30 We have also documented an increase in apoptotic cell death in HCV-infected, autophagy-impaired IHHs, and this reflects that autophagy promotes cell survival. It is possible

that HCV-mediated autophagy may sustain cell viability during virus-induced stress in order to prevent apoptosis. IFN-α can induce cell death by modulating the Janus kinase/signal transducer and activator of transcription (STAT) or phosphoinositide 3-kinase/protein kinase B signaling pathway, STAT3 activation, or cytokine induction.38 RAD001 concentration Therefore, IFN induction in HCV-infected, autophagy-impaired cells may mediate apoptotic cell death. Autophagy has been suggested to extend the survival time of human parvovirus B19–infected erythroid cells during viral expansion.39 Hepatitis B virus–encoded transcriptional transactivator

protein X up-regulates BCN1 expression and stimulates autophagy.40 We have shown previously that HCV infection enhances BCN1.12 Therefore, it is plausible that HCV induces autophagy to prolong cell survival. This process may help to initiate the development of liver disease progression, including hepatocellular carcinoma, through an as yet uncharacterized mechanism. In conclusion, the results from this study reveal that Selleckchem Tyrosine Kinase Inhibitor Library HCV infection in autophagy-knockdown cells induces the IFN signaling pathway and enhances hepatocyte death. Therefore, autophagy serves as a pivotal entity that may help HCV in establishing persistent infection, reducing antiviral innate immunity, and promoting cell survival. The interaction of the virus with the autophagy machinery involves multiple pathways that have only just begun to be characterized. However, other mechanisms, either simultaneously or subsequently, may also be involved in the establishment Oxalosuccinic acid of chronic HCV infection in humans. The authors thank Charlie Rice, Takaji Wakita, and Chen Liu for providing the HCV clones and HCV NS5A antibody and Leonard Grosso for helping to measure the genome copy number of HCV (IU/mL). “
“Single nucleotide polymorphisms (SNPs) located in lncRNA CASC8 gene may influence the process of splicing and stability of mRNA conformation,

resulting in the modification of its interacting partners. Genome-wide association studies (GWAS) have identified the SNP rs10505477 and SNP rs1562430 in CASC8 were associated with risk of the colorectal cancer (CRC) and breast cancer, respectively. In the present study, we genotyped the 940 surgically resected gastric cancer patients to explore the association between these two SNPs (e.g., rs10505477 and rs1562430) and survival of gastric cancer in a Chinese population. We found that the patients carrying rs10505477 GG genotype survived for a longer time than those with the GA and AA genotypes (log-rank P = 0.030). The similar result was also found in the dominant model (GA/AA versus GG, HR = 1.32, 95% CI = 1.08–1.63, log-rank P = 0.008).

Bifid Triple Viable, the combination of bacillus acidophilus, bifidobacterium bifidum, and fecal streptococci, made in Shanghai Xinyi pharmacy Inc. of China, are usually used in patients with diarrhea, alteration of intestinal flora, but has not been known if it is safe and valid in treating acute pancreatitis. Objective: Goal of this study is to determine if Bifid Triple Viable, coupled with enema, is capable of preventing infectious complications Nutlin3 in severe acute pancreatitis. Methods: Fifty patients

with severe acute pancreatitis were randomized into experimental group (n = 25) and control group (n = 25). All the patients received routine treatment, including fasting, acid suppressing, antibiotics, Rhubarb and Salvia miltiorrhiza treatment. Beyond that, the patients in the treatment group will receive a daily probiotic enema with 0.5 g Bifid Triple Viable diluted in 50–100 ml normal saline until discharge. Serum amylase level, C reactive protein (CRP) value, and abdominal pain were examined, recorded and compared between two groups in order to evaluate the effectiveness

