Blood and breath samples were collected at baseline and at 30, 60 and 120 min after ingestion of 100 mg 13C-labeled glucose and 75 g glucose. Results:  There SCH772984 cell line was a strong correlation between the change in the concentrations

at 2 h for the measured 13C-glucose breath test (2h-BT) and the 2 h plasma glucose level (r = −0.60, P < 0.0001). In a receiver–operator curve analysis using the 2h-BT, the area under the curve was determined to be 0.88, with a sensitivity and specificity (cut-off value of 3.5‰) of 82% and 85%, respectively, for the detection of DM. Multivariate analysis showed the 2h-BT to be an independent parameter to identify DM. Conclusion:  The 13C-glucose breath test is a useful tool and has the potential to become a routine outpatient examination for the screening of DM in cirrhotic patients. "
“Recently, the beneficial

effects of increased physical activity (PA) on non-alcoholic fatty liver disease (NAFLD) in obese subjects have been reported. However, the optimal strength and volume of PA in lifestyle modification to improve NAFLD pathophysiology and be recommended as an appropriate management of this condition are unclear. The primary goal of this retrospective GSK2126458 nmr study was to estimate the beneficial effects of a varying volume of moderate- to vigorous-intensity PA (MVPA) on the improvement of NAFLD. A total of 169 obese, middle-aged men were enrolled in a 12-week weight reduction program through lifestyle modification consisting of dietary MCE公司 restriction plus aerobic exercise. Among these obese subjects, 40 performed MVPA for <150 min·wk-1, 42 performed MVPA for 150-250 min·wk-1, and 87 performed MVPA for >250 min·wk-1. The subjects in the MVPA ≥250

min·wk-1 group, in comparison with those in the MVPA <250 min·wk-1 group, showed significantly attenuated levels of hepatic steatosis (-31.8% vs. -23.2%). This attenuation was likely independent of the detectable weight reduction. MVPA for ≥250 min·wk-1 in comparison with that for <150 min·wk-1 led to a significant decrease in the abdominal visceral adipose tissue severity (-40.6% vs. -12.9%), levels of ferritin (-13.6% vs. +1.5%), and lipid peroxidation (-15.1% vs. -2.8%), and a significant increase in the adiponectin levels (+17.1% vs. +5.6%). In association with these changes, the gene expression levels of sterol regulatory element-binding protein-1c and Carnitine palmitoyltransferase-1 in peripheral blood mononuclear cells also significantly decreased and increased, respectively. Conclusions: MVPA for ≥250 min·wk-1 as part of lifestyle management improves NAFLD pathophysiology in obese men. The benefits seem to be acquired through reducing inflammation and oxidative stress levels and altering fatty acid metabolism. (Hepatology 2014) "
“Autoimmune pancreatitis (AIP) is a distinct form of pancreatitis, which has a typical histopathology and excellent response to corticosteroids. AIP is sub-classified into Type 1 and 2 forms.

ASK1, apoptosis signal-regulating kinase 1; DAMP, damage-associated molecular pattern; DEN, diethylnitrosamine; DSB, double-strand break; GFP, green fluorescent protein; γ-H2A.X, phosphorylated histone H2A.X; HCC, hepatocellular carcinoma; IFN-γ,

interferon-γ; IL, interleukin; LPS, lipopolysaccharide; NF-κB, nuclear factor kappa B; NHEJ, nonhomologous end joining; p38 MAPK, p38 mitogen-activated protein kinase; PAMP, pathogen-associated molecular pattern; PCNA, proliferating cell nuclear antigen; ROS, reactive oxygen species; KU-60019 mw TLR4, Toll-like receptor 4; TLR4mut, TLR4 mutant; TUNEL, terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling; WT, wild-type. To explore the role of TLR4 in liver tumorigenesis, TLR4mut or WT mice at age 15 days were subjected to DEN-induced HCC, a well-established chemical carcinogenesis protocol.11 HCC developed in all of newborn WT or TLR4mut male mice injected with DEN (25

