6 mm; range, 8−20 mm). All had fewer than 5 mitoses per 50 high-power fields, suggesting a low risk of recurrence. The most common complication was subcutaneous emphysema and pneumomediastinum (verified by CT) (15/72, 20.8%). No adverse pulmonary events related to CO2 insufflations. No local recurrence and distant

metastasis occurred during 24 months’ follow-up. Conclusion: Our study showed that STER was safe and effective, provided accurate histopathologic evaluation, and was curative for SMTs of the deep MP layers at the EGJ. CO2 gas insufflation is recommended. Key Word(s): 1. submucosal CHIR 99021 tunneling endoscopic resection; 2. submucosal tumors; 3. esophagogastric junction Presenting Author: MEI DONG XU Additional Authors: CHEN ZHANG, PING HONG ZHOU, LI QING YAO Corresponding Author: HUI LIU Affiliations: Zhongshan Hospital, Zhongshan Hospital, Zhongshan Hospital Objective: We previously reported

a new technique, submucosal tunneling endoscopic resection (STER), for the resection of upper gastrointestinal SMTs originating from the muscularis propria layer, but the outcomes of this technique performed in a large number of cases have not been studied. Methods: From September 2010 to June 2013, a total of 290 patients with submucosal tumors (SMTs) originating from the muscularis propria of the upper gastrointestinal tract were included in the retrospective study in Zhongshan AZD2014 in vivo Hospital of Fudan University. Clinicopathological characteristics, en bloc resection, procedure time, complications were assessed in the present study. In addition, factors related the piecemeal resection were analyzed using MCE公司 logistic regression. Results: The male-to-female ratio was 2.05:1. The mean age was 49.0 years (range, 18–79 years). The mean time of STER procedure was 56 ± 38 minutes (median 45 minutes, range 15–200 minutes). The overall rates

of en bloc resection and piecemeal resection were 95.4% and 4.6% respectively. The pathology results were 226 leimyomas (77.9%), 53 gastrointestinal stromal tumors (GISTs, 18.4%), 3 glomus tumors, 5 Sehwannoma and 3 cases of calcifying fibrous tumors. Procedure related complications included mucosal injury (n = 3), subcutaneous emphysema (n = 61), pneumothorax (n = 22), pleural effusion (n = 49), and so on. Local recurrence or distant metastasis has not occurred during follow−up. Based on statistical analysis: i) the upper-GI SMT size and shape had significant impacts on the en bloc rate of STER, ii) the SMT with large size and irregular shape were the significant risk factors for the long-time procedure, iii) the piecemeal resection rate was significantly high in the patients with irregular tumor, large tumor or long-term procedure time, iv) tumor with irregular shape and long-time procedure time were the significant contributors to STER-related complications. Conclusion: STER is an effective and a safe method for the upper-GI SMTs with diameter size <35 mm (length ≤7 cm).

As mechanisms of iron handling were better defined and were examined in individual families affected

by NH, primary defects in these mechanisms appeared less likely. Awareness grew at the same time that recurrence rates of NH within sibships were too high for Mendelian single-gene recessive disease. Reports appeared of mothers by whom two men successively fathered infants with NH,4, 5 and mothers with autoimmune disease who bore infants with NH were described.5, 6 If NH were a unitary disorder, then single-gene models of defective iron handling did not accommodate important characteristics of NH.5 The analogic map of NH drawn by Cottier as “ein der Hämochromatose vergleichbares Krankheitsbild” no longer fit, clinically Tanespimycin in vivo or histopathologically,

the increasingly better explored territories of iron storage disorders of NH itself. In recent years, Whitington and coworkers7 have offered a new map, that of maternal immunity against a fetal antigen, not necessarily one involved in iron handling. This new paradigm defines Lorlatinib research buy NH as an alloimmune disorder, analogous to some instances of neonatal thrombocytopenia, in which transplacental transmission of a maternal antibody against an isoantigen results in cellular injury. It accounts for non-Mendelian occurrence and classes NH as an instance of liver failure with clinical and histopathological particularities explained by placentomaternal

