study on some biologically and chemically induced hepatic dysfunctions

The present work was planned to study the influence of either hepatitis B virus [HBV] infection or occupational exposure to vinyl chloride [VC] on the detoxification capacity of the liver and on immunologic response. Also, the present study was an attempt to differentiate between biologically- and chemically-induced hepatic dysfunctions. In HBV infected patients, chronic or acute, and VC-workers, whole blood reduced glutathione [GSH] level, serum activity of gamma-glutamyl transferase [GGT], and Glutathione-S-Transferase [GST] and liver function tests were measured. Also, T-lymphocyte count and determination of serum level of interleukin-1[beta] [IL-1beta] were carried out. From the present study, it was concluded that exposure to environmental factors that cause hepatic damage, either biological or chemical, affected much its detoxifying capacity through GSH and its related enzymes GGT and GST. The involvement of GSH in detoxification of reactive VC metabolites or reactive oxygen species liberated during HBV infection led to its depletion. The increase in the GST serum activity reflects its de novo synthesis and its release into circulation in response to hepatic damage. The observed change in GGT level is an adaptive mechanism in which an increase in GGT activity acts to restore GSH used in the detoxification of xenobiotic and reactive oxygen species. The results also showed that exposure to these environmental factors had its deteriorating effects on the immunoresponse which was observed by the significant reduction in the T-lymphocyte count and the significant increase in the serum level of IL-1beta

study on hepatitis B surface [Bs] antigen and auto-antibodies in patients with fascioliasis

A considerable, unexplained liver damage was reported in human fascioliasis. The present work explored the probability of adjoined hepatitis B surface [HB[S]] antigen and auto immunity in intensification of this pathological state. Nineteen patients with chronic infection were examined clinically. The intensity of infection and specific antibody level determined. The haematological parameters and liver functions were studied. Search for HB[S] antigen, anti nuclear and anti mitochondrial antibodies was undertaken. Hepatitis B surface [HB[S]] antigen and antimitochondrial antibodies were not detected in any case. Antinuclear antibodies were observed in cases with relatively high infection intensity. It was concluded that an auto immune process might intensify the liver injury initiated by fasciola infection