of probiotic enema in the treatment of severe acute pancreatitis. Results: Of the patients in the control group, serum amylase level returned to normal in 3.6 ± 0.7 days averagely, whereas it only took 1.9 ± 0.9 days in the experimental group. The differences were statistically significant with P < 0.05. CRP became normal in 7.8 ± 2.2 and 5.3 ± 1.4 days in control and experimental groups, respectively. Moreover, the symposium of abdominal pain disappeared

in 5.1 ± 1.6 days for the patients in PCI-32765 price the control group, while in 3.7 ± 1.1 days for those in the Alanine-glyoxylate transaminase experimental groups. All the differences were statistically significant with P < 0.05. Conclusion: On the basis of routine treatment, combination of Bifid Triple Viable and enema treatment exerted significant beneficial effects on severe acute pancreatitis. Key Word(s): 1. Bifid Triple Viable; 2. Enema; 3. Probiotics; 4. SAP; Presenting Author: CHAI SOON NGIU Additional Authors: KIAT HON LIM, DAMIEN TAN Corresponding Author: DAMIEN TAN Affiliations: Department of Gastroenterology & Hepatology, Singapore General Hospital; Department of Pathology, Singapore General Hospital; Department of Gastroenterology & Hepatology, Singapore General Hospital Objective: Endoscopic ultrasound (EUS) has become an important diagnostic tool for management of SMT. With the addition of fine needle aspiration (FNA), the accuracy of can improved up to 98%. However, EUS-FNA is not without risk and complications. We illustrate a rare complication of EUS-FNA in which a patient with pancreatic heterotopia presented with acute pancreatitis post EUS-FNA. Methods: A 57-year-old man presented with incidental finding a 2 cm submucosal tumour at the antrum during screening endoscopy.

0% of the anticipated dose.[10] In another phase III study in Japan for patients who had not achieved SVR to prior IFN therapy, dose reduction of RBV was required due to anemia in 98.6% of the patients.[11] In comparison to these reports, although our study did not include a control (non-EPO) group, patients who required RBV dose reduction due to anemia were 13.6% (3/22) and the total RBV dose was 97.5% of the anticipated amount, which

indicated that EPO administration was apparently successful for preventing RBV dose reduction. Inosine triphosphatase SNP HIF inhibitor has been identified as a marker for susceptibility to anemia in patients who receive PEG IFN/RBV therapy.[14] The mechanism of anemia is hypothesized to occur due to accumulation of RBV triphosphate in red blood cells inducing oxidative stress that results in hemolysis. ITPA, the substrate for ITPase, which also accumulates in red blood cells, may prevent RBV conversion to the triphosphate form. ITPase deficiency is considered to be protective against RBV-induced anemia. Here, we show that the CC genotype of ITPA revealed significantly rapid progression of anemia during the early phase in agreement with the case of PEG IFN/RBV combination therapy. Both the CC and non-CC groups, however,

seemed to show no further Hb decline after administration of EPO, and whereas the CC genotype is more prone to develop anemia, the Hb levels in the two groups became comparable probably because of the higher total EPO dose used for patients of the CC genotype. These findings indicated that EPO could control the RBV-induced learn more anemia regardless of the ITPA genotype. We next compared the Hb decline of the Protein kinase N1 patients

given 1500 mg and 2250 mg in each ITPA group to investigate the effect of TVR on Hb decline. TVR has been shown to increase the incidence of RBV-induced anemia. In the non-CC group, the changes in Hb concentration were very similar for patients dosed with 1500 mg and 2250 mg. On the other hand, in the CC group, after week 3, the Hb level tended to be lower in the 2250-mg dosed patients. We assume that augmentation of the hemolytic effect of RBV by TVR may not be enough to result in a difference of Hb decline in the non-CC patients, who have the protective ITPA allele against RBV-induced anemia. In the CC group, however, because the patients were more susceptible, the higher dose of TVR might more strongly induce hemolysis. Because the number of patients was very small, it may reflect individual variability and further investigation with a large number of patients is needed to clarify this. Ribavirin is the key drug in the current IFN therapy to achieve SVR. In patients with genotype 1 and high viral load, the SVR rate of PEG IFN/RBV combination therapy is approximately 50%, while without RBV, it is approximately 20%.

