nature publishing group CLINICAL AND SYSTEMATIC REVIEWS REVIEW 590 The American Journal of GASTROENTEROLOGY VOLUME 106 | APRIL 2011 www.amjgastro.com INTRODUCTION Crohn’s disease (CD) and ulcerative colitis (UC) are chronic inflammatory bowel diseases whose exact etiologies remain unclear. e population prevalence of these disorders in the United States is somewhere between 150 and 250 per 100,000 (1–4). Both CD and UC carry a high burden of morbidity because of their lifelong duration and relapsing and remitting natural history. Patients oſten experience intermittent flares of disease activity, impacting on their quality of life and ability to function normally. Glucocorticosteroid drugs were first used over 60 years ago (5), and the first controlled trial demonstrating their efficacy in patients with active inflammatory bowel disease was conducted in the 1950s (6). e effect of glucocorticosteroids in these condi- tions stems from their ability to modulate the immune response, via interaction with glucocorticoid receptors in the cell nucleus. ey inhibit expression of adhesion molecules and trafficking of inflammatory cells to target tissues, including the intestine (7). However, they have significant short-term adverse effects, includ- ing risk of opportunistic infection (8), and their longer-term use is Glucocorticosteroid Therapy in Inflammatory Bowel Disease: Systematic Review and Meta-Analysis Alexander C. Ford , MBChB, MD, MRCP 1,2 , Charles N. Bernstein , MD 3 , Khurram J. Khan , MD, FRCPC 4 , Maria T. Abreu , MD 5 , John K. Marshall , MD, MSc, FRCPC 4 , Nicholas J. Talley , MD, PhD 6 and Paul Moayyedi , BSc, MBChB, PhD, MPH, FRCP, FRCPC 4 OBJECTIVES: The use of glucocorticosteroids to treat both Crohn’s disease (CD) and ulcerative colitis (UC) is widespread, but no systematic review and meta-analysis has examined the issue of efficacy of these agents in its entirety. METHODS: MEDLINE, EMBASE, and the Cochrane central register of controlled trials were searched (through December 2010). Randomized controlled trials (RCTs) recruiting adults with active or quiescent CD comparing standard glucocorticosteroids or budesonide with placebo or each other, or comparing standard glucocorticosteroids with placebo in active UC, were eligible. Dichotomous data were extracted to obtain relative risk (RR) of failure to achieve remission in active disease, and RR of relapse of activity in quiescent disease, with a 95% confidence interval (CI). Adverse events data were extracted where reported. RESULTS: The search identified 3,061 citations, and 20 trials were eligible. Only one trial was at low risk of bias. Standard glucocorticosteroids were superior to placebo for UC remission (RR of no remis- sion = 0.65; 95% CI 0.45–0.93). Both trials of standard glucocorticosteroids in CD remission reported a statistically significant effect, but because of heterogeneity between studies, the overall effect was not significant (RR = 0.46; 95% CI 0.17–1.28). Budesonide was superior to placebo for CD remission (RR = 0.73; 95% CI 0.63–0.84), but not in preventing CD relapse (RR = 0.93; 95% CI 0.83–1.04). Standard glucocorticosteroids were superior to budesonide for CD remission (RR = 0.82; 95% CI 0.68–0.98), but glucocorticosteroid-related adverse events were commoner (RR = 1.64; 95% CI 1.34–2.00). CONCLUSIONS: Standard glucocorticosteroids are probably effective in inducing remission in UC, and may be of benefit in CD. Budesonide induces remission in active CD, but is less effective than standard glucocorticosteroids, and is of no benefit in preventing CD relapse. Am J Gastroenterol 2011; 106:590–599; doi:10.1038/ajg.2011.70; published online 15 March 2011 1 Leeds Gastroenterology Institute, Leeds General Infirmary , Leeds, UK; 2 Leeds Institute of Molecular Medicine, University of Leeds, Leeds, UK; 3 University of Manitoba, Winnipeg, Manitoba, Canada; 4 Gastroenterology Division, McMaster University, Health Sciences Center , Hamilton, Ontario, Canada; 5 Miller School of Medicine, University of Miami, Miami, Florida, USA; 6 Faculty of Health, University of Newcastle, Newcastle, New South Wales, Australia. Correspondence: Alexander C. Ford, MBChB, MD, MRCP , Leeds Gastroenterology Institute, D Floor, Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK. E-mail: alexf12399@yahoo.com Received 22 November 2010; accepted 13 February 2011 CME