It is hoped selleck products that the consensus strategies will be updated regularly and adopted by health authorities to improve the care of patients with HCCA in many other countries outside the Asia–Pacific region as well. “
“We read the excellent article by Harrison et al.,1 who showed that elevated baseline low-density lipoprotein levels are associated with higher sustained virological response (SVR) rates. In our experience with 32 transplant patients who suffered hepatitis C recurrence and were treated with peginterferon

alfa-2b and ribavirin, the total cholesterol (TC) levels (mg/dL) did not influence SVR.2 In this particular group of patients, the importance of parameters such as the body mass index (BMI; kg/m2), triglyceride (TGC) levels (ng/mL), and hepatic percentage of steatosis in the response to antiviral therapy was demonstrated. Ten patients (31.2%) stopped their therapy because of side effects. The observed BMI values, TC levels, TGC levels, and percentages of steatosis were confirmed to be normally distributed by the one-sample Kolmogorov-Smirnov

goodness-of-fit test procedure. Comparisons of the BMI values, TC levels, TGC levels, and percentages of steatosis screening assay between nonresponse (NR), SVR, and sustained biochemical response (SBR) groups were analyzed by analysis of variance with the post hoc Bonferroni test, and correlations between variables were tested with the Pearson test. A univariate analysis was

performed to estimate the chance of a response according to the aforementioned variables. The BMI values (26.8 ± 3.3 kg/m2), TGC levels (245.3 ± 84.4 ng/mL), and percentages of steatosis (26.8% ± 23.6%) in the NR group (nine cases) were higher than those observed in the SVR group [six cases; 20.4 ± 2.6 kg/m2 (P < 0.001), 108.3 ± 48.4 ng/mL (P = 0.002), and 5.75% ± 2.2% (P = 0.027), respectively] and in the SBR group [seven cases; 21.5 ± 1.6 kg/m2 (P = 0.003), 132.4 ± 51.2 ng/mL (P = 0.008), and 6.2% ± 2.4% (P = 0.033), respectively]. The differences selleck inhibitor between the SVR and SBR groups were not significant for the aforementioned variables. As for cholesterol, no significant differences were registered between the NR group (197.6 ± 47.3 mg/dL), the SVR group (149.3 ± 37 mg/dL), and the SBR group (153.4 ± 41.5 mg/dL). The Pearson correlation test (correlation coefficient >0.7, P < 0.001 for every correlation) showed a strong correlation between the BMI values, cholesterol levels, TGC levels, and percentages of steatosis. For patients with a BMI <25 kg/m2 and TGC levels < 160 ng/mL, the chance of SVR was 48 times higher than the chance of NR.

10 The association of malignancy with mural nodules on EUS was also reported in other studies.11,39 Yamao et al. reported that the combination of EUS and intraductal ultrasonography showed great accuracy in the diagnosis of invasive IPMN.12 Hara et al. showed that by intraductal ultrasound, 88% of lesions protruding 4 mm or more were malignant.13 Contrast-enhanced harmonic EUS is often used to examine the microvasculature and perfusion in the pancreas, and could prove to have a role in the diagnosis of malignant versus benign pancreatic cysts.14 Indeed, using contrast-enhanced EUS, Ohno et al. was able to classify

mural nodules of IPMN into four types. The diagnosis of IPMN with a type III or IV mural nodule had a sensitivity of 60%, specificity of DMXAA 92.9%, and accuracy of 75.9% for predicting malignancy.15 However, Song et al., in their study of 75 patients, showed that large mural nodules (≥ 10 mm) were observed in six (50%) of 12 patients with malignant IPMN versus three (30%) of 10 patients with benign IPMN, but the difference

was not statistically significant.32 In Korea, Kang et al. used cyst growth rate to predict malignancy of branch type IPMN. Cysts that grew more than 2 mm/year had a higher risk of malignancy (5-year risk of 45.5% vs 1.8%; P < 0.001).25 The latter is an interesting finding, and deserves further studies to provide corroborative evidence. Pancreatic cyst fluid viscosity, cytology, pancreatic

