In addition

to the tumor progression, hypoxia that impairs vitamin K uptake is known to induce DCP and this mechanism may explain DCP elevation by CHIR-99021 chemical structure sorafenib. In this study, we tried to evaluate the effect of sorafenib treatment using a new marker, NX-DCP, which is specific to vitamin K absence. Serum DCP and NX-DCP were measured in 50 consecutive HCC patients before and 1 week after starting sorafenib, and compared with the treatment effect using the modified Response Evaluation Criteria in Solid Tumors guidelines. DCP and NX-DCP increased 1.58- (median, range 0.21–28.7) and 1.20-fold (median, range 0.41–14.2) after the administration of sorafenib, respectively. The increases of both markers were less than twofold in approximately half of the patients (low-elevation group). However, 12 patients showed over twofold increase of both DCP and NX-DCP (double-elevation SCH727965 price group), and eight patients showed over twofold increase of DCP alone (DCP-elevation group). The disease

control rate (DCR) of the DCP-elevation group (12.5%) was significantly lower than those of the double-elevation group (75.0%, P = 0.020) and the low-elevation group (60.0%, P = 0.042). Progression-free survival (PFS) was significantly shorter in the DCP-elevation group than in the double-elevation group (P = 0.006) and the low-elevation group (P = 0.001). NX-DCP in combination with DCP could be a useful biomarker of sorafenib treatment for advanced HCC. “
“Background and Aim:  To obtain diagnostic performance of diffusion-weighted magnetic resonance imaging (DWI) and fluorine 18 fluorodeoxyglucose (FDG) positron emission tomography/computed medchemexpress tomography (PET/CT) in the detection of pancreatic malignancy.

Methods:  We performed a meta-analysis of all available studies of the diagnostic performance of DWI and PET/CT for pancreatic malignancy. MEDLINE, EMBASE, Cochrane library and some other databases were searched for initial studies. We determined sensitivities and specificities across studies, calculated positive and negative likelihood ratios (LR+ and LR−), and constructed summary receiver operating characteristic curves (SROC) using hierarchical regression models. Results:  Across 16 studies with 804 patients, PET/CT sensitivity was 0.87 (95% confidence interval [CI], 0.82, 0.81) and specificity was 0.83 (95% CI, 0.71, 0.91). Overall, LR+ was 5.84 (95% CI, 4.59, 7.42) and LR− was 0.24 (95% CI, 0.17, 0.33). DWI sensitivity was 0.85 (95% CI, 0.74, 0.92) and specificity was 0.91 (95% CI, 0.71, 0.98). LR+ was 9.53 (95% CI, 2.41, 37.65) and LR− was 0.17 (95% CI, 0.09, 0.32). In subgroup analysis, the sensitivity of enhanced versus unenhanced PET/CT in the detection of pancreatic cancer was 0.91 (95% CI, 0.86, 0.96) versus 0.84 (95% CI, 0.78, 0.90) (P > 0.05), the specificity 0.88 (95% CI, 0.73, 1.00) versus 0.81 (95% CI, 0.69, 0.94) (P > 0.05).

pylori other than exogenous, as many authors reported an inverse relation between H. pylori infection and asthma in children. It is known that H. pylori infection is implicated in many nutritional matters, including iron absorption and metabolism [19]. Boyanova [20], in fact, have recently proposed how virulent strains of H. pylori, such as find protocol those harboring CagA and VacA, work concurrently to provide both iron acquisition from interstitial holotransferrin and enhanced bacterial colonization

of host cells apically. Xia et al. [21] have conducted a survey on anemia and H. pylori infection in adolescent girls from the Chinese region Suhia, reporting a significant association between H. pylori and iron-deficient anemia (IDA), while Malik et al. [22] clearly showed that the administration of iron in patients with IDA and concomitant H. pylori infection is less effective in comparison with the results Ulixertinib supplier obtained when patients are successfully cured of H. pylori infection. Finally, the association between H. pylori infection and IDA is so strong that

even the British Society of Gastroenterology guidelines for the management of IDA indicate H. pylori infection to be sought in IDA patients if endoscopy is negative and to be eradicated if present [23]. On the other hand, the role of H. pylori in iron deficiency seems to be different in adult and children. In fact, there are several studies showing the absence of a positive association between iron stores and H. pylori infection among children [24-28]. Finally, the role of H. pylori infection

