[51] evaluated the HpSA monoclonal EIA (Diagnostic Bioprobes Sri) in a series of 87 Turkish children, but they found its performance (Table 1) and a blood-based beta-catenin inhibitor serological test (H. pylori immunoglobulin G, HpIgG; Radim, Pomezia-Rome, Italy) to be poor compared with the UBT pre and posteradication. Calvet et al.

evaluated three monoclonal stool tests in 88 patients compared with breath test or histology at least 8 weeks posteradication treatment. The rapid in-office test RAPID Hp STAR (Oxoid Ltd.) and the laboratory-based Enzyme Immunoassay Amplified IDEIA HpStAR (Oxoid Ltd.) both had 100% sensitivity and therefore, can reliably indicate eradication; however, the ImmunoCard STAT1 HpSA (Meridian Diagnostics) had a lower sensitivity of 90%. All the tests had a specificity of over 92%, but all the tests gave some false positives post-treatment with quite low positive predictive values (62–69%)

[47]. Shimoyama et al. sought to evaluate the Premier Platinum HpSA Plus EIA (HpSA ELISA II; Meridian Diagnostics) which uses multiple monoclonal antibodies in Japanese patients post-H. pylori eradication [52]. They found this test could detect fewer numbers of check details H. pylori organisms in spiked fecal specimens than another stool antigen with a single monoclonal antibody (Testmate pylori antigen EIA; Wakamoto Pharmaceutical Co. Ltd., Tokyo, Japan), but interestingly they found that both tests produced ten false negatives and the same negative predictive value. The Testmate produced more false positives (six compared with one), and therefore, the positive predictive value of the Premier Platinum was higher at 97% when it was recalculated (Table 1) [52]. The alkyl hydroperoxide reductase protein AhpC gene was amplified by Pourakbari et al. and used as the basis of a new stool antigen test.

This test had similar specificity and sensitivity to the other stool antigen tests (Table 1) [28]. Most of these diagnostic studies do not have sufficient numbers to give statistical power to determine 上海皓元医药股份有限公司 which test is superior. A meta-analysis of the results of the available studies post-treatment would help to determine which is the most accurate test in this clinical scenario. Fecal calprotectin was measured in patients with chronic gastritis and healthy volunteers but could not be identified as a marker of gastritis [53]. Only two studies evaluated H. pylori IgG-based kits. In a very large comparative study from the Zhuanghe region of North China, an area with high gastric cancer risk, Gong et al. compared serology (Hp-ELISA, Biohit Co, Finland) with histology in 7241 patients [54]. However, this serological kit from Finland was only positive in 42% of patients compared with 70% by histology, demonstrating the very important point that kits developed with H.

[51] evaluated the HpSA monoclonal EIA (Diagnostic Bioprobes Sri) in a series of 87 Turkish children, but they found its performance (Table 1) and a blood-based selleck chemicals llc serological test (H. pylori immunoglobulin G, HpIgG; Radim, Pomezia-Rome, Italy) to be poor compared with the UBT pre and posteradication. Calvet et al.

evaluated three monoclonal stool tests in 88 patients compared with breath test or histology at least 8 weeks posteradication treatment. The rapid in-office test RAPID Hp STAR (Oxoid Ltd.) and the laboratory-based Enzyme Immunoassay Amplified IDEIA HpStAR (Oxoid Ltd.) both had 100% sensitivity and therefore, can reliably indicate eradication; however, the ImmunoCard STAT1 HpSA (Meridian Diagnostics) had a lower sensitivity of 90%. All the tests had a specificity of over 92%, but all the tests gave some false positives post-treatment with quite low positive predictive values (62–69%)

[47]. Shimoyama et al. sought to evaluate the Premier Platinum HpSA Plus EIA (HpSA ELISA II; Meridian Diagnostics) which uses multiple monoclonal antibodies in Japanese patients post-H. pylori eradication [52]. They found this test could detect fewer numbers of INCB024360 clinical trial H. pylori organisms in spiked fecal specimens than another stool antigen with a single monoclonal antibody (Testmate pylori antigen EIA; Wakamoto Pharmaceutical Co. Ltd., Tokyo, Japan), but interestingly they found that both tests produced ten false negatives and the same negative predictive value. The Testmate produced more false positives (six compared with one), and therefore, the positive predictive value of the Premier Platinum was higher at 97% when it was recalculated (Table 1) [52]. The alkyl hydroperoxide reductase protein AhpC gene was amplified by Pourakbari et al. and used as the basis of a new stool antigen test.

