Cirrhosis, a pathological condition defined by deranged hepatic architecture resulting from progressive fibrosis, is the final common pathway through which nearly all chronic diseases of the liver produce morbidity and mortality. It is now recognized that hepatic stellate cells of liver are primarily responsible for hepatic fibrosis and subsequent progression to cirrhosis.1 Cirrhosis secondary to hepatitis C (HCV) appeared to have regressed in response to treatment with interferon (INF), as seen on paired biopsies.2 The mean fibrosis score decreased from 5.8 to 0.5 (P = 0.004), and the mean grading score decreased from 10.8 to 3.2 in cirrhosis due to chronic hepatitis B in patients who responded to antiviral therapy.3
In our country, chronic liver disease (CLD) carries a high in hospital mortality.4 We, therefore, need to address this growing population of our nation who have carried the hepatitis C virus for years leading to this end stage liver disease. Available therapies for many patients of CLD are ineffective, with liver transplantation as the only option, which is not available in our country. Novel approaches that attack the scarring response are therefore urgently needed. Optimism in this effort is fueled by major insights into the pathogenesis of fibrosis and by accumulating evidence that even cirrhosis is reversible in many patients.1-3 Most evolving antifibrotic therapies are aimed at inhibiting the activated hepatic stellate cell, which is responsible for the fibrotic response to injury.5
Cirrhosis, fibrosis, stellate cells.