• Miroslava Valentová, Stephan von Haehling, Wolfram Doehner, Ján Murín, Stefan D Anker, and Anja Sandek.
• Applied Cachexia Research, Department of Cardiology, Charité Medical School, Campus Virchow-Klinikum, Berlin, Germany.
• Nutrition. 2013 Feb 1;29(2):370-8.

AbstractHeart failure is a multifaceted pathophysiologic syndrome, with prevalent dysfunction of other vital organs and systems. The role of the liver in this disease has been little investigated, although up to 80% of patients with heart failure present with some form of liver dysfunction. In addition to its multiple metabolic functions, the liver has a crucial role in the removal of circulating endotoxins and in regulating immune responses and iron homeostasis. Kupffer cells that constitute 80% to 90% of tissue macrophages in the human body play an important role in this regard. A disturbed microcirculation of the liver may decrease endotoxin clearance and increase the hepatic secretion of proinflammatory cytokines. Such an immune activation may in turn alter the expression of hepcidin in the liver, resulting in iron deficiency. The proinflammatory state also is associated with an augmented free radical formation. However, the antioxidant capacity of the liver seems to be inadequate because there is evidence for selenium deficiency in patients with heart failure. The aim of this article was to summarize the various aspects of liver dysfunction in heart failure and to highlight the role of liver-derived factors in the development of specific nutritional deficiencies. Nutritional strategies opposing these deficiencies might present promising additive treatments of heart failure.Copyright © 2013 Elsevier Inc. All rights reserved.

34 keywords...

hide…