This test had similar specificity and sensitivity to the other stool antigen tests (Table 1) [28]. Most of these diagnostic studies do not have sufficient numbers to give statistical power to determine MCE公司 which test is superior. A meta-analysis of the results of the available studies post-treatment would help to determine which is the most accurate test in this clinical scenario. Fecal calprotectin was measured in patients with chronic gastritis and healthy volunteers but could not be identified as a marker of gastritis [53]. Only two studies evaluated H. pylori IgG-based kits. In a very large comparative study from the Zhuanghe region of North China, an area with high gastric cancer risk, Gong et al. compared serology (Hp-ELISA, Biohit Co, Finland) with histology in 7241 patients [54]. However, this serological kit from Finland was only positive in 42% of patients compared with 70% by histology, demonstrating the very important point that kits developed with H.

The initial treatment for liver cirrhosis is long term continuous entecavir therapy. Even if they are HBeAg positive, asymptomatic carriers in the immune tolerance phase with ALTs consistently within the normal range present few abnormal histological findings. Furthermore, irrespective of AZD2014 price the NAs or IFN, seroconversion rates from antiviral therapy are low at <10%.[217-222] For these reasons, treatment is not indicated in asymptomatic carriers.[223] HBV DNA, HBeAg and ALT levels should be monitored at 3–6 month intervals, and treatment considered

if ALT levels rise.[32, 224-227] Treatment is indicated in patients with HBeAg positive chronic hepatitis B with HBV DNA levels ≥4.0 log copies/mL and ALT ≥31 U/L.[4, 30-32] If there is no evidence of advanced fibrosis, and the patient is not considered at risk of fulminant hepatitis, it may be advisable to withhold treatment for another year while monitoring ALT, HBeAg and HBV DNA levels, anticipating natural HBeAg seroconversion, since the annual likelihood of natural HBeAg seroconversion is 7–16% per annum.[4, selleck chemicals 30-32] However, if HBeAg seroconversion does not occur, persistent hepatitis may cause progression of hepatic fibrosis,[2, 4, 228] necessitating treatment to prevent this. HBeAg positivity and elevated HBV DNA levels are independent risk factors for hepatocellular carcinogenesis and progression to liver cirrhosis,[2, 34, 37, 211, 229-231]

and patient age (≥40 years) is also a risk factor for progression of liver cirrhosis and HCC.[2, 36, 37] The risk of HCC is also higher in patients

with platelet counts <150 000, reflecting progression of hepatic fibrosis, or a family history of HCC.[38, 39] Accordingly, treatment should be positively considered in patients with any MCE公司 of the abovementioned risk factors, even if they do not meet the criteria for commencement of treatment. Liver biopsy (or noninvasive alternative) should be performed as an optional investigation to determine the extent of fibrosis, and treatment is indicated if hepatic fibrosis is diagnosed. Treatment should be commenced immediately, without a monitoring period, in patients with acute exacerbations of hepatitis associated with jaundice, or if there are concerns about liver failure. Recommendations Treatment is not indicated in HBeAg positive asymptomatic carriers. Treatment is indicated in patients with HBeAg positive chronic hepatitis cases with HBV DNA levels ≥4.0 log copies/mL and ALT ≥31 U/L. When ALT levels increase in patients with HBeAg positive chronic hepatitis, if there is no evidence of advanced fibrosis, and the patient is not considered at risk of fulminant hepatitis, one option is to defer treatment for approximately one year. However, if HBeAg seroconversion does not occur naturally, treatment is indicated to prevent progression of hepatic fibrosis due to persistent hepatitis.