mg/kg) within 6 months (Fig. 1A). However, only 20% of female WT littermates developed with HCC as described18 (data not shown). Notably, TLR4mut www.selleckchem.com/products/GDC-0980-RG7422.html mice developed two-fold more visible tumor nodules than WT mice (37.76 ± 5.83 versus 18.09 ± 1.69, P < 0.01) (Fig. 1B). Also, an earlier onset of liver tumors was observed in the TLR4mut mice than WT mice: 60% of WT male mice developed HCC at the end of 5th month after DEN treatment but all of TLR4mut male mice developed HCC (data not show). Moreover, the number of HCC tumor nodules was also found increased in TLR4mut mice than their WT littermates (Fig. 1B).

Most tumor nodules were basophilic HCC (Fig. 1A), and two-fold more tumor area (percentage) was detected in the TLR4mut mice compared with WT mice (39.35 ± 6.42 versus 16.85 ± 3.42; P < 0.01) (Fig. 1B). Consistently, TLR4mut mice displayed a persistent hepatic injury than the WT mice as indicated by increase in the serum alanine aminotransferase (data not shown). Therefore, TLR4mut 上海皓元医药股份有限公司 mice with HCC exhibited significantly shorter mean survival times than WT mice (Fig. 1C). Programmed cell death, including apoptosis and autophagy-associated cell death, is a crucial defense mechanism against tumorigenesis. Compared with WT mice, TLR4mut mice exhibited a remarkable decrease in apoptosis as marked by TUNEL staining (11.12 ± 0.84 versus 4.35 ± 0.45 [P < 0.01], 9.93 ± 0.18 versus 3.84 ± 0.29 [P < 0.01], and 10.35 ± 0.84 versus 4.30 ± 0.62 [P < 0.001], at month 1, 3, and 6 after DEN injection, respectively) (Fig. 1D) as well as a decrease in apoptotic cell death marked by cleaved caspase-3 (Supporting Fig. 1A,B). Moreover, TLR4mut livers displayed a persistent increase in proliferation biomarker proliferating cell nuclear antigen (PCNA) as indicated by immunohistochemistry staining (Fig. 1E) and immune blotting (Supporting Fig. 1A,C).

60,61 Rinderknecht

initially alleged that mesotrypsin can degrade trypsinogens, but later he withdrew this claim and attributed the trypsinogen-degrading activity to enzyme Y.60 Rinderknecht believed that enzyme Y was probably a degradation fragment of cationic trypsin,61 perhaps complexed with pancreatic secretory trypsin inhibitor,62 although he acknowledged the possibility of contamination with an unknown protease.61 Our findings indicated that CTRC is in fact enzyme Y, and following Rinderknecht’s theory, CTRC protects the pancreas by decreasing trypsinogen concentrations during inappropriate zymogen activation (Fig. 1). CTRC-mediated trypsinogen degradation is more likely to play a protective role against pancreatitis than CTRC-mediated trypsin inactivation, because the former reaction is much faster, Acalabrutinib molecular weight and trypsinogen concentrations are much higher. When trypsinogen autoactivation is measured in the presence of CTRC, the ultimate trypsin levels generated are lower and depend on the trypsinogen/CTRC ratio and the calcium concentration. Thus, in essence, CTRC regulates Pritelivir trypsinogen autoactivation through degradation. The cationic trypsinogen mutation p.R122H, which causes hereditary chronic pancreatitis,13 eliminates the Arg122 autolytic cleavage site,

and thereby blocks CTRC-mediated trypsin and trypsinogen degradation. Autoactivation of p.R122H mutant trypsinogen in the presence of CTRC results in higher