dependence and fetal physiology. The new map also has permitted predictions about the mechanisms of the disease and about effective treatment of mothers at risk of bearing infants with NH. The report by Pan et al.8 in the current issue of HEPATOLOGY, filling in a blank space on that map, describes an immunohistochemical search for signs of complement activation in the livers of children with NH who died or underwent transplantation. Complement comprises over 40 sequentially interacting proteins whose activation is key in the pathogenesis of immune-mediated tissue damage.9 Once determined by insensitive measurements of intact C3 and C4 factors, complement activation is currently assessed directly by detection MCE of activation fragments, neoantigens, or complexes formed only when complement is activated.10 That hepatocyte surfaces bear C5b-C9 as an activated final assemblage unit proves that the complement system has been fully activated and can punch holes into the plasma membrane of hepatocytes that will inexorably undergo osmotic lysis. Is the pathogenesis of NH solved? Not yet. We learn from this article that complement is fully activated in the acute liver failure of NH, but in the absence of sufficient numbers of acute liver failure controls without NH, we can not say if this finding is NH-specific.

Even with such early tumors, approximately one-third will present with either vascular invasion,

satellite tumors, or both. It is these patients in particular who cannot be identified preoperatively by imaging, in whom anatomic resection is associated with a lower rate of recurrence. Additional Supporting Information may be found in the online version of this article. “
“Inflammatory bowel disease (IBD) is increasing in many parts of the Asia-Pacific region. There is a need to improve the awareness of IBD and develop diagnostic and management recommendations relevant to the region. This evidence-based consensus focuses on the definition, epidemiology and management of ulcerative colitis (UC) in Asia. A multi-disciplinary group developed the consensus statements, reviewed the relevant literature, and voted on them anonymously using the Delphi method. The finalized statements were reviewed to determine the level of consensus, evidence quality and strength Selleck BMN 673 of recommendation. Infectious colitis BMS-907351 manufacturer must be excluded prior to diagnosing UC. Typical histology and macroscopic extent of the disease seen in the West is found in the Asia-Pacific region. Ulcerative colitis is increasing in many parts of Asia with gender distribution and age of diagnosis

similar to the West. Extra-intestinal manifestations including primary sclerosing cholangitis are rarer than in the West. Clinical stratification of disease severity guides management. In Japan, leukocytapheresis is a treatment option. Access to biologic agents remains limited due to high cost and concern over opportunistic infections. The high

endemic rates of hepatitis B virus infection require stringent screening before initiating immune-suppressive agents. Vaccination and prophylactic therapies should be initiated on a case-by-case basis and in accordance medchemexpress with local practice. Colorectal cancer complicates chronic colitis. A recent increase in UC is reported in the Asia-Pacific region. These consensus statements aim to improve the recognition of UC and assist clinicians in its management with particular relevance to the region. Inflammatory bowel disease (IBD) is uncommon in Asia but the recent literature has shown that the disease is increasing in both incidence and prevalence. The Asia Pacific Working Group on Inflammatory Bowel Disease was established in Cebu, Philippines, at the Asia Pacific Digestive Week conference in 2006 under the auspices of the Asian Pacific Association of Gastroenterology (APAGE) with the goal of coordinating research and raising awareness of IBD in the region. The aim of this Consensus Group was to develop recommendations for the diagnosis and management of ulcerative colitis (UC) with specific relevance to the Asia-Pacific region and provide some updates on the IBD Consensus drafted in Sanya, China, in 2005.1 A modified Delphi process was adopted to develop the consensus.