enzymes, and tumor markers could aid in the diagnosis of pancreatic cysts.40,41 The reported rate of correct diagnosis based on the cytology Selleckchem Selumetinib of cyst fluid by EUS-FNA varied from 54% to 97%, according to various reports.42–48 The specificity for the diagnosis of the presence of malignancy in mucinous cystic lesions ranged from 89% to 100%, and the sensitivity ranged from 22% to 100%.47–49 For patients with nodules, in addition to cytology, tissue diagnosis could be performed. Attempts had been made to improve the rate of correct diagnosis with brushing cytology for cysts50 and cystic wall biopsy.51 Of the pancreatic enzymes, amylase and lipase are the most well studied.52 As there is no clear standard for the cut-off learn more value for the diagnosis of mucinous cysts, a differential diagnosis based on a combination of values is necessary. In a pooled analysis of 450 patients, cyst fluid amylase concentration < 250 U/L virtually excluded pseudocysts.53 The American Society for Gastrointestinal Endoscopy guidelines stated that the measurement of cyst fluid amylase and lipase might provide clinically useful information about the cyst, but it could not provide a definitive diagnosis or determine the potential for malignancy.54 The most studied tumor markers are carcinoembryonic antigen (CEA) and CA19-9. The reported cut-off values varied significantly, and the data should not be applied without modification to the standards of various institutions.

3C). To determine the source of cholesterol, we assayed de novo cholesterol synthesis in Cyp7a1-tg mice. An increased bile acid pool should inhibit de novo cholesterol synthesis as observed in bile acid feeding experiments. However, hepatic de novo cholesterol synthesis rate was markedly increased by ∼11-fold (Fig. 3D), consistent with approximately seven-fold induction of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HmgCoAR) expression in Cyp7a1-tg mouse livers (Table 1). An increased bile acid pool normally should stimulate intestine fractional absorption of cholesterol. Surprisingly, we found that intestine fractional cholesterol absorption was similar between Cyp7a1-tg

mice and wild-type mice (Fig. 3E). These

results suggest that Cyp7a1-tg mice have Fulvestrant mouse selleck chemicals llc increased hepatic de novo cholesterol synthesis. Excess cholesterol is metabolized to bile acids, which are efficiently secreted into bile. Thus, the increased fecal cholesterol excretion in Cyp7a1-tg mice more likely resulted from increased biliary secretion of cholesterol rather than decreased intestine cholesterol absorption. Furthermore, plasma total cholesterol was decreased by 60% in Cyp7a1-tg mice, suggesting that increased hepatic cholesterol uptake may also contribute to hepatic cholesterol input. To investigate the mechanism of increased biliary bile acid and cholesterol secretion in Cyp7a1-tg mice, we first analyzed selleck chemicals messenger RNA (mRNA) expression of bile acid and cholesterol transporters in the liver and intestine. Cyp7a1-tg mice had significantly higher Abcg5 (2.7-fold) and Abcg8 (1.7-fold) mRNA expression in the liver, but not in the intestine (Table 1). Hepatic Abcg5/g8 protein levels were higher in Cyp7a1-tg mice than their wild-type littermates, whereas intestine Abcg5/g8 protein expression showed no difference (Fig. 4A). Expression of Sr-b1 mRNA increased 1.9-fold in Cyp7a1-tg mouse livers, but not in the intestine (Table 1). Expression of bile salt export pump (Bsep or Abcb11), a major biliary bile acid efflux transporter was significantly increased (1.7-fold) in Cyp7a1-tg mice (Table 1). Expression of liver sinusoidal

Na+-dependent taurocholate cotransport peptide (Ntcp), which reabsorbs bile salts from sinusoidal blood, did not change in Cyp7a1-tg mice. Expression of a hepatic phospholipid flipase (Abcb4) or multidrug resistance protein 2 (Mdr2), which is required for efficient biliary cholesterol secretion, did not change (Table 1). This is consistent with the observance of no significant increase of biliary phospholipid secretion in Cyp7a1-tg mice (Fig. 3C). In the intestine, mRNA expression levels of Niemann-Pick–like 1 protein (Npc1l1), which is an intestine cholesterol absorption transporter, and apical sodium-dependent bile salt transporter (Asbt), which reabsorbs bile salts from the lumen, were not changed in Cyp7a1-tg mice (Table 1).