Recognition, cessation of further attempt, and prophylactic antibiotics are adequate for management in most cases.60 If bleeding does not stop after a period of observation, application of pressure or EUS-guided injection of epinephrine

at the bleeding site are possible options to achieve hemostasis.60,61 Lee et al. reported a case of retroperitoneal bleed, where the patient presented with abdominal pain and responded to blood transfusion. It was associated with aspirin and prednisone intake.62 The overall complication rate due to hemorrhage is between 0.2% and 6%.60,61 All reported cases of fever as a complication responded to antibiotics, including one case of aspiration pneumonia.61 Antibiotic BVD-523 molecular weight prophylaxis should be given for EUS-FNA of pancreatic cysts.54 A fluoroquinolone given for 3 days after the procedure seems to be the most common practice. The overall infectious complication rate is between 0.2% and 5%.59,61 Acute pancreatitis occurs between 0.6% and 2.6%, and involves mainly

cysts in the pancreatic head and uncinate process.61,62 This is due to the longer distance the Selleckchem HIF inhibitor needle passes through in normal pancreatic tissue during aspiration.62 Most cases have mild to moderate pancreatitis, which respond to conservative measures within 2–3 days.61,62 However, Lee et al. reported one case of severe acute pancreatitis with possible necrosis on computed tomography that required total parenteral nutrition. The overall complication rate for EUS-guided pancreatic cyst FNA is between 1% and 6%.59–62 The type of cyst, size, presence of septations or mass, and same day endoscopic retrograde cholangiopancreatography are not predictors of complications.62 Most complications do not require surgery.62 Pancreatic cysts can either be observed or resected depending on the benign or malignant nature, or malignant potential of the lesions. As early as 1993, EUS monitoring of pancreatic cyst every 6 months was performed on 82 patients with small (< 2 cm) asymptomatic pancreatic cysts. Of the 31 patients who completed 3 years of follow Axenfeld syndrome up, 26 (84%) were non-progressive. Only one patient’s cyst

progressed, and surgical intervention diagnosed a retention cyst.17 Subsequently, improvements in technology have provided much better resolution and image clarity, and thus, characterization of IPMN. Wakabayashi et al.18 followed up pathologically-proven IPMN. They found that main duct type tumors (n = 9) were histological adenomas or adenocarcinoma. For those with branch duct-type tumors showing mural nodules or a tumor diameter of 3 cm or more (n = 26), a high malignant potential was found in 25 of 26 patients (96%). Surgical resection should be considered for such patients. However, for the patients with tumors < 3 cm and no mural nodules (n = 23), 17 of 23 had no apparent progression on follow-up EUS. Okabayashi et al.19 studied the risk factors of malignancy in 23 patients who were diagnosed with IPMN.

Sequential therapy also cured significantly more patients harboring strains resistant only to clarithromycin than triple therapy (p = .0216). Five randomized trials took place comparing sequential therapy to standard therapy across three countries. Although sequential therapy is thought to be especially useful in overcoming Rucaparib clarithromycin resistance, a study from China showed that this may be negated when dual clarithromycin and metronidazole resistance is present [19]. In this study, there was no significant difference between the eradication rates achieved with standard triple therapy (66.4%)

and sequential (72.1%) in either the ITT or the PP analysis. Sequential therapy achieved significantly higher eradication rates (88.8%; 95% CI: 51.7–88.7) than triple therapy (43.7%; 95% CI: 19.7–70) in patients harboring strains resistant only to clarithromycin. However, in patients harboring strains resistant

to clarithromycin and metronidazole, neither treatment was able to reach an eradication rate >55%. In Morocco, two randomized studies were performed comparing sequential to standard therapy. In both, sequential therapy performed impressively against standard triple, with ITT eradication rates of 65.9% in the standard triple therapy group and 82.8 in the sequential therapy group in one, and 94.2% for sequential and 70% for metronidazole-based triple therapy and 78% for clarithromycin-based