as a possible cause of idiopathic thrombocytopenic purpura (ITP) still remains significant. In fact, Saito et al. [29] demonstrated that the absolute number medchemexpress of plasmacytoid dendritic cells (pDCs), which is generally reduced in patients with ITP, is also reduced in patients with ITP and concomitant H. pylori infection. Interestingly, the number of pDCs resulted to be significantly increased after the eradication of H. pylori infection in ITP patients [29]. In another study, Sato et al., [30] reported that the development of corpus atrophic gastritis may be associated with H. pylori-related ITP, while Kikuchi et al. [31] in a 8-year follow-up of patients with ITP and previous H. pylori infection clearly showed that the prognosis of patients who positively increased their platelet count after the eradication of H. pylori is usually excellent. Similar results have been reported by Russo et al. [32] on children. Nonetheless, Ohe and Hashino [33] postulated that the administration of macrolides in patients with ITP may increase the platelet count independently from H. pylori infection, through an immunomodulatory effect intrinsic to the drug. Deretzi et al. [34] have been explaining the link of neurodegenerative disorders and neuroinflammation that could be potentially initiated by peripheral conditions through disrupted blood–brain barrier.

It is also important to establish the most effective and safest way to manage any risk and it is likely this will only be achieved through prospective observational studies requiring wide collaboration. “
“Summary.  In oral surgery, patients with inherited bleeding disorders have historically had factor cover where possible. Factor support is expensive, time consuming to administer and places the patient at a potential risk of complications of therapy. A protocol employing rigorous local

measures and minimal factor replacement was used to obtain haemostasis following simple and complex oral surgery on 50 consecutive patients with inherited bleeding disorders, referred to this website the Alfred Health Dental Unit from the Ronald Sawers Haemophilia Centre, selleck compound Alfred Health, Melbourne. Excellent haemostasis was achieved using standardized local measures of 5% tranexamic acid solution, surgicel

and monocryl sutures. Oral surgery may be considered safe to perform in patients with inherited bleeding disorders using minimal factor support and meticulous local haemostatic measures. “
“Summary.  The history behind the production of clotting factor concentrates produced differences in the prevalence of Hepatitis C Virus (HCV) and other blood-borne infections in haemophilic patients. Prevalence rates of HCV infection up to 100% were reported in patients treated 上海皓元医药股份有限公司 with concentrates before 1985. Conversely, nowadays, viral inactivation and recombinant technologies have effectively prevented transfusion-transmitted viral pathogens. Recently, new HCV infections in three young brothers were observed. In the absence of any other risk of transmission, their HIV/HCV coinfected uncle, who was living in the same house, was subject to

study. Plasma samples of the four relatives were investigated in order to test whether the infections have a common source. A phylogenetic approach using the most variable (E2) viral sequences was carried out using samples from the four family members. The HCV sequences from the study resulted highly related, being those obtained from the uncle the most ancestral ones. Because of the chronological order in which the infections occurred and the relatedness of the sequences, an infection from the uncle to his nephews is the most likely explanation. Special cares must be applied in the case of household contact among members of a family with inherited bleeding disorders. “
“The immune response against therapeutic clotting factors VIII and IX (FVIII and FIX) is a major adverse event that can effectively thwart their effectiveness in correcting bleeding disorders. Thus, a significant number of haemophilia patients form antibodies, called inhibitors, which neutralize the procoagulant functions of therapeutic cofactors FVIII (haemophilia A) or FIX (haemophilia B).

4.5; Carl Zeiss Microimaging, Thornwood, NY). Hepatic leukocytes were isolated using established procedures19, 21 with minor modifications (refer to the Supporting Material). All staining specified below was performed in 5% fetal bovine serum (FBS) in sterile phosphate-buffered saline (PBS) at 4°C in the dark. Hepatic leukocytes were stained with violet LIVE/DEAD Fixable Aqua Dead Cell stain kit (Invitrogen, Carlsbad, CA) for 30 minutes then blocked with 0.5 μg of anti-CD16/CD32 (2.4G2, BD Pharmingen, San Diego, CA) for 15 minutes. They were then stained for 45 minutes with 0.5 μg each of APC-Cy7-conjugated anti-CD11b

(M1/70, BD Pharmingen), Alexa 488-conjugated anti-CD11c (N418, eBioscience, San Diego,