Dissection of the fibrosis is made along an imaginary line at the top of the “mountain” which is the pulled up muscularis. PCM has two advantages including maintenance of the thick GDC 0068 submucosal layer with a minimal mucosal incision preventing leakage of injection solution, and providing good traction, thus stretching the submucosal tissue and facilitating the submucosal dissection. SUBJECT: From September 2009 to December 2013,

88 sessile or subpedunculated lesions >20 mm in size were treated by ESD at Jichi Medical University Hospital. PCM was performed for 29 lesions (P-group) and conventional ESD was performed for 59 lesions (C-group). Results: The mean tumor size was 44.9 mm in the P-group and 41.6 mm in the C-group. The F2 rate (Hiroshima University Classification for degree of submuscosal fibrosis, =F2/F0+F1) was higher in the P-group (51.7% vs 28.8%, p = 0.04). En-bloc resection rate and resection speed (resection area/time) were not significantly different in the two groups. Perforation rate was almost the same in both groups (10.3% vs 10.2%). Conclusion: PCM had outcomes similar to ESD, even when

a significantly greater number of lesions had submucosal fibrosis, suggesting that PCM may be a superior technique. These results support further study of this technique. Key Word(s): 1. ESD Pocket-Creation method Presenting Author: YAMAYO TADA Additional Authors: TOSHIYASU IWAO, TOMOKI KYOSAKA, KATSUYA HIROSE Corresponding Author: YAMATO TADA Affiliations: Aidu Chuo Hospital, Aidu this website Chuo Hospital, Aidu Chuo Hospital Objective: A 79-year-old man who had alcoholic pancreatitis was diagnosed with a pancreatic pseudocyst around the tail of the pancreas. Methods: As the pseudocyst was infected, we performed endoscopic ultrasound-guided cyst drainage (EUS-CD). EUS showed a large blood vessel in the puncture route, and we therefore made the puncture MCE taking care to avoid the vessel. A guidewire was left in place through the route, and we attempted to dilate it with a diathermic sheath; however, we could not move the sheath smoothly

owing to resistance. Electrification for 20–30 s was required to dilate the whole route. After we successfully expanded the route and passed the diathermic sheath, we completed the procedure with a nasal cyst drainage tube left in place. At 2 d after the procedure, we detected bloody drainage from the tube, and After 7 d, the patient vomited blood. We performed upper gastrointestinal endoscopy to stop the bleeding and found that the hole of the puncture was the source of the bleeding; however, we could not stop the bleeding via the endoscope. We then performed angiography and embolized the splenic artery using coils. To clarify the process of damage, we performed an experiment for examining vascular injury by a diathermic sheath using uncured ham and porcine blood vessels.

Schalk van der Merwe, Werner Van Steenbergen, Johan Fevery; for Hospital Vall d’Hebron: Meritxell Selleck STI571 Ventura; for Hospital de la Santa Creu I Sant Pau: Rubén Guerrero, Cristina Romero and Eva Román; for the Royal Free Sheila Sherlock Liver Center: Dominic Yu;

for the University College London Hospitals: Rajeshwar Mookerjee, Roger Williams; for Hospital Clinic Barcelona: Marta Burrel, Maribel Real, Xavier Muntanya, Maria Angeles Garcia-Criado, Anna Darnell, Susana Seijo, AnnaLisa Berzigotti. “
“Background:  Despite pharmaceutical treatment with NTBC (2-2-nitro-4-fluoromethylbenzoyl-1,3-cyclohexanedione), a high incidence of liver malignancies occur in humans and mice suffering from hereditary tyrosinemia type 1 (HT1) caused by mutation of the fumarylacetoacetate hydrolase (fah) gene. Methods:  To evaluate the efficacy of a definitive treatment for HT1, we transfected fah knockout mice with naked plasmid DNA using high volume tail-vein injection. This approach was chosen to reduce the occurrence of insertional mutagenesis that is frequently observed when using other (retro-)viral vectors. To prolong gene expression, the fah gene was cloned between adeno-associated virus (AAV)-specific inverted terminal