trypsin levels than those observed with wild-type cationic trypsinogen, suggesting that mutation p.R122H exerts its pathogenic effect by interfering with the CTRC-dependent defense mechanism of trypsinogen degradation. Human digestive carboxypeptidases CPA1, CPA2, and CPB1 are secreted by the pancreas as inactive proenzymes containing a 94–96 amino-acid-long propeptide.63 Activation of procarboxypeptidases is initiated by proteolytic cleavage at the C-terminal end of the propeptide by trypsin. The trypsin-cleaved propeptide is still inhibitory, suppressing approximately 90% of carboxypeptidase activity. Recently, we demonstrated that CTRC induces nearly a 10-fold increase in the activity of trypsin-activated CPA1 and CPA2.64 CTRC exerts its effect by proteolyzing the α-helical connecting segment of the propeptide, which 上海皓元 becomes accessible only after tryptic activation. As a result, the propeptide dissociates and becomes completely degraded, resulting in full carboxypeptidase activity. CTRC cleaves the connecting segment in the propeptide at multiple sites, but the critical cleavage appears to be at the conserved Leu96–Leu97 peptide bond. Other human pancreatic chymotrypsins (CTRB1, CTRB2, CTRL1) or elastases (ELA2A, ELA3A, ELA3B) are inactive or markedly less effective at promoting procarboxypeptidase activation. Taken together, these observations indicate that CTRC is an essential co-activator of proCPA1 and proCPA2.

60,61 Rinderknecht

initially alleged that mesotrypsin can degrade trypsinogens, but later he withdrew this claim and attributed the trypsinogen-degrading activity to enzyme Y.60 Rinderknecht believed that enzyme Y was probably a degradation fragment of cationic trypsin,61 perhaps complexed with pancreatic secretory trypsin inhibitor,62 although he acknowledged the possibility of contamination with an unknown protease.61 Our findings indicated that CTRC is in fact enzyme Y, and following Rinderknecht’s theory, CTRC protects the pancreas by decreasing trypsinogen concentrations during inappropriate zymogen activation (Fig. 1). CTRC-mediated trypsinogen degradation is more likely to play a protective role against pancreatitis than CTRC-mediated trypsin inactivation, because the former reaction is much faster, B-Raf mutation and trypsinogen concentrations are much higher. When trypsinogen autoactivation is measured in the presence of CTRC, the ultimate trypsin levels generated are lower and depend on the trypsinogen/CTRC ratio and the calcium concentration. Thus, in essence, CTRC regulates ICG-001 manufacturer trypsinogen autoactivation through degradation. The cationic trypsinogen mutation p.R122H, which causes hereditary chronic pancreatitis,13 eliminates the Arg122 autolytic cleavage site,

and thereby blocks CTRC-mediated trypsin and trypsinogen degradation. Autoactivation of p.R122H mutant trypsinogen in the presence of CTRC results in higher

trypsin levels than those observed with wild-type cationic trypsinogen, suggesting that mutation p.R122H exerts its pathogenic effect by interfering with the CTRC-dependent defense mechanism of trypsinogen degradation. Human digestive carboxypeptidases CPA1, CPA2, and CPB1 are secreted by the pancreas as inactive proenzymes containing a 94–96 amino-acid-long propeptide.63 Activation of procarboxypeptidases is initiated by proteolytic cleavage at the C-terminal end of the propeptide by trypsin. The trypsin-cleaved propeptide is still inhibitory, suppressing approximately 90% of carboxypeptidase activity. Recently, we demonstrated that CTRC induces nearly a 10-fold increase in the activity of trypsin-activated CPA1 and CPA2.64 CTRC exerts its effect by proteolyzing the α-helical connecting segment of the propeptide, which MCE becomes accessible only after tryptic activation. As a result, the propeptide dissociates and becomes completely degraded, resulting in full carboxypeptidase activity. CTRC cleaves the connecting segment in the propeptide at multiple sites, but the critical cleavage appears to be at the conserved Leu96–Leu97 peptide bond. Other human pancreatic chymotrypsins (CTRB1, CTRB2, CTRL1) or elastases (ELA2A, ELA3A, ELA3B) are inactive or markedly less effective at promoting procarboxypeptidase activation. Taken together, these observations indicate that CTRC is an essential co-activator of proCPA1 and proCPA2.