triple in the other [20, 21]. Another two randomized, Selleck BTK inhibitor prospective studies carried out in India also showed significantly better eradication rates for sequential therapy [22, 23]. One study on patients with all causes of dyspepsia showed an advantage for sequential next therapy with an ITT eradication rate of 88.2 vs 79.1% for triple [22]. A second study looking at patients with documented peptic ulcer disease also found sequential therapy superior although the raw ITT eradication rates were less impressive (76.0 vs 61.9%) [23]. Three meta-analyses examining the efficacy of sequential versus standard triple therapy in Asia were also published this year, all of which favored sequential therapy. One included all studies with Asian adults and reported a pooled RR of 1.1 for eradication with sequential therapy over standard triple with an NNT of 14 [24]. In a second meta-analysis limited to nine studies conducted in Asia, the odds ratio (OR) for eradication of H. pylori with sequential therapy over standard triple was 1.8 [25]. A further meta-analysis of Korean studies only also favored of sequential therapy with an OR of 1.8 [26]. Concomitant therapy was evaluated in one article published this year from an area of high antibiotic resistance and found to have an ITT eradication rate in first-line therapy of 91.5 and 60.6% as second therapy [27].

Aim: To investigate the correlation of HBV and fatty liver in the different demographics of age and BMI. Methods: We enrolled consecutive subjects who had received health check details check-up services at the Taipei Veterans General Hospital

from 2002 to 2009 and ultrasonography was used to diagnose fatty liver according to the practice guidelines of the American Gastroenterological Association. Results: Among the 33, 439 subjects enrolled in this study, fatty liver was diagnosed in 43.9% of the population and 38.9% of patients with chronic HBV infection. Multivariate analysis showed that BMI, age, waist circumference, systolic blood pressure, fasting glucose, cholesterol, alanine aminotransferase (ALT) levels, and platelet counts were positively associated, while hepatitis B surface antigen (HBsAg) positivity was inversely associated with fatty liver, especially for subjects with BMI> 22.4 kg/m2 and age>50 years. On the contrary, HBV infection was positively correlated with the presence of elevated serum ALT levels in subjects BYL719 datasheet with fatty

liver disease regardless of their age and BMI. Conclusions: Metabolic factors are important determinants for the prevalence of fatty liver. Patients with HBV infection were inversely associated with fatty liver disease than the general population, especially in older and obese patients. Furthermore, metabolic factors and HBV infection were associated with elevated serum ALT levels in fatty liver disease. Age distribution of fatty Pregnenolone liver stratified by HBV status. Disclosures: The following people have nothing to disclose: Chien-Wei Su, Yuan-Jen Wang, Jaw-Ching Wu, Teh-la Huo, Yi-Hsiang Huang, Han-Chieh Lin, Fa-Yauh Lee, ShouDong Lee Background and aim: To

test the association of carotid atherosclerosis with gene variants influencing hepatic fat accumulation and the severity of liver damage in patients with NAFLD. Methods: We assessed anthropometric, metabolic and histological data(Kleiner score) in 162 consecutive, biopsy-proven Sicilian NAFLD patients. Intima-media thickness(IMT), IMT thickening(IMT>1 mm) and carotid plaques(focal thickening of >1.3mm at the level of common carotid artery) were evaluated using ultrasonography. IL28B rs12979860 C>T, PNPLA3 rs738409 C>G, GCKR rs780094 C>T, LYPLAL1 rs12137855 C>T, and NCAN rs2228603 C>T single nucleotide polymorphisms were also assessed. The results were validated in a cohort of 267 subjects with clinical or histological diagnosis of NAFLD from Northern Italy, 63 of whom had follow-up examinations. Results: Carotid plaques, IMT thickening and mean maximum IMT were similar in the two cohorts, whereas the prevalence of diabetes, obesity, NASH, and PNPLA3 GG polymorphism(21 %vs.1 3%, p=0.02) were significantly higher in the Sicilian cohort.