repeats (ITRs). Results:  All animals treated with high volume plasmid DNA injections could be successfully weaned off NTBC and survived in the long term without any further pharmacological support. Up to 50% fah positive hepatocytes were detected in livers of naked plasmid DNA-treated animals and serum liver function tests approximated those of wild-type Fulvestrant controls. Conclusions:  Naked plasmid DNA transfection offers a promising alternative treatment 上海皓元医药股份有限公司 for HT1. Minimizing side-effects makes this approach especially appealing. “
“Aim:  Sonazoid is a new contrast agent for ultrasonography (US). Contrast-enhanced ultrasonography (CEUS) using Sonazoid enables Kupffer imaging, which improves the sensitivity of hepatocellular carcinoma (HCC) detection. However, there are no studies on the cost-effectiveness of

HCC surveillance using Sonazoid. Methods:  We constructed a Markov model simulating the natural history of HCV-related liver cirrhosis (LC) patients, and compared three strategies (no surveillance, US surveillance and CEUS surveillance). The transition probability and cost data were obtained from published data. The simulation and analysis were performed using TreeAge pro 2009 software. Results:  When compared to the no surveillance group, the US and CEUS surveillance groups increased the life expectancy by 1.67 and 1.99 quality-adjusted life-years (QALY), respectively, and the incremental cost effectiveness ratio (ICER) were 17 296 $US/QALY and 18 384 $US/QALY, respectively. These results were both less than the commonly-accepted threshold of $US 50 000/QALY.

50/1.82–188.39, P = 0.014). Host IL-28B genetic variants played a role in Asian relapsers but not nonresponders retreated with peginterferon/ribavirin. Direct antiviral

agents might be possibly avoidable in Asian relapsers with favorable IL-28B genotype. “
“Aim:  A genetic polymorphism of inosine triphosphate pyrophosphatase (ITPA) has been associated with pegylated-interferon/ribavirin (PEG-IFN/RBV)-induced anemia in chronic hepatitis C patients. However, correlation of the genetic variant with anemia following liver transplantation has not been determined. Methods:  Sixty-three hepatitis Metformin C virus (HCV)-positive patients who underwent liver transplantation and PEG-IFN/RBV therapy were enrolled. The rs1127354 was determined for each individual. Results:  There was no relationship with anemia or RBV dosage in patients carrying the CC allele (CC group, n = 43) and those carrying the CA allele (CA group, n = 20). The incidence of hemoglobin CH5424802 price (Hb) decline >3 g/dL (CC: 4.7%, CA: 0%) was relatively low, whereas the incidence of Hb levels <10 g/dL (CC: 18.6%, CA: 30.0%) was high. Univariate analysis revealed that splenectomy inversely correlated with Hb levels <10 g/dL at 4 weeks (P = 0.04). Among the 22 patients who did not undergo splenectomy, the incidence of Hb levels <10 g/dL tended to be lower in the seven patients carrying the CA allele (28.6%)

than in the 15 patients with the CC allele (60.0%). Conclusion:  The ITPA genetic polymorphism does not correlate with post-transplant PEG-IFN/RBV-induced anemia. Splenectomy is useful in preventing anemia regardless of the ITPA genotype. “
“Background and Aim:  Previous medchemexpress studies investigating the association between the glutathione S-transferase Tl (GSTT1) null genotype and colorectal cancer (CRC) risk in the Asian population have reported controversial results.

