3% (65/82), 84.2% (69/82) and 92.7% (76/82); the HBV-DNA loads were (3.108 ± 1.394), (2.637 ± 0.571) and (2.670 ± 0.982) log10 copies/ml; the rates of HBV DNA clearances were 65.9% (54/82), 81.7% (67/82) and 89.0% (73/82) respectively. And for the 60 cases of HBeAg positive patients, during the end of the therapy of year 1, 2 and 3, the rates of HBeAg loss were 18.3% (11/60), 43.3% (26/60) and 41.7% (25/60); the rates of HBeAg seroconversion were 16.7% (10/60), 28.3% (17/60) and 31.7% (19/60) respectively. Conclusion: Continuous entecavir treatment in nucleos(t)ide-naïve

chronic hepatitis B patients could inhibit HBV replication effectively, enhance ALT normalization and HBeAg seroconversion. And prolongationg of treatment may increase the rates of HBV DNA clearances, HBeAg loss and HBeAg seroconversion.

find more Key Word(s): 1. Hepatitis B; 2. Chronic; 3. Entecavir; 4. Efficacy; “
“Antidiabetic thiazolidinediones (TZD) have in vitro antiproliferative selleck compound effect in epithelial cancers, including hepatocellular carcinoma (HCC). The effective anticancer properties and the underlying molecular mechanisms of these drugs in vivo remain unclear. In addition, the primary biological target of TZD, the ligand-dependent transcription factor peroxisome proliferator-activated receptor γ (PPARγ), is up-regulated in HCC and seems to provide tumor-promoting responses. The aim of our study was to evaluate whether chronic administration of TZD may affect hepatic carcinogenesis Galeterone in vivo in relation to PPARγ expression and activity. The effect of TZD oral administration for 26 weeks was tested on tumor formation in PPARγ-expressing and PPARγ-deficient mouse models of hepatic carcinogenesis.

Proteomic analysis was performed in freshly isolated hepatocytes by differential in gel electrophoresis and mass spectrometry analysis. Identified TZD targets were confirmed in cultured PPARγ-deficient hepatocytes. TZD administration in hepatitis B virus (HBV)–transgenic mice (TgN[Alb1HBV]44Bri) reduced tumor incidence in the liver, inhibiting hepatocyte proliferation and increasing apoptosis. PPARγ deletion in hepatocytes of HBV-transgenic mice (Tg[HBV]CreKOγ) did not modify hepatic carcinogenesis but increased the TZD antitumorigenic effect. Proteomic analysis identified nucleophosmin (NPM) as a TZD target in PPARγ-deficient hepatocytes. TZD inhibited NPM expression at protein and messenger RNA levels and decreased NPM promoter activity. TZD inhibition of NPM was associated with the induction of p53 phosphorylation and p21 expression. Conclusion: These findings suggest that chronic administration of TZD has anticancer activity in the liver via inhibition of NPM expression and indicate that these drugs might be useful for HCC chemoprevention and treatment. HEPATOLOGY 2010 Hepatocellular carcinoma (HCC) is the most frequent solid tumor of the liver.

HA-tagged Cas FL and Cas ΔSH3 (Fig. 4A)28 were retrovirally introduced into NP31 cells, and the expression levels of their protein products were examined by western blotting with an anti-HA antibody that detects exogenous Cas and selleck inhibitor also with an anti-Cas antibody that detects endogenous and exogenous Cas. As shown in Fig. 4B, Cas FL and Cas ΔSH3 were expressed at almost comparable levels (left panel) that were approximately 5 to 6 times greater than those of endogenous Cas (right panel). To examine the effect of SH3 deletion on Cas-mediated signaling, cells were plated onto fibronectin (FN)-coated dishes, and the cell lysates were subjected to immunoprecipitation

followed by western blotting. As shown in Fig. 4C, anti-HA and anti-Cas2 immunoprecipitates blotted by an anti-phosphotyrosine antibody (4G10) find more showed that Cas ΔSH3 was much less tyrosine-phosphorylated than Cas FL (left panel), and tyrosine phosphorylation of endogenous Cas was barely detectable in Cas ΔSH3–expressing cells (right

panel). In addition, as shown in Fig. 4D, anti-CrkII immunoprecipitates blotted by anti-HA or anti-Cas2 antibodies revealed that Cas ΔSH3 was far less efficiently coprecipitated with CrkII than Cas FL (left panel), and CrkII did not detectably coprecipitate endogenous Cas in lysates from Cas ΔSH3–expressing cells (right panel). These findings indicate that Cas ΔSH3 functions as a reduction-of-function molecule in NP31 cells as CasΔex2/Δex2 does in mouse embryonic fibroblasts (MEFs).32 To examine the suppressive function of Cas ΔSH3 on actin stress fiber formation, parental,