CA), eFluor 450-conjugated anti-Gr-1 Selleck NVP-BKM120 (RB6-8C5, eBioscience), and PE-conjugated anti-sialic acid-binding immunoglobulin-like lectin-F (Siglec-F) (E50-2440, BD Pharmingen) or corresponding isotype controls. Cells were then fixed with BD Cytofix solution (BD Biosciences). Live cell events (2 × 105 per liver) were measured on an LSRII flow cytometer (BD Biosciences) and data were analyzed with FCS Express 3 (De Novo Software, Pexidartinib Los Angeles, CA). Cells gated as CD11c− CD11b+ Gr-1low Siglec-Fhigh were quantified to be eosinophils, based on the established method29 with minor changes. Cells gated as CD11c− CD11b+ Gr-1high Siglec-Flow/neg were quantified to be neutrophils, based on previous reports20, 30 with minor changes. The absolute number of each cell type was calculated by multiplying their percentage by the total number of viable hepatic leukocytes per liver. Hepatic leukocytes were isolated and pooled from 5 female Balb/cJ mice sacrificed 24 hours after halothane treatment. Eosinophils and neutrophils were stained identically as outlined above yielding CD11c− CD11b+ Gr-1low Siglec-Fhigh eosinophils and CD11c−

CD11b+ Gr-1high Siglec-Flow/neg neutrophils that were sorted from live cells only using an Aria II fluorescent-activated cell sorter (BD Biosciences). Sorted cells (50,000) in 100 μL of 5% FBS in PBS 上海皓元医药股份有限公司 were placed in a prewetted cytofunnel (Thermo Scientific, Rockford, IL) and centrifuged at 300g for 5 minutes at 4°C in a Cytospin 3 centrifuge (Thermo Scientific). Slides were stained with DiffQuik (Siemens, Newark, DE), dehydrated, and mounted using Shandon Consul-Mount Cytology permanent mounting media (Thermo Scientific). Eosinophils and neutrophils were visualized by light microscopy. Total RNA was isolated from 25 mg of liver sections, freshly preserved in 1 mL of RNAlater solution, by use of miRNeasy kits (Qiagen, Valencia, CA) following the manufacturer’s procedures. In a separate experiment, RNA was also isolated from livers and infiltrating hepatic leukocytes (1 × 106 cells total) using mRNeasy kits (Qiagen).

As noted in the article by Davenport et al.,[1] in addition to “BASM,” another term for infants with BA and stereotypical syndromic abdominal and vascular anomalies is “biliary atresia laterality sequence.” Given that only 70% of our patients with laterality defects actually had splenic anomalies, the latter term might be preferable in the future to RO4929097 “BASM” to describe this stereotypical group of infants. The Canadian Pediatric Hepatology Research group has recently reported their analysis of 382 infants with BA and the associated anomalies.[22] Forty-four (13%) had

associated anomalies, only 25 (6.5%) of which were associated with SM. The authors concluded that BA infants with anomalies demonstrated a spectrum of laterality defects and suggested that the meaning of the acronym BASM be modified to “biliary atresia structural malformation.” Our conclusions are somewhat similar in that a total of 16% of our infants were in the anomaly Groups 2 and 3. On the other hand, the main difference between our observations and those of the Canadian group was that Group 2 infants frequently exhibited major birth defects Veliparib price of the genitourinary and/or gastrointestinal systems, not considered part of defective lateralization, suggesting that this group may represent a different etiopathogenesis than Groups 1 and 3. Group 3

infants were younger at the time of initial evaluation compared to Group 1. The associated anomalies in Group 3, especially the cardiac lesions associated with murmurs or cyanosis, probably brought the patient to medical attention sooner than the infants with isolated cholestasis. An unexpected finding was the high incidence of

autoimmunity in first-degree relatives of all BA groups (average 44%). The occurrence of autoimmune diseases in relatives provides circumstantial evidence that a candidate disease (i.e., BA) may be autoimmune in nature.[23] The incidence of autoimmunity in first-degree relatives is much higher than that found in the general population, where autoimmunity rates vary from 2.5%-9%.[26, 27] Importantly, the incidence of autoimmunity medchemexpress in first-degree relatives of BA patients was similar to the rate of 37%-43% identified in autoimmune hepatitis[26] and 25.5% in type-1 diabetes mellitus.[25] This intriguing finding of autoimmunity in first-degree relatives of BA patients warrants further investigation. The fact that there was no difference in autoimmunity rates between the three groups suggests that the autoimmune hypothesis of BA may be relevant to the pathogenesis of all types of BA and is a clue to be pursued in further studies. It is also possibly that the high incidence simply resulted from our rigorous questionnaire containing a long list of autoimmune diseases and not being of pathogenetic significance.

