In refractory GERD patients, the treatment of weakly acid and weakly alkaline reflux is more effective to PPI treatment. Key Word(s): 1. GERD; 2. PPI; Presenting Author: RAJESHKUMAR PARAMASIVAM Additional Authors: SHASHIKUMAR MENON, SARAVANAN ARJUNAN, OOI TIAM, NORHANIZA BAKAR, MAYLENE WONG, CHAN KAI Corresponding Author: RAJESHKUMAR PARAMASIVAM Affiliations: UiTM Objective: To determine presence of celiac disease (CD) among high risk patients in Kuala Lumpur General Hospital from December 2011 to March

2012. Methods: Patients from 12–70 years of age, presenting with unexplained iron deficiency anemia (IDA), chronic diarrhea or weight loss were recruited. A gastroscopy with total of 6 biopsies from 2nd part of duodenum was performed. Patients with other causes for IDA, chronic diarrhea and weight loss were excluded. All of them had anti-transglutaminase antibody (anti-tTG) and anti-gliadin LBH589 concentration antibody (AGA) tested using immunoblot test. Patients with positive anti-tTG, with or without

duodenal histopathological changes were diagnosed as classical or atypical CD respectively. Results: Total of 29 patients were recruited for this study. 13 were excluded. 16 patients were analyzed, 11 had IDA and 5 presented with unexplained chronic diarrhea with weight loss. The mean (SD) hemoglobin was 8.4 (1.5) g/dl among the IDA patients. Indians were the largest group (n = 7). 2 (12.5%) patients had positive anti-tTG comprising of 1 Malay and 1 Indian. Duodenal histology showed chronic duodenitis and the other was normal; sufficient PD0325901 concentration to be diagnosed as atypical CD. Total of 5 patients had positive AGA antibody. Neither transferrin saturation (P value = 0.122) nor race (P value = 0.95) showed statistical difference. Conclusion: Celiac disease is not uncommon among high risk population in Malaysia. Larger scale studies are required to determine the prevalence of CD among high risk population. Duodenal

biopsy and celiac serology the must be done routinely in high risk patients. Key Word(s): 1. Celiac disease; 2. Presence; 3. Malaysia; 4. High risk; Presenting Author: HAEWON KIM Additional Authors: JIE-HYUN KIM Corresponding Author: HAEWON KIM Affiliations: Gangnam Severance Hospital Objective: Locally advanced esophageal cancer is highly aggressive and fatal, because they often persist or recur after definitive concurrent chemoradiation (CCRT). But, little is known about the failure patterns after definitive CCRT, especially in esophageal squamous cell carcinoma (SCC). Thus, we evaluated treatment failure patterns after definite CCRT and predictive factors of treatment response in esophageal SCC. Methods: We retrospectively evaluated 136 patients with esophageal SCC treated with definitive CCRT at Severance and Gangnam Severance Hospital from January 2005 to December 2010. We analyzed the factors which affected the complete remission after CCRT.

No adverse effects were seen in this acute study. In a repeated administration toxicity study, male Sprague Dawley rats were treated iv with PEG-60 in doses up to 11.0 mg kg−1 every other day for 4 weeks. Clinical parameters and laboratory assays as noted above and postmortem examination, such as necropsy, organ weight analysis and light microscopic histopathology of all organs and tissues, were conducted to assess potential adverse

changes. The highest dose of 11 mg kg−1 used in the repeated administration study is in the range of the total expected cumulative lifetime dose of PEG-60 EPZ-6438 ic50 to be given with BAY 94–9027 in humans. Rats received up to 11 mg kg−1 every other day for 4 weeks and no adverse effects or histopathological changes were observed after treatment with PEG-60. Standard genotoxicity studies with the PEG-60 part of BAY 94–9027 were negative. In addition, the non-clinical programme with BAY 94-9027 assessed systemic toxicity, including male reproductive organ effects (addressing reproduction and fertility) and local tolerance. BAY 94–9027 did not induce any protein- or PEG-related adverse effects. No vacuolation of any organ or tissue was seen. Carcinogenicity studies were not considered necessary, as neither the protein (FVIII) nor