Cas FL–expressing, and Cas ΔSH3–expressing NP31 cells were subjected to cytoskeletal staining. As shown in Fig. 5A, prominent actin stress fiber formation was detected in parental cells and to a comparable extent in Cas FL–expressing cells (indicated by arrows in the lower left and middle panels). In contrast, no obvious actin stress fibers were formed and only dotlike actin filaments were observed in Cas ΔSH3–expressing NP31 cells (indicated by arrowheads in the lower right panel). We then investigated the formation BCKDHA of fenestrae in NP31 cells by electron microscopy because the architectural control of fenestrae is regulated by the actin cytoskeleton.1, 3, 7 Parental and Cas FL–expressing NP31 cells exhibited a number of fenestrae of various diameters (left and middle panels in Fig. 5B). Counting of the fenestrae per square micrometer showed that although the number of fenestrae in Cas FL–expressing cells was slightly higher than that in parental cells (5.80 ± 0.37 for parental cells and 6.13 ± 0.39 for Cas FL–expressing NP31 cells), the difference was not statistically significant (left and middle bars in Fig. 5C).

HA-tagged Cas FL and Cas ΔSH3 (Fig. 4A)28 were retrovirally introduced into NP31 cells, and the expression levels of their protein products were examined by western blotting with an anti-HA antibody that detects exogenous Cas and Selleckchem Sorafenib also with an anti-Cas antibody that detects endogenous and exogenous Cas. As shown in Fig. 4B, Cas FL and Cas ΔSH3 were expressed at almost comparable levels (left panel) that were approximately 5 to 6 times greater than those of endogenous Cas (right panel). To examine the effect of SH3 deletion on Cas-mediated signaling, cells were plated onto fibronectin (FN)-coated dishes, and the cell lysates were subjected to immunoprecipitation

followed by western blotting. As shown in Fig. 4C, anti-HA and anti-Cas2 immunoprecipitates blotted by an anti-phosphotyrosine antibody (4G10) Selleck Target Selective Inhibitor Library showed that Cas ΔSH3 was much less tyrosine-phosphorylated than Cas FL (left panel), and tyrosine phosphorylation of endogenous Cas was barely detectable in Cas ΔSH3–expressing cells (right

panel). In addition, as shown in Fig. 4D, anti-CrkII immunoprecipitates blotted by anti-HA or anti-Cas2 antibodies revealed that Cas ΔSH3 was far less efficiently coprecipitated with CrkII than Cas FL (left panel), and CrkII did not detectably coprecipitate endogenous Cas in lysates from Cas ΔSH3–expressing cells (right panel). These findings indicate that Cas ΔSH3 functions as a reduction-of-function molecule in NP31 cells as CasΔex2/Δex2 does in mouse embryonic fibroblasts (MEFs).32 To examine the suppressive function of Cas ΔSH3 on actin stress fiber formation, parental,

Cas FL–expressing, and Cas ΔSH3–expressing NP31 cells were subjected to cytoskeletal staining. As shown in Fig. 5A, prominent actin stress fiber formation was detected in parental cells and to a comparable extent in Cas FL–expressing cells (indicated by arrows in the lower left and middle panels). In contrast, no obvious actin stress fibers were formed and only dotlike actin filaments were observed in Cas ΔSH3–expressing NP31 cells (indicated by arrowheads in the lower right panel). We then investigated the formation Liothyronine Sodium of fenestrae in NP31 cells by electron microscopy because the architectural control of fenestrae is regulated by the actin cytoskeleton.1, 3, 7 Parental and Cas FL–expressing NP31 cells exhibited a number of fenestrae of various diameters (left and middle panels in Fig. 5B). Counting of the fenestrae per square micrometer showed that although the number of fenestrae in Cas FL–expressing cells was slightly higher than that in parental cells (5.80 ± 0.37 for parental cells and 6.13 ± 0.39 for Cas FL–expressing NP31 cells), the difference was not statistically significant (left and middle bars in Fig. 5C).

