Doctor-to-patient transmission of viral hepatitis B: Is it a problem, is there a solution?

It is well-established that hepatitis B may be transmitted from surgeons to their patients. Clear strategies are needed to reduce the risk of transmission whilst not discriminating unnecessarily against surgeons who may pose no risks to their patients. This review outlines the current position and provides a blueprint for action that may reduce the risks to patients whilst minimizing the impact on practising surgeons

Antiviral agents in hepatitis B virus transfected cell lines: Inhibitory and cytotoxic effect related to time of treatment

The antiviral and cytotoxic effects of ara-arabinoside monophosphate, 2′,3′, dideoxy-cytidine, ganciclovir, 9-2(-phosphonylmethoxyethyl) adenine, 2′,3′-dideoxy-3′-thiacytidine and recombinant interferon-alpha were studied using two human hepatitis B virus transfected hepatoma cell lines, HepG2 2.2.15 and HB 611. After 9 days of exposure, starting on day 3 after seeding, inhibition of extracellular HBV-DNA expressed as ID50 was in the 0.1–1.0 μM range for 2′,3′-dideoxy-3′-thiacytidine and 9-2(-phosphonylmethoxyethyl) adenine and >10 μM for dideoxy-cytidine, ara-arabinoside monophosphate and ganciclovir in both cell lines. At 2.500 U/ml recombinant interferon-alpha showed less than 20% inhibition in both cell lines. The HBV-DNA inhibitory effects of 2′,3′-dideoxy-3′-thiacytidine and 9-2(-phosphonylmethoxyethyl) adenine were also investigated after 1 and 3 days of exposure. In t

45CaCl2 autoradiography in brain from rabbits with encephalopathy from acute liver failure or acute hyperammonemia

In experimental hepatic encephalopathy and hyperammonemia, extracellular levels of glutamate are increased in hippocampus and cerebral cortex. It has been suggested that overstimulation of glutamate receptors causes a pathological entry of calcium into neurons via receptor-operated (NMDA- and AMPA-type) or voltage-dependent calcium channels leading to calcium overload and cell death. Neurodegeneration as a result of exposure to excitotoxins, including glutamate, can be localized and quantified using45CaCl2 autoradiography. This approach was used to study cerebral calcium accumulation in rabbits with acute liver failure and acute hyperammonemia. Acute liver failure was induced in 6 rabbits, acute hyperammonemia in 4 rabbits; 4 control rabbits received sodium-potassium-acetate. At the start of the experiment 500 µCi45CaCl2 was given intravenously. After development of severe encephalopathy, the animals were killed by decapitation. All rabbits with acute liver failure or acute hyperammonemia developed severe encephalopathy, after 13.2±1.7 and 19.3±0.5 hours respectively (mean±SEM). Plasma ammonia levels were 425±46 and 883±21 µmol/l, respectively (p<0.05). Control rabbits maintained normal plasma ammonia levels (13±5 µmol/l), demonstrated normal behaviour throughout the study and were sacrificed after 16 hours.45Ca2+-autoradiograms of 40 µm brain sections were analyzed semiquantitatively using relative optical density and computerized image analysis. As compared to background levels45Ca was not increased in hippocampus or any other brain area of rabbits with severe encephalopathy from acute liver failure or acute hyperammonemia. This suggests that, despite increased extracellular brain glutamate levels in these conditions, glutamate neurotoxicity was not important for the development of encephalopathy in these rabbits

Immunoprophylaxis to limit a hepatitis B epidemic among women undergoing in vitro fertilization

Abstract Women (175) who participated in an in vitro fertilization (IVF) programme were possibly exposed to hepatitis B virus. Later it became evident that 79 women had a hepatitis B infection, 49 were exposed but not infected and 47 were not exposed. Hepatitis B immunoglobulin (HBIg) and recombina