the PEG part of BAY 94–9027 has any genotoxic potential, nor do they express any mechanism that is related with tumour formation. The non-clinical safety programme is based on the ICH Selleckchem Hydroxychloroquine S6 (R1) guideline of biotechnology products and accepted practice in biotechnology industry. The majority of published metabolism studies have investigated low molecular weight PEGs [13]. Although no data have been published on the metabolism of PEGylated biologics, there is evidence that the protein part is degraded by proteases with release of their PEG-moieties much [12, 13]. The only comprehensive

and often cited data set on the elimination of different molecular weight PEGs have been generated in mice by Yamaoka et al. [38, 39]. Polyethylene glycol in the range of 50 kDa had a long half-life in circulation, but lower organ accumulation compared with PEGs of other molecular weights (higher and lower). The following summarizes some of their findings in mice: Small PEG molecules are more rapidly cleared from circulation than large ones (which are still cleared, but slower), e.g. the half-life for a 3 kDa PEG increases from 18 min to 24 h for a 190 kDa PEG. PEG excretion is closely related to the half-life in circulation. Larger PEG molecules do not permeate into tissue to the degree as smaller PEGs of molecular weight 20 kDa and below.

Despite this disadvantage, ASL estimates of CBF appeared to be of sufficient quality to localize regions of highest vascularity when compared with DSC. A statistically significant, positive linear correlation was observed between ASL and DSC estimates of mean normalized CBF within both FLAIR hyperintense (Pearson’s correlation coefficient, R2 = .706, P < .0001) and contrast-enhancing regions (Pearson's correlation coefficient, R2 = .809, P < .0001) on a per patient basis (Figs 2A, B). The selleck linear slope that best explained the correlation between normalized

ASL and DSC estimates of CBF in all tumors was .72 ± .04 standard error of the mean (SEM) for FLAIR hyperintense and .68 ± .03 SEM for contrast-enhancing selleck kinase inhibitor regions, suggesting DSC had about a 3:1 higher dynamic range of CBF measurements

compared to ASL. Similarly for glioblastoma patients, a statistically significant linear was observed in FLAIR (Pearson’s correlation coefficient, R2 = .829, P < .0001) and contrast-enhancing regions (Pearson's correlation coefficient, R2 = .872, P < .0001). The linear relationship between ASL and DSC estimates of CBF in glioblastomas was similar to that of all tumors, measuring .74 ± .05 SEM for FLAIR and .66 ± .04 SEM for contrast-enhancing regions. These results suggest overall estimates of tumor blood flow may be similar between the two techniques, albeit to a different level of sensitivity and dynamic range. Surprisingly, only a minority of patients examined in the current study demonstrated a statistically significant linear correlation between DSC and ASL measurements of relative CBF on a voxel-wise basis for areas of FLAIR and contrast-enhanced regions. As illustrated in Figure

3A, some patients did illustrate a strong voxel-wise association Tenoxicam between the two measurements of CBF, specifically showing a 2:1 correspondence (slope ∼.5) between DSC and ASL DSC. The vast majority of patients, however, had voxel-wise relationships similar to those illustrated in Figure 3B, where no apparent linear relationship was evident. Approximately 31% of glioblastoma patients (4 of 13) demonstrated a significant voxel-wise linear correlation between DSC and ASL measurements of CBF with FLAIR hyperintense regions and only 38% of glioblastoma patients (5 of 13) showed a significant correlation in contrast-enhancing regions (Chi-Squared Goodness of Fit, χ2red > 1.0, P < .05). Interestingly, both patients with anaplastic astrocytoma (WHO III) had a significant voxel-wise correlation between DSC and ASL measurements of CBF in both FLAIR and postcontrast regions of interest (Chi-Squared Goodness of Fit, χ2red > 1.0, P < .05).

This result is consistent with the observation that LCMV-induced IFN-α secretion in mice has been shown to increase STAT1 expression in NK cells, resulting in preferential STAT1 over STAT4 phosphorylation.6, 9, 11 It also extends the findings by Miyagi et al. on preferential STAT1 phosphorylation in HCV-infected patients,11 because we show that IFN-α exposure in vivo results in increased pSTAT1 levels, and that it correlates to increased TRAIL production and degranulation and decreased IFN-γ production

