HOME
Return to Table of Contents
BUDESONIDE FOR THE INDUCTION OF REMISSION IN CROHN’S DISEASE – A SYSTEMATIC REVIEW & METANALYSIS
CH Seow1,2, EI Benchimol3, AM Griffiths3, AR Otley4, AH Steinhart1
1IBD Center, Mount Sinai Hospital, Toronto, Ontario; 2University of Western Australia, Perth, Australia; 3Hospital for Sick Children, Toronto, Ontario; 4Dalhousie University, Halifax, Nova Scotia
AIM: To systematically evaluate the efficacy and safety of budesonide (a glucocorticoid with limited systemic availability) for inducing remission in CD.
METHODS: Randomized controlled trials of budesonide (BUD) for the induction of remission in active CD were reviewed. Remission was defined as a CDAI <=150 or PCDAI <=10. Electronic databases (MEDLINE, EMBASE, Cochrane Central Register, ClinicalTrials.gov), review articles, and conference proceedings were searched. Two independent investigators reviewed studies for eligibility, extracted data and assessed study quality using Jadad’s criteria. A random or fixed effects model was chosen based on an assessment of heterogeneity. Studies were then weighted using the DerSimonian & Laird or Mantel-Haenszel method.
RESULTS: Twelve studies in patients with CD involving ileum ± right colon were eligible for inclusion. (A further two studies were secondary analyses of included studies but provided further outcome data). Nine studies compared BUD with conventional corticosteroids, two studies made comparisons with placebo, and one study compared BUD with mesalamine. After 8 weeks of treatment, BUD was twice as likely to induce remission compared with placebo (RR 1.96; 95% CI 1.19-3.23) and was more effective than mesalamine (RR 1.63; 95% CI 1.23-2.16). At 8 weeks, 9 mg BUD was less effective than conventional steroids in inducing remission (RR 0.86, 95% CI 0.76-0.98), particularly among patients with initially severe disease (CDAI >300) (RR 0.52, 95% CI 0.28 - 0.95). In 3 studies with follow up to 12 weeks and varied dosage tapering, the percentage of patients still in remission in each group was equivalent (RR 1.02, 95% CI 0.81-1.30). There was no difference in the proportion of BUD patients experiencing adverse events compared to placebo (RR 0.99, 95% CI 0.78-1.25). There were fewer adverse events in those treated with BUD compared to conventional steroids (RR 0.64, 95% CI 0.54-0.76) and BUD was able to preserve adrenal function (RR for abnormal ACTH test 0.65, 95% CI 0.55-0.78).
CONCLUSIONS: BUD is more effective than placebo or mesalamine in inducing remission of Crohn’s disease. Although short-term efficacy is less than with conventional steroids, particularly in those with moderate to severe disease, the likelihood of adverse effects and adrenal suppression is lower.