Thus, a meta-analysis was performed to clarify the effect of the GSTT1 null genotype on CRC risk in the Asian population. Methods:  A comprehensive study was conducted, and 12 case-control studies were finally included, involving a total of 4517 CRC cases and 6607 controls. Subgroup analyses were performed by the sample size. Results:  A meta-analysis of all 12 studies showed that the GSTT1 null genotype was significantly associated with an increased CRC risk in the Asian population (odds ratio [OR] = 1.10, 95% confidence interval [CI] = 1.02–1.19, the P-value of the OR [POR] = 0.02, the value of the heterogeneity analysis [I2] = 42%). A more obvious association was observed after the heterogeneity was eliminated by excluding one study (OR = 1.15, 95% CI: 1.06–1.25, POR = 0.001, I2 = 0%). This association was further identified by both subgroup analyses and a sensitivity analysis. Conclusions:  This meta-analysis suggests that the GSTT1 null genotype contributes to an increased colorectal cancer risk in the Asian population.

Blood glucose levels remained unchanged upon treatment Forskolin cost in

lean mice. Fasting insulin levels (not shown) were unchanged and decreased, respectively, in colesevelam-treated lean and db/db mice. Nonesterified fatty acid and very low-density lipoprotein TG levels (Supporting Fig. 1) were significantly reduced in colesevelam-treated db/db mice compared with untreated controls but remained unchanged in lean mice. Control db/db mice showed increased feces production and a higher fecal bile salt output, representing hepatic bile salt synthesis, compared with lean controls (Fig. 1A,B). As expected, colesevelam treatment led to massive increases in fecal bile salt output (Fig. 1B). Untreated lean and db/db mice had similar bile flow rates and biliary bile salt output rates (Fig. 1C,D) that remained unchanged in both models upon sequestrant treatment. Direct end products PD98059 of de novo bile salt synthesis are the primary bile salts cholate (CA) and chenodeoxycholate (CDCA). Modifications of these bile salts in the liver and intestine give rise to differentially structured primary and secondary bile salts, respectively.

Supporting Table 1 provides details on biliary and fecal bile salt compositions. In short, sequestrant treatment resulted in a strongly increased relative content of fecal deoxycholate in both groups. Cholate remained the major biliary bile salt species in both models upon sequestrant treatment. Next, we determined relevant kinetic parameters 上海皓元医药股份有限公司 of CA,23 the major primary bile salt species in mice. Untreated db/db mice displayed a larger pool size and a higher synthesis rate of CA compared with untreated lean mice (Fig. 2). Importantly, CA pool size remained unchanged upon colesevelam treatment in both models. Synthesis rates of CA were massively increased upon sequestrant treatment (+375% and +172%, lean and db/db mice, respectively) and completely compensated for the increased fecal bile salt loss induced by colesevelam. The calculated amount of CA reabsorbed from intestines of colesevelam-treated lean

and db/db mice was reduced by about 30% compared with untreated controls (Fig. 2D). Decreased plasma bile salt levels further reflect a reduced flux of bile salts returning to the liver (Fig. 2E). To gain insight into colesevelam-induced changes in total bile salt pool composition and synthesis of bile salts derived from the primary bile salt species CA and CDCA, we calculated the amount of CA- and CDCA-derived bile salts in the pool as well as their synthesis rates (for details on calculation, see Supporting Materials and Methods). Upon sequestrant treatment, the total pools of bile salts remained unchanged in both models (Fig. 3A). Nevertheless, the pool size of CDCA-derived bile salts was decreased. The synthesis of CA-derived bile salts was massively increased, whereas synthesis of CDCA-derived bile salts remained unchanged in sequestrant-treated mice compared with untreated controls (Fig. 3B).

