Direct acting antivirals for decompensated cirrhosis. Efficacy and safety are now established.

Chronic liver injury of any etiology most commonly results in liver fibrosis and eventually cirrhosis and portal hypertension with the attendant risks of decompensated liver failure, hepatocellular carcinoma (HCC) and death. Several studies have shown that successful treatment or removal of the underlying liver injury can result in regression of liver fibrosis and cirrhosis in some patients [1]. Reversal of liver cirrhosis was observed in 49% of patients with compensated hepatitis C virus (HCV) cirrhosis treated with interferon (IFN) based therapy. Sustained virological response (SVR) was the only independent predictor of reversal [2]. Eradication of HCV infection with IFN based therapy also reduces the risk of liver failure, HCC, liver-related mortality, all cause mortality and the need for liver transplantation (LT) in those patients with compensated liver cirrhosis [3,4]. The improved SVR rates and safety profiles of all oral direct acting antivirals (DAA) has led to the treatment of some patients who would not have received widespread treatment in the IFN era. One such group is the decompensated cirrhotic patients, who have a poor prognosis, have limited treatment options and make up a large proportion of those awaiting LT [5]. Several open label clinical trials of DAA in decompensated HCV patients have recently demonstrated SVR rates above 80% and improvements have been observed in the Child-Pugh-Turcotte (CPT) and/or model for end-stage liver disease (MELD) scores in a significant proportion of patients after relatively short follow up [6–9]. These improvements are largely attributable to changes in biochemical parameters of serum bilirubin and albumin. The results for SVR observed in these studies are indeed impressive given that the majority of these patients had several characteristics that would predict poor response. However, there are some limitations to the studies that make it hard to draw definitive conclusions about benefits other than viral eradication. The absence of comparator control groups makes it difficult to determine if viral eradication and improvement in MELD and CPT scores result in improved survival. The effects of viral eradication on the clinical aspects of hepatic decompensation are not well represented in