(Fig. 3). The clinical relevance of IFN-α signaling in NK cells is suggested by our observation that NK cell responsiveness and refractoriness correlate with the first-phase virological response to IFN-α-based therapy (Fig. 5). This analysis of NK cells is relevant for current research on biomarkers predicting IFN responsiveness and treatment outcome. Advantages of using NK cells check details as biomarkers

of IFN responsiveness are that they are readily accessible from the peripheral blood, and that both in vivo and in vitro NK cell responsiveness can easily be assessed in a short, standardized flow-cytometry–based assay by checking pSTAT1 levels. How does our system compare to other biomarkers of IFN responsiveness? A well-established biomarker for IFN responsiveness is the intrahepatic expression of interferon-stimulated genes (ISGs). Typically, ISGs are most highly expressed PD0332991 in vivo pretreatment in HCV-infected patients who respond poorly to IFN-α-based therapy.17 As a potential explanation, it has been proposed that high baseline activation of the endogenous IFN system does not allow a further increase of ISGs during IFN-based therapy, possibly because the ISG response has already reached maximal levels and/or inhibitory autocrine feedback mechanisms have been induced.18 In contrast to these ISG data, we did not find any evidence that pretreatment pSTAT1 levels or in vitro inducibility differed among HCV-infected patients (data not shown). Thus,

pSTAT1 induction is an independent measure for IFN responsiveness and may complement ISG analysis. How does the NK cell response correlate to the treatment response? Because all patients in our study achieved an EVR to PegIFN/RBV Flucloronide therapy at week 12, we were not able to assess NK cell responses in the context of the ultimate treatment outcome. On the other hand, we believe that late time points of PegIFN/RBV therapy are less relevant for our study, because NK cells exhibited their greatest response within the first days of therapy in parallel to the first-phase virological response (Figs. 1-4). Our data clearly indicate that near-maximal NK cell activation can be reached within hours of the first injection of PegIFN, because the response to additional in vitro stimulation with IFN-α was significantly reduced at later treatment time points (Fig. 4).

This result is consistent with the observation that LCMV-induced IFN-α secretion in mice has been shown to increase STAT1 expression in NK cells, resulting in preferential STAT1 over STAT4 phosphorylation.6, 9, 11 It also extends the findings by Miyagi et al. on preferential STAT1 phosphorylation in HCV-infected patients,11 because we show that IFN-α exposure in vivo results in increased pSTAT1 levels, and that it correlates to increased TRAIL production and degranulation and decreased IFN-γ production

(Fig. 3). The clinical relevance of IFN-α signaling in NK cells is suggested by our observation that NK cell responsiveness and refractoriness correlate with the first-phase virological response to IFN-α-based therapy (Fig. 5). This analysis of NK cells is relevant for current research on biomarkers predicting IFN responsiveness and treatment outcome. Advantages of using NK cells Gemcitabine datasheet as biomarkers

of IFN responsiveness are that they are readily accessible from the peripheral blood, and that both in vivo and in vitro NK cell responsiveness can easily be assessed in a short, standardized flow-cytometry–based assay by checking pSTAT1 levels. How does our system compare to other biomarkers of IFN responsiveness? A well-established biomarker for IFN responsiveness is the intrahepatic expression of interferon-stimulated genes (ISGs). Typically, ISGs are most highly expressed Palbociclib in vivo pretreatment in HCV-infected patients who respond poorly to IFN-α-based therapy.17 As a potential explanation, it has been proposed that high baseline activation of the endogenous IFN system does not allow a further increase of ISGs during IFN-based therapy, possibly because the ISG response has already reached maximal levels and/or inhibitory autocrine feedback mechanisms have been induced.18 In contrast to these ISG data, we did not find any evidence that pretreatment pSTAT1 levels or in vitro inducibility differed among HCV-infected patients (data not shown). Thus,

pSTAT1 induction is an independent measure for IFN responsiveness and may complement ISG analysis. How does the NK cell response correlate to the treatment response? Because all patients in our study achieved an EVR to PegIFN/RBV selleck therapy at week 12, we were not able to assess NK cell responses in the context of the ultimate treatment outcome. On the other hand, we believe that late time points of PegIFN/RBV therapy are less relevant for our study, because NK cells exhibited their greatest response within the first days of therapy in parallel to the first-phase virological response (Figs. 1-4). Our data clearly indicate that near-maximal NK cell activation can be reached within hours of the first injection of PegIFN, because the response to additional in vitro stimulation with IFN-α was significantly reduced at later treatment time points (Fig. 4).

