Hepatitis B Reactivation in HBsAg-negative Anti-HBc-positive patients receiving cytotoxic chemotherapy for solid tumors.

PURPOSE: The prevalence of hepatitis B virus (HBV) reacti- vation in HBsAg-negative/anti-HBc-positive patients receiving chemotherapy for solid tumors is not fully known. The aim of this study was to investigate the incidence and outcomes of HBV reactivation in these patients. METHODS: Data among 645 HBsAg-negative/ anti-HBc-positive patients who underwent intravenous chemotherapy were retrospectively analyzed. Patients were categorized into two groups, based on received antiviral prophylaxis (n = 43) or not (n = 602). HBV reactivation was defined as the presence of detectable serum HBV DNA or HBsAg seroconversion from negative to positive, with or without increased liver enzymes. RESULTS: HBV reactivation was detected in 3 patients (0.49%) among non-antiviral prophylaxis group and in none of those with antiviral prophylaxis. Two of the HBV reactivation detected patients were successfully treated with rescue therapy, while the third died due to liver failure. CONCLUSIONS: HBV reactivation is rare in HBsAg-negative and anti-HBc-positive patients receiving chemotherapy for solid tumors. However, considering the fatal outcomes patients must be closely monitored in terms of HBV-DNA positivity and/or HBsAg seroreversion and pre-emptive antiviral therapy must be initiated as soon as HBV reactivation occurs.

Differences in nephrotoxicity risk and renal effects among anti-viral therapies against hepatitis B.

BACKGROUND: Results are conflicting with respect to the renal effects of anti-viral agents used for hepatitis B virus infection. AIM: To compare short and long-term renal effects in real-life settings and to determine risk factors for renal impairment during treatment. METHODS: 2221 treatment-naïve patients were enrolled. Among these, 895 (302 lamivudine, 27 telbivudine, 282 entecavir, 273 tenofovir and 11 adefovir initiated patients) had 'repeated measures' of creatinine (baseline, 1st, 6th, 12th and 24th month of treatment). Telbivudine and adefovir groups were excluded from further analysis because of the low number of patients. We calculated the glomerular filtration rate (GFR) using the Modification of Diet in Renal Disease (MDRD) formula at each time point. Hypophosphataemia was also recorded. Risk factors for renal impairment were analysed. RESULTS: Tenofovir caused a decline in GFR at each time point when compared to baseline levels. However, lamivudine and entecavir did not change GFR. GFR-shifting from ≥90 to 60-89 mL/min/1.73 m(2) was comparable among groups. The proportion of patients whose baseline creatinine increased more than 25% was comparable among all anti-virals. GFR showed a decline in patients who switched from entecavir to tenofovir. One patient with compensated cirrhosis needed to change from tenofovir because of renal safety. Seven and three patients developed transient hypophosphataemia in the tenofovir and lamivudine groups, respectively. CONCLUSIONS: Although tenofovir caused a decline in GFR, differences between the anti-viral agents do not appear to be so impressive. In patients with and without renal risk factors at baseline, there is no impact of anti-virals, including tenofovir.

Effect of vitamin E and pentoxifylline on glycerol-induced acute renal failure.

The pathogenesis of acute renal failure may involve, among other causes, ischemia, vascular congestion, arachidonic acid pathways, and reactive oxygen metabolites. The aim of this study is to evaluate the effects of pentoxifylline and vitamin E on the prevention of experimental acute renal failure induced by glycerol. Eighty-five Sprague-Dawley rats weighing 170-230 g were included in the study. The rats were randomly divided into four groups: group 1 was given 1 ml saline; group 2, glycerol; group 3, glycerol plus vitamin E, and group 4, glycerol plus pentoxifylline. Extent of histological renal tubular necrosis and regeneration in each animal were graded. Blood urea nitrogen, serum creatinine, and creatine kinase concentrations were measured. Mean blood urea nitrogen and serum creatinine concentrations and tubular injury scores were significantly lower in group 1 than in groups 2-4 (p < 0.001), but there were no significant differences among groups 2-4. We conclude that postinsult administration of vitamin E and pentoxifylline does not have a beneficial effect on prevention and severity of acute renal failure and that controlled, multicenter studies involving a large number of patients are needed to clarify this subject.