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Large amounts of new data on the natural history and treatment of chronic hepatitis B virus (HBV) infection have become available since 2005. These include long-term follow-up studies in large community-based cohorts or asymptomatic subjects with chronic HBV infection, further studies on the role of HBV genotype/naturally occurring HBV mutations, treatment of drug resistance and new therapies. In addition, Pegylated interferon α2a, entecavir and telbivudine have been approved globally. To update HBV management guidelines, relevant new data were reviewed and assessed by experts from the region, and the significance of the reported findings were discussed and debated. The earlier “Asian-Pacific consensus statement on the management of chronic hepatitis B” was revised accordingly. The key terms used in the statement were also defined. The new guidelines include general management, special indications for liver biopsy in patients with persistently normal alanine aminotransferase, time to start or stop drug therapy, choice of drug to initiate therapy, when and how to monitor the patients during and after stopping drug therapy. Recommendations on the therapy of patients in special circumstances, including women in childbearing age, patients with antiviral drug resistance, concurrent viral infection, hepatic decompensation, patients receiving immune-suppressive medications or chemotherapy and patients in the setting of liver transplantation, are also included.

Background Replication of hepatitis B virus (HBV) is the primary driver of disease progression and clinical outcomes in patients with chronic hepatitis B (CHB), but other factors, such as hepatitis B e antigen (HBeAg) status, also influence disease course. The importance of HBeAg seroconversion is underscored by current CHB treatment guidelines that recommend limiting the duration of antiviral therapy in HBeAg-positive patients who achieve seroconversion. Aims A 2-day meeting of leading hepatologists with extensive experience managing patients with CHB in the Asia-Pacific region was held with the overall goals of reviewing and evaluating (1) available data on the relationship between HBeAg seroconversion and clinical outcomes for patients with HBeAg-positive CHB, and (2) the ways in which seroconversion should influence patient management. Conclusions It was agreed that HBeAg seroconversion is an important serologic end point for patients with CHB and that achieving this goal should be an important consideration in treatment selection. Patients with HBeAg-positive CHB should consider pegylated interferon if they are aged <40 years (especially women), have lower HBV DNA levels, can afford this treatment, and have a lifestyle that would support adherence to injection therapy. Alternatively, nucleos(t)ide analogs are recommended in patients with alanine aminotransferase levels ≥2 × the upper limit of normal, HBV DNA levels <9 log₁₀ IU/ml, and compensated CHB. Entecavir, telbivudine, and tenofovir may be used as first-line therapy; they can be administered as a finite therapeutic course in HBeAg-positive patients who seroconvert. Telbivudine and tenofovir should be considered in women of child-bearing potential.

The Asian-Pacific Association for the Study of the Liver (APASL) convened an international working party on the “APASL consensus statements and recommendation on management of hepatitis C” in March, 2015, in order to revise “APASL consensus statements and management algorithms for hepatitis C virus infection (Hepatol Int 6:409–435, 2012)”. The working party consisted of expert hepatologists from the Asian-Pacific region gathered at Istanbul Congress Center, Istanbul, Turkey on 13 March 2015. New data were presented, discussed and debated to draft a revision. Participants of the consensus meeting assessed the quality of cited studies. Finalized recommendations on treatment of hepatitis C are presented in this review.

Induction of curative immune responses by therapeutic vaccination in chronic viral infections such as chronic hepatitis B (CHB) is expected to be facilitated by reduction of viral load by antiviral treatment. In this open label, controlled, randomized study, 195 patients with HBeAg positive CHB were randomized to receive 12 doses of HBsAg with AS02B adjuvant candidate vaccine plus lamivudine daily for 52 weeks or lamivudine daily alone. The combined administration of vaccine and lamivudine was safe and well tolerated, but did not improve the HBe seroconversion rate (18.8%) when compared to treatment with lamivudine alone (16.1%) ( p = 0.6824). Despite induction of a vigorous HBsAg-specific lymphoproliferative response, cytokine production and anti-HBs antibodies, therapeutic vaccination with an adjuvanted HBsAg vaccine administered concomitantly with lamivudine did not demonstrate superior clinical efficacy in HBeAg positive CHB patients as compared to lamivudine therapy alone.

After 48 weeks of treatment and 24 weeks of follow-up, patients treated with peginterferon either alone or in combination with lamivudine were more likely to have HBeAg seroconversion than patients treated with lamivudine alone (32 percent and 27 percent vs. 19 percent) and more likely to have HBV DNA levels below 100,000 copies per milliliter (32 percent and 34 percent vs. 22 percent). A 48-week course of peginterferon alfa-2a is more effective than 48 weeks of lamivudine for HBeAg-positive chronic hepatitis B. A 48-week course of peginterferon alfa-2a is more effective than 48 weeks of lamivudine for HBeAg-positive chronic hepatitis B. More than 400 million people worldwide are chronically infected with hepatitis B virus (HBV). 1 Effective therapy is necessary to prevent the progression of chronic hepatitis B to cirrhosis, hepatocellular carcinoma, and death. Current consensus guidelines from Asia, Europe, and the United States recommend lamivudine, adefovir, or conventional interferon alfa for the treatment of chronic hepatitis B. 2 – 5 Lamivudine and adefovir suppress HBV replication and result in an improvement in liver architecture on microscopical evaluation during therapy. However, rates of hepatitis B e antigen (HBeAg) seroconversion, an end point that has been associated with improved long-term clinical outcomes, 6 , 7 are generally . . .