Changes in bilirubin levels showed

a 10% improvement in the C/EBPα-saRNA group when compared to the control groups. Additionally, Selleckchem AZD0530 a 10% improvement in AST levels and 30% improvement in ALT levels were observed in the C/EBPα-saRNA-treated group when compared to the control groups. More significant was the reduction in tumor burden and the inhibition of preneoplastic lesions as detected by a 40% reduction in GST-p staining in the liver sections from the C/EBPα-saRNA-treated group. From a clinical perspective, this represents a very attractive therapeutic avenue since the expression level of C/EBPα in matched tumor tissues and nontumor tissues of HCC patients is down-regulated in the majority of tumor specimens. Moreover, patients with tumor samples showing higher levels of C/EBPα have a longer survival rate than those patients with tumor samples in which the expression of the C/EBPα is lower.[41] Our data support this evidence, suggesting

that up-regulation of C/EBPα provides a strong antiproliferative role in hepatocytes.[14, 42] To better understand the global molecular effect of C/EPBα-saRNA more specific to liver cancer, we performed a liver cancer pathway gene expression profile analysis. Such analysis of whole tumors is frequently confounded by the presence of cell types other than those with a transformed Liproxstatin-1 molecular weight phenotype.[43] Therefore, we profiled the gene expression changes brought about by C/EPBα-saRNA in HepG2 cells. The expression pattern of the liver cancer genes varied greatly between untransfected and C/EPBα-saRNA-transfected HepG2 cells. After normalization and cluster analysis, several important genes were significantly altered in expression. From the list of 20 genes that were up-regulated, 18 were known tumor suppressor genes. Of note was the up-regulation of RB, TP53, BID, and BAX to regulate cell cycle and apoptosis. The down-regulation of key genes were also noted, in particular ADAM17, a metalloproteinase reported as being a pathological feature of HCC.[44] ADAM17

is known to cause the shedding of receptor ligands such as epidermal TCL growth factor (EGF) and tumor necrosis factor alpha (TNFα),[45, 46] thus preventing regulation of key signaling events for normal cell signaling. Upon further analysis of the tumor suppressor genes, we noticed a pathway-defined trend where key effector genes of the tumor suppressors were down-regulated. Examples of this included repression of RHOA following up-regulation of the tumor suppressor DLC1, or up-regulation of RUNX3 to reverse expression of the oncogenes involved in EMT. Here we observed down-regulation of CTNB1 (β-catenin), HGF, SMAD7, and TGFB1. We also observed increased expression of the tumor suppressor SOC3, a known regulator of apoptosis and cell adhesion. Concomitantly, we also observed down-regulation of the associated SOC3 oncogenes including STAT3, cyclin-D1 (CCND1), XIAP, BIRC5, and MCL1.

In animal models, cells engraft and differentiate into hepatocyte-like cells expressing OTC enzyme. HHALPC improve bilirubin levels in Gunn rats. Hepastem was investigated in an open label, phase I/II safety study in patients with urea cycle

disorders (UCD) and Crigler-Najjar syndrome (CN) with preliminary efficacy secondary endpoints. Methods: Primary objective was safety at 6 months and secondary objectives, beside safety at 12 months, included efficacy at 6 and 12 months. Readouts included measure of de novo urea production in UCD patients based on 13C incorporation into urea up to 120 minutes after 1 dose of oral Na [1-13C] acetate (expressed as [13C] blood urea Area

Under the Curve or AUC-120), measures of blood ammonia and see more glutamine in UCD patients, natural protein intake in UCD patients, blood total find more bilirubin in CN patients, as well as evaluation of quality of life (QoL) by PedsQL™ for both diseases. A dose equivalent to 0.4 to 6.1% of the liver mass was infused in the portal vein through a transhepatic catheter placed under radioguidance. Over 1 to 4 consecutive days, 1 cycle of cells was infused to 14 UCD patients (1.5m to 17yrs, 8 boys, 6 girls, ) and 6 CN patients (3.5yrs-9yrs, 2 boys, 4 girls). Results: Adverse events were more frequent during the infusion cycle and within 14 following days, e.g. abnormal lab values, non-specific symptoms, and transient metabolic decompensations. Two patients had a thrombotic event: one had a non-occlusive portal thrombus resolving after 1 month; one had a left portal vein thrombosis with stable liver function tests during 6 month follow-up. Rate of infection was within the expected incidence for the studied population. [13C] blood urea AUC-120, highly variable between patients at baseline, increased in all Erythromycin but one patient

