Acute alcoholic hepatitis (AH) is a distinct clinical entity amongst patients with chronic alcohol abuse. Patients with severe AH are at risk of dying in about 20%-25% cases despite specific treatment with corticosteroids and/or pentoxifylline. Clearly, a need for an additional more effective treatment option is unmet currently. Liver transplantation (LT), a definitive treatment option for alcoholic cirrhosis requires 6 mo abstinence. However, this rule cannot be applied to patients with AH as these patients are actively drinking prior to their presentation. Shortage of donors, ethical issues, and fear of recidivism after transplantation with less than 6 mo pre-transplant abstinence are some of the reasons behind this rule of 6 mo of abstinence and hesitancy of transplanting patients with AH. These issues are debated at length in this manuscript. Further, retrospective studies have shown that patients undergoing transplantation for alcoholic cirrhosis and having histological changes of AH have been shown to fare as well when compared to patients without these histological changes. Recently, French workers have reported a case matched prospective study showing encouraging data on the usefulness of LT for patients who are non-responders to corticosteroid and/or pentoxifylline therapy. Future studies are needed to identify patients with severe AH who are going to benefit most with LT. In the light of emerging data on the efficacy of LT in improving survival of patients with severe acute AH who do not respond to corticosteroids, the time is ripe to re-evaluate our policy of LT in patients with AH.

Acute alcoholic hepatitis (AH) is a distinct clinical syndrome that manifests as jaundice, abdominal pain, fever and acute hepatic decompensation of variable degrees depending on the severity of the disease, and may commonly be associated with underlying chronic liver disease[1]. It is caused by excessive alcohol consumption of prolonged duration which is invariably heavy and increased in the last few weeks to months prior to presentation[1]. Patients with mild to moderate AH may respond to conservative management and abstinence. However, patients with severe disease (discriminant function index or Maddrey score of ≥ 32) have an overall mortality of about 40% within 6 mo[1]. Current available treatment options are corticosteroids and pentoxifylline but have limited efficacy, with a survival benefit of only around 50%[2,3]. Clearly, there is a need for more effective and definitive treatment options in order to improve prognosis and outcome of patients with severe AH.

Liver transplantation (LT) is a definitive treatment option for patients with end-stage liver disease who have > 10% risk of dying within 1 year. LT is an accepted treatment modality for patients with alcohol related chronic liver disease (ALD). The outcome after LT for ALD is as good as for other causes of liver disease[4]. However, LT as a treatment option for patients with severe AH remains controversial despite the fact that it is an established treatment option for most etiologies of acute liver failure (ALF)[1]. Many issues preclude physicians and transplant hepatologists to uniformly adopt this treatment modality for this group of acutely sick patients. These issues are related to (1) ethical concerns of transplanting patients with active alcohol abuse; (2) lack of applicability of 6 mo abstinence rule to these patients as by definition AH occurs among people who are currently actively drinking until at least a few weeks prior to presentation; and (3) risk of recidivism to alcohol drinking after LT that affects the graft and patient survival.

Before implementing and rethinking our policy of LT in patients with severe AH, let us first examine the available data on the outcome of patients with AH after OLT. These data are limited and restricted to retrospective analyses. In one such study, among a series of 246 cases of ALD, 110 underwent OLT. About 7.2% (8 cases) had histological evidence of AH on the explants. Comparison of these 8 cases with the remaining 102 cases without histological AH in the explants showed similar patient survival post-OLT recidivism[20]. Similar data have been reported by other investigators[21-23]. Recidivism rates were similar irrespective of presence or absence of AH in the explant[21]. Further, there were no differences on the outcome between patients with mild AH and severe AH[21]. The problems with these studies is their retrospective design and the fact that histological changes of AH can persist for a long duration even after response to treatment[23]. Prospective data on the use of LT in this group of patients with severe AH are scant. In a recently reported study at the American association for the study of liver disease 2009 in Boston from the French group, 18 patients with severe AH non-responsive to steroids (NRS: defined as ≥ 0.45 Lille score) were studied prospectively to assess the role of LT[24]. Each case was matched to a control patient (who did not undergo LT and continued to receive medical management) for age, sex, DFI and Lille score. Patients received LT within an average of 9 d from the day they were labeled as NRS. At the end of 1 year, patient survival in the transplanted group was higher compared to those not receiving LT (83% vs 44%, P = 0.009)[24]. Among the non-transplanted patients, 50%-90% deaths occurred within first 2 mo. Only one patient relapsed to drinking about 2.5 years after LT. That patient was classified a social drinker without any impact on the graft function[24].

AH remains, for the moment, a contraindication for transplant in the majority of liver centers in the United States. However, we think that the time is right to re-evaluate our policy[12]. Current data clearly show that LT is a definitive treatment option for the group of patients with severe AH who continue to deteriorate despite intensive medical treatment. Further, 6 mo of abstinence does not affect recidivism after OLT. However, before we routinely use this modality of definitive treatment for severe AH, we need to (1) derive long-term outcome of patients and graft in this setting; (2) determine the best criteria to identify candidates with the least risk of recidivism to harmful drinking; and (3) develop homogeneity in the definition of harmful drinking, drinking patterns and alcohol abuse questionnaires. Then we will be able to implement guidelines that are fair and scientifically sound for the optimal utilization of available organs in the setting of AH in the same way we are doing for other etiologies of ALF. Although the destination is far, there seems to be light at the end of the tunnel which will allow us to make the right decision and a life or death difference in many cases of severe AH.