title: Basiliximab does not increase efficacy of corticosteroids in patients with steroid-refractory ulcerative colitis.
abstract: OBJECTIVE
  Basiliximab is a chimeric monoclonal antibody that binds CD25 and thereby inhibits interleukin (IL)-2-mediated proliferation of lymphocytes. IL-2 might contribute to the resistance of T cells to corticosteroids. We investigated the efficacy and safety of basiliximab as a corticosteroid-sensitizing agent in patients with corticosteroid-refractory ulcerative colitis (UC).
  
  
  METHODS
  We studied 149 patients with moderate to severe UC (Mayo score ≥6 and endoscopic subscore ≥2) despite treatment for at least 14 days with oral prednisone (40-50 mg/day). Subjects were randomly assigned to groups that were given 20 mg (n = 46) or 40 mg (n = 52) basiliximab or placebo (n = 51) at weeks 0, 2, and 4. All subjects received 30 mg/day prednisone through week 2; the dose was reduced by 5 mg each week to 20 mg/day, which was maintained until week 8. At week 8, we compared the rates of clinical remission (Mayo score ≤2, no subscore >1) for patients given basiliximab with the rate for patients given placebo.
  
  
  RESULTS
  Twenty-eight percent of patients given placebo, 29% of those given the 40-mg dose of basiliximab, and 26% of those given the 20-mg dose of basiliximab achieved clinical remission (P = 1.00 vs placebo for each dose). Basiliximab was generally well tolerated. Six subjects who received basiliximab had serious adverse events (6.1%) compared with 2 who received placebo (3.9%; P = .72). In subjects given basiliximab, incomplete saturation of CD25 (<50%) on peripheral T cells was associated with the presence of anti-basiliximab antibodies (odds ratio, 21; 95% confidence interval, 2.4-184).
  
  
  CONCLUSIONS
  Basiliximab does not increase the effect of corticosteroids in the induction of remission in outpatients with corticosteroid-resistant moderate to severe UC.
authors.affiliation: Mount Sinai School of Medicine, New York, NY, USA. bruce.sands@mssm.edu
authors.forename: Bruce E
authors.initials: BE
authors.lastname: Sands
authors.forename: William J
authors.initials: WJ
authors.lastname: Sandborn
authors.forename: Tom J
authors.initials: TJ
authors.lastname: Creed
authors.forename: Colin M
authors.initials: CM
authors.lastname: Dayan
authors.forename: Ashwin D
authors.initials: AD
authors.lastname: Dhanda
authors.forename: Gert A
authors.initials: GA
authors.lastname: Van Assche
authors.forename: Miloš
authors.initials: M
authors.lastname: Greguš
authors.forename: Ajit
authors.initials: A
authors.lastname: Sood
authors.forename: Gourdas
authors.initials: G
authors.lastname: Choudhuri
authors.forename: Mary Jean
authors.initials: MJ
authors.lastname: Stempien
authors.forename: Daniel
authors.initials: D
authors.lastname: Levitt
authors.forename: Christopher S
authors.initials: CS
authors.lastname: Probert
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000493:pharmacokinetics / Q000627:therapeutic use*; D000077552:Basiliximab; D003093:Colitis, Ulcerative / Q000188:drug therapy*; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D004334:Drug Administration Schedule; D004359:Drug Therapy, Combination; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D007166:Immunosuppressive Agents / Q000493:pharmacokinetics / Q000627:therapeutic use*; D060828:Induction Chemotherapy; D008297:Male; D008875:Middle Aged; D011241:Prednisone / Q000627:therapeutic use*; D011993:Recombinant Fusion Proteins / Q000493:pharmacokinetics / Q000627:therapeutic use*; D012720:Severity of Illness Index; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D000911:Antibodies, Monoclonal; D005938:Glucocorticoids; D007166:Immunosuppressive Agents; D011993:Recombinant Fusion Proteins; D000077552:Basiliximab; D011241:Prednisone