between baseline and six months (101 % increase (95%CI Lower Limit: 28%, Upper Limit 217%, p value: 0.004). Compared to 1 year pre-infusion available data, median ammonia post-infusion tended to decrease in <12yo UCD patients. Four patients increased slightly their natural protein tolerance. In CN patients median bilirubin values decreased in 3/6 CN (∼−40,−30 & −10%). Overall, QoL results remained stable. Conclusion: One cycle of hepastem (dose 0.4% to 6.1% of liver mass) is safe and preliminary data show functional metabolic changes in UCD and CN patients. Disclosures: Etienne M. Sokal – Board Membership: Promethera Biosciences; Management Position: Promethera Biosciences; Patent Held/Filed: Promethera Biosciences Patrick J.

Members include: J. Gregory Fitz, MD, Co-Chair Gary L. Davis, MD, Co-Chair Kenneth D. Chavin, MD, PhD Mark J. Czaja, MD Adrian M. Di Bisceglie, MD, FACP Marc G. Ghany, MD Mary E. Rinella, MD Ronald J. Sokol, MD Gyongyi Szabo, MD, PhD Rebecca T. Wells, MD The overall goal of The Liver Meeting® is to provide a forum for the exchange of groundbreaking research and clinical information in diseases of the liver and biliary tract and in liver

transplantation. The Liver Meeting® 2013 is designed for physicians, surgeons, scientists, educators, nurses, physician assistants, and all other hepatology health professionals. AASLD takes responsibility for the content, quality, and scientific integrity of this CME activity.

Provide a forum for exchange of groundbreaking Selleckchem EPZ6438 basic and clinical research in liver disease Create an arena for the BGB324 cell line presentation and interchange of opinions on state-of-the-art care and management of the full spectrum of patients with liver disease The American Association for the Study of Liver Diseases (AASLD) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. AASLD designates these live activities for AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Annual Meeting

(State-of-the-Art Lectures; President’s Choice; General Hepatology Update; Advances for Practitioners; Plenaries and Parallel Sessions; Global Forum; Federal Focus; and Emerging Trends) 18. 0 CME Credits Postgraduate Course 12. 0 CME Credits/***11. 75 Contact Hours Basic Research Workshop4. 0 CME Credits AASLD/IASL Program*4. 0 CME Credits Hepatology Associates Course5. 5 CME Credits/***5. 0 Contact Hours AASLD/ILTS Transplant Course* 7. 5 CME Credits/***6. 0 Contact Hours AASLD/NASPGHAN Pediatric Symposium** 3. 0 CME many Credits AASLD/ASGE Endoscopy Course** 6. 5 CME Credits Maintenance of Certification 2. 0 CME Credits *These activities have been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of the American Association for the Study of Liver Diseases (AASLD), and the International Liver Transplantation Society (ILTS) and the International Association for the Study of the Liver (IASL). AASLD is accredited by the ACCME to provide continuing medical education for physicians. **Co-sponsored activity: The American Association for the Study of Liver Diseases (AASLD) is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Of 312 patients, 176 (56.4%) were diagnosed with non-alcoholic

steatohepatitis. During a median follow-up period of 4.8 years Doxorubicin (range, 0.3–15.8), six patients (1.9%) developed HCC, and 20 (6.4%) developed extrahepatic cancer. Multivariate analysis identified fibrosis stage (≥3; hazard ratio [HR], 12.3; 95% confidence interval [CI], 1.11–136.0; P = 0.041) as a predictor for HCC and type IV collagen 7s (>5 ng/mL; HR, 1.74; 95% CI, 1.08–2.79; P = 0.022) as a predictor for extrahepatic cancer. Eight patients (2.6%) died during the follow-up period. The most common cause of death was extrahepatic malignancy. None died of cardiovascular disease. Multivariate analysis identified type IV collagen 7s (>5 ng/mL; HR, 3.38; 95% CI, 1.17–9.76; P = 0.024) as a predictor for mortality. The incidence of extrahepatic cancer was higher than that of HCC. Severe

