Search

SUMMARYBackgroundHepatic fibrosis occurs in response to chronic liver injury, regardless ofthe cause. An impressive amount of knowledge concerning the patho-genesis and treatment of liver fibrosis has emerged over the past fewyears. The hallmark of this event is the activation of the hepatic stellatecell. The latter event causes accumulation of extracellular matrix andformation of scar, leading to deterioration in hepatic function.AimTo assess chronic liver injury, many invasive and non-invasive methodshave been suggested.MethodsAlthough transient elastography, image analysis of fractal geometry andfibrotest with actitest have been used in clinical practice, liver biopsyremains the recommended choice, especially when histological stagingof fibrosis or response to treatment is needed.ConclusionsThe recent advances in anti-viral therapy have resulted in many reportson fibrosis and even on cirrhosis regression, especially early and inyoung people. A number of new agents have been suggested for thetreatment of fibrosis, with promising results in animals; however, theirefficacy in humans remains to be elucidated. The investigation of hetero-geneity and plasticity of hepatic stellate cells is a topic of scientificinterest and may result in improvements in patient management.

Eighteen patients with presumed childhood acquisition of chronic hepatitis B virus infection were initially entered into this randomized controlled trial. Twelve were treated with prednisolone for 4 weeks followed, after a 2-week gap, by thrice weekly lymphoblastoid alpha-interferon for 12 weeks. Two of these had previously acted as untreated controls. Three of the 12 patients (25%) [who were initially hepatitis B virus (HBV) surface antigen (HBsAg), 'e' antigen (HBeAg) and HBV-DNA positive] became HBeAg and HBV-DNA negative during therapy and remained so after 12 months post-therapy follow-up. One of these also lost HBsAg. A further two patients lost HBeAg and HBV-DNA during therapy but relapsed 6 and 9 months later. Two additional patients were HBV-DNA negative but HBeAg positive at the end of follow-up. None of the eight untreated control patients seroconverted during an identical follow-up period. Two further patients were HBsAg and HBeAg positive but HBV-DNA negative at the start of therapy. These were omitted from the final analysis: both subsequently lost HBeAg. The treatment response was associated with a rise in aspartate aminotransferase, peaking 2-6 weeks after prednisolone withdrawal, loss of HBV-DNA 0-8 weeks later and subsequent normalization of liver function tests. Treatment was well tolerated.