Those studies are expected to have a significant impact on the optimization of treatments for patients with inhibitor as well as for patients with thrombophilia. Replacement therapy with factor VIII (FVIII) concentrates prepared from plasma or with recombinant FVIII (rFVIII) can elicit the production of specific antibodies neutralizing FVIII function, also called inhibitors

[1]. Different types of anti-FVIII antibodies have been distinguished. Type I and type II inhibitors have been defined as antibodies inhibiting FVIII activity completely or partially, respectively BMN-673 [2]. The mechanisms of action of type II inhibitor are still only partially understood and are still intensively studied. Competition with von Willebrand factor (VWF) has been demonstrated as one such mechanism [2]. Conversely, some inhibitors rely on the presence of VWF to inhibit FVIII activity [3,4]. A detailed analysis of the specificity of FVIII inhibitors has proven to be difficult because of the large diversity of the humoral response, including antibodies which do not interfere with FVIII activity [5]. Moreover, anti-idiotypic antibodies have been described that can neutralize FVIII inhibitors check details [6,7]. To circumvent difficulties inherent to the use

of polyclonal antibodies, we produced human monoclonal antibodies directed towards FVIII and representative of patients’ pathogenic antibodies by immortalizing memory B cells from haemophilia A patients with inhibitor [8]. We have applied that strategy to characterize at the clonal level the relation between alteration of FVIII B cell epitopes and humoral response of a mild haemophilia A patient (LE) with inhibitor, who maintained significant endogenous FVIII activity ASK1 despite the presence of a high level of FVIII inhibitor [9]. The FVIII gene

mutation carried by patient LE was located in the C1 domain. When we started those experiments, mutations in that FVIII region were known to be associated with a high incidence of inhibitors in mild/moderate haemophilia A patients [10], although the reason for such an association was unclear. Moreover, inhibitor antibodies recognizing the C1 domain had never been demonstrated and no role of the latter domain in FVIII function and/or stability had been determined [11,12]. Clonal characterization of patient LE antibodies offered therefore the potential of determining whether epitopes recognized by inhibitor antibodies were located in the C1 domain, but also provided an opportunity to analyse the structure/function relationship of a FVIII domain whose function was still completely unknown. In this review, the properties of a type II human monoclonal antibody derived from patient LE will be examined in details. The importance of an unusual glycosylation in the antigen binding site of the antibody will be highlighted. This review will also emphasize how that study unexpectedly improved understanding of FVIII structure/function relation.

Those studies are expected to have a significant impact on the optimization of treatments for patients with inhibitor as well as for patients with thrombophilia. Replacement therapy with factor VIII (FVIII) concentrates prepared from plasma or with recombinant FVIII (rFVIII) can elicit the production of specific antibodies neutralizing FVIII function, also called inhibitors

[1]. Different types of anti-FVIII antibodies have been distinguished. Type I and type II inhibitors have been defined as antibodies inhibiting FVIII activity completely or partially, respectively Z-VAD-FMK manufacturer [2]. The mechanisms of action of type II inhibitor are still only partially understood and are still intensively studied. Competition with von Willebrand factor (VWF) has been demonstrated as one such mechanism [2]. Conversely, some inhibitors rely on the presence of VWF to inhibit FVIII activity [3,4]. A detailed analysis of the specificity of FVIII inhibitors has proven to be difficult because of the large diversity of the humoral response, including antibodies which do not interfere with FVIII activity [5]. Moreover, anti-idiotypic antibodies have been described that can neutralize FVIII inhibitors PD0325901 [6,7]. To circumvent difficulties inherent to the use

of polyclonal antibodies, we produced human monoclonal antibodies directed towards FVIII and representative of patients’ pathogenic antibodies by immortalizing memory B cells from haemophilia A patients with inhibitor [8]. We have applied that strategy to characterize at the clonal level the relation between alteration of FVIII B cell epitopes and humoral response of a mild haemophilia A patient (LE) with inhibitor, who maintained significant endogenous FVIII activity RAS p21 protein activator 1 despite the presence of a high level of FVIII inhibitor [9]. The FVIII gene

mutation carried by patient LE was located in the C1 domain. When we started those experiments, mutations in that FVIII region were known to be associated with a high incidence of inhibitors in mild/moderate haemophilia A patients [10], although the reason for such an association was unclear. Moreover, inhibitor antibodies recognizing the C1 domain had never been demonstrated and no role of the latter domain in FVIII function and/or stability had been determined [11,12]. Clonal characterization of patient LE antibodies offered therefore the potential of determining whether epitopes recognized by inhibitor antibodies were located in the C1 domain, but also provided an opportunity to analyse the structure/function relationship of a FVIII domain whose function was still completely unknown. In this review, the properties of a type II human monoclonal antibody derived from patient LE will be examined in details. The importance of an unusual glycosylation in the antigen binding site of the antibody will be highlighted. This review will also emphasize how that study unexpectedly improved understanding of FVIII structure/function relation.