Investigators have reported findings similar to ours in an ischemia/reperfusion model of injury.13 Kuboki and others13 demonstrated that CXCR2 knockout mice had significantly less liver injury after ischemia/reperfusion, and this was related to accelerated hepatocyte proliferation in the knockout mice. This

was associated with increased NF-KB and signal transducers and activators of transcription-3 activation and was not associated with changes in inflammation.13 These investigations suggested that low MIP2 concentrations protected against cell death, whereas high MIP2 concentrations induced cell death; these effects were absent in the CXCR2 knockout mice.13 Similarly, Ishida and colleagues14 also demonstrated that CXCR2 knockout mice had a lower mortality rate after buy 17-AAG APAP injury than control Selleckchem SCH 900776 mice but a higher mortality rate than neutropenic mice. These findings are similar to ours in that the CXCR2 knockout genotype confers protection against hepatic injury. Our experiments did not demonstrate differences in hepatocyte proliferation, although there were significant decreases in cellular death, and the NF-κB pathway appeared to be involved in this process.

Our experiments confirm the presence of the CXCR2 receptor on hepatocytes in the wild-type mice. The CXCR2 ligands, MIP2 and KC, were significantly increased after APAP in both wild-type and CXCR2 knockout mice, with the most significant increases seen in the knockout animals. The increased levels in the knockout animals did not appear to have any detrimental hepatic effects; this was similar to the results of Kuboki and colleagues.13 Our experiments suggest that the survival advantage conferred by the CXCR2 knockout genotype is related to decreased hepatocyte apoptosis. This was confirmed by a decrease in activated caspase-3 and increases in the prosurvival protein XIAP in CXCR2 knockout mice, and

this provides a potential mechanism for decreased apoptosis. MCE The IAP family of proteins protects against apoptosis in many systems, and this is linked to the BIF domains of these molecules, which bind to and inhibit caspases.3 In our model, this links the decrease in activated caspase-3 to the increased XIAP levels in the knockout mice. XIAP is known to potently inhibit caspase-3, caspase-7, and caspase-9, and this also correlates with our data.15 Another mechanism for XIAP-conferred protection against apoptosis is a positive feedback mechanism by which XIAP induces NF-κB with the additional recruitment of other target genes.4 XIAP as well as cIAP can activate NF-κB. cIAP is also up-regulated in our model, although this was seen in wild-type and knockout mice, so it does not provide as much of a clear explanation of the differences in these two genotypes.

Most studies concerning the relationships between lifestyle or dietary factors and FD are based on symptom intensities evaluated by questionnaire or on physiological studies involving particular foods or components. Further prospective studies are necessary to clarify the details of these pathogenetic factors and the role of dietary therapy in the management of FD. Statement 22. An integrated approach

addressing physiological, biological, psychological and social factors is recommended for all patients with functional dyspepsia. (SeeFig. 2) Grade of evidence: low. Strength of recommendation: probably do it. Level of selleck screening library agreement: a: 84.2%; b: 10.5%; c: 5.3%; d: 0%; e: 0%; f: 0%. As the pathogenesis of FD is multi-factorial, treatment should be individualized, with an effort to identify as many possible putative factors as possible. There have been no direct data to support this approach to managing FD in general. On the other hand, there have been studies on IBS that demonstrate a favorable response to treatment when physicians make an effort to address possible contributing factors such as past GI infection (biological), psychosocial stressors (psychological) and dietary changes (social), to reassure the patient by providing reasonable evidence that he or she does not have a life-threatening condition, and to explain the diagnosis with appropriate

pathophysiological (physiological) models. In view of the overlap in symptoms, patient demographics and putative pathophysiology, it is reasonable to recommend a similar approach to FD, as was recommended in the recent Metformin research buy Asian IBS Consensus.137–139 There is a study to support adopting a combination of intensive medical therapy with psychological intervention in patients with refractory FD. Haag et al.,140 in a prospective randomized, controlled trial, compared the long-term outcome of intensive medical therapy (with or without cognitive-behavioral or muscle relaxation therapy) versus standard medical therapy in patients with refractory FD and found that in FD patients with refractory symptoms, intensified medical management involving function testing and psychological

intervention yielded superior long-term outcomes. There is also a study from China that showed psychological intervention to be superior to prokinetic therapy.141 MCE公司 Statement 23. Where socio-economic conditions allow, Helicobacter pylori testing and eradication should be part of the management strategy for all patients in Asia who present with dyspepsia. (SeeFig. 2) Grade of evidence: high. Strength of recommendation: do it. Level of agreement: a: 58.0%; b: 42.0%; c: 0%; d: 0%; e: 0%; f: 0%. Helicobacter pylori eradication has a statistically significant effect on symptom relief in patients with FD. Cochrane meta-analysis on 17 randomized controlled trials (n = 3566) found a small but statistically significant benefit of H.