Recent work has identified the NALP3 inflammasome as a critical pathway in the generation of proinflammatory signals during liver injury. Moreover, IL-1 generated through this pathway exerts profibrogenic activities through the modulation of TIMP-1 and MMP9. Aim of this study was to evaluate the role of CCR5

in mediating inflammasome activation in response to gp120, in cells involved in liver tissue repair, including HSC. Myofibroblastic human HSCs were isolated from normal human liver tissue and cultured on plastic until fully activated. PBMC were separated from human whole blood. Gene expression was measured by qPCR. Protein IL-1 β protein levels were assayed by ELISA. HSCs or PBMC were exposed to 500 ng/ml recombinant M-tropic gp120 PS341 (CN54) for 2, 8 and 24 hours showed a time-dependent, significant up-regulation of pycard and NALP3, critical proteins for the assembly

of NALP3-dependent inflammasome, and of cas-pase-1 and IL-1 β. gp120 efficiently induced secretion of mature IL-1β, as shown by ELISA tests performed on the supernatants of both cell types. Notably, pre-incubation of HSCs with TAK779, a CCR5 receptor antagonist or with neutralizing α-CCR5 antibody reverted gp120-mediated IL-1 β production, indicating a primary role for this receptor in the activation of inflammasome Paclitaxel price complex. Interestingly, when HSC were stimulated with CCL5 (RANTES), a natural agonist of CCR5, we also found a significant up-regulation of IL-1 b, confirming that CCR5 may mediate activation of this inflammatory complex in HSC. In conclusion, HIV-gp1 20 significantly increases the expression of components of the NALP3 Avelestat (AZD9668) inflammasome pathway in human HSC and PBMC, through activation of CCR5. These data identify a novel mechanism by which HIV-gp1 20 may directly influence hepatic

necroinflammation and fibrosis during HCV/HIV coinfection, i.e. through increased production of IL-1 β. Moreover, these data establish for the first time a direct link between the inflammasome complex, HIV proteins and CCR5. We thank aid-sreagent.org for the kind gift of gp120. Disclosures: Fabio Marra – Advisory Committees or Review Panels: Abbott; Consulting: Bayer Healthcare, Gilead; Grant/Research Support: ViiV The following people have nothing to disclose: Andrea Cappon, Raffaele Bruno, Sandra Gessani, Andrea Masotti Matrix metalloproteinases (MMPs) are involved in various processes such as modulation of inflammation, tissue remodeling and collagen turnover. MMP-8 plays a yet ill-defined role in liver fibrogenesis and fibrolysis. Thus, we investigated the role of MMP-8 in toxin-induced liver fibrosis and spontaneous fibrosis regression using MMP-8 knock-out mice. Six week old female MMP-8 KO mice (n=10/group,C57/BL6 background) were treated according to an optimized CCl4 and TAA fibrosis-induction protocol for 4 and 8 weeks. For fibrosis regression, mice were harvested 5 days, 2 weeks, and 4 weeks after discontinuation of toxin treatment.

Results: A total of 250 subjects were included (male 143, aged 55.3 ± 13.5 yrs, obscure gastrointestinal bleeding 106, abdominal pain 82, diarrhea 50 and others 12) and no capsule retention occurred. The prolonged recording time is 826.2 ± 62.8 (628–960) min, median pylorus transit time is 45 [2–501] min GW-572016 research buy and small bowel transit time is 380.0 ± 134.8 (97–882) min. Compared with 8 h recording time, prolonged recording time has a significantly higher completion rate of SBCE (noted in table). Conclusion: Prolonged recording time increases the complete examination rate of SBCE, which may be helpful to improve its diagnostic yield. Key Word(s): 1. capsule endoscopy;