4 patients (3.3%) of those who received diclofenac sodium developed post-ERCP pancreatitis, compared to 7 patients (5.8%) in the group not received the drug. The risk of pancreatits was lower in the NSAID group than in the controlled group but statistically insignificant. No deaths or NSAID-related complications were noted. Conclusion: Prophylactic NSAIDs were ineffective in preventing PEP. Widespread prophylactic administration of these agents may not significantly reduce thei ncidence of PEP. Given current scepticism regarding the efficacy of any prophylactic medication for ERCP, additional multicentre studies are needed for confirmation

prior to widespread adoption of this strategy. Key Word(s): 1. GSK1120212 clinical trial NSAIDs; 2. ERCP; 3. pancreatitis; 4. prophylactic; Presenting Author: KEN ITO Additional Authors: YOSHINORI IGARASHI, TAKAHIKO MIMURA, SEIICHI HARA, KENSUKE TAKUMA, YUI KISHIMOTO, NAOKI OKANO Corresponding Author: KEN ITO Affiliations: Toho

University Omori Medical Center Objective: The efficacy of electrohydraulic lithotripsy (EHL) is well documented for the treatment of chronic pancreatitis lithiasis when endoscopic lithotripsy failed. As an alternative method, we attempt extracorporeal shock wave lithotripsy (ESWL) on an outpatient basis in our institution. We retrospectively evaluated the efficacy of the EHL as a second attempt and that of ESWL Ixazomib order on an outpatient basis as a third attempt for treatment of pancreatic duct stones. Cetuximab molecular weight Methods: The indication

of EHL and ESWL on an outpatient basis was considered for the failed cases of the combination treatment of endoscopic lithotomy and ESWL during admission (combination treatment), failed cases of endoscopic pancreatic stenting due to stone impaction or severe main pancreatic duct (MPD) stricture. We retrospectively evaluated the 98 patients with symptomatic pancreatic duct stones that was treated at our institution between May 2005 and December 2012. We analyzed the outcomes of the MPD stone clearance in the cases treated by EHL or ESWL on an outpatient basis. Results: The successful results were obtained in 67 of 98 patients (74.5%) by combination treatment, 7 of 14 patients (7.1%) by EHL, and 6 of 6 patients (6.1%) by ESWL on an outpatient basis, respectively. Sixteen patients were out of indication, 12 cases had radiolucent stones, and 4 cases failed in selective pancreatic duct cannulation with radiolucent stones. A total of 87.7% of the patients (80 of 98 patients) resulted in MPD stone clearance. The multivariate analysis showed that GW negotiation across the stone was a statistically significant factor for the stone clearance (odds ratio, 14.1; 95% CI, 0.46 to 43.2; P 0.0003). Conclusion: EHL and ESWL on an outpatient basis, compared with combination treatment of endoscopic lithotomy and ESWL during admission, increased the composite rate of MPD stones clearance. Key Word(s): 1. EHL; 2.

4 patients (3.3%) of those who received diclofenac sodium developed post-ERCP pancreatitis, compared to 7 patients (5.8%) in the group not received the drug. The risk of pancreatits was lower in the NSAID group than in the controlled group but statistically insignificant. No deaths or NSAID-related complications were noted. Conclusion: Prophylactic NSAIDs were ineffective in preventing PEP. Widespread prophylactic administration of these agents may not significantly reduce thei ncidence of PEP. Given current scepticism regarding the efficacy of any prophylactic medication for ERCP, additional multicentre studies are needed for confirmation

prior to widespread adoption of this strategy. Key Word(s): 1. LY294002 mouse NSAIDs; 2. ERCP; 3. pancreatitis; 4. prophylactic; Presenting Author: KEN ITO Additional Authors: YOSHINORI IGARASHI, TAKAHIKO MIMURA, SEIICHI HARA, KENSUKE TAKUMA, YUI KISHIMOTO, NAOKI OKANO Corresponding Author: KEN ITO Affiliations: Toho