All of these factors, accompanied by the present

evidence that attacks may transpire in just a matter of minutes, might certainly explain the lack of in situ observations of this behavior in the field to date. In the Moray Firth population, infanticidal events may be orchestrated by single males (as seen in the present report and by Wilson1) or by several cooperating males at once (e.g., Eisfeld 2003). Nonetheless, all events essentially involve the same prolonged chasing, repeated ramming, tossing out of the water, and attempted asphyxiation of targeted newborns. Nery and Simão (2009) reported similar coercive strategies used by marine tucuxi (Sotalia guianensis) towards an early newborn calf. Moreover, HKI-272 the mechanisms used by other delphinids in predatory and nonpredatory interspecific events alike (e.g., killer whale, Orcinus orca, attacks on baleen whales as described by Ford et al. 2005 and Barrett-Lennard et al. 2011, and lethal attacks on harbor porpoises, Phocoena phocoena, by bottlenose dolphins, e.g., Ross and Wilson 1996, Cotter et al. 2012) are clearly comparable, in both method and execution, to the event described herein. The present paper contributes a valuable, first-hand

account of infanticidal behavior in free-ranging bottlenose dolphins, adding further to our understanding of the mechanisms and conditions Selleckchem AZD6244 that may elicit such responses in these highly-social, aquatic mammals. All observations were made during boat surveys under license number 9380 from Scottish Natural Heritage. Field support was provided by Jamie Vaughan, MCE公司 Elizabeth Wheeler, Marilynne Eichinger, and Gisa Scheschonka. Many thanks to David Janiger for providing bibliographic references, Kirsten Henry

for proof reading, Colin MacLeod, Paul Thompson, Paul Jepson and Mark Simmonds for constructive comments on the initial manuscript, and Care for the Wild International for ongoing financial and moral support. Thank you also to the three anonymous reviewers whose valuable input and advice resulted in this much improved final paper. “
“Long-term passive acoustic monitoring of marine mammals on navy ranges provides the opportunity to better understand the potential impact of sonar on populations. The navy range in Tongue of the Ocean (TOTO), Bahamas contains extensive hydrophone arrays, potentially allowing estimation of the density of deep diving, vocally active species such as the sperm whale (Physeter macrocephalus). Previous visual surveys in TOTO have been of limited spatio–temporal coverage and resulted in only sporadic sightings of sperm whales, whereas passive acoustic observations suggest the species is present year round. However, until now the means of acoustically determining the specific number of individuals in each cluster has been limited. We used recently developed algorithms to identify the number of echolocating whales present during a 42 d study period.

While delayed or secondary PPH is rare, occurring after <1% of deliveries [10,11], it has been reported in 20–25% of women with VWD [12,13], 2–11% of haemophilia carriers [14,15] and 24% of women with factor XI deficiency [14]. Carriers are another significant and often neglected member of the global bleeding disorder check details family. Women who have the haemophilia gene are called carriers, and they can pass the gene on to their children. In recent decades, it has been recognized that carriers may also

have low levels of factor VIII (FVIII) or factor IX (FIX), meaning by definition that they too have haemophilia. Although most carriers will be asymptomatic in day-to-day life, some experience significant bleeding symptoms, including excessive bleeding during menstruation, childbirth and with surgical intervention. The reported incidence of carriers per male with haemophilia varies significantly in the literature. The difficulty in accurately defining this figure lies in the fact that most women who are not mothers or daughters of someone with haemophilia do not know whether or not they are or might be carriers. Estimates range from 1.56 [16] to 5 [17] true genetic carriers per male born with selleck chemicals llc haemophilia within a pedigree. Based upon the WFH global estimate of 400 000 people worldwide with haemophilia, this means there are potentially 625 000–2 000 000 carriers worldwide that could require on-going management

