N-acetylcysteine in acute hepatic failure (non-paracetamol-induced)

Acute liver failure is a serious condition associated with poor prognosis. It may be associated with changes in systemic hemodynamics, i.e., tissue hypoxia, which contributes to multiple-organ failure. Recent studies have shown that N-acetylcysteine administered to patients with fulminant hepatic failure (paracetamol-induced) increases oxygen delivery and improves survival. The aim of this pilot study was to evaluate N-acetylcysteine administration to patients with non-paracetamol-induced acute liver failure and assess its effect on the clinical course and outcome.

N-acetylcysteine was administered at presentation to 7 patients with non-paracetamol-induced acute liver failure. Patients were followed for changes in clinical parameters (grade of encephalopathy), coagulation factors, biochemical parameters and outcome.

Clinically, 3 patients who initially had grade O/II encephalopathy, did not progress, and have fully recovered. The mean peak prothrombin time, serum factor V, aspartate aminotransferase and alanine aminotransferase levels, all significantly improved. Four patients (57%) have recovered fully (1 patient, although fully recovered, died later from an unrelated cause). Two patients required orthotopic liver transplantation and 1 patient died. N-acetylcysteine administration may have prevented progression to grade III/IV encephalopathy and improved serum coagulation factors. This may account for its beneficial effect on survival in patients who had poor prognostic criteria at base-line. No side effects of the drug were noted.

This study suggests that N-acetylcysteine administration should be considered in all patients with acute liver failure.