Relationship of increased serum brain natriuretic peptide levels with hepatic failure, portal hypertension and treatment in patients with cirrhosis.

Background/aims: Brain natriuretic peptide is a cardiac neurohormone secreted from ventricles in response to end diastolic pressure and increased volume. It has diuretic, natriuretic and vasodilator effects. In cirrhosis, a hyperdynamic circulation occurs because of hemodynamic and hemostatic alterations. The increase in brain natriuretic peptide concentration shows parallelism with the stage of cirrhosis. The aim of this study is to investigate the relation of increased brain natriuretic peptide level with the pathophysiologic components of cirrhosis and treatment.

Methods: Ninety-five cirrhotic patients in different stages (Child-A: 33; Child-B: 25; Child-C:37) and age and sex matched 86 healthy individuals were recruited for the study. Brain natriuretic peptide concentration was measured with brain natriuretic peptide-Triage test device using fluoresan immune assay method.

Results: Brain natriuretic peptide levels of patients with hepatic cirrhosis were significantly higher compared to control group (288.5±329.2/60.2±29.5/p=0.000, respectively). Serum brain natriuretic peptide levels were positively correlated with Child score (Child A-B-C; 201.2±266/258.7±233.6/386.5±407.7, respectively). A negative correlation was observed between brain natriuretic peptide and albumin levels (p=0.002). Brain natriuretic peptide concentration was significantly correlated with the grade of esophagus varices, and presence of ascites and collateral circulation (p=0.006; p=0.001; p=0.002; respectively). Patients receiving with beta-blocker and diuretic treatments had significantly higher brain natriuretic peptide levels.

Conclusions: High brain natriuretic peptide levels in patients with cirrhosis may be due to hepatocellular insufficiency or portal hypertension, but a cardiomyopathy developing insiduously should not be regarded.