April 25, 2016
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Early alcoholic relapse post-liver transplant leads to severe graft injury

Liver transplant recipients who experienced alcoholic relapse within 5 years of transplant had increased risk for developing severe allograft injury, according to findings published in Liver Transplantation.

“Severe alcoholic relapse usually occurs in the early years after [liver transplantation] and is responsible for severe graft injury in a very few years. Our results strongly reinforce the need for an early alcohol assessment post-[liver transplant] and multidisciplinary interventions to maintain abstinence and prevent graft injury,” Jérôme Dumortier, MD, PhD, of the Fédération des Spécialités Digestives, Hôpital Edouard Herriot, Hospices Civils de Lyon, Université Claude Bernard Lyon 1, France, and colleagues wrote.

In this retrospective study, Dumortier and colleagues enrolled 369 patients who underwent alcoholic liver disease (ALD) -related liver transplant (LT) between 1990 and 2010. Each patient survived at least 1-year post-transplant and underwent liver biopsy at 1, 5 and every 5 years post-transplant. The median follow-up post-transplant was 11 years.

“[This is] one of the largest [studies] which evaluated liver graft injury after post-LT alcoholic relapse, based on histological analysis of sequential liver biopsies,” the researchers wrote.

Seventy-three patients experienced severe alcoholic relapse (20%), of which 56 had available histological evaluation and were included in the final analysis. The median delay to observed alcoholic relapse was 3 years post-LT. Of the patients, 75% drank continuously and 25% drank intermittently post-LT.

Liver biopsies showed graft steatosis rates of 61% at 1-year post-LT and 87% at 5 years. Graft steatosis was 83% at 1-year post-alcoholic relapse and 87% at 5 years. Steatosis grade was higher in patients who were actively drinking 1 year before biopsy (P < .001). According to the research, 48% of those passively drinking had grade 3 steatosis.

“Our present results strongly confirm that steatosis and steatohepatitis of the graft are very frequent in cases of heavy drinking,” the researchers wrote.

Eighteen patients experienced recurrent alcoholic cirrhosis (32%), 5% of all the patients who underwent LT for alcoholic liver disease. The median delay between LT and recurrent alcoholic cirrhosis was 6 years and 4.5 years after severe alcoholic relapse. The median cumulated years of alcohol use before recurrent alcoholic cirrhosis was 3.5 years.

In the first 2 years post-LT, a majority of patients has grade F0 or F1 fibrosis. However, at 3 years post-LT, 25% of patients had developed F3 or F4 fibrosis. Recurrent alcoholic cirrhosis was observed in 14% of patients 2 years after alcoholic relapse and 40% at 7 years or more after alcoholic relapse. The cumulative risk for F4 fibrosis was 15% at 3 years, 32% at 5 years and 54% at 10 years after severe alcoholic relapse.

“Our results strongly support that severe alcoholic relapse is responsible for a rapid progression of fibrosis post-LT. … Identifying predictive factors of fibrosis progression may help to explain the very rapid evolution of fibrosis after LT,” the researchers wrote.

The only variables associated with recurrent alcoholic relapse were younger age at LT (younger than 50 years; P = .01) and heavy drinking within 3 years post-LT (P = .02), according to univariate analysis.

Disclosure: The researchers report no relevant financial disclosures.