6% in 1997 to 0.3% in 2003 after the implementation of a universal infant vaccination program

in 1990.15 Recent data in Hawaii show a reduction of 97% in the prevalence of HBsAg since the start of infant hepatitis B vaccination program in 1991. The incidence of acute HBV infections in children and adults was reduced from 4.5/100 000 in 1990 to zero in the period between 2002 and 2004 in Hawaii.16 In Taiwan, where universal vaccination of newborn was started in 1983–1985, the HBsAg prevalence in children younger than 15 years of age decreased from 9.8% in 1984 to 0.7% in 1999, Acalabrutinib in vivo and further to 0.5% in 2004.17 Mainland China is perhaps an excellent example where a lengthy process is required before the universal infant immunization program can be implemented. The Ministry of Health in China has recommended a 3-dose active HBV immunization to all infants since 1992, but families had to pay for such vaccination. In 2002, the Chinese

government fully integrated HBV vaccine into the routine immunization program (Expanded Programme on Immunization, EPI), in which free HBV vaccine was provided to all infants, but the families still had to pay for the service of the vaccination procedure. In 2005, the central government issued the “Regulation on Vaccine Circulation and Immunization Management”, which finally waived all vaccination-associated charges. Eventually, infants born after June 2005 were offered completely PLX4032 concentration free HBV vaccination. With the efforts of the government and free vaccination implemented, HBV vaccine coverage rate in children increased gradually from about 30% in 1992 to 90% in 2005.18 Because of the uneven economic development

across different regions, immunization coverage still remained relatively low in rural areas and in the western part of China. However, by the end of 2005, the coverage of HBV vaccination was believed to be 90%, 80%, and 70% in urban, rural and click here remote areas, respectively. In 2006, a national survey of HBV seroepidemiology already showed a decrease in general prevalence of HBsAg from 9.75% in 1992 to 7.18% in 2006, and a decrease in the prevalence of HBsAg in children ≤ 5 years old from 9.67% in 1992 to 0.96% in 2006.19 Perinatally acquired chronic hepatitis B is traditionally classified into three phases.20 The immune tolerance phase marks the initial two to three decades when hepatitis B e antigen (HBeAg) is positive, HBV DNA is very high, alanine aminotransferase (ALT) is normal, and histologic injury is minimal. It is followed by the immune clearance phase when host immune clearance leads to a reduction in HBV DNA and elevation of ALT. Patients who have prolonged, unsuccessful immune clearance will have progressive liver fibrosis, which eventually develops into liver cirrhosis.

Disclosures: Mario Pirisi – Advisory Committees or Review Panels: Merck; Speaking and Teaching: Gilead, Bristol-Myers-Squibb The following people have nothing to disclose: Andrea Maqri, Michela E. Burlone, Lisa Franzosi, Elisa Boccato, Simone Bocchetta, Rosalba Minisini Aim: to evaluate the baseline similarities and differences between the two HCV-1 subtypes, 1a vs 1b, on pre-treatment of response to peg-interferon and 1184 with HCV genotype-1 infection were treated with PEG-IFN α-2a or α-2b in combination with daily ribavirin (1000-1200 mg/day). A total of 15 centers in Italy, selected by

voluntary participation between January 2005 and December 2010, took part into the

study. The study included 155 (13%) see more patients infected with subtype 1a (M/F 114/41, median age 47 yrs, range 18-78) and 1029 (87%) patients infected with subtype 1b (M/F 574/455, median age 57 yrs, range 18-84). Results: At multivariate analysis, the baseline characteristics differentiating patients with genotype 1a vs 1b were younger age (<50 yrs) and male sex, learn more being more frequently observed in genotype 1a. Of note, the IL28B polymorphisms and the RVR resulted equally distributed between the two HCV 1 subtype. SVR was achieved by 38% of genotype 1b and by 45% of genotype 1a even in this difference of 7% is not statistically significant. At the multivariate analysis of pre-treatment and on-treatment predictors of SVR, three factors were independently associated in subtype 1a: female gender (OR = 2.829, Cl: 1.146-6.983),

