazard ratio (HR): 0.486, 95% CI: 0.256-0.925, VX-809 research buy p=0.028), CP score (HR: 1.2, 95% CI: 1.057-1.365, p=0.005), albumin

(HR: 0.578, 95% CI: 0.346-0.967, p=0.037), PVT (HR: 0.323, 95% CI: 0.125-0.836, p=0.02) and ATPD stratified by gender (HR: 0.969, 95% CI: 0.944-0.994, p=0.015). In the multivariate analysis, higher CP score (HR: 1.2, 95% CI: 1.021-1.41, p=0.027) and lower ATPD stratified by gender (HR: 0.965, 95% CI: 0.936-0.995, p=0.023) were predictors of mortality. Conclusion: Muscle fat infiltration is a negative predictive factor

for survival in liver cirrhosis. There is a need for further investigation ABT-888 cost of the predictive value of indicators of nutritional status in the every-day clinical practice in patients with liver cirrhosis. Disclosures: The following people have nothing to disclose: Christos K. Triantos, Andreas Karatzas, Maria Kalafateli, Paraskevi Tselekouni, Georgios Tsiaoussis, Nikolaos Koukias, Efstratios Koutroumpakis, Konstatinos Thomopoulos, Vasiliki Nikolopoulou, Christina Kalogeropoulou, Chrisoula Labropoulou-Karatza C Background: Staging hepatic fibrosis is important in the management of chronic hepatitis C. The elastic modulus of liver has been shown to correlate well with histologic fibrosis stage. Supersonic shear imaging CYTH4 (SSI) is based on the acoustic radiation

force imaging technique to generate shear waves in liver tissue and is able to quantify the elastic modulus of liver. Thus SSI seems promising for the quantification of liver stiffness. Methods: Chronic hepatitis C patients na’fve to anti-viral therapy were enrolled. Liver stiffness, expressed in kPa, was measured with SSI using a SuperSonic Imagine Aixplorer diagnostic ultrasound scanner. Liver stiffness measurement with Fibroscan system was simultaneously performed for comparison. Liver histological examinations performed within 2 years were evaluated for the correlation of liver stiffness with METAVIR fibrosis stage. Results: A total of 191 chronic hepatitis C patients (97 men and 94 women; mean age, 63.1 years) were enrolled. Liver stiffness values measured by SSI and Fibroscan had a good correlation (r = 0.8653, P<0.0001). Seventy patients had received liver histological examination within 2 years. The mean ±SD of SSI liver stiffness for each fibrosis stage was 6.9±1.9 (F1), 10.3±2.4 (F2), 12.7±2.7 (F3), and 21.6±6.9 (F4), respectively.

39,40 The use of adefovir as a first line agent for treatment naïve CHB patients is limited by its modest antiviral suppressive effect and its potential renal toxicity. It has mainly been used in lamivudine-resistant disease. While waiting for more promising NA for treatment approval for CHB, a new formulation of IFN-α, pegylated IFN-α2a was approved in 2005. (It had been approved for the treatment of chronic hepatitis C in January 2001.)

Since then, conventional IFN-α has been gradually replaced by pegylated Caspase-independent apoptosis IFN-α2a. Although there are more updated data on the determinants of the development of long-term CHB complications, the criteria of starting pegylated IFN-α are based on the findings from studies using conventional IFN-α, i.e. ALT > 2 ULN. The duration of pegylated IFN-α therapy is again arbitrarily chosen, this time as 48 weeks rather than the 16–24 weeks for conventional IFN-α. Even with the extension of the duration of treatment to 48 weeks, it has shown learn more that the HBeAg seroconversion rate (33%) is almost identical to that of conventional IFN-α as determined in a meta-analysis (32%). In addition, after 3 years of follow-up for HBeAg-negative patients with lower baseline HBV DNA levels, the rate of undetectable HBV