Nonetheless, the ablation strategies employed in our study (1) avoid common side effects described for DC ablation[26] due to our use of CD11c-DTR chimeric mice and 120G8 antibody, (2) address the role of both cDC and pDC, and (3) investigate the role of cDCs in

two common models of liver fibrosis. Our study contains several limitations. First, because we observed more than 1,400 HM-regulated genes, it is likely that genes besides NF-κB–regulated genes affect HSC responses. Further studies are required to unravel the relevance of NF-κB–independent genes and pathways regulated by HM. These may include additional mediators secreted from selleckchem HMs such as IL-6 and transforming growth factor β.[35, 42] Accordingly, our IPA analysis revealed Stat1/3/5 as an HM-activated pathway. Second, our studies were performed in mouse models, and further studies are required to determine whether HM-induced NF-κB activation plays a role in human fibrogenesis. As patients develop fibrosis slowly over decades, pathways that promote long-term myofibroblast survival may be particularly relevant. IL-1 and TNF inhibitors may be considered for antifibrotic therapies but may cause severe side effects. In conjunction with previous studies,[32, 43] our data support the concept that targeting the NF-κB pathway in HSCs and subsequent induction

of HSC apoptosis may be a more suitable antifibrogenic 上海皓元 BYL719 solubility dmso strategy. In conclusion, our study shows

that HMs provide a novel link between inflammation, HSC survival, and liver fibrosis and suggests that inflammatory signaling pathways may provide additional targets for antifibrotic therapies in the liver. Future studies are needed to determine whether macrophage-mediated promotion of myofibroblast survival also promotes fibrosis in other organs. Additional Supporting Information may be found in the online version of this article. “
“Background and Aim:  Insulin resistance and diabetes mellitus (DM) are known to contribute to the progression of non-alcoholic fatty liver disease (NAFLD). However, the relationship between glucose metabolism and NAFLD is not well known. In this study, we investigated whether secretion patterns of glucose and insulin could influence the histological severity in NAFLD patients without prior known type 2 DM. Methods:  A 75-g glucose tolerance test was performed on 173 biopsy-proven NAFLD patients without prior known type 2 DM. Plasma glucose and insulin levels were analyzed periodically for 3 h after oral glucose loading. Results:  Of the 173 NAFLD patients, 168 had non-alcoholic steatohepatitis, whereas no patient had cirrhosis. Irrespective of the hemoglobin A1c levels, impaired glucose tolerance, including DM, was detected in 60% of the NAFLD patients.

We aimed to evaluate the clinical performance of the recently developed real-time kinetic polymerase chain reaction (kPCR) assay: VERSANT HCV RNA 1.0 Assay (Siemens, Erlangen, Germany). Methods: Pre- and on-treatment serum samples from patients with HCV genotype 1-infection treated with telaprevir-based triple therapy were tested by three commercially available real-time PCR assays according to the respective manufacturers’ instructions: kPCR, the COBAS AmpliPrep/COBAS TaqMan HCV v2.0 test (CAP/ CTM) and the Abbott RealTime HCV assay (ART).

Results: Overall, Napabucasin mw kPCR showed excellent agreement with CAP/CTM (mean difference: 0.07 log10 IU/ml; 95% limits of agreement: −0.29 and 0.43) and ART (mean difference: 0.17 log10 IU/ml; 95% limits of agreement: −0.24 and 0.58) for the quantification of HCV-RNA (n=106). Concordance analyses showed that 17% and 38% of samples undetectable by kPCR were positive by CAP/CTM and ART, respectively while none of the samples undetectable by CAP/CTM or ART were positive by kPCR. At treatment week 4 (TW4), 82%, 45% and 16% of samples had undetectable HCV-RNA according to kPCR, CAP/CTM and ART, respectively. Thus, rapid virologic response (RVR) rates differed between kPCR and CAP/CTM in

14/38 (37%) patients and between kPCR and ART in 25/38 (66%) patients. Conclusions: kPCR showed excellent agreement with CAP/ CTM and ART for the quantification of HCV-RNA. However, significant differences in RVR rates were seen between all three assays, with the greatest observed discrepancy between kPCR and ART. These data may have significant implications for response-guided triple Cetuximab price therapies when using different commercial assays. Disclosures: Stefan Zeuzem – Consulting: Abbvie, Boehringer Ingelheim GmbH, Bristol-Myers Squibb Co., Gilead, Novartis Pharmaceuticals, Merck