IL28B polymorphism (OR = 5.216, Cl: 1.765-15.410), and RVR (OR =5.066, Cl: 1.926-13.328); and three factors independently associated in subtype 1b: IL28B polymorphism (OR = 3.303, Cl: 2.256 −4.834), RVR (OR = 7.139, Cl: 4.721-10.796), and low baseline serum selleck products HCV-RNA concentration (< 400.000 IU/ mL)(OR = 2.123, Cl: 1.474-3.059). In subtype 1b the RVR status emerges as the most predictive characteristic of SVR, its strength outweighing the power of IL28 polymorphisms; on the contrary, in subtype 1a the two previous predictors appear to have an identical efficiency in predicting SVR. Conclusion: Our study conducted in a large nation-wide cohort of naīve patients with HCV subtype 1a and 1b infections shows that genotype 1a are more frequently observed in young male patients. The study also pinpoints some differential predictive features of SVR between the two subtypes, a finding which would imply that the two subtypes be separately evaluated in future therapeutic trials. Disclosures: Giovanni B.

05). Anti-HEV positivity was not associated with race, sex, ethnicity, country of birth and primary language. Conclusion: Seroprevalence of HEV increased with age and was higher in patients with chronic liver disease of viral etiology compared to other etiologies. There is considerable variation in the seroprevalence of HEV depending on the assay used, ranging from 14%-26% among chronic liver disease patients- similar to the general U.S. population. Wantai and NIH assays had the highest inter-test concordance. Understanding test performance characteristics of these assays is crucial to see more the interpretation of HEV prevalence. Comparison

of 3 assays P value: a vs d = 0.0003, b vs d = 0.3, b vs c = 0.4 Disclosures: The following people

have nothing Raf activity to disclose: Niharika Samala, Elizabeth C. Wright, Joni Trenbeath, Ronald E. Engle, Nancy Fryzek, Harvey J. Alter, Jay H. Hoofnagle, Marc G. Ghany The impact of liver diseases (LDs) on health-related quality of life (HRQoL) is an important aspect to understand the burden of these conditions and to improve their management. A well characterized impact of the major LDs on HRQoL of the general population is still lacking. The aim of our study was to fill this gap. A dataset with HRQoL data of a representative sample of the general population of most populated Italian region was matched with the dataset from a multicenter study conducted selleck chemicals in the same region and

time period to generate and validate a set of health care outcomes indicators for the major LDs (hepatitis B (HBV), hepatitis C (HCV), compensated cirrhosis (CC), decompensated cirrhosis (DC), hepatocellular carcinoma (HCC), autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC), NAFLD/ NASH and patients listed for liver transplant (LTL)). Within both datasets, HRQoL data were collected using the EQ-5D-3L, a generic instrument that enables HRQoL to be compared within and between clinical conditions and with the general population. It generates a health profile made up of 5 domains (Mobility, Self-care, Usual activities, Pain/discomfort, Anxiety/ depression). It also consists of a visual analogue scale (EQ-5D VAS) which measures overall HRQoL. Further, results from the EQ-5D health profile can be converted to utility index, useful to conduct economic evaluations. Multivariate logistic and linear regressions were then performed adjusting for possible confounders (age, sex, education and working status). A total of 6,800 “healthy subjects” and 3,105 subjects with LDs (625 HCV, 287 HBV, 614 CC, 531 DC, 647 HCC, 59 LTL, 229 NAFLD/NASH, 68 PBC, 55 PSC, and 49 AIH) were included in the analyses. Multivariate logistic analyses showed that DC, HCC, and LTL had significantly (p<0.05) higher risk to have problems in mobility, self-care, and usual activities compared to “healthy subjected”.

“
“Ponds, streams and other water bodies are known to attract high numbers of bats of various species and all foraging guilds. PR-171 price The attractiveness of these riparian habitats for bats lies in their providing the required large amounts of drinking water for successful reproduction and a potentially high supply of both aquatic and terrestrial prey insects compared to the surrounding habitats, and in the lower ultrasound interference over water than in forest habitats, important for foraging of open-habitat bat species. The actual abundance of prey depends strongly on the productivity of the aquatic ecosystem, and therefore eutrophic riparian habitats are highly

attractive to bats, but little is known about the reasons for the attractiveness of oligotrophic habitats. Here, we compared the bat activity, bat foraging activity and insect abundance around oligotrophic and less-prey-rich ponds in acidic near-natural Rapamycin solubility dmso environments to two structurally similar, simple habitats, that is, clear-cuts and meadows, by simultaneously recording echolocation calls and light trapping of insects. Our generalized linear mixed models showed no differences in prey abundance but higher bat activity at ponds than at meadows and clear-cuts, and all locally indigenous