8 to 2.5 times increased odds of having no surveillance. Patients

with complete surveillance had a significantly (p<0.05) greater number of physician visits during follow-up when stratified by hepatic decompensation status: 1) no hepatic decompensation: mean-1.8 visits (complete surveillance), 1.1 (incomplete), and 0.6 (none); 2) prior hepatic decompensation: mean-2.8 visits (complete), 1.5 (incomplete), and 1.1 (none). In linear regression models, non-GI provider, non-PPO/POS health insurance, and increasing age were associated with decreased PUTDS, while a history of a hepatic decompensation, presence of any component of the metabolic syndrome, and diagnosis of hepatitis B PD98059 datasheet or C were associated with increased PUTDS. Conclusions: HCC surveillance rates in commercially insured at-risk patients remain poor despite EGFR inhibitor formalized guidelines. Improving access to appropriate specialized care should

be targeted for quality improvement interventions. Disclosures: David S. Goldberg – Grant/Research Support: Bayer Healthcare Adriana Valderama – Employment: Bayer Sujit S. Sansgiry – Consulting: Bayer Pharmaceuticals James D. Lewis – Grant/Research Support: Bayer The following people have nothing to disclose: Rajesh Kamalakar, Svetlana Babajanyan Background: The United Network for Organ Sharing (UNOS) provides patients (pts) with HCC who are listed for LT with exemption MELD points that can place them at an advantage for earlier LT compared to pts listed for non-malignant indications. Aim: Identify medchemexpress a scoring system that achieves survival benefit equity among pts with and without HCC who are listed for LT. Methods: We defined LT survival benefit as the difference between life expectancy if transplanted and life expectancy if the subject remains on the waiting list (WL). Adult pts listed for LT in the United States between 2003 and 2012 were identified from the UNOS database, including HCC pts meeting exemption policy 3.6.4.4 (stage T2). A univariable analysis was performed to assess differences between HCC and non-HCC pts; this was done for WL and LT populations. Pre-LT survival

was modeled using competing risks analysis and post-LT survival was assessed using Cox regression. Using these models, life expectancy on WL and after LT was estimated for each patient by calculating the area under the survival curve up to 5 years using the trapezoidal rule. Linear regression was used to obtain a regression model defining 5-year LT survival benefit based on MELD score for non-HCC pts and based on MELD and AFP for HCC pts. These 2 models were equated to obtain an adjusted HCC-MELD score which matches the LT survival benefit of HCC pts to non-HCC pts having the same biochemical MELD. Results: 101,458 pts were included in the analysis. Average age at time of listing was 53 ± 10 years, 65% were male and 13% had HCC. 69% of HCC pts underwent LT compared to 47% of non-HCC pts.

29 Thus, the matrix chemistry transitions from its start point in the stem cell

niche having labile matrix Pictilisib chemistry associated with high turnover and minimal sulfation to stable matrix chemistries and having increasing amounts of sulfation with progression towards the pericentral zone. We hypothesize that maintenance of the natural architecture and matrix chemistry correlating with histology will facilitate recellularization in tissue engineering processes by guiding cells to specific sites on the biomatrix scaffolds and/or providing the proper mix of signals to drive differentiation into mature cells. The biomatrix scaffolds can be prepared from any tissue, normal or diseased, and from any species. In the supplement we show biomatrix scaffolds from human pancreas, biliary tree, and duodenum and from rat pancreas (Supporting Figs. S6-S9). Figures 5–7 and Supporting Fig. S5 show effects of bovine or rat liver biomatrix scaffolds on hepatic cells. In addition, biomatrix scaffolds have been prepared from human abdominal aorta, iliac vein,

and from rat and pig intestine (data not shown). Histological, ultrastructural, and immunohistochemical studies on the biomatrix scaffolds suggested a marked tissue specificity, but not species specificity, in their structure, chemical composition, and functions (data not shown). Plating hHpSCs onto dishes with sections of liver biomatrix scaffolds and in HDM tailored for adult liver cells resulted in essentially 100% of the viable cells attached within a few hours onto Galunisertib in vivo biomatrix scaffolds, whether intact or after cryogenic pulverization. The colonies of cells that initially formed on the sections of scaffolds retained some of their stem cell phenotype, as the cells in the center of the colonies

