• Antifibrotic therapy
• cirrhosis
• fibrosis marker
• HALT-C
• HCV
• liver fibrosis
• non-responder
• progression
• serum marker
• fibrogenesis
• fibrosis
• hepatitis C
• liver cirrhosis

As in other chronic liver diseases, the clinically relevant end point for patients with chronic hepatitis C infection who have failed antiviral therapy, is progressive hepatic fibrosis and finally cirrhosis; with impending hepatic decompensation, liver failure and the development of hepatocellular carcinoma.1–3 Of note, the natural history of liver fibrosis progression has been studied in greatest detail in the hepatitis C population. The course is variable with decades of viraemia causing mild fibrosis in some patients to post-transplant hepatitis C, where cirrhosis can develop within a few years post transplant. Percutaneous liver biopsy has been the reference standard for liver fibrosis staging since its general introduction by Menghini in the 1950s. The liver biopsy has the additional benefit of providing information on A. aetiology, B. grading of inflammation, C. steatosis and D. iron overload, making it a valuable diagnostic test. However, there are important limitations with liver biopsy that include a small but significant morbidity and mortality rate, which creates anxiety in patients, but most importantly a significant sampling variability coupled with intraobserver and interobserver variation in pathology reporting.1 3 4

Serum markers were originally developed to identify the degree of liver fibrosis as an alternative to liver biopsy. The idea of developing a simple blood test to identify and stage liver fibrosis, and to act as a surrogate marker of clinical severity of liver disease superior to conventional liver function tests has enormous potential. There have been many different serum marker panels studied in the hepatitis …