TY - JOUR
T1 - N-acetylcysteine in acute hepatic failure (non-paracetamol-induced)
AU - Ben-Ari, Ziv
AU - Vaknin, Hanna
AU - Tur-Kaspa, Ran
PY - 2000
Y1 - 2000
N2 - Background/Aims: 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. Methodology: 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. Results: 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. Conclusions: This study suggests that N-acetylcysteine administration should be considered in all patients with acute liver failure.
AB - Background/Aims: 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. Methodology: 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. Results: 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. Conclusions: This study suggests that N-acetylcysteine administration should be considered in all patients with acute liver failure.
KW - Acute liver failure
KW - N-acetylcysteine
UR - http://www.scopus.com/inward/record.url?scp=0034124433&partnerID=8YFLogxK
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C2 - 10919033
AN - SCOPUS:0034124433
SN - 0172-6390
VL - 47
SP - 786
EP - 789
JO - Hepato-Gastroenterology
JF - Hepato-Gastroenterology
IS - 33
ER -