Liver fibrosis.

|Only 20% of patients with chronic hepatitis C (CHC) progress to cirrhosis [1]. Progressive fibrosis is the hallmark of an unfavorable course and is related to several factors such as male gender, contracting the disease at an older age, features of the metabolic syndrome, iron overload, ethanol abuse, and co-infection with hepatitis B or human acquired immunodeficiency viruses. However, the course of the disease is highly variable from individual to individual. Liver biopsy remains the gold standard for evaluating necroinflammation (grade) and fibrosis (stage) in CHC [2]; however, this pre-eminence is currently being examined due to its intrinsic risks and limitations. Liver biopsy is an invasive procedure that carries a risk of complications, although rarely severe. The biopsy provides a very small specimen of liver tissue and has both a significant rate of sampling error, especially when the cylinder obtained is less than 25 mm in length, and interobserver variability. The risk-benefit ratio of liver biopsy is insufficient to maintain it as a firstline procedure, and new and non-invasive criteria for the evaluation of liver fibrosis are urgently needed [3]. A discussion on the molecular pathobiology of liver fibrogenesis is beyond the scope of this article (for a review see references [4] and [5]. The ideal marker for liver fibrosis must be specific to fibrosis of the liver, not influenced by co-morbidities, sensitive, reproducible, and informative for both the current stage of fibrosis as well as the rate of fibrogenesis activity [6]. For practical purposes, non-invasive fibrosis markers can be classified as direct (Class I biomarkers), indirect (Class II biomarkers), and imaging methods [7].