During long-term follow-up, new telangiectasias or rectal bleeding were easily controlled. No major complications resulted. Conclusion: Bipolar heater probe is safe and effective relative

to medical therapy for palliation of patients with lower gastrointestinal bleeding from radiation colitis, all patients improved in ability to travel and day to day working and in their overall impression of their health. Key Word(s): 1. BIPOLAR HEATER PROBE; 2. RADIATION COLITIS; Presenting Author: VIJAY SHARMA Additional Authors: RICHA SHARMA, BHARATRAJ SHARMA Corresponding Author: VIJAY SHARMA Affiliations: Regional Institute of Health, Medicine & Research; S K Soni Hospital Objective: Hemorrhoids are common in Alcoholic liver disease. Band ligation is an established nonoperative Akt inhibitor method for treatment of symptomatic internal LY2109761 haemorrhoids. There is a few data in Alcoholic Liver disease patients. This study assessed the efficacy and safety of indigenous multiband ligator for endoscopic hemorrhoidectomy in Alcoholic liver cirrhosis. Methods: Patients with symptomatic internal haemorrhoids were treated

by retroflexed endoscopic multiple band ligation. Symptoms (prolapse, bleeding, pain with defecation) were graded from 0 to 3. Indigenously produced pneumatiic endoscopic multiband ligation device with six bands loaded to the olympusUGI scope, in retroflexed position hemorrhoid underwent suction and ligation. As many ligations as possible up to six performed in the same session. At four weeks the patients were assessed for symptoms, grade. Patients with rectal varices, coagulopathy, thrombocytopenia, grade 4 hemorrhoids, immunocompromised patients, rectal prolapse, prior injection therapy or anorectal surgery were excluded. Results: Total 73 Alcoholic liver disease patients with symptomatic (bleed, pain, prolapse) internal hemorrhoids were included in study, 53 were male and 20 were female. Among them

grade I were; 11, grade II; 51, and grade III; 11. Mean age of the patients was 44 years (Range 19 to 77 years). Mean number of bands placed was four (range 2 to 6). 62 patients underwent single session only, while only 11 patients underwent second session due to recurrent bleed and prolapse, 10 of them were grade 3. Patient satisfaction score and follow up endoscopy eradication scores were very click here high. Symptom and endoscopic scores improved at 4 weeks : bleeding, from 1.29 to 0.49 (p < 0.01); prolapse, from 1.83 to 0.5 (p < 0.01); pain, from 1.19 to 0.93 (p = 0.57); Grade of the hemorrhoids improved in most. Low grade fever in 4, managed with oral antibiotics and antipyretics. Severe pain in 17 patients, requiring analgesics. Conclusion: Indigenously produced multiband ligators are cheap, easily available and they can be safely and effectively used in Alcoholic liver disease patients with symptomatic internal hemorrhoids. Key Word(s): 1. internal hemorrhoids; 2. liver cirrhosis; 3.

Overall, 15(9.2%) were HCV antibody positive. Among 87 individuals born between 1945 and 1965 (the CDC “birth cohort”), 11.5% were HCV antibody positive. Of note, among 62 individuals born prior to 1945, 4 selleck chemical (6.5%) were HCV antibody positive, and all denied a prior history of injection drug use or prior HCV testing. 14 of 15 patients who

screened HCV antibody positive had confirmatory HCV RNA testing; of whom 12 (85.7%) were viremic. 10 (67%) individuals who screened HCV positive were previously unaware of their infection and did not consider themselves at risk for HCV. 10(67%) visited/ contacted the STD clinics for HCV RNA results/linkage to HCV care services within 4 weeks of testing. Conclusion Models Y-27632 cost are needed to improve the number of persons aware of and cured of HCV infection. These results suggest that in some cities the birth cohort should be expanded and that senior centers could be important venues for detection of unrecognized HCV infection. Additional research is needed to ascertain the medical impact of HCV treatment in this demographic group. Disclosures: Mark S. Sulkowski – Advisory Committees or Review Panels: Merck, AbbVie, Idenix, Janssen,

Gilead, BMS, Pfizer; Grant/Research Support: Merck, AbbVie, BIPI, Vertex, Janssen, Gilead, BMS The following people have nothing to disclose: Oluwaseun Falade-Nwulia, Risha Irvin, Ayesha M. McAdams-Mahmoud, Shruti H. Mehta, Jackline Joy M. Lasola, Dorcas Baker, Arnold Eppel, Patrick Chaulk, Kathleen R. Page, David L.