bat species visited the ponds. The foraging activity of bats evaluated as the proportion of feeding buzzes to commuting passes positively correlated with prey abundance at meadows and clear-cuts but not at water bodies. We therefore conclude that ponds in acidic this website mountain areas are more

important to bats as a source of drinking water than as a source of prey. Our results indicate that bat monitoring in such a landscape by bat-call recording and probably by mist netting is highly promising around water bodies, and that bat conservation strategies should maintain a continuous network of water sources as an important habitat feature. “
“The ability of an organism to produce different phenotypes under different environmental conditions is a common adaptation in nature. Biotic factors like competition, community structure and predation can influence the survival and time to metamorphosis in amphibians. However, abiotic factors such as the hydroperiod and light intensity can be as important as biotic ones. We examine the influence of abiotic (light, hydroperiod) and biotic (density) factors on the morphology, growth and development of Argenteohyla siemersi pederseni tadpoles. Our main goal was to determine whether the morphology, growth and development vary in relation to changes in water volume, light intensity and number of conspecifics. The experiment was conducted under mesocosm conditions. We used a randomized block design with a factorial combination of two densities of tadpoles, two volumes of water and two light intensity conditions.

Some

studies have been published on GC in the last years, although more comprehensive studies are required. In a large cohort in China [17], three miRNAs (miR-221; miR-744, and miR-376c) were identified as being capable of distinguishing GC cases from controls with 82.4% sensitivity and 58.8% specificity. Another study [18] showed that the has-miR-335 had the potential to recognize the recurrence risk and could be related to the prognosis of GC patients. Genetic polymorphisms in several microRNA genes, such as miR-27a, miR-181a and miR-196a2, have also been found associated with GC and its prognosis [19-21] during the last year. Furthermore, polymorphisms in the miRNA-binding site of specific target genes have also been found associated with GC [22, 23]. Other genetic variants that have been associated with noncardia selleck screening library GC through GWAS and further replication analyses are rs2494938 at 6p21 and rs2285947 at 7p15.3, which also have a role in the susceptibility to other cancers [24]. Similarly, potentially functional variants at PLCE1 have been

confirmed to be associated with cardia GC [25]. It is well known that dietary factors play a role in gastric carcinogenesis. High consumption of fruit and vegetables has been associated with a reduction in GC risk, but mainly from case–control studies, while the effect from cohort Cisplatin chemical structure studies seems to be weaker. In a reanalysis in the EPIC cohort [26], based on 683 gastric adenocarcinomas, an inverse and significant association between the total vegetable and fruit intake and the GC risk was observed, between fresh fruit intake and the risk of diffuse type GC, and between citrus fruit intake and the risk of cardia GC. In the same study, a negative association was also found with dietary total antioxidant capacity [27] for both cardia and noncardia GC. In another study on the same selleck products EPIC cohort, a significant inverse association between

total flavonoid intake and GC risk was found in women but not in men [28]. In a systematic review of cohort and case–control studies among the Japanese population [29], a decrease in GC was associated with the consumption of green tea in women but not in men. Green tea is one of the sources of flavonoid intake. It is believed that salt and salt-rich foods probably increase the risk of GC. A meta-analysis of prospective studies [30] found a positive and significant association between the amount of habitual salt intake and GC risk, with a progressively increasing risk across consumption levels. The effect was stronger in Japanese studies. There is some evidence that high intake of pickled foods in Far East Asia increases the risk of GC. A systematic review and meta-analysis [31] confirmed this association, suggesting a potential 50% higher risk of GC associated with intake of pickled vegetables/foods and perhaps stronger associations in Korea and China.

Although PVT carries independent prognostic value for a poorer outcome, it is not a direct cause for aggravation. These data point to PVT and aggravation as discrete consequences of a common determinant for progression of cirrhosis, e. g. hepatic or intestinal microcirculatory dysfunction. Disclosures: Dominique Valla – Board Membership: Sequana Medical; Independent Contractor: IRIS; Speaking and Teaching: Mayoly

