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Human albumin: liver disease


Human albumin:


management of liver disease


Several studies have clearly established that albumin is effective in counteracting the hemodynamic dysfunction of advanced cirrhosis, which results from an arterial vasodilation mainly located in the splanchnic area, and represents the common background for several complications


Mauro Bernardi Manuel Tufoni Carmen Serena Ricci Maria Elena Bonavita Giacomo Zaccherini Department of Medical and Surgical Sciences, University of Bologna, Italy Email: mauro.bernardi@unibo.it


Hypoalbuminaemia is a typical feature


of cirrhosis and represents an important and adverse prognostic factor. It results from both a decreased synthesis by liver cells and, to a lesser extent, to other factors such as plasma volume expansion diluting the extracellular fluid protein content, due to the renal retention of sodium and water, and an increased trans-capillary escape rate of albumin, which leads the protein to be lost towards the extravascular space. Several studies have clearly established that albumin is effective in counteracting the hemodynamic dysfunction of advanced cirrhosis, which results from an arterial vasodilation mainly located in the splanchnic area, and represents the common background for several complications. These favourable effects are likely due not only to volume expansion, but also to the non-oncotic properties of albumin, such as anti- oxidant and scavenger activities, and its ability to preserve capillary integrity and permeability.1


Established indications to albumin administration in cirrhosis Prevention of renal failure in spontaneous bacterial peritonitis Spontaneous bacterial peritonitis (SBP) is


a frequent and life-threatening infection of ascitic fluid. The diagnosis is based on finding more than 250


polymorphonuclear cells/mmc in ascites, in the absence of an intra-abdominal source of infection or malignancy. Even without the occurrence of septic shock, SBP leads to a pro-inflammatory cytokine storm that further impairs cardiovascular dysfunction. The ensuing worsening in effective volaemia can lead to acute renal failure, with the phenotype of hepatorenal syndrome type 1 (HRS-1) or acute tubular necrosis, which occurs in about 30% of cases and represents a main cause of death. Indeed, SBP-related in-hospital mortality rates can be as high as 20%, despite the resolution of infection.2


A


prospective randomised study has shown the administration of a high dose of albumin (1.5 g/kg at diagnosis and 1 g/kg on day 3) in addition to antibiotic treatment decreases the incidence of renal failure (from 30% to 10%) and improves in-hospital and 3-month survival.3


The capacity of albumin to


improve the outcome of patients with SBP has been confirmed in a recent meta- analysis of randomised trials.4


The amount of albumin to be administered in this setting and whether all patients have to be treated have not been fully defined as yet. In fact, it would appear that only patients at high risk of developing renal failure (baseline bilirubin > 4 mg/dl and/or creatinine > 1.0 mg/dl) most benefit from albumin administration, suggesting that it could be restricted to high-risk patients. However, two large subsequent retrospective studies showed that the incidence of poor outcome in low-risk patients not treated with albumin is not negligible. It has also been reported that a reduced-dose regimen of albumin (1.0 g/ kg on day 1 and 0.5 g/kg on day 3) is as effective as the standard regimen in preventing renal failure and reducing mortality. However, these results still need to be confirmed by further prospective studies in larger patient populations. Thus, to date, the European Association for the Study of the Liver recommends that all patients with SBP should receive intravenous albumin at the higher dosage in addition to antibiotics.5


Diagnosis and treatment of hepatorenal syndrome HRS is a potentially reversible renal failure that occurs in patients with advanced cirrhosis, ascites and liver failure, associated with marked circulatory dysfunction. HRS is the clinical manifestation of a severe intra-renal vasoconstriction. This results from impaired effective volaemia secondary to both arterial vasodilation and cardiac dysfunction (cirrhotic cardiomyopathy), which lead to a striking compensatory activation of vasoconstrictor systems such as the


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