Thomas Background: The prevalence of hepatitis E virus antibodies (+HEV-IgG) in the US is estimated to be 6%, with an increased prevalence reported in patients with viral-induced chronic hepatitis. To our knowledge, the impact of +HEV-IgG in cancer patients with chronic hepatitis C virus (HCV) infection has not been studied. Hence, we sought to investigate the prevalence and predictors of HEV seropositivity along with the liver-related outcome of such patients. Methods: As part of a prospective study conducted at MD Anderson Cancer Center since 2012, characteristics associated with the development of cirrhosis, including co-infections with other hepatitis viruses, are being investigated in cancer patients with chronic HCV infection. Diagnosis of cirrhosis was made by non-invasive fibrosis this website markers, radiology or liver biopsy. Categorical variables were compared using χ2 test or Fisher’s exact test. Continuous variables were compared using Wilcoxon rank-sum test. Logistic regression modeling was used to determine predictors of cirrhosis. Results: Ninety-six HCV-infected cancer patients were enrolled; 11 of them (12%) had +HEV-IgG. When compared to -HEV-IgG, +HEV-IgG was significantly associated with advanced age (median, 60 vs 66; p= 0.019), Middle Eastern/Asian race (p= 0.01), birth in a developing country (Egypt, Vietnam, Laos, Qatar) (4% vs 36%; p= 0.

Methods: Vitamin D 25(OH)D was quantified in serum by liquid chromatographytandem mass spectrometry in 193 adults (>18 yrs) with well characterized, biopsy-proven NAFLD. Vitamin D Deficiency (VDD) was defined as <20ng/mL. Demographics, socioeconomic, and comorbidities (Type 2 DM and metabolic syndrome) were

compared between the VDD and non-VDD groups. Multivariable logistic regression analysis was used to investigate the association of VDD and the presence of definite nonalcoholic steatohepatitis (NASH) and individual features of NAFLD including steatosis, lobular inflammation, portal inflammation, ballooning degeneration and fibrosis, adjusting for age, sex, race, BMI, ALT, and PD98059 nmr diabetes status. Results: VDD was present in 55% of subjects and did not vary significantly among different demographic Natural Product Library concentration or socioeconomic groups or with the presence of comorbidities including diabetes type 2 and metabolic syndrome.

VDD subjects were more likely to have definitive NASH compared to non-VDD subjects (65% vs 35%, respectively, p=0.02). VDD was independently associated with definitive NASH (OR= 3.64, 95%CI=1.80-7.33, p<0.001), increased ballooning (OR= 2.49, CI=1.36-4.57, p=0.003) and a higher lobular inflammation grade (OR= 1.90, CI=1.02-3.51, p=0.042) after controlling for age, sex, diabetes, race, BMI and ALT. VDD subjects were more likely to have fibro-sis, but this failed to reach statistical significance (OR= 1.97, CI=0.94-4.11, p=0.072). Conclusions: VDD is highly prevalent among U.S. patients with NAFLD and is independently associated with a definitive diagnosis of NASH

and increased histological ballooning and inflammation scores. These data support further study of the mechanism for VDD in the pathogenesis of NASH and in dietary and/or lifestyle modifications to increase vitamin D levels in patients with NAFLD. Disclosures: Kris V. Kowdley – Advisory Committees or Review Panels: AbbVie, Gilead, Merck, Novartis, Trio Health, Boeringer Ingelheim, Ikaria, Janssen; Grant/Research Support: AbbVie, Beckman, Boeringer Ingelheim, BMS, Gilead Sciences, Ikaria, Janssen, Merck, selleck Mochida, Vertex The following people have nothing to disclose: James E. Nelson, Laura Wilson, Christian Roth, Matthew M. Yeh Background/aim: Non-alcoholic fatty liver disease (NAFLD) is an increasing health burden in western countries. The pathogenetic mechanisms remain widely unclear. Besides insulin resistance and dietary factors mutations of PNPLA3 (patatin-like phospholipase domain-containing 3 gene) were identified. Since preliminary data suggest that copper deficiency may contribute to the development of NAFLD, the aim of this study was to evaluate the association of hepatic copper content and PNPLA3 with histological features in patients with NAFLD. Methods: One-hundred and eight NAFLD patients (m/f: 75/33, mean age: 49.

