Hepatitis B core antibody‐positive donors in cardiac transplantation: a single‐center experience

Hepatitis B virus (HBV) core antibody (HBcAb)‐positive donors are increasingly utilized in solid organ transplantation. We report a single center's experience in cardiac transplantation with 18 HBcAb‐positive donors. Available follow‐up on recipients of cardiac allografts from HBcAb‐positive donors, including 2 donors with low‐level serum HBV DNA at the time of transplantation, demonstrated no documented donor‐derived HBV transmission.     

Hepatitis B virus and risk of non‐Hodgkin lymphoma: An updated meta‐analysis of 58 studies

Previous studies have focused on the relationship between hepatitis B virus (HBV) infection and non‐Hodgkin lymphoma (NHL). However, the results remain inconsistent and somehow conflicting in different subgroups. The aim of this study was to combine the findings of independent studies to comprehensively assess the association between HBV and NHL using a meta‐analysis. Relevant studies were identified through structured keyword searches in PubMed, EMBASE and the China National Knowledge Infrastructure (CNKI) database, and 58 studies with a total of 53 714 NHL cases and 1 778 591 controls were finally included. Pooled estimates indicated a significantly increased NHL risk in HBV‐infected individuals (summary odds ratio [sOR]: 2.50; 95% confidence interval [CI]: 2.20‐2.83) regardless of the study design (case–control studies: sOR: 2.47; 95% CI: 2.16‐2.82; cohort studies: sOR: 2.64; 95% CI: 1.78‐3.91). Considerable heterogeneity was observed across studies that was primarily attributed to the NHL subtypes (meta‐regression: P < .05). Overall, B‐cell NHL (sOR: 2.46; 95% CI: 1.97‐3.07) presented a stronger association with HBV infection than T‐cell NHL (sOR: 1.67; 95% CI: 1.34‐2.10). Within the B‐cell NHL subtypes, HBV infection was significantly associated with diffuse large B‐cell lymphoma (DLBCL, sOR: 2.06; 95% CI: 1.48‐2.88) and follicular lymphoma (FL, sOR: 1.54; 95% CI: 1.11‐2.12), but not with chronic lymphocytic leukaemia/small lymphocytic lymphoma (CLL/SLL) and Burkitt lymphoma. The results of this meta‐analysis support a positive link between HBV infection and NHL development. Further investigations for the mechanisms underlying HBV‐induced NHL are warranted.     

Hepatitis C virus eradication with direct‐acting antiviral improves insulin resistance

Sustained virological response (SVR) after interferon‐based therapy is associated with improvement of insulin resistance (IR) in HCV‐infected patients. Few data are available in the direct‐acting antivirals (DAAs) era, especially in cirrhotic patients. We prospectively evaluated the long‐term effect of DAAs on IR. Patients treated with DAAs between May 2015 and December 2016 in 3 tertiary care centres were recruited. Patients with diabetes were excluded. Biochemical and virological data were collected at baseline, 12/24/48 weeks (W) after the end of therapy (EOT). Presence of IR was defined by a ‘homeostasis model assessment index for IR’ [HOMA‐IR])> 2.5. Liver fibroscan was performed at baseline, at 24/48W after EOT. Hundred and thirty‐eight patients were enrolled (mean age 58 years, M/F 85/53, GT1 61%, 68.8% cirrhotic). Sixty‐eight patients (94/138) had IR. Patients with IR had significantly higher stiffness than patients without it (23 ± 12 vs 15 ± 8; P < .0001). SVR12 was achieved in 135 (98%) patients, and 124 (90%) patients reached the 48W post‐EOT. At this time point, the percentage of patients with IR significantly decreased to 49% (P = 0,01). HOMA‐IR was significantly lower than baseline (1.8 vs 3; P < .001), and this was related to a significant reduction of insulin level (11.7 ± 6.3 vs 16.4 ± 8.3). High BMI was associated with a significantly lower probability of achieving a non‐IR status at 24W (P = .05) and 48W (P = .03).In conclusion, SVR following DAAs led to a significant reduction of IR, even in patients with cirrhosis. Nevertheless, IR can persist after the achievement of SVR, especially in patients with high BMI.     