[12] A strong correlation between H. pylori infection and gastric cancer has been experimentally confirmed in animal models.[13, 14] We have previously reported that in the patients in whom H. pylori was eradicated, there was normalization in the numbers of both infiltrating Selleckchem Forskolin neutrophils and mononuclear cells.[15] Fukase et al.

conducted the multicenter, open-label, randomized controlled trial, and concluded that treatment to eradicate H. pylori may reduce the risk of developing new gastric carcinoma in patients who have a history of such disease and are thus at high risk for developing further gastric cancers.[5] They did not evaluate histological changes, however, so we assume that histological improvement of possible precancerous lesions would have inhibited the development

of metachronous gastric cancer. Our data did not directly show suppression of metachronous gastric cancer in the gastric remnant by H. pylori eradication; however, significant histological improvement in the scores of chronic inflammation and atrophy indicates H. pylori eradication may suppress the development of new gastric carcinoma in patients with a gastric remnant. In our study, all the patients underwent Billroth I reconstruction. Biliopancreatic reflux is regarded as the main cause of an inhospitable environment for H. pylori after gastric resection.[16, 17] Billroth click here II gastric resection favors biliopancreatic reflux, which creates different mucosal conditions to the Billroth I gastric resection. However, we assume Billroth I gastric resection still promotes biliopancreatic reflux, and this might be the reason why chronic inflammation scores improved more slowly than atrophy scores after eradication. All in all, our data showing H. pylori eradication improving possible precancerous lesions of the gastric remnant can be applied only to the gastric remnant after Billroth I reconstruction. Several

limitations of this study warrant mention. First, we did not directly show suppression of metachronous gastric cancer by 上海皓元医药股份有限公司 H. pylori eradication. Second, this study does not have controls with a gastric remnant that did not undergo H. pylori eradication therapy. To have controls was difficult because we assumed H. pylori eradication therapy would suppress metachronous gastric cancer and recommended patients for H. pylori eradication therapy. Third, we did not examine any patient with a gastric remnant after Billroth II reconstruction. By comparing the data for Billroth and Billroth II reconstructions, we would be able to determine the important role of H. pylori eradication on prevention of metachronous gastric cancer development in the gastric remnant. In conclusion, prophylactic H. pylori eradication in the gastric remnant may be useful in preventing the development of metachronous gastric carcinoma. Further study remains to be done to clearly demonstrate the effect of H.

Demographics, ulcer size and location of ulcers were compared between patients with and without symptoms, and between patients with uPUD and BPU. Univariate associations with symptoms were initially explored using the χ2-test with the Yates correction for continuity, where appropriate, and a Kruskal–Wallis

one-way Gemcitabine anova was used to determine differences in cumulated symptom response to nutrient challenge test among the three groups where appropriate at a significance level of P ≤ 0.05. The primary hypothesis tested was that there is a difference between patients with BPU and uPUD for the cumulated symptom response to a standardized 800-ml nutrient challenge. We thus compared the response to a standardized nutrient challenge for patients with BPU, uPUD and HC and between patients with and without symptoms. anova adjusting for age, gender and body mass index (BMI) was used to compare the cumulative symptom response. P-values ≤ 0.05 were considered significant. Data are presented as mean ± standard error of the mean. For the statistical analysis sas Version 6.12 (sas Institute, Cary, NC, USA) and spss Version 12 (spss, OTX015 manufacturer Chicago, IL, USA) were used. Demographic data, the characteristics of the ulcers and the various factors that could potentially determine the symptoms of patients with BPU and uPUD are shown in Table 1. All patients had peptic ulcer