fibrosis was a predictor for HCC. Patients with NAFLD and elevated type IV collagen 7s levels are at increased risk for extrahepatic cancer and overall mortality. “
“Association between genetic variations in alcohol-related enzymes find more and impaired ethanol biodisposition has not been unambiguously proven, and the effect of many newly described polymorphisms remains to be explored. The aims of this study are to elucidate the influence of genetic factors in alcohol biodisposition and effects. We analyzed alcohol pharmacokinetics and biodisposition after the administration of 0.5 g/kg ethanol; we measured ethanol effects on reaction time and motor time in response Cediranib (AZD2171) to visual and acoustic signals, and we analyzed 13 single nucleotide polymorphism (SNPs) in the genes coding for ADH1B, ADH1C, ALDH2, and CYP2E1 in 250 healthy white individuals. Variability in ethanol pharmacokinetics and biodisposition is related to sex, with

women showing a higher area under the curve (AUC) (P = 0.002), maximum concentration (Cmax) (P < 0.001) and metabolic rate (P = 0.001). Four nonsynonymous SNPs are related to decreased alcohol metabolic rates: ADH1B rs6413413 (P = 0.012), ADH1C rs283413 (P < 0.001), rs1693482 (P < 0.001), and rs698 (P < 0.001). Individuals carrying diplotypes combining these mutations display statistically significant decrease in alcohol biodisposition as compared with individuals lacking these mutations. Alcohol effects displayed bimodal distribution independently of sex or pharmacokinetics. Most individuals had significant delays in reaction and motor times at alcohol blood concentrations under 500 mg/L, which are the driving limits for most countries. Conclusion: Besides the identification of new genetic factors related to alcohol biodisposition relevant to whites, this study provides unambiguous identification of diplotypes related to variability in alcohol biodisposition. (HEPATOLOGY 2010;51:491–500.) Effects of alcohol drinking vary among individuals.

Sporadic MSI cancers also differ in that they arise on a background of widespread gene promoter hypermethylation termed the CpG island methylator phenotype (CIMP).7 Of the mismatch repair gene family, only MLH1 is targeted for promoter hypermethylation,

so sporadic MSI cancers are all MLH1-deficient, unlike Lynch syndrome cancers where the mission protein may be MLH1, MSH2, MSH6 or PMS2. A clinical, histological and molecular testing algorithm for the identification of Lynch syndrome is suggested in Figure 1. The article by Yoon and colleagues in this issue of the Journal focuses on sporadic MSI cancer, methods of identification and clinicopathological associations.8 Critical selleck compound library to the findings of any such studies are the methods used to identify MSI cancers and the protocols in place to select a homogeneous DMXAA manufacturer study population. Immunohistochemical staining for

mismatch repair proteins is inexpensive and offered routinely in pathology laboratories. MLH1 and MSH2 are the two most commonly targeted proteins in Lynch syndrome, although the addition of MSH6 and PMS2 to the staining panel increases the number of Lynch cancers identified and where possible should be undertaken. MLH1 immunostaining is sufficient to detect sporadic disease. It is therefore surprising that Yoon et al. chose to include 85 patients (41% of study cases) with loss of MSH2 expression as these cases most likely represent Lynch syndrome despite the family history not meeting the Amsterdam criteria. The MLH1 immunostain in particular may be subject to technical variation. Yoon et al. make the important observation that technical issues, such as delayed fixation, are important for Urease staining efficacy. Some difficult-to-interpret cases may be resolved if staining is scored by a specialist pathologist, and

further clarified by addition of PCR-based MSI testing of tumors with indefinite staining patterns.9 PCR-based MSI testing is more expensive to perform and available in fewer testing centers. The MSI five-marker panel used by Yoon et al. and criteria of two positive markers to determine MSI reflects standard practice and the recommendations of the NCI Workshop on Microsatellite Instability conducted in 1998.10 In 2008, Nagasaka and colleagues subtly refined this definition of MSI to require at least one positive mononucleotide repeat tract mutation and one other marker of the NCI panel.11 This modified definition highlights the specificity of mononucleotide repeat tracts in detecting MSI and would reduce the small number of false positives arising due to mutation of two dinucleotide markers. Patient exclusion is as important as inclusion when designing a study to better understand a particular tumor subgroup. Yoon et al. used Amsterdam I or II criteria to exclude hereditary cases.