4F and Supporting Fig. 4D). These data reinforce IL-10 as a potential RXDX-106 factor in the early response to BMC infusion therapy for treatment of hepatic fibrosis in mice as well as humans. To further investigate IL-10 expression by BMCs in vitro, we analyzed the subsets of BMCs after coculturing with HSCs. Since the major sources of IL-10 among infused BMCs were identified as CD11b+Gr1highF4/80− and CD11b+Gr1+F4/80+ cells in vivo (Fig. 3C), we investigated whether adherent and floating BMCs contained both types of cells. In FACS analyses after coculturing, adherent BMCs contained a higher fraction of CD11b+Gr1+F4/80+ cells (18%) than those of floating cells (6%), while the frequency of CD11b+Gr1highF4/80−

cells (87%) in floating BMCs exceeded that of adherent cells (50%) at 6 hours (Fig. 5A and Supporting Fig. 5A). After 6 hours of coculture, IL-10–positive cells in adherent and floating BMCs were higher than those of control BMCs, respectively (Fig. 5B and Supporting Fig. 5B). Therefore, we further analyzed IL-10–positive cells of BMCs using antibodies to CD11b, Gr1, and F4/80. After coculturing with HSCs, the frequencies of CD11b+IL-10+ cells in adherent (8%) and floating (5%) BMCs were much higher than those (4.7% and 1.8%) of control BMCs; CD11b+Gr1+F4/80+ cells and CD11b+Gr1highF4/80− cells were identified as major IL-10–producing cells in adherent and floating

BMCs, respectively (Fig. 5C,D and Supporting Fig. 5C). However, CD11b−IL-10+

cells in control and cocultured BMCs showed PF-02341066 cell line similar frequencies, which were mostly recognized as CD11b−Gr1+F4/80+ cells (Supporting Fig. 5D). To characterize the morphologies of IL-10–producing BMCs, CD11b+Gr1+F4/80+ and CD11b+Gr1highF4/80− cells were sorted and then stained with Giemsa followed by immunocytochemistry for IL-10. Using Giemsa staining, monocytic cells with vesicles and granules were the major types among the CD11b+Gr1+F4/80+ adherent BMCs, in which monocytic cells with nonindented nuclei were positive for IL-10 (Fig. 5E, upper panels). In contrast, granulocytic cells and their precursor cells were the main cell types among CD11b+Gr1highF4/80− floating BMCs, in which precursor type cells were positive for IL-10 find more (Fig. 5E, lower panels). In addition, in further analyses of BMCs with additional antibodies to Ly6G and Ly6C, the CD11b+Gr1+F4/80+ and CD11b+Gr1highF4/80− cells were identified as CD11b+Ly6G−Ly6Chigh and CD11b+Ly6G+Ly6Clow cells, respectively (Supporting Fig. 5E). Based on these findings, adherent and floating BMCs expressing IL-10 might be monocytic and granulocytic MDSC-like cells, respectively. Other Gr1lowF4/80− BMCs were identified as precursor cells for granulocytes and monocytes (Supporting Fig. 5F). To confirm the antifibrotic role of infused BMC-derived IL-10 in liver fibrosis, we infused IL-10–deficient BMCs in mice with CCl4-induced liver fibrosis.