Hepatitis C virus infection and risk of multiple myeloma: Evidence from a meta‐analysis based on 17 case‐control studies

Hepatitis C virus (HCV) infection is a leading cause of chronic liver damage and is associated with other diseases. Some studies reported that patients with HCV have a significantly increased risk of multiple myeloma while others do not report an association. We aimed to clarify the association between HCV and multiple myeloma and analyse the factors that affect the controversial conclusions through a meta‐analysis. We conducted a systematic literature search of HCV and myeloma in the databases of PubMed/MEDLINE, Cochrane Library, EMBASE, Wanfang and China National Knowledge Infrastructure (CNKI) from inception to September 2016. Outcomes were expressed as odds ratios (ORs) and 95% confidence intervals (95% CIs). A positive correlation between HCV infection and risk of developing multiple myeloma was revealed (OR=2.67, 95% CI=1.35‐5.26, P=.005) based on meta‐analysis of 17 case‐control observational studies. When the data were stratified by source of control, significant associations were observed in hospital‐based studies, but not population‐based studies. Further subgroup analyses showed increased risk of multiple myeloma in HCV patients when studies were conducted in high HCV prevalent countries, but not in low or moderate HCV prevalent countries. In addition, similar positive association was detected in studies performed in the East Asia and in intermediate‐quality studies. In summary, the association of HCV infection with increased risk of multiple myeloma depended on several factors, including study design, quality and environmental HCV prevalence. Further large‐scale, well‐designed studies are needed to validate the role of HCV in the aetiology of multiple myeloma.     

Hepatitis B virus reactivation associated with anti‐neoplastic therapy

Reactivation of hepatitis B virus (HBV) infection is a known complication during and after anti‐cancer therapy. This condition can affect two patient populations: it is most commonly seen in patients who are seropositive for hepatitis B surface antigen (HBsAg), but it is also being increasingly reported among patients who are HBsAg‐negative but who have prior infection, as evident by seropositive status for antibody to hepatitis B core antigen (anti‐HBc), irrespective of their anti‐HBs (antibody to HBsAg) status. The clinical course can vary from asymptomatic hepatitis to fulminant hepatic failure that can be potentially fatal. With the increasing use of biological agents in addition to potent cytotoxic chemotherapy in the armamentarium of anti‐cancer treatments, reactivation of hepatitis B has become a common clinical situation that is faced by both oncologists and hepatologists especially in HBV endemic areas. In this review, we discuss the clinical course of reactivation in the two HBV‐infected sub‐populations, and the role of anti‐virals in the prevention and management of HBV reactivation in association with cytotoxic chemotherapy and biological therapies.     

Hepatitis B virus genotype and basal core promoter/precore mutations are associated with hepatitis B‐related acute‐on‐chronic liver failure without pre‐existing liver cirrhosis

Summary. The study was undertaken to investigate the features and clinical implications of hepatitis B virus (HBV) genotypes, basal core promoter (BCP) and precore (PC) mutations in hepatitis B‐related acute‐on‐chronic liver failure (HB‐ACLF). Samples from 75 patients with HB‐ACLF and without pre‐existing liver cirrhosis and 328 age‐matched patients with chronic hepatitis B (CHB) were analyzed. HBV genotype and BCP/PC mutations were determined by direct sequencing. Mutations at 8 sites of the BCP/PC region were compared between the two groups of patients. A significantly higher ratio of genotype B to C was found in patients with HB‐ACLF than in patients with CHB (30.7–69.3%vs16.5–82.6%, P < 0.01). Single mutations including T1753V (C/A/G), A1762T, G1764A, G1896A and G1899A and triple mutations T1753V/A1762T/G1764A and A1762T/G1764A/C1766T (or T1768A) were more frequently detected in patients with HB‐ACLF than in patients with CHB. Correspondingly, BCP/PC wild‐type sequences were absent in patients with HB‐ACLF in contrast to 27.1% in patients with CHB. The BCP/PC mutations were found to be associated with increased HBeAg negativity, higher alanine aminotransferase level and lower viral load. Patients with HB‐ACLF infected with the PC mutant virus had a higher mortality. The findings suggest that patients with CHB infected with genotype B with BCP/PC mutations were more likely to develop HB‐ACLF than those with genotype C with wild‐type BCP/PC regions, and patients with HB‐ACLF with the PC mutation had increased risk of a fatal outcome.