by an HTC. It is recognized that the median clotting factor level in carriers is 50%. Thus, half of the carriers are at increased risk of bleeding and, some estimates are higher [18–20]. Twenty percent of true genetic carriers have factor levels under 30% (Carol Kasper MD, Private communication). If one assumes a robust outreach and genetic counselling programme is taking place and utilize the definition that those with a factor level of 30% or less have mild haemophilia,

these ratios would suggest that an HTC MCE公司 with 100 patients with haemophilia could have between 30 and 100 carriers* with a low factor level requiring on-going management for possible bleeding problems similar to men with mild haemophilia. Additionally, other carriers with higher factor levels in the range of 40–60% of normal may have an increased bleeding tendency and also require occasional intervention and counselling [19]. To address this need, more refined estimates of the true incidence of carriers are needed. Additionally, these estimates do not reflect all those in need of carrier testing. For example, in regions of the world where very large families are common, such as Iran, 4000 female relatives for 1500 haemophilia patients have been reported [21]. Because of the unknown carrier status of grandmothers, mothers, aunts, sisters, daughters and nieces of a person with haemophilia must all be considered for screening to establish their carrier status and factor levels.

GT EVERSON,1 KD SIMS,2 M RODRIGUEZ-TORRES,3 C HÉZODE,4 E LAWITZ,5 M BOURLIÈRE,6 V LOUSTAUD-RATTI,7 V RUSTGI,8 H SCHWARTZ,9 H TATUM,10 P MARCELLIN,11 S POL,12 PJ THULUVATH,13 T ELEY,2 X WANG,2 SP HUANG,14 F MCPHEE,15 M WIND-ROTOLO,14 E CHUNG,2 C PASQUINELLI,2 DM GRASELA,2 DF GARDINER2

1University of Colorado Denver, Aurora, CO, USA, 2Bristol-Myers Squibb, Hopewell, NJ, USA, 3Fundación de Investigación, San Juan, Puerto Rico, 4CHU Henri Mondor, Service d’Hépato-Gastroentérologie, Créteil, France, 5Alamo Medical Research, San Antonio, TX, USA, 6Hôpital Saint Joseph, Service d’Hépato-Gastroentérologie, Marseille, France, 7University Hospital of Limoges, Limoges, France, 8Metropolitan Research, Arlington, VA, USA, 9Miami Research Associates, South Miami, FL, USA, 10Options Health Research, Tulsa, OK, USA,

11Hôpital Beaujon, Clichy, France, 12Université Paris Descartes, PD-0332991 nmr INSERM U1610 and Liver Unit, Hôpital Cochin, Ivacaftor Paris, France, 13Mercy Medical Center, Baltimore, MD, USA, 14Bristol-Myers Squibb, Princeton, NJ, USA, 15Bristol-Myers Squibb, Wallingford, CT, USA Introduction: The IFN- and RBV-free regimen of DCV (NS5A inhibitor), ASV (NS3 protease inhibitor) and BMS-791325 (non-nucleoside NS5B polymerase inhibitor, 75 mg BID) for 24 or 12 weeks was well tolerated and achieved SVR4 and SVR12 >90% in treatment-naïve, hepatitis C virus (HCV) genotype (GT) 1 patients. We present safety and SVR following 24 or 12 weeks of this treatment using two BMS-791325 doses (75 vs 150 mg BID). Methods: This phase 2 study randomized treatment-naive, HCV GT1, non-cirrhotic patients (N = 32) 1 : 1 to DCV 60 mg QD, ASV 200 mg BID, and BMS-791325 75 mg BID for 24 (Group 1) or 12 (Group 2) weeks. Following safety evaluation, 34 additional patients were randomized to DCV, ASV, and BMS-791325 150 mg BID for 24 (Group 3) or 12 (Group 4) weeks. The primary end point was HCV