DNA by PCR assay, is only 18%.41 Though 8% of these patients also have HBsAg seroconversion, data from entecavir and tenofovir give similar rates of HBsAg seroconversion in comparable (largely European) cohorts. Lamivudine as the first line agent for treatment naïve CHB patients, and additional adefovir for those with lamivudine-resistant disease, were the main treatment strategies

during the period between 1998 and 2004. In 2005, entecavir came in the arena of CHB treatment. It has two outstanding characteristics. It is a nucleoside belonging to a new subgroup, cyclopentane, and has an extremely high anti-HBV suppressive effect, rendering 67% of HBeAg-positive and 90% of HBeAg-negative patients to have unquantifiable HBV DNA (by PCR assays) after one year of therapy.42,43 A recent study showed that over 91% of patients have unquantifiable HBV DNA (< 12 IU/mL) after three years of entecavir treatment.44 This high rate of undetectable HBV DNA levels persists after five years of continuous Pazopanib in vitro entecavir therapy.45 The potent antiviral effect is probably related to its rapid intracellular phosphorylation to the active triphosphate derivative, as well as its triple action in the inhibition of HBV DNA synthesis, starting with the priming of the HBV DNA polymerase.46 This potent viral suppression has now been shown to be effective in not only reducing necroinflammation, but also reversing fibrosis and cirrhosis in 57 patients on continuous entecavir treatment with a third liver biopsy (45 of the third biopsies at year 6 of therapy).

7% (4 out of 109 patients), the mean value of the program was estimated 4,1 ± 0,2%. HE occurred in 11 (10.1%) patients, the estimated risk rate was 10,8 ± 0,3%. Bleeding from the EGV in early postshunting period was observed in 4 (3.7%) patients, the estimated risk for this group was 4,2 ± 0,2%. Increase the risk of ascites according to the program was 13,2 ± 0,5%, the true value was 12.8% (14).

Mortality was 3.7% (4), whereas the calculated risk was 4,1 ± 0,2%. Summary of calculated survival according to the program amounted to 91,2 ± 0,4%, while the true figure – 93.0%. After the central shunting the true frequency of liver failure was 3.8% (3 out of 80 patients), value of the program 3,6 ± 0,1%. HE occurred in 12 (15.0%) patients, the estimated risk rate was 16,2 ± 0,4%. Bleeding from the EGV in early selleck screening library postshunting period was observed in 2 (2.5%) patients, the estimated risk for this group was 2,7 ± 0,1%. Increase the risk of ascites according to the program was 5,9 ± 0,2%, while the true value was 6.3% (5). Mortality was 2.5% (2), whereas the calculated risk was 2,8 ± 0,1%. Summary survival was calculated – 90,2 ± 0,3%, while the true figure is also not significantly different –

91.2%. Conclusion: Thus, the developed integrated risk assessment program of cirrhotic patients, allows to calculate the risk of developing specific postshunting complications, mortality, survival PD0325901 mw and prognosis, with accuracy equal to 85,6–98,3% – for selective types of bypass surgery and 88,0–98,9% – options for central decompression. Key Word(s): 1. LIVER CIRRHOSIS; Presenting Author: FERUZGAFUROVICH NAZIROV Additional Authors: DEVYATOVANDREY VASILEVICH, BABDJANOVAZAM HASANOVICH Corresponding Adenosine triphosphate Author: FERUZGAFUROVICH NAZIROV Affiliations: Republican Specialized Center of Surgery named after acad. V.Vahidov Objective: Degree of progression of the pathological process in

the liver in the absence of the risk of bleeding from esophageal and gastric varices (EGV) is a main predictor of survival in patients with liver cirrhosis (LC). In view of generally accepted indications for liver transplantation, which should be performed in patients with decompensated LC, compensated state function of hepatocytes allows for dynamic monitoring with conservative therapy. Against this background, nivelation of the risk of hemorrhagic syndrome is a priority task for the solution of which will reduce the need for liver transplantation or to delay its implementation. Methods: To assess the severity and prognosis of survival after portosystemic shunt (PSSh) used MELD. Analyzed figures from 32 patients operated on at 2011 and traced for a year after PSSh. The mean age was 30,97 ± 3,12 years. Results: Before PSSh mean value MELD score was 10,19 ± 0,24 points. Implementation of PSSh in the immediate postoperative period did not result in a significant deterioration of the MELD (10,94 ± 0,23).