& Co., Idenix, Janssen, Roche Pharma AG, Vertex Pharmaceuticals Christoph Sarrazin – Advisory Committees or Review Panels: Boehringer Ingelheim, Vertex, Janssen, Merck/MSD, Gilead, Roche, Boehringer Ingelheim, Achillion, Janssen, Merck/MSD, Gilead, Roche; Consulting: Merck/MSD, Novartis, Merck/MSD, MCE公司 Novartis; Grant/Research Support: Abbott, Intermune, Roche, Merck/MSD, Gilead, Janssen, Abbott, Roche, Merck/MSD, Vertex, Gilead, Janssen; Speaking and Teaching: Bristol-Myers Squibb, Gilead, Novartis, Abbott, Roche, Merck/MSD, Janssen, Siemens, Falk, Boehringer-Ingelheim, Bristol-Myers Squibb, Gilead, Novartis, Abbott, Roche, Merck/MSD, Janssen, Siemens, Falk, Boehringer-Ingelheim The following people have nothing to disclose: Johannes Vermehren, Simone Susser, Dany Perner Background: In patients with chronic hepatitis C (CHC), clinical outcome is associated with age of patient, gender, genotype, alcohol abuse, late testing, coinfection with human immunodeficiency virus (HIV) and the stage of disease at presentation.

In experimentally infected nonhuman primates, HEV RNA is observed in serum, bile, and feces before the elevation of aminotransferases; the HEV antigens Gefitinib mw first appear in hepatocytes around day 7 postinfection, followed by rapid spread to 70%-90% of hepatocytes. It appears that HEV, like other hepatitis viruses, is not directly cytopathic, and liver injury results from the host immune response. Pathogenetic events leading to increased mortality after HEV infection during pregnancy are not fully understood;

endotoxin-mediated hepatocyte injury and elevated T-helper type 2 responses may have some role.22 Distinct epidemiological patterns are identified in regions where the disease is highly endemic and where it is not; these differ in routes of transmission, affected population groups, and disease characteristics (Table Erlotinib 1). HEV is endemic to tropical and subtropical countries in Asia, Africa, and Central America. In these areas, infection is most often transmitted through the fecal-oral

route, usually through contaminated water. Less frequent routes of transmission include contaminated food, transfusion of infected blood products, and materno-fetal transmission. Outbreaks of hepatitis E have been reported from the Indian subcontinent, China, Southeast and Central Asia, the Middle East, and northern and western Africa.1, 2, 23, 24 Two small outbreaks were recorded in Mexico during 1986-1987, but none have been reported thereafter. The epidemics are usually related to contamination of drinking water with human excreta. These vary from small unimodal outbreaks lasting a few weeks to multipeaked MCE公司 epidemics lasting many months with several thousand cases.2, 23 Water contamination is often related to heavy rainfall and floods,1, 2 diminution of water flow in rivers increasing the concentration of contaminants,23, 25 or leaky water pipes passing through sewage-contaminated soil. Occasional, small foodborne outbreaks

have been reported. During outbreaks, 1%-15% of the population may be affected. Young adults are most often affected. Infection in children is more often asymptomatic. Men usually outnumber women, possibly because of greater exposure to contaminated water. During the outbreaks, pregnant women have a higher disease attack rate and are more likely to develop fulminant hepatic failure (FHF) and die. In the 1978-1979 Kashmir outbreak, 8.8%, 19.4%, and 18.6% of pregnant women in the first, second, and third trimesters, respectively, had icteric disease, compared to 2.1% of nonpregnant women and 2.8% of men.26 Furthermore, pregnant cases developed FHF more often (22%) than nonpregnant women (0%) or men (3%). Once FHF appears, the case-fatality rate may be similar in pregnant women with hepatitis E or other causes of liver injury.27 Immunological or hormonal factors may be responsible for this specific predilection among pregnant women.