RNA <25 IU/mL at 12 weeks post-treatment (SVR12). Safety and SVR from Groups 1 (SVR12), 2 (SVR24) and 4 (SVR4) are MCE described, Groups 3 (SVR4) and 4 (SVR12) will be presented. Results: Patients were mainly GT1a (74%), white race (79%), and IL28B non-CC (70%). 64 of 66 patients had HCV RNA <25 IU/mL by Week 4 (Table 1). In this interim analysis, there was no difference in virologic responses between 12 and 24 weeks of treatment (Table 1). Overall, patients achieved SVR4 92% (46/50), SVR12 94% (30/32), and SVR24 94% (15/16). Three failures (Groups 3–4) were observed in patients receiving BMS-791325 150 mg (2-viral breakthrough, 1-relapse). No patients discontinued due to adverse events (AEs) related to DCV+ASV+BMS-791325. Most common AEs (≥10% total) were headache, asthenia, and gastrointestinal. Two serious AEs have been reported, both unrelated to DCV+ASV+BMS-791325. No hepatotoxicity or Grade 3/4 elevations of ALT/AST or bilirubin were reported.

GT EVERSON,1 KD SIMS,2 M RODRIGUEZ-TORRES,3 C HÉZODE,4 E LAWITZ,5 M BOURLIÈRE,6 V LOUSTAUD-RATTI,7 V RUSTGI,8 H SCHWARTZ,9 H TATUM,10 P MARCELLIN,11 S POL,12 PJ THULUVATH,13 T ELEY,2 X WANG,2 SP HUANG,14 F MCPHEE,15 M WIND-ROTOLO,14 E CHUNG,2 C PASQUINELLI,2 DM GRASELA,2 DF GARDINER2

1University of Colorado Denver, Aurora, CO, USA, 2Bristol-Myers Squibb, Hopewell, NJ, USA, 3Fundación de Investigación, San Juan, Puerto Rico, 4CHU Henri Mondor, Service d’Hépato-Gastroentérologie, Créteil, France, 5Alamo Medical Research, San Antonio, TX, USA, 6Hôpital Saint Joseph, Service d’Hépato-Gastroentérologie, Marseille, France, 7University Hospital of Limoges, Limoges, France, 8Metropolitan Research, Arlington, VA, USA, 9Miami Research Associates, South Miami, FL, USA, 10Options Health Research, Tulsa, OK, USA,

11Hôpital Beaujon, Clichy, France, 12Université Paris Descartes, CHIR-99021 supplier INSERM U1610 and Liver Unit, Hôpital Cochin, this website Paris, France, 13Mercy Medical Center, Baltimore, MD, USA, 14Bristol-Myers Squibb, Princeton, NJ, USA, 15Bristol-Myers Squibb, Wallingford, CT, USA Introduction: The IFN- and RBV-free regimen of DCV (NS5A inhibitor), ASV (NS3 protease inhibitor) and BMS-791325 (non-nucleoside NS5B polymerase inhibitor, 75 mg BID) for 24 or 12 weeks was well tolerated and achieved SVR4 and SVR12 >90% in treatment-naïve, hepatitis C virus (HCV) genotype (GT) 1 patients. We present safety and SVR following 24 or 12 weeks of this treatment using two BMS-791325 doses (75 vs 150 mg BID). Methods: This phase 2 study randomized treatment-naive, HCV GT1, non-cirrhotic patients (N = 32) 1 : 1 to DCV 60 mg QD, ASV 200 mg BID, and BMS-791325 75 mg BID for 24 (Group 1) or 12 (Group 2) weeks. Following safety evaluation, 34 additional patients were randomized to DCV, ASV, and BMS-791325 150 mg BID for 24 (Group 3) or 12 (Group 4) weeks. The primary end point was HCV

