This is a cross-sectional study to determine the prevalence and risk factors for transmission of hepatitis B virus (HBV) infection in the Gezira state of central Sudan prior to the introduction of blood screening and vaccination against HBV.The study was carried out on the population of Um Zukra village in Gezira state of Central Sudan. The village was surveyed on five consecutive days in Dec 2000. Epidemiological characteristics were recorded and participants were interviewed for risk factors of viral hepatitis. Blood samples were then collected and tested for HBsAg and HBcAb.A total of 404 subjects were screened with a mean age of 35 years; 54.9% were females, HBsAg and HBcAb were reactive in 6.9% and 47.5% of the studied population, respectively. Exposure to HBV increased with increasing age. The only significant risk factor for transmission of infection was a history of parenteral antischistosomal therapy.This study shows that prevalence of HBV infection is high in the studied population and it is hoped that introduction of blood screening and vaccination against HBV would decrease the carrier pool in the next few years.
Abstract1. After administration to mice of a hepatotoxic dose of paracetamol (400 mg/kg body wt, p.o.) peak plasma concentrations of the drug and its glucuronide were ∼900uM around one hour. Corresponding levels of the sulphate, mercapturate and cysteine conjugates were ∼100, 35 and 20uM, respectively.2. Urinary excretion accounted for 55% of the administered drug 31 h after dosing. Of this total, 64.7% was paracetamol glucuronide, 17.9% paracetamol cysteine, 10.4% paracetamol sulphate, 0.5% paracetamol mercapturate and 6.5% unchanged drug.3. One hour after acute ethanol administration (3g/kg, p.o., concomitantly with paracetamol) plasma levels of the glucuronide, cysteine and mercapturate conjugates were decreased by ∼50%. There were reductions in the urinary excretion of the glucuronide (-13%) and cysteine conjugates (-24%), but increases in the amounts of mercapturate (+52%), sulphate +11%) and unchanged drug (+81%).4. Chronic ethanol ingestion (15 g/kg per d for 28 d) caused a transient initial increase in plasma paracetamol cysteine (+32%) and mercapturate (+41%) concentrations, but the only substantial change in urinary excretion was a 29% increase in the amount of paracetamol glucuronide.5. After chronic ethanol consumption, acute ethanol administration had a transient inhibitory effect on paracetamol mono-oxygenation, but glucuronidation was unaffected (as judged by plasma concentrations). Only paracetamol mercapturate excretion was substantially affected (+64%)
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