Increased intestinal hydrolysis of urea in patients with alcoholic cirrhosis.

Fourteen patients with biopsy-proven alcoholic liver cirrhosis in a clinically stable phase but with compromised liver function entered the study, together with 10 control persons. All had normal creatinine clearance, and none received antibiotics or hormones. They ingested a diet containing 1 g of protein/kg body weight daily during the study. The fractional intestinal loss of newly synthesized urea, determined by a 14C-urea tracer method, was increased from 0.17 +/- 0.08 in controls to 0.26 +/- 0.08 in cirrhotics (mean +/- SD, P less than 0.02). Urea nitrogen synthesis rate, determined as urinary excretion rate, corrected for accumulation in the total body water and for fractional intestinal loss, was the same in controls and cirrhotics (26.1 +/- 3.8 and 22.1 +/- 6.8 mmol/h, respectively). The patients with cirrhosis had a significantly greater nitrogen balance than the control group (12.5 +/- 7.0 mmol/h versus 7.0 +/- 5.9 mmol/h; P less than 0.05). Furthermore, there was a positive correlation between intestinal loss and blood urea nitrogen concentration (r = 0.68, P less than 0.01) in patients with cirrhosis but not in controls. The increased endogenous ammonia load of cirrhotics corresponds to an extra protein intake of 30-35 g/day. In patients with cirrhosis prophylactic treatment with, for example, lactulose is rational before reduction in dietary protein.