71% respectively, the intervention group was significantly lower than the control group Conclusion: Through effective nursing intervention to reduce the incidence of postoperative adverse reactions, improves patient’s quality of life. Key Word(s): 1. Liver biopsy; 2. Adverse reactions; 3. Nursing intervention; Presenting Author: ODD HELGE GILJA Additional

Authors: FREDRIK SAEVIK, KIM NYLUND, TRYGVE HAUSKEN Corresponding Author: ODD HELGE GILJA Affiliations: Haukeland Palbociclib purchase University Hospital Objective: Crohn’s disease is characterized by periods of remission and relapse. To improve patient management objective measurements of the degree of local inflammation in the gastrointestinal wall should be made. Increased microvessel density and perfusion are typical features of acute inflammation. Indirect measurements of these parameters can be measured using contrast-enhanced ultrasound (CEUS). The aim of this study was to investigate whether CEUS can provide prognostic information about patients treated medically for an acute exacerbation of Crohn’s disease. Methods: 13 patients with Crohn’s disease were prospectively recruited in a pilot study at Haukeland University Hospital. All patients received medical treatment for an acute exacerbation with systemic steroids, adalimumab or infliximab. Patients who had to change treatment regime during

the follow-up were categorized as having lack of treatment effect. The Resveratrol patients were examined at time AZD6244 0, 1, 3 and 12 months after initiation of the treatment with clinical scoring, blood tests and CEUS. Ultrasound was performed with a Logiq E9 ultrasound scanner (GE Healthcare, Milwaukee, USA) and contrast agents (Sonovue, Bracco, Milan Italy). The perfusion analysis was performed with commercially available software (Vuebox, Bracco Suisse SA, Geneva Switzerland). The program analyzes the contrast intensity in a selected

area, fits the data to a standardized curve and derives variables such as peak contrast intensity, area under the curve and slope of the curve. Results: In six of the 13 patients, the treatment regime was changed during the study period. There were no significant differences in perfusion between the two groups at the start of the treatment or examinations after 3 and 12 months. There was, however, a significant difference between the two groups for peak contrast intensity (p < 0,022), area under the curve (p < 0,05), during the wash in phase (p < 0,014), wash out phase (p < 0,07) and slope (wash in rate: p < 0,035, wash out rate: p < 0,014, respectively) at the examination one month after the initiation of the treatment. Conclusion: CEUS enables high-resolution perfusion analysis of the intestinal wall. One month after starting treatment in patients with Crohn’s disease prognostic information regarding treatment response can be obtained. Key Word(s): 1. Ultrasound; 2. CEUS; 3. Crohn’s disease; 4.

The exact reason for this change is difficult to determine but reflects the growing affluence in Asia. Gastric acid secretion would have increased in a “healthier” population. In an interesting and important study, Kinoshita has shown an increase in both basal and maximal acid output in Japanese patients over a 20-year period.71 Dramatic socio-economic development in Asia has resulted in consequent lifestyle changes. A change in diet and physical activity and an increase in BMI and obesity have often been thought to be putative. Older age and male sex have been shown in many studies to be associated with GERD.22,29,31 In a region where life expectancy has now increased

markedly, a Palbociclib datasheet higher prevalence of GERD could also reflect the ageing of the population. This has often been linked to H. pylori infection, but the relationship has not been straightforward. Kinoshita et al. showed in their study that acid secretion had increased in both elderly and not elderly patients, regardless of H. pylori status, suggesting that H. pylori infection did not play a significant role in this change.71 However, cross-sectional and case-control studies studies from Asia

have shown an inverse relationship between BAY 57-1293 nmr the prevalence of H. pylori and GERD.72–74 Further support for the role of H. pylori infection is shown by the negative association with more virulent strains of Isoconazole H. pylori, as has been reported in the Western literature.75–77 However, there is an association between H. pylori eradication and GERD has been the subject of conflicting reports. Koike et al. have shown in two studies, an increase in gastric acid with H. pylori eradication and, conversely decreased acid secretion in the presence of H. pylori. They proposed

that this fall was protective against the development of erosive reflux esophagitis.78,79 Wu et al. showed that H. pylori eradication led to more “difficult-to- treat” cases of GERD.80 Hamada et al. and Inoue et al. have both shown an increase in incidence of erosive esophagitis after H. pylori eradication.81,82 However, Kim et al.83 reported no association with H. pylori eradication, and Tsukuda only found an association only in patients with hiatus hernia.84 H. pylori infection especially with the antral-predominant or duodenal ulcer phenotype, is associated with an increase in gastric acid secretion. This would normalize with H. pylori eradication. On the other hand, the pangastritis phenotype of H. pylori infection is associated with a decrease in gastric acid secretion, so that a rebound of acid secretion would occur with H. pylori eradication unless irreversible atrophic gastritis has already occurred.85 This difference in the phenotype of H. pylori infection likely underlies the variable outcomes of H. pylori eradication that have been reported.