After densitometric analysis corrected for GAPDH expression, the expression of MMP-12 showed no significant changes across all groups (data not shown). Given the tightly regulated activity of MMPs,9, 10 it was important to detect whether active MMP-12 was present. One of the main factors in determining MMP activity is the ratio with their tissue inhibitors, especially TIMP-1. TIMP-1 mRNA and protein (Fig. 3B) were increased after 8 and 12 weeks injury. In order to establish the degree of inhibition of MMP-12

by TIMP-1 in our model system, we coimmunoprecipitated the two proteins and analyzed the samples by zymography. After immunoprecipitation of MMP-12, casein zymography (Fig. 3C) showed a similar pattern to the samples used for western blot, indicating even efficiency of precipitation. R788 ic50 Additionally, when we immunoprecipitated TIMP-1 and performed casein zymography (Fig. 3C) the signal increased through 4 to 8 and 12 weeks (Fig. 3C), indicating that there is increasing amounts of TIMP-1 bound to MMP-12 in increasingly fibrotic liver. Thus, MMP-12

selleck kinase inhibitor is present in the liver but held in check by noncovalent binding to TIMP-1 with increasing duration of liver injury. Taken together, these data strongly suggest that the elastin content in scars is regulated by MMP-12-mediated degradation, with active MMP-12 being inhibited by increased interaction with TIMP-1 with worsening fibrosis in vivo. Previous work by Yoshiji et al.10, 28 using a TIMP-1 overexpression, however, suggests that the Timp-1 inhibition may not be maximal and MMP-mediated find more degradation still occurs

in remodeling during progressive fibrosis. MMP-12 has been reported to be expressed by macrophages.29 We confirmed this by immunocytochemistry on human monocyte-derived macrophages stained for both MMP-12 and the macrophage marker CD-68 (Fig. 4A1-2); 100% of the cells were positive for both proteins. To define which cells express MMP-12 in vivo, we stained serial sections of rat tissue for MMP-12 and CD-68 (Fig. 4A3-4). We found that the cells positive for MMP-12 were macrophages but that only a proportion of the CD-68-positive macrophages were also positive for MMP-12. To confirm the macrophage origin of MMP-12, we used the transgenic mouse CD11b-DTR in which macrophages can be selectively depleted as described.22 These mice show a 50% decrease in macrophage populations and increased accumulation of elastin compared with WT mice after CCl4 administration. Staining of liver following macrophage depletion showed a significant decrease in MMP-12-positive cells (Fig. 4B1-3). qPCR analysis of these tissues (Fig. 4B4) showed no significant changes in the expression of either tropoelastin or neutrophil elastase, whereas MMP-12 expression was significantly decreased. To further confirm that macrophages are the major hepatic source of MMP-12, we costained mouse liver after CCl4 injury for MMP-12 and key liver cell markers.

After densitometric analysis corrected for GAPDH expression, the expression of MMP-12 showed no significant changes across all groups (data not shown). Given the tightly regulated activity of MMPs,9, 10 it was important to detect whether active MMP-12 was present. One of the main factors in determining MMP activity is the ratio with their tissue inhibitors, especially TIMP-1. TIMP-1 mRNA and protein (Fig. 3B) were increased after 8 and 12 weeks injury. In order to establish the degree of inhibition of MMP-12

by TIMP-1 in our model system, we coimmunoprecipitated the two proteins and analyzed the samples by zymography. After immunoprecipitation of MMP-12, casein zymography (Fig. 3C) showed a similar pattern to the samples used for western blot, indicating even efficiency of precipitation. click here Additionally, when we immunoprecipitated TIMP-1 and performed casein zymography (Fig. 3C) the signal increased through 4 to 8 and 12 weeks (Fig. 3C), indicating that there is increasing amounts of TIMP-1 bound to MMP-12 in increasingly fibrotic liver. Thus, MMP-12