were able to resist staining with dyes (Supporting Fig. S4) and expressed classic hepatic progenitor markers, such as chemokine (C-X-C motif) receptor 4 (CXCR4) and epithelial cell adhesion molecule (EpCAM) (Fig. 5E). They divided once or twice and then transitioned into cell cycle arrest and into 3D cord-like morphologies typical for cultures of mature parenchymal cells (Figs. 5, 6 for stem cells differentiation; compare with Fig. 7 and Supporting Fig. S5 for maintenance of 上海皓元 mature hepatocytes). The HDM used did not require all the usual cytokines or growth factors because these are present bound to the biomatrix scaffolds. The transition to growth arrest correlated with staining throughout the colonies with viability dyes (Supporting Fig. S4), with loss of expression of EpCAM and CXCR4 (Fig. 5E) and with a steady increase in the expression of adult-specific hepatocytic and cholangiocytic genes such as urea and cytochrome P450 3A4 (Fig. 5F). Normal adult rat and human hepatocytes were plated onto type I collagen versus on biomatrix scaffolds from rat or bovine livers and into HDM for adult cells.

29 Thus, the matrix chemistry transitions from its start point in the stem cell

niche having labile matrix click here chemistry associated with high turnover and minimal sulfation to stable matrix chemistries and having increasing amounts of sulfation with progression towards the pericentral zone. We hypothesize that maintenance of the natural architecture and matrix chemistry correlating with histology will facilitate recellularization in tissue engineering processes by guiding cells to specific sites on the biomatrix scaffolds and/or providing the proper mix of signals to drive differentiation into mature cells. The biomatrix scaffolds can be prepared from any tissue, normal or diseased, and from any species. In the supplement we show biomatrix scaffolds from human pancreas, biliary tree, and duodenum and from rat pancreas (Supporting Figs. S6-S9). Figures 5–7 and Supporting Fig. S5 show effects of bovine or rat liver biomatrix scaffolds on hepatic cells. In addition, biomatrix scaffolds have been prepared from human abdominal aorta, iliac vein,

and from rat and pig intestine (data not shown). Histological, ultrastructural, and immunohistochemical studies on the biomatrix scaffolds suggested a marked tissue specificity, but not species specificity, in their structure, chemical composition, and functions (data not shown). Plating hHpSCs onto dishes with sections of liver biomatrix scaffolds and in HDM tailored for adult liver cells resulted in essentially 100% of the viable cells attached within a few hours onto ABT-888 cell line biomatrix scaffolds, whether intact or after cryogenic pulverization. The colonies of cells that initially formed on the sections of scaffolds retained some of their stem cell phenotype, as the cells in the center of the colonies

were able to resist staining with dyes (Supporting Fig. S4) and expressed classic hepatic progenitor markers, such as chemokine (C-X-C motif) receptor 4 (CXCR4) and epithelial cell adhesion molecule (EpCAM) (Fig. 5E). They divided once or twice and then transitioned into cell cycle arrest and into 3D cord-like morphologies typical for cultures of mature parenchymal cells (Figs. 5, 6 for stem cells differentiation; compare with Fig. 7 and Supporting Fig. S5 for maintenance of 上海皓元医药股份有限公司 mature hepatocytes). The HDM used did not require all the usual cytokines or growth factors because these are present bound to the biomatrix scaffolds. The transition to growth arrest correlated with staining throughout the colonies with viability dyes (Supporting Fig. S4), with loss of expression of EpCAM and CXCR4 (Fig. 5E) and with a steady increase in the expression of adult-specific hepatocytic and cholangiocytic genes such as urea and cytochrome P450 3A4 (Fig. 5F). Normal adult rat and human hepatocytes were plated onto type I collagen versus on biomatrix scaffolds from rat or bovine livers and into HDM for adult cells.