with a mucosal break at least 3 mm in diameter with visible depth confirmed by endoscopy. Most (15/25) of the patients with uPUD had been treated with PPI and in most instances, the ulcer had the appearance of being in the healing phase. Eighty-three

percent of the patients with BPU were asymptomatic prior the bleeding event. In contrast, all patients with uPUD presented with abdominal pain (P < 0.0001). Patients with BPU were significantly older than patients with uPUD (P = 0.01). There was no significant difference in mean age between HC and patients with uPUD or BPU. Patients with BPU had significantly larger ulcers (P < 0.01). Only two patients with BPU had diabetes MCE whose blood sugar had been well controlled by medication. There were no significant differences in gender, BMI, location of ulcers, number of ulcers, use of NSAIDs, or smoking between the groups. At the time of diagnosis, rates of H. pylori infection were not significantly different among the groups (uPUD = 48%, BPU = 57%). On the study day, two of patients with BPU, two uPUD patients and six HC tested positive to H. pylori (after receiving H. pylori eradication therapy). However, there were no significant differences in H. pylori infection among the groups (P > 0.99 between BPU and uPUD patients). After at least 8 weeks of treatment of the ulcer, and confirmation of healing of GU, most patients were asymptomatic. Twenty-five out of 30 (83%, 95%CI 65–94%) patients with BPU and 13/25 (52%, 95%CI 32–72%) patients with uPUD reported no symptoms on GIS and NDI.

Demographics, ulcer size and location of ulcers were compared between patients with and without symptoms, and between patients with uPUD and BPU. Univariate associations with symptoms were initially explored using the χ2-test with the Yates correction for continuity, where appropriate, and a Kruskal–Wallis

one-way Doxorubicin anova was used to determine differences in cumulated symptom response to nutrient challenge test among the three groups where appropriate at a significance level of P ≤ 0.05. The primary hypothesis tested was that there is a difference between patients with BPU and uPUD for the cumulated symptom response to a standardized 800-ml nutrient challenge. We thus compared the response to a standardized nutrient challenge for patients with BPU, uPUD and HC and between patients with and without symptoms. anova adjusting for age, gender and body mass index (BMI) was used to compare the cumulative symptom response. P-values ≤ 0.05 were considered significant. Data are presented as mean ± standard error of the mean. For the statistical analysis sas Version 6.12 (sas Institute, Cary, NC, USA) and spss Version 12 (spss, Dabrafenib research buy Chicago, IL, USA) were used. Demographic data, the characteristics of the ulcers and the various factors that could potentially determine the symptoms of patients with BPU and uPUD are shown in Table 1. All patients had peptic ulcer

with a mucosal break at least 3 mm in diameter with visible depth confirmed by endoscopy. Most (15/25) of the patients with uPUD had been treated with PPI and in most instances, the ulcer had the appearance of being in the healing phase. Eighty-three

percent of the patients with BPU were asymptomatic prior the bleeding event. In contrast, all patients with uPUD presented with abdominal pain (P < 0.0001). Patients with BPU were significantly older than patients with uPUD (P = 0.01). There was no significant difference in mean age between HC and patients with uPUD or BPU. Patients with BPU had significantly larger ulcers (P < 0.01). Only two patients with BPU had diabetes MCE公司 whose blood sugar had been well controlled by medication. There were no significant differences in gender, BMI, location of ulcers, number of ulcers, use of NSAIDs, or smoking between the groups. At the time of diagnosis, rates of H. pylori infection were not significantly different among the groups (uPUD = 48%, BPU = 57%). On the study day, two of patients with BPU, two uPUD patients and six HC tested positive to H. pylori (after receiving H. pylori eradication therapy). However, there were no significant differences in H. pylori infection among the groups (P > 0.99 between BPU and uPUD patients). After at least 8 weeks of treatment of the ulcer, and confirmation of healing of GU, most patients were asymptomatic. Twenty-five out of 30 (83%, 95%CI 65–94%) patients with BPU and 13/25 (52%, 95%CI 32–72%) patients with uPUD reported no symptoms on GIS and NDI.

