for the Foie-Alcool group of the Association Franc ¸aise pour l'Etude du Foie (AFEF)** Tumor necrosis factor-␣ (TNF-␣) may contribute to the progression of acute alcoholic hepatitis (AAH). The aim of this study was to evaluate the efficacy of an association of infliximab and prednisolone at reducing the 2-month mortality rate among patients with severe AAH. Patients with severe AAH (Maddrey score >32) were randomly assigned to group A receiving intravenous infusions of infliximab (10 mg/kg) in weeks 0, 2, and 4; or group B receiving a placebo at the same times. All patients received prednisolone (40 mg/day) for 28 days. Blood neutrophil functional capacities were monitored over 28 days. After randomization of 36 patients, seven patients from group A and three from group B died within 2 months. The probability of being dead at 2 months was higher (not significant [NS]) in group A (39% ؎ 11%) than in group B (18% ؎ 9%). The study was stopped by the follow-up committee and the sponsor (Assistance Publique-Ho ˆpitaux de Paris). The frequency of severe infections within 2 months was higher in group A than in group B (P < .002). This difference was potentially related to a significantly lower ex vivo stimulation capacity of neutrophils. There were no differences between the two groups in terms of Maddrey scores at any time point. In conclusion, three infusions of 10 mg/kg of infliximab in association with prednisolone may be harmful in patients with severe AAH because of the high prevalence of severe infections. (HEPATOLOGY 2004;39:1390 -1397.) A cute alcoholic hepatitis (AAH) is a serious acute liver disease, with a hospital mortality rate of up to 44%. 1 Considerable evidence suggests that tumor necrosis factor-␣ (TNF-␣) contributes to the progression of AAH. Ethanol administration promotes the translocation of endotoxin from the intestine and increases iron levels in Kupffer cells. These factors seem to play critical roles in the activation of nuclear factor B in Kupffer cells, resulting in the release of cytokines, including TNF-␣. 2,3 In male Wistar rats exposed to ethanol, levels of macrophage inflammatory protein-2 mRNA, a potent chemotactic factor for neutrophils regulated by TNF-␣, the serum aspartate transaminase levels and hepatic inflammation and necrosis are attenuated by anti-TNF-␣ antibody treatment. 4 Despite the ongoing controversy surrounding corticosteroid treatment, 5 there are many arguments in support that corticosteroids as the reference treatment for severe AAH. Three metaanalyses and an analysis that combined individual data from the three most recent randomized controlled trials of patients with a Maddrey score Ն32 concluded that corticosteroids improved the short-term survival of patients with severe AAH. [6][7][8][9] Furthermore, representatives of the American College of Gastroenterology recently recommended corticosteroids for patients with severe AAH. 10 However, although corticosteroids have been shown to improve survival, mortality at 2 months remains approximately 30%.