RNA <25 IU/mL at 12 weeks post-treatment (SVR12). Safety and SVR from Groups 1 (SVR12), 2 (SVR24) and 4 (SVR4) are MCE公司 described, Groups 3 (SVR4) and 4 (SVR12) will be presented. Results: Patients were mainly GT1a (74%), white race (79%), and IL28B non-CC (70%). 64 of 66 patients had HCV RNA <25 IU/mL by Week 4 (Table 1). In this interim analysis, there was no difference in virologic responses between 12 and 24 weeks of treatment (Table 1). Overall, patients achieved SVR4 92% (46/50), SVR12 94% (30/32), and SVR24 94% (15/16). Three failures (Groups 3–4) were observed in patients receiving BMS-791325 150 mg (2-viral breakthrough, 1-relapse). No patients discontinued due to adverse events (AEs) related to DCV+ASV+BMS-791325. Most common AEs (≥10% total) were headache, asthenia, and gastrointestinal. Two serious AEs have been reported, both unrelated to DCV+ASV+BMS-791325. No hepatotoxicity or Grade 3/4 elevations of ALT/AST or bilirubin were reported.

Up to week 16, 41% of patients developed grade 1–4 anaemia, with 20% Grade 3–4 cases (1 grade 4 case); 33 patients (41%) dose-reduced ribavirin, 2 (2%) received EPO, 8 (10%) were transfused and 2 (2%) discontinued treatment for anaemia. Results by baseline disease stage are

shown below [Table].: Up to week 16, 26% of patients developed grade 3 or 4 adverse events including 6 patients (7%) who developed grade 3 or 4 rash; 11% of patients had serious adverse events. Nine patients (11%) discontinued TVR due to adverse events, including 5 patients (6%) who discontinued due to rash. No deaths occurred during the study. Conclusions: In this telaprevir early access program for patients with severe fibrosis or compensated cirrhosis, Grade 3 Hydroxychloroquine price or 4 anaemia was reported in 20% of patients, but discontinuation for anaemia was rare (2%). Anaemia was principally managed by ribavirin dose reduction. Type of anaemia Definition F3 patients (n = 20) F4 patients (n = 57) Total (n = 81)* *Includes 4 patients with F1/F2 fibrosis K WILLIAMS,1 T LEE,1 J MCDONALD1 1Department of Gastroenterology, The Wollongong Hospital, Wollongong, Australia Background: Vertical transmission of hepatitis

B virus is the main cause of chronic hepatitis B. Recent evidence suggests a role of maternal treatment in late pregnancy in addition to standard MLN2238 clinical trial passive and immuno-prophylaxis in women with high viral load (HBV DNA >106 IU/mL) to further reduce the risk of mother to child transmission. Objectives: To assess the burden of chronic hepatitis B and how this is managed in our local antenatal population, with a particular view to whether maternal treatment could be incorporated into our local practices. Method: A retrospective single centre study of antenatal records over a 5 year period. After appropriate ethics approval, the Antenatal Department data bank was reviewed for all deliveries at The Wollongong Hospital between 2008 and 2012. Data collected 上海皓元 included maternal demographics, HBsAg status at booking

visit and HBeAg status where recorded, as well as neonatal date and time of birth, Apgar scores, administration of hepatitis B immunoglobulin (HBIG) and birth dose of monovalent hepatitis B vaccine. Hospital electronic medical records were then reviewed to confirm or clarify HBsAG status. Gastroenterology Department electronic records were searched for evidence of follow-up of women identified as HBsAg positive during their pregnancy. Results: There were 11,955 deliveries by 9494 women at The Wollongong Hospital between 2008 and 2012. HBsAg screening occurred in 99.6% pregnancies. HBsAg was positive in 35 pregnancies (28 women) giving a prevalence of 0.29%. A majority of these women were born in high endemic areas. HBeAg was checked in 32/35 cases, with 21 positive results. HBV DNA levels were checked in 5 cases but were not required to be recorded on the antenatal booking data sheet.