The main contraindications for PAIR are superficially located cysts (because of the risk

of rupture), cysts with multiple, thick internal septations, and cysts communicating with the biliary tree.1 The cyst in this case did have a relative contraindication to PAIR with a somewhat superficial location (which increased the risk of intra-abdominal spillage of cyst contents). The initially suspected internal MLN0128 in vivo septations were actually detached cyst membranes; thus, a complication was less likely. Furthermore, the risk of PAIR seemed less in comparison with the risk of right hepatectomy. Therefore, PAIR was performed, and the aspirated cyst fluid showed hydatid sand consisting of a protoscolex with prominent hooklets (Panel B) and free-floating, selleck chemicals calcific hooklets (Panel C) from the degeneration of protoscolices. A diagnosis of E.granulosus was confirmed by the characteristic appearance of the protoscolex in the cyst fluid. E.granulosus is

a tapeworm infection found in areas in which dogs are used to raise livestock. Adult tapeworms develop in definitive hosts, which include dogs and other carnivores. Dogs are infected through the consumption of organs of sheep or cattle with hydatid cysts. In intermediate hosts (sheep and cattle) and humans, the larval forms penetrate the intestinal mucosa and enter the portal circulation, through which they travel to the liver and form hydatid cysts. Humans

acquire the infection through the consumption of vegetables contaminated by dog feces containing parasite eggs. Most individuals with hydatid liver cysts are asymptomatic. As the cyst enlarges, they may develop a fever, pain, tender hepatomegaly, and eosinophilia. The diagnosis relies on epidemiological data, clinical manifestations, radiological imaging, and serological tests. However, the detection of protoscolices or hooklets in cyst fluid, as in this case, is diagnostic.2 Daughter cysts develop from the inner germinal layer of hydatid cysts, as do cystic 上海皓元 structures called brood capsules. New larvae, which are called protoscolices, develop in large numbers within the brood capsule. Protoscolices bud off from the cyst wall and have the potential to form other cysts or to develop into adult tapeworms if they are ingested by a host (usually a dog). Surgery by which the cyst is removed without leakage of the cyst contents is the preferred definitive treatment. Cyst leakage during removal can cause fatal anaphylactic reactions, and because of this complication, percutaneous aspiration of these cysts has been contraindicated. However, in expert hands with the use of concomitant antihelminthic therapy, percutaneous aspiration for both diagnosis and therapy has been shown to be safe.3 PAIR is a procedure that can be performed safely with long-term control of echinococcal cysts.

21/64 patients (33%) did not fulfil the safety criteria for NL treatment, eight of these due to medical and eight due to psychiatric comorbidity. 13/78 patients (17%) were unsuitable for treatment in the SOC arm, ten of these due to medical comorbidity. Wnt inhibitor Of those offered treatment in the SOC arm 63% (38/60) accepted treatment and 12% (9/60) started treatment. In the NL arm 47% (18/38) accepted and 21% (8/38) started treatment (p=ns). One patient in the SOC arm and two patients in the NL arm had to discontinue treatment early. Conclusions Treatment rates were low in both arms, and nurse led therapy did not significantly increase the number of patients starting treatment.

Further results including SVR rates are awaited as the trial is still on-going. Disclosures: Graham R. Foster – Advisory Committees or Review Panels: GlaxoSmithKline, Novartis, Boehringer Ingelheim, Tibotec, Chughai, Gilead, Janssen, Idenix, GlaxoSmithKline, Novartis, Roche, Tibotec, Chughai, Gilead, Merck, Janssen, Idenix, BMS; Board Membership: Boehringer Ingelheim; Grant/Research Support: Chughai, Roche, Chughai; Speaking and Teaching: Roche, Gilead, Tibotec, Merck, BMS, Boehringer Ingelheim, Gilead, Janssen The following