2. complete examination; Comparison between Prolonged and 8 h recording time   Prolonged recording time 8 h recording time P value Pylorus transit rate 100% (250/250) 98.4% (246/250) >0.05 Complete examination rate of

small bowel 98.0% (245/250) 80.4% (201/250) <0.001 Presenting Author: SYEDZEA-UL-ISLAM FARRUKH Additional Authors: ARIFRASHEED SIDDIQUI, SAADKHALID NIAZ Corresponding Author: SYEDZEA-UL-ISLAM FARRUKH, ARIFRASHEED SIDDIQUI, SAADKHALID NIAZ Affiliations: Patel Hospital Karachi Objective: Ultrasound (U/S) remains the first choice in the study of biliary obstructive diseases, due to its accessibility, speed, ease of performance and low cost. In Pakistan the standard is thought to be variable in U/S results between tertiary and smaller U/S centers. No study is locally available validating the usefulness of U/S in diagnosing obstructive biliary disease in comparison to ERCP. Objective: find more To evaluate the overall results of U/S from different centers of our province and validate with ERCP. Methods: Patients and Methods: Study design: Cross-Sectional study. Setting: GNE-0877 Gastroenterology Unit, Patel hospital Karachi. Sample Size and collection: 200 patients were included, Ultrasounds were performed in various

centers of Sindh and ERCPs by a single operator. Results: Results: In our study of 200 patients, ultrasound showed biliary obstruction in 187 patients with a sensitivity of 93.50%. In comparison to ERCP, U/S showed Common bile duct (CBD) stone in 109 cases, sensitivity of 77.45%, specificity of 69.39% and positive predictive value of 72.48%. On U/S 36 patients showed dilated CBD without cause of obstruction while on ERCP 29 of these patients showing reason for obstruction giving sensitivity of 36.84% and negative predictive value of 92.68%. On u/s CBD sludge was noted in 3 patients, comparing to ERCP, sensitivity is 50.00% and negative predictive value of 98.98%. Comparing with ERCP findings, U/S showed biliary stricture level correctly in 100% of patients but in determining cause of stricture sensitivity is only 51.72%. All 13 patients reported as normal U/S, have biliary tract obstruction on ERCP.

Measured QOL was analyzed by z-test or Student’s t-test between each group. Data analysis was performed using JMP ver. 5.1J (SAS Institute Japan, Tokyo, Japan) and P < 0.05 was considered statistically significant. THE MEAN BMI of all patients with liver cirrhosis was 23.1 ± 3.4 kg/m2.

The ratio of obese subjects with BMI of 25 or higher was 30.6% and that of less than 18.5 kg/m2 was 5.1%, respectively NVP-AUY922 chemical structure (Fig. 1). We then excluded patients with ascites, edema or HCC to match the present cohort with those reported in 2002.[4] The number of patents in this cohort was 95, and Child–Pugh grades A, B and C were 71:22:2, respectively. Mean BMI was 23.6 ± 3.6 kg/m2, and BMI of less than 18.5 kg/m2 and 25.0 kg/m2 or higher were observed in 9.2% and 33.7%, respectively (Fig. 2). We examined nutritional status in 181 patients with liver cirrhosis that underwent indirect calorimetry. In these patients, the male : female ratio was 112:69, HCC was present in 94, and Child–Pugh grades A : B : C were 90:58:33. When protein malnutrition was defined as serum albumin level of less than 3.5 g/dL and energy malnutrition as a non-protein respiratory quotient of less than 0.85, protein malnutrition was found in 61%, energy malnutrition

in 43% and PEM in 27% (Table 2). Similarly, among 87 patients without HCC (Child–Pugh grades A : B : C, 36:27:24), 67% had protein malnutrition, 48% had energy malnutrition and 30% had PEM (Table 3). We examined health-related QOL in 114 patients with liver cirrhosis (64 Cell Cycle inhibitor men and 50 women) using the SF-8. Sixty-two patients had HCC, and Child–Pugh grades A : B : C were 63:26:25. Quality of life of all subjects was significantly lower on all subscales than Japanese national standard values (Table 4),[24] but no difference was observed between the presence and the absence of HCC (Table 5). PROTEIN-ENERGY