University Omori Medical Center Objective: The efficacy of electrohydraulic lithotripsy (EHL) is well documented for the treatment of chronic pancreatitis lithiasis when endoscopic lithotripsy failed. As an alternative method, we attempt extracorporeal shock wave lithotripsy (ESWL) on an outpatient basis in our institution. We retrospectively evaluated the efficacy of the EHL as a second attempt and that of ESWL Ibrutinib nmr on an outpatient basis as a third attempt for treatment of pancreatic duct stones. Thymidylate synthase Methods: The indication

of EHL and ESWL on an outpatient basis was considered for the failed cases of the combination treatment of endoscopic lithotomy and ESWL during admission (combination treatment), failed cases of endoscopic pancreatic stenting due to stone impaction or severe main pancreatic duct (MPD) stricture. We retrospectively evaluated the 98 patients with symptomatic pancreatic duct stones that was treated at our institution between May 2005 and December 2012. We analyzed the outcomes of the MPD stone clearance in the cases treated by EHL or ESWL on an outpatient basis. Results: The successful results were obtained in 67 of 98 patients (74.5%) by combination treatment, 7 of 14 patients (7.1%) by EHL, and 6 of 6 patients (6.1%) by ESWL on an outpatient basis, respectively. Sixteen patients were out of indication, 12 cases had radiolucent stones, and 4 cases failed in selective pancreatic duct cannulation with radiolucent stones. A total of 87.7% of the patients (80 of 98 patients) resulted in MPD stone clearance. The multivariate analysis showed that GW negotiation across the stone was a statistically significant factor for the stone clearance (odds ratio, 14.1; 95% CI, 0.46 to 43.2; P 0.0003). Conclusion: EHL and ESWL on an outpatient basis, compared with combination treatment of endoscopic lithotomy and ESWL during admission, increased the composite rate of MPD stones clearance. Key Word(s): 1. EHL; 2.

70 Unlike many other enterically-transmitted

infections, person-to-person buy MG-132 transmission of HEV appears to be uncommon.71,72 Thus, secondary attack rates among household contacts of patients with hepatitis E are only 0.7% to 2.2%, as compared to 50% to 75% for hepatitis A. Even when multiple cases occur in a family, the time interval between cases is usually short, indicating a shared primary water-borne infection rather than person-to-person spread.71 Materno-fetal73 and transfusion-related transmission74 of HEV are well documented. However, the contribution of these routes to the overall disease burden appears to be small. In the US, Europe (including UK, France, the Netherlands, Austria, Spain and Greece), and developed countries of Asia-Pacific

(Japan, Taiwan, Hong Kong, Australia), hepatitis E is responsible for only occasional cases with acute viral hepatitis. Initially, most such cases were found to be related to travel to high-endemic areas. However, in recent years, solitary cases or small case series related to autochthonous (locally-acquired) hepatitis E in these regions have been reported.25–27 In the UK, a seasonal variation with peaks in spring learn more and summer has been reported.75 These rare autochthonous cases of hepatitis E in these areas are believed to be caused by zoonotic spread of infection from wild or domestic animals,75,76 since HEV isolates from them are genetically related to swine isolates.25–27 Experimental cross-species transmission of human isolates to pigs, and of swine HEV to primates supports this view.27,57 A cluster of Japanese cases among persons who had consumed inadequately-cooked deer meat a few weeks prior to the onset of illness has been reported.51 The genomic sequences of HEV isolated from these cases were identical to those from the left-over frozen meat, establishing food-borne transmission; these isolates also had a high (99.7%)

genomic sequence homology with those from a wild boar and another Oxymatrine wild deer from the forest where the implicated deer had been hunted, suggesting transmission between wild boars and deer.77 A proportion of commercial packets of pig liver sold in Japanese and US grocery stores have been shown to contain genotype 3 or 4 HEV.78,79 This finding, along with the reported association of sporadic hepatitis E cases with eating uncooked or undercooked pig livers in case-control studies, suggests that at least some autochthonous cases are related to consumption of contaminated meat. Contaminated shellfish has also been proposed as a potential vehicle. The reservoir of HEV responsible for maintaining the disease in hyperendemic populations has not been clearly determined. Protracted viremia and prolonged fecal shedding of HEV have been suggested; however, we found that viral shedding in feces lasts for only a short period.