people have nothing to disclose: Jan Kunkel, Heather Hedgehog antagonist Lewis, Mandie Wilkinson Purpose: Fifty to 75% of individuals chronically infected with HGV are unaware MCE they are infected. New GDG guidelines recommending HCV testing for baby boomers will help promote HCV testing among individuals who already access primary care; however, many individuals at highest risk for HGV do not have a primary care provider and therefore may never be tested for HGV. Understanding the demographic factors and risk behaviors of HCV positive individuals in the most heavily impacted communities of the US can help inform development of HCV testing, linkage to care and treatment programs for individuals with limited access to health services. Methods: The “Do One Thing” Campaign is a testing, linkage to care, and treatment program that stimulates demand for and provides

HIV and HCV testing in non-clinical settings across an entire zip code in a heavily impacted neighborhood of Southwest Philadelphia. From December 2012 to May 2013, 466 participants 18 years and older were screened for HCV using the Oraquick rapid HGV antibody test; we also conducted confirmatory testing for all individuals with reactive results. After providing informed consent, individuals completed a 20-minute survey. Demographic and risk behavior data was collected on an iPad via an online secure survey. We used multivariable logistic regression models to explore the strongest predictors of testing positive for HCV. Results: Anti-HCV seroprevalence in this population was 4%. Ninety percent of individuals tested were African American, 62% were insured, and 53% were male.

8 years. In their study, gastric cancer developed in persons infected with H. pylori but not in the uninfected persons, which is a conclusive evidence that H. pylori has a crucial role in the development of gastric cancer. In Japan,

intestinal type mucosal gastric cancer without concomitant lymph node metastasis is usually treated with endoscopic resection,[4] which removes the tumor and surrounding mucosa such that metachronous gastric cancer could develop at sites other than that of the endoscopic resection. Fukase et al.[5] investigated the prophylactic effect of H. pylori eradication on the development of metachronous gastric carcinoma after endoscopic resection for early gastric cancer. After endoscopic treatment, they randomly assigned patients to receive H. pylori eradication regimen or not. The cumulative incidence selleck chemicals of gastric cancer was significantly higher in the non-eradication therapy group than in the group undergoing eradication treatment. They concluded BI6727 that prophylactic eradication of H. pylori after endoscopic resection of early gastric cancer should be performed to prevent the development of metachronous gastric carcinoma. As to the gastric remnant, the effect of H. pylori eradication on the development of metachronous gastric carcinoma has not been clearly determined.

Evaluation of the risk of cancer in the intact stomach mucosa requires monitoring of atrophic or intestinal metaplastic changes. In the remnant stomach, however, evaluation can be confounded by H. pylori infection and by reflux of bile, intestinal juice or pancreatic juice, both of which are important risk factors for secondary carcinogenesis in the remnant stomach mucosa.[6, 7] It has been reported that H. pylori infection plays a major role in gastritis of the remnant stomach after Billroth I anastomosis, whereas 上海皓元 bile reflux is the major cause after the Billroth II procedure.[8] The remnant stomach after Billroth II anastomosis is a complicated circumstance because it is affected by H. pylori infection and bile reflux. Kato et al.[9] measured

the gastric juice pH of the patients who had undergone distal gastrectomy and H. pylori eradication therapy. pH levels in these patients were normalized after eradication in the remnant stomach, and they predicted that this effect may reduce the risk of secondary stomach carcinogenesis. Our hypothesis is that H. pylori infection triggers the development of histological inflammation in the remnant stomach after Billroth I anastomosis, which increases the risk of gastric carcinogenesis. The aim of this study was to clarify whether eradicating the bacteria results in normalization of the histological abnormalities, which may consequently reduce the risk of cancer in the remnant stomach. To more clearly understand the role of H. pylori rather than bile acid in the development of metachronous gastric carcinoma, we focused on patients with a remnant stomach after Billroth I anastomosis.