title: Clinical significance of C-reactive protein levels in predicting responsiveness to iron therapy in patients with inflammatory bowel disease and iron deficiency anemia.
abstract: BACKGROUND
  Iron deficiency anemia (IDA) is a common complication of inflammatory bowel disease (IBD). In clinical practice, many patients receive initial treatment with iron tablets although intravenous (i.v.) iron supplementation is often preferable.
  
  
  OBJECTIVE
  This study investigated whether systemic inflammation at initiation of treatment (assessed by C-reactive protein [CRP] and interleukin-6 [IL-6] measurements) predicts response to iron therapy.
  
  
  METHODS
  Data from a previously published phase III trial were retrospectively analyzed after stratification of patients according to baseline CRP (> 4 vs. ≤ 4 mg/L) and IL-6 (> 6 vs. ≤ 6 pg/mL) levels. The study population consisted of patients with Crohn's disease or ulcerative colitis and IDA (Hb ≤ 110 g/L and TSAT < 20 % or serum ferritin < 100 ng/mL), randomized to either oral (ferrous sulfate) or i.v. iron (ferric carboxymaltose).
  
  
  RESULTS
  A total of 196 patients were evaluated (oral iron: n = 60; i.v. iron: n = 136). Baseline CRP and IL-6 levels were independent of patients' initial Hb levels and iron status (serum ferritin and TSAT; all p > 0.05). Among iron tablet-treated patients, Hb increase was significantly smaller in the high- versus low-CRP subgroup (1.1 vs. 2.0, 2.3 vs. 3.1, and 3.0 vs. 4.0 g/dL at weeks 2, 4, and 8, respectively; all p < 0.05). Differences were less pronounced with stratification according to baseline IL-6. Response to i.v. iron was mainly independent of inflammation.
  
  
  CONCLUSIONS
  Patients with high baseline CRP achieved a lower Hb response with oral iron therapy. Our results suggest that CRP may be useful to identify IBD patients who can benefit from first-line treatment with i.v. iron to improve their IDA.
authors.affiliation: Department of Gastroenterology, University Hospital Birmingham, Vincent Drive, Birmingham, B15 2TH, UK, T.H.IQBAL@bham.ac.uk.
authors.forename: Tariq
authors.initials: T
authors.lastname: Iqbal
authors.forename: Jürgen
authors.initials: J
authors.lastname: Stein
authors.forename: Naveen
authors.initials: N
authors.lastname: Sharma
authors.forename: Stefanie
authors.initials: S
authors.lastname: Kulnigg-Dabsch
authors.forename: Senthil
authors.initials: S
authors.lastname: Vel
authors.forename: Christoph
authors.initials: C
authors.lastname: Gasche
mesh_terms: D061605:Administration, Intravenous; D000284:Administration, Oral; D018798:Anemia, Iron-Deficiency / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis*; D017326:Clinical Trials, Phase III as Topic; D003093:Colitis, Ulcerative / Q000097:blood / Q000175:diagnosis / Q000276:immunology*; D003424:Crohn Disease / Q000097:blood / Q000175:diagnosis / Q000276:immunology*; D005290:Ferric Compounds / Q000008:administration & dosage*; D005296:Ferrous Compounds / Q000008:administration & dosage*; D006397:Hematinics / Q000008:administration & dosage*; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008320:Maltose / Q000008:administration & dosage / Q000031:analogs & derivatives*; D016032:Randomized Controlled Trials as Topic; D012189:Retrospective Studies; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D005290:Ferric Compounds; D005296:Ferrous Compounds; D006397:Hematinics; D006454:Hemoglobins; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; C020748:ferrous sulfate; C522335:ferric carboxymaltose; D008320:Maltose; D002097:C-Reactive Protein