1042 Original article A pilot study comparing hydrocortisone premedication to concomitant azathioprine treatment in preventing loss of response to infliximab Gerassimos J. Mantzaris a , Nikolaos Viazis b , Kalliopi Petraki c , Konstantinos Papamichael a , Ioannis Theodoropoulos a , Anastassios Roussos a , Christos Karakoidas a , Stavroula Koilakou a , Nikolaos Raptis a , Alexandros Smyrnidis a , George Agalos a and Dimitrios G. Karamanolis b Objectives Antibodies to infliximab may lead to loss of response to infliximab (IFX) in Crohn’s disease. Azathioprine (AZA) coadministration prevents the formation, whereas hydrocortisone (HC) premedication reduces the levels of antibodies to IFX. This pilot study aims at assessing the efficacy of these strategies to prevent loss of response to IFX. Methods Eligible patients had active steroid-dependent luminal Crohn’s disease and received IFX (5 mg/kg at weeks 0, 2, and 6 for induction and then scheduled q8 week for remission maintenance). Patients were stratified in a 1 : 1 ratio to oral AZA (2–2.5 mg/kg/day, stratum A) or HC premedication (250 mg intravenously, stratum B). Stratum A included only patients naive to AZA; stratum B included both AZA naive and intolerant patients. Steroids were tapered within 6–8 weeks. Patients were followed up with monthly clinical assessments, laboratory tests, Crohn’s Disease Activity Index calculations, adverse-events check up, and adherence to treatment. Results Overall, 23 patients received IFX/HC and 23 IFX/ AZA. There were no differences at baseline in any patient- related or disease-related parameters. Seventeen (74%) patients on IFX/AZA completed the study; six patients were withdrawn for primary nonresponse (one patient), lost response to IFX (two patients), or AZA-related adverse events. Eighteen (78%) patients on IFX/HC completed the study; five patients were withdrawn for primary nonresponse (one patient), loss of response (two patients), or infusion reactions to IFX. No significant differences emerged between strata in clinical remission rates or lost response to IFX. Conclusion This prospective 2-year pilot study has not confirmed superiority of any available strategy to maintain the efficacy of IFX. Eur J Gastroenterol Hepatol 21:1042–1048  c 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins. European Journal of Gastroenterology & Hepatology 2009, 21:1042–1048 Keywords: azathioprine, Crohn’s disease, hydrocortisone, infliximab, loss of response a First Department of Gastroenterology, b Second Department of Gastroenterology, Evangelismos Hospital, Athens and c Department of Histopathology, Metropolitan Hospital, Piraeus, Greece Correspondence to Gerassimos J. Mantzaris, MD, PhD, MACG, AGAF, A’ Gastroenterology Clinic, GHA ‘Evangelismos’, 45-47 Ypsilantou Street, Kolonaki 10676, Athens, Greece Tel: + 30 210 7201604; fax: + 30 210 7239716; e-mail: gman195@yahoo.gr Received 27 November 2008 Accepted 7 January 2009 Introduction Crohn’s disease (CD) is an idiopathic inflammatory bowel disease characterized by a chronic relapsing or unremit- ting course, segmental transmural inflammation of the intestinal wall with granuloma formation and occasionally extraintestinal manifestations and/or fistulae. As there is no definitive treatment, therapy aims at inducing and maintaining remission by reducing active inflammation and healing the intestinal mucosa because this reduces the rate of hospitalizations and surgical interventions, and improves quality of life. Infliximab (IFX), an immuno- globulin G1 mouse/human chimerical monoclonal anti- body to tumor necrosis factor (TNF)-a may achieve most of these therapeutic targets and has greatly improved the management of patients with luminal and/or fistulizing CD who are refractory to all previous therapies including conventional steroids and azathioprine (AZA) [1–5]. Recent studies indicate that the administration of IFX early in the course of luminal CD induces mucosal healing, which in turn may prevent the development of permanent structural damage to the intestinal wall, thus altering the natural course of disease at least in the short term [6,7]. As a chimerical antibody, IFX is immunogenic and induces inevitably the formation of antibodies to infliximab (ATI). In clinical trials, ATI occur in 13–18% of patients [8]. Although additional mechanisms may be involved, such as host factors, route of administration, dosing schedule, concomitant medications, binding 0954-691X  c 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins DOI: 10.1097/MEG.0b013e32832937e3 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.