EASL Clinical Practice Guidelines

Introduction

Hepatitis C virus (HCV) infection is one of the main causes of chronic liver disease worldwide. The long-term impact of HCV infection is highly variable, from minimal changes to extensive fibrosis and cirrhosis with or without hepatocellular carcinoma (HCC). The number of chronically infected persons worldwide is estimated to be about 160 million, but most of them are unaware of their infection. The implementation of extended criteria for screening of HCV, such as targeting birth cohorts, is the subject of major debate among different stakeholders. Clinical care for patients with HCV-related liver disease has advanced considerably during the last two decades, thanks to an enhanced understanding of the pathophysiology of the disease, and because of developments in diagnostic procedures and improvements in therapy and prevention.

These EASL Clinical Practice Guidelines (CPGs) are intended to assist physicians and other healthcare providers, as well as patients and other interested individuals, in the clinical decision-making process by describing the optimal management of patients with acute and chronic HCV infections. These guidelines apply to therapies that are approved at the time of their publication. Two protease inhibitors (PIs) have completed phase III development for patients infected with HCV genotype 1, and are currently registered for use in Europe and elsewhere. Therefore, these EASL CPGs on the management of HCV infection have been updated to include guidance on the use of these two drugs, and will be updated regularly based on approval of additional new therapies and clinical experience with them. Also, substance users are increasingly considered as a treatable patient group at risk. The EASL CPGs have been updated in this respect. The preceding HCV CPGs were published as recently as 2011 [1]. These updated CPGs have built upon the earlier published work, so much remains unchanged. In particular, dual therapy remains the standard of care for patients with genotype non-1, and for some patients with genotype 1 infection. The authors of the current CPGs acknowledge the work undertaken by Professor Craxi and the authors of the 2011 CPGs which forms the basis of the current revision.