Among patients with hepatitis B e antigen (HBeAg)–negative chronic hepatitis B, the rates of suppression of hepatitis B virus DNA to below 20,000 copies per milliliter were 43 percent with peginterferon alfa-2a alone, 44 percent with peginterferon alfa-2a plus lamivudine, and 29 percent with lamivudine alone after 48 weeks of treatment and 24 weeks of follow-up; the rates of suppression to below 400 copies per milliliter were 19 percent, 20 percent, and 7 percent, respectively. Peginterferon alfa-2a was more effective than lamivudine for HBeAg-negative chronic hepatitis B. Chronic infection with hepatitis B virus (HBV) is a major global health problem, affecting more than 400 million people worldwide. 1 Chronic hepatitis B is associated with serious complications, including liver failure, cirrhosis, and hepatocellular carcinoma. Hepatitis B e antigen (HBeAg)–negative chronic hepatitis B represents a late phase of the infection that is characterized by progressive liver damage 2 , 3 and viral variants with changes in the precore or core promoter region, 4 , 5 which abolish or suppress the expression of HBeAg. Spontaneous, sustained remissions are rare in HBeAg-negative chronic hepatitis B, 6 which has a poor prognosis. HBeAg-negative chronic hepatitis B occurs throughout . . .

The Asian Pacific Association for the Study of the Liver (APASL) convened an international working party on “APASL consensus statements and recommendations for management of hepatitis C” in March 2015 to revise the “APASL consensus statements and management algorithms for hepatitis C virus infection” (Hepatol Int 6:409–435, 2012). The working party consisted of expert hepatologists from the Asian–Pacific region gathered at the Istanbul Congress Center, Istanbul, Turkey on 13 March 2015. New data were presented, discussed, and debated during the course of drafting a revision. Participants of the consensus meeting assessed the quality of the cited studies. The finalized recommendations for hepatitis C prevention, epidemiology, and laboratory testing are presented in this review.

Hepatitis due to hepatitis B virus reactivation after cytotoxic or immunosuppressive therapy is a serious cause of liver-related morbidity and mortality. With the characterization of the underlying pathogenesis, much progress in the management of this important clinical problem has been made in the past 2 decades. By year 2008, it is mandatory to screen for hepatitis B surface antigen status before initiating intensive chemotherapy or immunosuppressive therapy. All those who are hepatitis B surface antigen positive should be started on preemptive nucleos(t)ide analogues. However, there remains important issues, such as the type and duration of nucleos(t)ide analogue therapy, which need to be understood. As not all hepatitis B surface antigen-positive patients will suffer from HBV reactivation, it is therefore useful to identify risk factors related to HBV reactivation so that patients will not be treated unnecessarily with nucleos(t)ide analogues. To date, a high baseline level of viral replication, as reflected by high serum HBV DNA level, positive serum hepatitis B e antigen, and a high intrahepatic covalently closed circular DNA level, is the most important predictor for HBV reactivation. Recently, there has been an increased awareness of reactivation of occult hepatitis B virus, especially in hepatitis B virus endemic area, such as the Asia-Pacific region. Careful epidemiological study will be needed to clarify the impact of occult hepatitis B infection in patients treated with cytotoxic or immunosuppressive therapy.

Estimated hepatitis C virus (HCV) infection rates in the general populations were 1.3, 0.9, 0.4–1.0, 14.7, 0.1–0.3, 0.9–1.9, 1.0–2.0, 5, 4.4–8.6 and 0.5–1.3 % in Australia, Bangladesh, Mainland China, Egypt, Hong Kong, India, Japan, Pakistan, Taiwan and Turkey, respectively. The main HCV genotypes (Gs) are G1, G3, G1b, G4, G1b, G3, G1b, G3, G1b and G2, and G1 in Australia, Bangladesh, Mainland China, Egypt, Hong Kong, India, Japan, Pakistan, Taiwan and Turkey, respectively. Of IL28B genotypes, favorable alleles are ~50 % in Australia and Turkey, but 60–70 % in most of the other Asian countries. Peginterferon plus ribavirin is available in all ten Asian Pasific countries. In addition, HCV NS3/4A protease inhibitors with peginterferon plus ribavirin are currently available in several countries. Clinical trials of interferon-free regimens for HCV are ongoing in most of the ten Asian Pacific countries.

The use of low-dose aspirin as prophylaxis against cardiac events or stroke and the presence of Helicobacter pylori infection are both risk factors for upper gastrointestinal tract bleeding from ulcers. In this study, patients taking low-dose aspirin who had both bleeding from ulcers and H. pylori infection had the latter eradicated and were then randomly assigned to receive lansoprazole (62 patients) or placebo (61 patients) and were followed for a median of 12 months while the low-dose aspirin treatment was continued. There was one recurrence of ulcer complications in the lansoprazole group and nine in the placebo group (P=0.008). After the eradication of H. pylori infection, low-dose aspirin therapy can be continued more safely if lansoprazole is added to the therapeutic regimen. The efficacy of low-dose aspirin (less than 325 mg daily) in the prevention of cardiovascular and cerebrovascular diseases is well established. 1 Patients who are taking low-dose aspirin, however, have an increased risk of ulcer complications, 2 and some of these patients should be given prophylactic treatment. One of the available options for preventing these ulcer complications is the simultaneous use of proton-pump inhibitors, which reduce gastric acidity substantially. In a recent epidemiologic study, the use of a proton-pump inhibitor was found to be associated with a decrease of 80 percent in the risk of gastrointestinal bleeding in subjects taking low-dose aspirin. . . .