Dabrafenib is present in the liver but held in check by noncovalent binding to TIMP-1 with increasing duration of liver injury. Taken together, these data strongly suggest that the elastin content in scars is regulated by MMP-12-mediated degradation, with active MMP-12 being inhibited by increased interaction with TIMP-1 with worsening fibrosis in vivo. Previous work by Yoshiji et al.10, 28 using a TIMP-1 overexpression, however, suggests that the Timp-1 inhibition may not be maximal and MMP-mediated selleck chemicals degradation still occurs

in remodeling during progressive fibrosis. MMP-12 has been reported to be expressed by macrophages.29 We confirmed this by immunocytochemistry on human monocyte-derived macrophages stained for both MMP-12 and the macrophage marker CD-68 (Fig. 4A1-2); 100% of the cells were positive for both proteins. To define which cells express MMP-12 in vivo, we stained serial sections of rat tissue for MMP-12 and CD-68 (Fig. 4A3-4). We found that the cells positive for MMP-12 were macrophages but that only a proportion of the CD-68-positive macrophages were also positive for MMP-12. To confirm the macrophage origin of MMP-12, we used the transgenic mouse CD11b-DTR in which macrophages can be selectively depleted as described.22 These mice show a 50% decrease in macrophage populations and increased accumulation of elastin compared with WT mice after CCl4 administration. Staining of liver following macrophage depletion showed a significant decrease in MMP-12-positive cells (Fig. 4B1-3). qPCR analysis of these tissues (Fig. 4B4) showed no significant changes in the expression of either tropoelastin or neutrophil elastase, whereas MMP-12 expression was significantly decreased. To further confirm that macrophages are the major hepatic source of MMP-12, we costained mouse liver after CCl4 injury for MMP-12 and key liver cell markers.

In 14 patients of regular follow-up, no bleeding occurred related to EV. Conclusion: ESCI

could effectively control acute esophageal variceal bleeding without heterotopic embolism. Glue extrusion was commonly began 2∼3 weeks after the operation, and early glue extrusion would cause esophageal obstruction which need to be alerted. Key Word(s): 1. Esophageal varices; 2. sclerotherapy; 3. NBCA injection; 4. glue extrusion; Presenting Author: RAJIV BAIJAL Additional Authors: DEEPAK AMARAPURKAR, PRAVEEN KUMAR, NIKHIL PATEL, PRAFUL KAMANI, MAYANK JAIN, SANDEEP KULKARNI, NIMISH SHAH, DEEPAK GUPTA, MRUDUL DHAROD, SOHAM DOSHI Corresponding Author: RAJIV BAIJAL Affiliations: Indian Railways; None; Choitraram Hospital;

India Railways; Bombay Hospital Objective: Background: Bacterial infection, especially with intestinal-type bacterial flora, is a common complication Dabrafenib nmr in patients with cirrhosis. Recent data suggest that between 15% and 35% of cirrhotic patients admitted to hospital develop Selleckchem PD332991 nosocomial bacterial infection. Infections are important modifiable cause for morbidity and mortality in patients with cirrhosis of liver. Aim: To assess the incidence, predisposing factors, types of infection, prognostic factors and mortality in patients with infections in cirrhosis of liver. Methods: All patients diagnosed as cirrhosis of liver from 1st January 2013 to 31 st march 2013 coming to five different centers in India were included in this multicentre observational study. All patients were evaluated for clinical profile, etiology of cirrhosis

of liver, thorough laboratory investigations and imaging studies at baseline and after 30 days of presentation. Blood, urine and whenever necessary sputum cultures were sent on admission and 30 day mortality was also recorded. Results: Out of total of 380 patients with check details cirrhosis of liver, 287 (75.52%) were male and 93 (24.48%) were female. Average age was 53.5 years. 97 (25.52%) patients had infections. Out of these 48 (49.48%) patients had community acquired and 49 (50.52%) patients had hospital acquired infection. 83 (85.56%) patients seen as indoor and 14 (14.44%) as outdoor had infection. In 25 patients cultures were positive. Out of 97 patients- SBP(24), UTI(24), Pneumonia(12), Cellulites(12), Diarrhea(5), Tuberculosis(5), Malaria(9), Meningitis(2), Septic arthritis(3),Dengue(1), Skin infections(4), Pericarditis(1), Sepsis with source not identified(12). 17 patients had more tah one infections. Acconding to etiology number of patients who had systemic infections were alcohol (45/138), autoimmune(5/29), cryptogenic(22/68),hepatitis B(8/65), hepatitis C(1/22),NASH(14/48),Biliary cirrhosis(2/5), Wilsons(0/5). In all 380 patients, 32 (8.4%) patients expired out of which 24 (75%) had infections.