Abstract
Objective:
To provide an understanding of the detrimental impact of cirrhosis and its complications, strengths and weaknesses of current treatment options for the management of these complications, and new developments in this rapidly changing field.
Research design and methods:
Relevant publications were identified via PubMed and Cochrane databases, with additional references obtained by reviewing bibliographies from selected articles.
Results:
Cirrhosis, a progressive liver disease, is characterized by fibrosis caused by chronic liver injury. Liver fibrosis impairs hepatic function and causes structural changes that result in portal hypertension. Most patients with cirrhosis remain asymptomatic until they develop decompensated cirrhosis. At this stage, patients experience complications associated with portal hypertension (i.e., the abnormal increase in portal vein pressure), including ascites, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy (HE), hepatorenal syndrome, portopulmonary hypertension, or variceal bleeding. In addition, intestinal microbial translocation in patients with cirrhosis might also cause SBP and HE. Because the survival rate for patients with cirrhosis substantially decreases once complications develop, the key goals in treating patients with cirrhosis include both managing the underlying liver disease and preventing and treating related complications. In patients with compensated cirrhosis, the management strategy is to prevent variceal bleeding and other complications that can lead to decompensated cirrhosis. Patients with decompensated cirrhosis are typically referred for liver transplantation, and the main focus of pre-transplant management is to eliminate the cause of cirrhosis (e.g., excess alcohol consumption, hepatitis virus) and prevent the recurrence of each decompensating complication.
Conclusions:
Although substantial progress has been made to prevent the complications and mortality associated with cirrhosis, liver transplantation in combination with resolution of the etiology of cirrhosis remains the only curative option for most patients. Emerging therapies such as anti-fibrotic agents hold promise in potentially halting or reversing the progression of cirrhosis, even in patients with decompensated cirrhosis.
Transparency
Declaration of funding
Funding for editorial support was provided by Salix Pharmaceuticals, Inc., Raleigh, NC. The author was not provided funding for development of this review.
Declaration of financial/other relationships
F.F.P. received grant/research support from Abbvie, Achillion Pharmaceuticals, Anadys Pharmaceuticals, Biolex Therapeutics, Boehringer Ingelheim, Bristol-Myers Squibb, Genentech, Gilead Sciences, GlaxoSmithKline, GlobeImmune, Idenix Pharmaceuticals, Idera Pharmaceuticals, Intercept Pharmaceuticals, Janssen Pharmaceuticals, Inc, Medarex, Medtronic, Merck, Novartis, Santarus Pharmaceuticals (a wholly owned subsidiary of Salix Pharmaceuticals, Inc.), Scynexis Pharmaceuticals, Vertex Pharmaceuticals, and ZymoGenetics; is a speaker for Gilead, Kadmon, Merck, Onyx/Bayer, Genentech, GSK, Salix, and Vertex; and a consultant/advisor for Abbvie, Achillion Pharmaceuticals, Anadys Pharmaceuticals, Biolex Therapeutics, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, GlobeImmune, Idenix, Merck, Novartis, Tibotec/Janssen, Theravance, and Vertex. CMRO Peer Reviewers on this manuscript have no relevant financial or other relationships to disclose.
Acknowledgments
Technical editorial and medical writing assistance was provided by Pratibha Hebbar, PhD, Synchrony Medical Communications, LLC, West Chester, PA.