Spindler, MSD, Janssen Pharmaceuticals The following people have nothing to disclose: Filipe G. Nery, Cendrine Chaffaut, Bertrand Condat, Emmanuelle de Raucourt, Larbi Boudaoud, Pierre-Emmanuel Rautou, Aurelie Plessier, Dominique Roulot, Jean Claude Trinchet, Sylvie Chevret Background EX 527 purchase and Aims: The current definitions

for AKI and Hepatorenal syndrome (HRS) have been derived from patients with cirrhosis (CLD). There is paucity of data on AKI in patients with ACLF. We investigated the prevalence, spectrum, natural history and outcome of AKI in patients with ACLF [Asian Pacific Association for Study of Liver, (APASL), definition] and compared it with a cohort of hospitalized patients with cirrhosis. We also compared outcome and response to terlipressin in HRS (International Ascites Club) in both the groups. Methods: AKI was defined according to Acute Kidney Injury Network (AKIN )criteria. Serial creatinine until improvement or upto day 30 was recorded for all patients. Results: Patients with AcLF (n=534) were predominantly Gefitinib ic50 males (p<0.0001), younger (p<0.0001) with higher serum bilirubin (p<0.0001), INR (p<0.0001), hepatic encephalopathy (p<0.0001), GI bleed (p<0.0001) and mortality (p<0.0001) as compared to CLD (n=2083). AKI

at baseline was significantly more common in patients with ACLF (50.5% vs. 32.3%; p<0.0001) and associated with increased risk of mortality (59.9% vs. 41.3%; p<0.0001) as compared to CLD. A significant difference was also observed in the spectrum of AKI (p<0.0001) with sepsis related AKI as commonest cause in ACLF (160; 58.8%) and prerenal (289; 43%) in CLD. Presence of ACLF (vs CLD) was associated with a six-fold increased risk of AKI (p<0.0001, OR 95% CI 4.9-8.3) on multivariate analysis. There was no significant difference seen in the AKIN stage at baseline (Stage 1 : 61% vs 69%; Stage 2: 29.5% vs 23.5%; Stage 3: 9.9% vs 8.5%), decrease in serum creatinine at selleck screening library 48 hours (67.3% vs 65.3%) and in the overall progression of AKI (48.5%vs 45.1%), however, requirement of renal replacement therapy (RRT) and progression to AKIN stage 3 (23.5% vs 12.6%) was significantly more common in ACLF (p<0.0001). Presence of HRS (28.7% vs 29.2%) and response to terlipressin (44.1% vs 44.3%) was not significantly different in both the groups, however HRS in ACLF was characterized by an increased mortality (67.9% vs 45.9%; p=0.001) and progression to acute tubular necrosis (ATN) with higher need of RRT (53.8%vs 20.4%; p<0.

These changes may be enhanced by a bottleneck effect over HBV-quasispecies variant populations due to OLT, and prophylactic treatment pressure. (1)Buti M, J. Hepatol. 2003;38:811-817. Funding by Instituto de Salud Carlos III and the European Regional Development

Fund (ERDF), grant PI11/01973. Disclosures: Maria Buti – Advisory Committees or Review Panels: Gilead, Janssen, Vertex, MSD; Grant/Research Support: Gilead, Janssen; Speaking and Teaching: Gil-ead, Janssen, Vertex, Novartis Martin Prieto – Advisory Committees or Review Panels: Bristol, Gilead Jose Ignacio Herrero – Speaking and Teaching: Roche, Astellas, Novartis; Stock Shareholder: Roche, Novartis, Abbott, GlaxoSmitthKline Rafael Esteban – Speaking and Teaching: MSD, BMS, Novartis,

Gilead, Glaxo, MSD, BMS, Novartis, Gilead, Glaxo, Janssen The following people have nothing to disclose: selleckchem David Tabernero, Rosario Casil-las, Antoni Mas, Maria Homs, Fernando Casafont, Antonio Gonzalez, Manuel Miras, Lluis Castells, Francisco selleck compound Rodriguez-Frias Background: In HBV life cycle, viral core proteins, pregenomic RNA, reverse-transcriptase and host factors form icosahedral nucleocapsid, which plays an important role in HBV DNA replication and progeny virus production. Previous reports revealed that core protein-core protein hydrophobic interaction was required for capsid assembly initiation. In this study, we identified two acidic amino acids E77, D78 of HBV core proteins, located at the tip of the capsid spike, played vital roles in capsid formation and function. E77K/R, D78K/R mutations, which changed the charge of the region, completely blocked the capsid formation,

