Chronic hepatitis B (CHB) infection is the major cause of hepatocellular carcinoma (HCC). Primary prevention of hepatitis B infection by vaccination is effective in reducing the incidence of HCC. In persons with CHB infection, the two accepted treatment modalities are interferon alpha (IFN-α) given subcutaneously for a limited period and nucleoside/nucleotide analogs given orally on a long-term basis. These treatments are effective in suppressing viral activity and improving disease markers in short-term studies. The long-term effect on the development of liver cancers with these two forms of treatment appears to be different. However, there are no studies directly comparing IFN-α and nucleoside/nucleotide analogs. Comparisons across studies are inevitably limited by differences in the baseline characteristics of the study cohorts. Long-term follow-up studies of IFN-α therapy show inconsistent results. The beneficial effect in reducing the development of liver cancer is observed mainly in treatment responders who have preexisting cirrhosis of the liver. The long-term studies of lamivudine (and adefovir) show a consistent reduction in the development of liver cancers in patients with, and without, cirrhosis. This beneficial effect is blunted by the development of resistance. The effects of the newer nucleoside/nucleotide analogs, with higher potency and minimal risk of resistance development, are, as yet, unknown.
Abstract Aim: To correlate liver stiffness with demographical factors and routine liver biochemistry and to assess the predictive value of these as potential markers of fibrosis. Methods: Transient elastography was performed in 1268 chronic hepatitis B (CHB) patients. According to a previous validated study for CHB, liver stiffness of >8.1 and >10.3 kPa were used as cut‐off values for defining severe fibrosis and cirrhosis respectively. Results: Liver stiffness correlated positively with bilirubin, alkaline phosphatase (ALP), γ‐glutamyl transpeptidase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), globulin, α‐fetoprotein (AFP) and HBV DNA levels and negatively with albumin and platelet levels ( P <0.05 for all correlations). From 13 parameters (age, sex, platelet, AST, ALT, GGT, AFP, albumin, globulin, bilirubin, ALP, HBV DNA and hepatitis B e‐antigen), four best parameters (AST, platelet, GGT and AFP) were used to derive a liver stiffness model. Using log (index)=1.44+0.1490(GGT)+0.3308 log (AST)−0.5846 log (platelets)+0.1148 log (AFP+1) to predict both severe fibrosis and cirrhosis had area under the receiver operating characteristics curve of 0.85. Conclusion: Routine liver biochemistry correlated well with liver stiffness in Asian CHB patients. A model using simple serum markers can predict liver stiffness, and further studies are required to validate the usefulness of these simple tests as non‐invasive markers of fibrosis in CHB.
SUMMARY Four thousand and one hospital staff were screened for hepatitis B virus (HBV) markers in a vaccination programme in Hong Kong. The seropositivity rate for HBsAg, anti-HBs and anti-HBc were significantly higher in the 3160 existing hospital staff than in 841 new recruits. Of the subjects negative for HBV markers, 605 were randomized to receive three doses of either 10 or 20 μg of the Merck Institute vaccine (HB-VAX). Compared with the 20 μg dose, vaccination with the 10 μg dose results in equal immunogenicity and efficacy at the completion of the three injections but induced a slower response rate and lower anti-HBs titres with the first two doses. The commonest side-effect of local soreness was less with the 10 μg dose. We conclude that (1) hospital staff working in high endemic areas should be vaccinated on recruitment and (2) the 10 μg dose of HB-VAX can replace the recommended 20 μg dose for adults, being cheaper and as efficacious.
1 The haemodynamic responses to a bolus intravenous injection of 400 mg cimetidine were studied in eight subjects with normal lung function and sixteen with chronic obstructive airway disease (COAD), under continuous systemic and pulmonary arterial monitoring. In all subjects there were significant immediate but transient (less than 10 min) drops in the systemic and pulmonary arterial pressures (both systolic and diastolic), the systemic vascular resistance and total pulmonary resistance. The percentage drops were significant more marked in the COAD group in the following: systemic arterial pressures (systolic and diastolic), systemic vascular resistance and total pulmonary resistance. The cardiac output showed no significant change in the group with normal lung function but rose significantly in the COAD group. None of the subjects had any symptoms associated with the haemodynamic changes. 2 These results can be explained by a generalized vasodilatory effect of cimetidine, but the relationship to its H2‐ receptor blocking effect is undetermined. Hypoxia and/or hypercapnia may sensitize an individual to the vasodilatory effect of cimetidine.
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