We thank all those authors for their contributions to this field, and we apologize for not being able to mention them directly in this article. “
“Chronic hepatitis B virus (HBV) infection is a major health problem in the Asia-Pacific region. In the past decade, much progress has been made in the understanding and management of this disease. The introduction of universal vaccination has significantly reduced the incidence of perinatal infection in most Asia-Pacific countries. As the majority of the adult population have not been immunized at birth, we are still facing a large

selleck inhibitor population of young HBV-infected patients in the coming two decades. The study of long-term longitudinal databases has provided deeper insight into the clinical significance of HBV DNA suppression, hepatitis B e antigen (HBeAg) seroconversion and hepatitis B surface antigen (HBsAg) seroclearance in chronic hepatitis B. With a better understanding on the natural history of HBV infection, one can now stratify the risk of chronic hepatitis B patients for adverse clinical outcomes and use this to individualize management. The introduction

of non-invasive assessment of liver fibrosis can potentially reduce the necessity of liver biopsy. There have also been great advances in the development of antiviral therapy in the past decade. However, the high cost of HBV antiviral drugs poses major challenges to health authorities in many Asia-Pacific countries. Properly performed cost-effective analysis www.selleckchem.com/products/dorsomorphin-2hcl.html and understanding on the best timing of stopping antiviral drugs will be important to facilitate the most appropriate allocation of resources. Chronic hepatitis B virus (HBV) infection is a major global health problem whose greatest impact is in the Asia-Pacific region. Much progress has been made in the understanding and management of this disease in the past decade. MCE The introduction of universal vaccination in the late 80s to early 90s has significantly changed the prevalence of HBV infection in children and young adults. With the availability of sensitive HBV DNA assays and studies based on

long-term longitudinal databases, the natural history of chronic HBV infection has become much better understood. The advances in antiviral therapy have also greatly improved the prognosis of this dreadful condition. Nonetheless, many challenges still remain. This review article summarizes the recent progress in the epidemiology, understanding of the natural history and the challenges of management of chronic hepatitis B in the Asia-Pacific region. It is estimated that at least 2 billion people or one third of the world population have been exposed to HBV infection. Approximately 400 million people worldwide or about 6% of the world population are chronically infected with HBV.1,2 Globally, 57% of cirrhosis is caused by either HBV (30%) or hepatitis C virus (HCV) (27%), and 78% of hepatocellular carcinoma (HCC) is caused by HBV (53%) or HCV (25%) infection.

We thank all those authors for their contributions to this field, and we apologize for not being able to mention them directly in this article. “
“Chronic hepatitis B virus (HBV) infection is a major health problem in the Asia-Pacific region. In the past decade, much progress has been made in the understanding and management of this disease. The introduction of universal vaccination has significantly reduced the incidence of perinatal infection in most Asia-Pacific countries. As the majority of the adult population have not been immunized at birth, we are still facing a large

Selleck Pirfenidone population of young HBV-infected patients in the coming two decades. The study of long-term longitudinal databases has provided deeper insight into the clinical significance of HBV DNA suppression, hepatitis B e antigen (HBeAg) seroconversion and hepatitis B surface antigen (HBsAg) seroclearance in chronic hepatitis B. With a better understanding on the natural history of HBV infection, one can now stratify the risk of chronic hepatitis B patients for adverse clinical outcomes and use this to individualize management. The introduction

of non-invasive assessment of liver fibrosis can potentially reduce the necessity of liver biopsy. There have also been great advances in the development of antiviral therapy in the past decade. However, the high cost of HBV antiviral drugs poses major challenges to health authorities in many Asia-Pacific countries. Properly performed cost-effective analysis Palbociclib clinical trial and understanding on the best timing of stopping antiviral drugs will be important to facilitate the most appropriate allocation of resources. Chronic hepatitis B virus (HBV) infection is a major global health problem whose greatest impact is in the Asia-Pacific region. Much progress has been made in the understanding and management of this disease in the past decade. 上海皓元医药股份有限公司 The introduction of universal vaccination in the late 80s to early 90s has significantly changed the prevalence of HBV infection in children and young adults. With the availability of sensitive HBV DNA assays and studies based on

long-term longitudinal databases, the natural history of chronic HBV infection has become much better understood. The advances in antiviral therapy have also greatly improved the prognosis of this dreadful condition. Nonetheless, many challenges still remain. This review article summarizes the recent progress in the epidemiology, understanding of the natural history and the challenges of management of chronic hepatitis B in the Asia-Pacific region. It is estimated that at least 2 billion people or one third of the world population have been exposed to HBV infection. Approximately 400 million people worldwide or about 6% of the world population are chronically infected with HBV.1,2 Globally, 57% of cirrhosis is caused by either HBV (30%) or hepatitis C virus (HCV) (27%), and 78% of hepatocellular carcinoma (HCC) is caused by HBV (53%) or HCV (25%) infection.