while E77K/A, D78K/A mutations form irregular core protein aggregates with a larger molecular weight than wild type capsid. The corresponding core protein selleck mutants (E77K/R, D78K/R) can also effectively interfere wild type capsid formation, HBV DNA replication and progeny virus production. Methodology: Based on HBc capsid spatial structure (PDB Accession Number: 1QGT.), HBc E77, D78 spatial location was analyzed using Swiss-PdbViewer v4.0. Plasmid pHBV1.2 (AY518556) contained a 1.2-length HBV adw genome inserted into the vector PUC18. Plasmid pHBV1.2-core- was derived from pHBV1.2 by introducing a stop codon(TAT—>TAG) into the C gene at Y38 position, prevented the production of core proteins. Plasmid 1-183flag directed the expression of the HBV core gene with a flag tag at the C terminal. Core protein mutations were generated by site-directed mutagenesis based on plasmid 1-183flag. HepG2 cells were cultivated in DMEM-F12 medium and all transient tansfections were performed using FuGENE HD transfection agent. HBV capsid was detected by anti-core serum (DAKO B0586).

The hazard ratio for all-cause mortality compared with controls was 2.2, 95% CI: [1.8; 2.7], P < 0.001 for the entire group Selleck AZD5363 of patients and 1.7, 95% CI: [1.3; 2.2], P < 0.001 when patients with HIV and/or viral hepatitis were excluded. The corresponding figures for the severe haemophilia subgroup were 6.6, 95% CI: [4.5; 10.0], P < 0.001

and 8.2, 95% CI [3.2; 20.8], P < 0.001 respectively. The most common causes of death were related to malignancies and the haemostatic defect. People with haemophilia were 57% less likely to die from ischaemic heart disease than controls. People with haemophilia in Sweden demonstrate higher mortality over time, independent of HIV and viral hepatitis, despite relatively advantageous access to clotting factor concentrates. "
“Summary.  Acquired factor XIII (FXIII) deficiency, arising from an autoantibody against factor XIII, is a rare bleeding disorder. This

autoimmune disorder most commonly occurs in the elderly. Patients who develop such acquired FXIII inhibitors may present with catastrophic bleeding events and are hard to be diagnosed with the normal general coagulation tests. Though the disease is relatively rare, it is known to cause ABT-888 mw significant mortality. In this article we briefly describe a patient who presented with extensive bleeding and a normal activated partial thromboplastin time and prothrombin time (PT), but had an acquired inhibitor to FXIII; selleck compound her primary disease was systemic lupus erythematosus (SLE). Also, we will focus on the clinical features, treatment modalities, fibrin structure and epitope identification for acquired factor XIII inhibitor with a review of the literature. “
“Summary.  Changes in articular cartilage after haemarthrosis

have not been completely elucidated in haemophilic arthropathy. Insights into the pathophysiological mechanisms of blood-induced joint damage mainly derived from histological, inflammatory and biochemical investigations. A structure–function relationship is another reasonable way to determine the joint overall health status. Cartilage, a viscoelastic connective tissue, is at least a biphasic material that should also work under minimal friction. Pendulum friction tester measures the mechanical aspects of joint lubrication and quantifies the biotribological properties of the joint. Indentation test is an in situ method characterizing the biomechanical properties of the cartilage. Gross, biotribological and biomechanical properties were determined in a rabbit model of experimental haemarthrosis. A sample of 1 mL of fresh autologous blood was injected in the left knee of rabbit’s joint twice weekly for four consecutive weeks. The right knee and animals in the control group were left untreated. After 8 days, joint perimeter, biotribological and biomechanical tests were performed. In a consistent manner, all data showed detrimental effects of the blood on the overall cartilage function under loading.

5F, groups 4, 6, 8). We observed that stimulation with LPS

induced TNF-α also in IRF3-deficient LMNCs (Fig. 5E, group 4), whereas no induction was observed in IRF3-deficient livers of alcohol-fed mice (Figs. 1C, 2D,E). This finding suggests a context-specific role for IRF3: whereas IRF3 is crucial for the synergism of ethanol and LPS in induction of TNF-α from monocytes/macrophages, other transcription factors likely induce TNF-α in monocytes/macrophages that are stimulated only with LPS.21 To further evaluate if regulation of IL-10 by Type I IFNs is preserved across species, we stimulated RAW264.7 murine macrophages or human PBMCs with LPS and Type I IFN and identified a significant increase of IL-10 in the presence of Type I IFN compared to stimulation with LPS alone in both species Selleck PI3K Inhibitor Library (Fig. 6A,B). We found that expression of TNF-α was significantly decreased in RAW264.7 murine macrophages stimulated with LPS in the presence of recombinant IL-10, whereas neutralization of the IL-10 receptor (IL-10R) with anti-IL10R antibody significantly up-regulated TNF-α (Fig. 6C). We also observed a dose-dependent inhibition of TNF-α and IL-1β by IL-10 in human PBMCs (Fig. 6D). Further, a 50% inhibitory concentration (IC50) of IL-10 caused a significant Tyrosine Kinase Inhibitor high throughput screening inhibition of LPS-triggered

