Ecstasy-induced brain death and acute hepatocellular failure: multiorgan donor and liver transplantation.

摘要

BACKGROUND: Ecstasy is a neurotoxic and hepatotoxic drug. Brain edema and fulminant hepatic failure are two of the most serious complications associated with the consumption of ecstasy. Acute ecstasy intoxication can transform a patient into an organ donor or a hepatic graft recipient. MATERIALS AND METHODS: In the last 5 years in our centers, we have had two multiorgan donors who died from ecstasy-induced brain edema and three patients who required urgent orthotopic liver transplantation for treatment of severe acute hepatocellular failure induced by this drug. We performed eight transplantations using the organs of these two brain-dead donors: one heart, one bipulmonary, three kidneys, one kidney-pancreas, and two livers. RESULTS: Toxicity caused by ecstasy was not observed in any of the eight patients who underwent transplantation. The clinical state and the graft function of the heart, two liver, renopancreatic, and three kidney recipients were normal for a follow-up period that ranged between 7 months and 4.5 years. The lung recipient died from multiorgan failure secondary to bilateral pneumonia 5 days after the transplantation, and one of the kidney transplant patients died as a result of intestinal lymphoma 6 months after transplantation. The three liver transplantations in the three patients with ecstasy-induced fulminant hepatic failure were performed successfully using orthotopic transplantation. These three recipients are asymptomatic and have normal-functioning hepatic grafts after follow-up of 3.5 years, 15 months, and 11 months, respectively. CONCLUSIONS: The thoracic and abdominal organs of people dying from ecstasy intoxication can be viable for transplantation. The short- and medium-term survival of the graft and of the recipient have been similar to that of other organ donors. Urgent liver transplantation is an effective therapeutic option in patients with ecstasy-induced acute hepatocellular failure.