Position statement on the use of albumin in liver cirrhosis
Graciela Castro‐Narro, Carlos Moctezuma‐Velázquez, R. Malé-Velázquez, R. Trejo-Estrada, Francisco Javier Bosques, R. Moreno-Alcántar, Heriberto Rodríguez-Hernández, Aleida Bautista-Santos, Carlos Alejandro Cortéz-Hernández, Eira Cerda‐Reyes, Juanita Pérez-Escobar, J.M. Aldana-Ledesma, Jonathan Aguirre-Valádez, J.A. Velarde-Ruiz Velasco, Raúl Contreras-Omaña, Godolfino Miranda-Zazueta, M. Reyes-Bastidas, J. Meza‐Cardona, Norberto C. Chávez‐Tapia, N.J. Fernández-Pérez, E.S. García-Jiménez, Aldo Torre
Abstract
Cirrhosis is characterised by a prolonged asymptomatic period in which the inflammation persists, increasing as the disease progresses. Characteristic of this is the increase in pro-inflammatory cytokines and pro-oxidant molecules which are determining factors in the development of multiple organ dysfunction. In the early development of cirrhosis, splanchnic arterial vasodilation, activation of vasoconstrictor systems (renin-angiotensin-aldosterone) and the sympathetic nervous system (noradrenaline) bring about bacterial translocation and systemic dissemination via portal circulation of bacterial products, and molecular patterns associated with damage, which exacerbate the systemic inflammation present in the patient with cirrhosis. Albumin is a molecule that undergoes structural and functional changes as liver damage progresses, affecting its antioxidant, immunomodulatory, oncotic and endothelial stabilising properties. Our knowledge of the properties of albumin reveals a molecule with multiple treatment options in patients with cirrhosis, from the compensated then decompensated phases to multiple organ dysfunction. Its recognised uses in spontaneous bacterial peritonitis, post-paracentesis circulatory dysfunction, acute kidney injury and hepatorenal syndrome are fully validated, and a treatment option has opened up in decompensated cirrhosis and in acute-on-chronic liver disease.