In this article we will critically discuss recent findings in genomic hepatology with special focus on the (epi)genetic contribution to the fibrogenic evolution of CLDs. (C) 2011 Elsevier Ltd. All rights reserved.”
“This article contains a review of major new developments
in drug treatment and the impact they could have www.selleckchem.com/products/gsk923295.html for the general cardiologist. New treatments for arrhythmias, chronic ischemic heart disease, and secondary prevention are changing the practice of clinical cardiology. In addition, recent publications on treatment adherence and therapeutic inertia are discussed. Finally, the work of the Clinical Cardiology and Outpatient Section of the Spanish Society of Cardiology during the last year is described.”
“Liver cirrhosis is a frequent consequence of the long clinical course of all chronic liver diseases and is characterized by tissue
fibrosis and the conversion of normal liver architecture selleck compound into structurally abnormal nodules. Portal hypertension is the earliest and most important consequence of cirrhosis and underlies most of the clinical complications of the disease. Portal hypertension results from an increased intrahepatic resistance combined with increased portal (and hepatic arterial) blood flow. The fibrotic and angio-architectural modifications of liver tissue leading to increased intrahepatic resistance and the degree of portal hypertension seem to be highly correlated until HVPG values of 10-12 mm Hg are reached. At this stage, which broadly represents the turning point between ‘compensated’ and ‘decompensated’ cirrhosis, additional extra-hepatic Vadimezan factors condition the further worsening of PH. Indeed, a HVPG >= 10-12 mm Hg represents a critical threshold beyond which chronic liver disease becomes a systemic disorder with the involvement of other organs and systems. The progressive failure of one of the fundamental functions of the liver, i.e. the detoxification of potentially harmful substances received from the splanchnic circulation and particularly bacterial end-products, is responsible for the establishment of a systemic pro-inflammatory state further accelerating disease
progression. The biology of liver cirrhosis is characterized by a constant stimulus for hepatocellular regeneration in a microenvironment characterized by chronic inflammation and tissue fibrosis, thus representing an ideal condition predisposing to the development of hepatocellular carcinoma (HCC). In reason of the significant improvements in the management of the complications of cirrhosis occurred in the past 20 years, HCC is becoming the most common clinical event leading to patient death. Whereas evidence clearly indicates reversibility of fibrosis in pre-cirrhotic disease, the determinants of fibrosis regression in cirrhosis are not sufficiently clear, and the point at which cirrhosis is truly irreversible is not established, either in morphologic or functional terms.