TNF-α and IL-1β (Fig. 6D-F), whereas inhibition of IL-10 receptors using IL-10R antibody significantly up-regulated secretion of inflammatory cytokines in human PBMCs (Fig. 6E,F). These data confirmed that Type I IFN potentiates the LPS-induced IL-10 both in human and mouse systems. Taken together, these data demonstrate

that parenchymal cell-derived click here Type I IFNs up-regulate IL-10 and down-regulate inflammatory cytokines in nonparenchymal cells in the liver. More important, they outline the paradigm of intercellular cooperation and regulation in the liver, where hepatocytes control the inflammatory potential of immune cells. Chronic consumption of ethanol is tightly linked to liver inflammation and steatosis in human disease as well as in experimental models. Whereas activation of TLR4-dependent pathways by gut-derived LPS and induction of inflammatory cytokines has been traditionally attributed to BM-derived Kupffer cells,22 the role of crosstalk between parenchymal and nonparenchymal (BM-derived immune cells) in ALD remains elusive. Here we demonstrate that liver response to insults is a multistep process: IRF3 in parenchymal cells drives Type I IFN induction in the liver and parenchymal cell-derived Type I IFN leads to a modulation of inflammatory cytokines in nonparenchymal BM-derived cells (Fig. 7). Our novel findings outline a link between parenchymal and liver immune cells in modulation of innate immune signaling in ALD.

The authors thank Department of Clinical selleck products Biochemistry, Copenhagen University Hospital, Hvidovre (Copenhagen, Denmark) for quantifying IgG. The authors thank Anne-Louise Sørensen, Lotte Mikkelsen, and Lubna Ghanem (Copenhagen University Hospital, Hvidovre) for their general laboratory support as well as assistance locating samples and reagents, Jens Ole Nielsen and Ove Andersen (Copenhagen University Hospital, Hvidovre) for their support of the project, and Charles Rice (Rockerfeller University, New York, NY) and Takaji Wakita (National Institute of Infectious Diseases, Tokyo, Japan) for providing

reagents. Additional Supporting Information may be found in the online version of this article. “
“The traditional Chinese herbal medicine Sho-saiko-to is a mixture of seven herbal preparations that has long been used in the treatment of chronic liver disease. Various clinical trials

have shown that Sho-saiko-to protects against the development of hepatocellular carcinoma in cirrhotic patients. However, the mechanism by which Sho-saiko-to protects hepatocytes against hepatic fibrosis and carcinoma is not yet known. Basic science studies have demonstrated that Sho-saiko-to reduces hepatocyte necrosis and enhances liver function. Sho-saiko-to significantly inhibits hepatic fibrosis by inhibiting the activation of stellate cells, the major producers of collagen in the liver, as well as by inhibiting hepatic lipid peroxidation, promoting matrix degradation, and suppressing extracellular matrix BTK high throughput screening (ECM) accumulation. Furthermore, clinical trials have shown that

Sho-saiko-to lowers the rate of hepatocellular carcinoma (HCC) development in patients with cirrhosis and increases the survival of patients with HCC. Unfortunately, some case reports have shown the side selleck chemicals llc effects of Sho-saiko-to. Most of the side effects were interstitial pneumonia and acute respiratory failure induced by Sho-saiko-to in Japan. As a result of analyzing these case reports, the incidence and risk are increased by co-administration of interferon, duration of medication, and, high in an elderly population. This review discusses the properties of Sho-saiko-to with regards to the treatment of chronic liver diseases and suggests the side effects of Sho-saiko-to “
“The use of biological agents in inflammatory bowel diseases across the Asia-Pacific region is increasing. As new molecules and targets are identified, knowledge regarding the indications, utility, optimization and adverse effects of biological agents grows. Careful patient selection, attention to communication and patient education will maximize the benefit of these drugs. Tertiary referral centers with specific interest in inflammatory bowel diseases and experience play an important role in their use.