MALNUTRITION is a common manifestation in cirrhotic patients with reported incidences as high as 50–87%.[1, 2] Protein nutrition is usually evaluated by serum albumin level and, for energy nutrition, indirect Megestrol Acetate calorimetry is recommended for precise analysis.[13] Energy malnutrition typically shows reduced carbohydrate oxidation, increased fat oxidation and decline in npRQ measured by indirect calorimetry. It is reported that PEM worsens prognosis and QOL in patients with liver cirrhosis.[3, 4] Thus, intervention for PEM is an important issue in the clinical management of liver cirrhosis. For this purpose, BCAA administration for protein malnutrition raises the serum albumin level and improves QOL and survival of patients with liver cirrhosis.[5-8] LES for energy malnutrition improves npRQ, liver dysfunction and QOL.[9, 10] Thus, many guidelines[11-13] recommend such nutritional therapy for liver cirrhosis.

Measured QOL was analyzed by z-test or Student’s t-test between each group. Data analysis was performed using JMP ver. 5.1J (SAS Institute Japan, Tokyo, Japan) and P < 0.05 was considered statistically significant. THE MEAN BMI of all patients with liver cirrhosis was 23.1 ± 3.4 kg/m2.

The ratio of obese subjects with BMI of 25 or higher was 30.6% and that of less than 18.5 kg/m2 was 5.1%, respectively check details (Fig. 1). We then excluded patients with ascites, edema or HCC to match the present cohort with those reported in 2002.[4] The number of patents in this cohort was 95, and Child–Pugh grades A, B and C were 71:22:2, respectively. Mean BMI was 23.6 ± 3.6 kg/m2, and BMI of less than 18.5 kg/m2 and 25.0 kg/m2 or higher were observed in 9.2% and 33.7%, respectively (Fig. 2). We examined nutritional status in 181 patients with liver cirrhosis that underwent indirect calorimetry. In these patients, the male : female ratio was 112:69, HCC was present in 94, and Child–Pugh grades A : B : C were 90:58:33. When protein malnutrition was defined as serum albumin level of less than 3.5 g/dL and energy malnutrition as a non-protein respiratory quotient of less than 0.85, protein malnutrition was found in 61%, energy malnutrition

in 43% and PEM in 27% (Table 2). Similarly, among 87 patients without HCC (Child–Pugh grades A : B : C, 36:27:24), 67% had protein malnutrition, 48% had energy malnutrition and 30% had PEM (Table 3). We examined health-related QOL in 114 patients with liver cirrhosis (64 BGB324 order men and 50 women) using the SF-8. Sixty-two patients had HCC, and Child–Pugh grades A : B : C were 63:26:25. Quality of life of all subjects was significantly lower on all subscales than Japanese national standard values (Table 4),[24] but no difference was observed between the presence and the absence of HCC (Table 5). PROTEIN-ENERGY

MALNUTRITION is a common manifestation in cirrhotic patients with reported incidences as high as 50–87%.[1, 2] Protein nutrition is usually evaluated by serum albumin level and, for energy nutrition, indirect Florfenicol calorimetry is recommended for precise analysis.[13] Energy malnutrition typically shows reduced carbohydrate oxidation, increased fat oxidation and decline in npRQ measured by indirect calorimetry. It is reported that PEM worsens prognosis and QOL in patients with liver cirrhosis.[3, 4] Thus, intervention for PEM is an important issue in the clinical management of liver cirrhosis. For this purpose, BCAA administration for protein malnutrition raises the serum albumin level and improves QOL and survival of patients with liver cirrhosis.[5-8] LES for energy malnutrition improves npRQ, liver dysfunction and QOL.[9, 10] Thus, many guidelines[11-13] recommend such nutritional therapy for liver cirrhosis.