title: Low free and total insulinlike growth factor I (IGF-I) and IGF binding protein-3 levels in chronic inflammatory bowel disease: partial normalization during prednisolone treatment.
abstract: OBJECTIVE
  Catabolism and growth impairment are well known complications of chronic inflammatory bowel disease (CIBD). This may be caused by disease activity itself and/or the medical treatment, which may lead to changes in the growth hormone and insulinlike growth factor I (IGF-I) axis. Interest has focused on corticosteroids, as they are known to influence the growth hormone/IGF-I axis.
  
  
  METHODS
  The aim of the present study was to examine changes in total and free IGF-I, IGF binding proteins (IGFBPs), and IGFBP-3 protease activity in 10 patients with severe acute activity in colon CIBD before and during high dose prednisolone treatment (1 wk) and 3 months tapering. Eight healthy subjects served as controls.
  
  
  RESULTS
  Total and free IGF-I were significantly reduced by 35% and 53%, respectively, before prednisolone treatment (p < 0.05), and free IGF-I remained reduced even by the end of the study period relative to controls (p < 0.05). IGFBP-3 was reduced by 16% before (p < 0.05), with normalization during prednisolone treatment and tapering relative to controls. There was no evidence of increase in IGFBP-3 protease activity. IGFBP-1 was increased before and tended also to be increased during prednisolone treatment and tapering.
  
  
  CONCLUSIONS
  Marked changes in serum total and free IGF-I and IGFBPs were demonstrated in patients with severe exacerbation of CIBD without complete normalization during high dose prednisolone treatment and tapering. These changes may partly be involved in the catabolism of active CIBD patients.
authors.affiliation: Medical Department V (Gastroenterology & Hepatology), Aarhus University Hospital, Denmark.
authors.forename: H
authors.initials: H
authors.lastname: Grønbek
authors.forename: T
authors.initials: T
authors.lastname: Thøgersen
authors.forename: J
authors.initials: J
authors.lastname: Frystyk
authors.forename: H
authors.initials: H
authors.lastname: Vilstrup
authors.forename: A
authors.initials: A
authors.lastname: Flyvbjerg
authors.forename: J F
authors.initials: JF
authors.lastname: Dahlerup
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D002908:Chronic Disease; D004305:Dose-Response Relationship, Drug; D010450:Endopeptidases / Q000097:blood / Q000187:drug effects; D005260:Female; D006130:Growth Disorders / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000097:blood* / Q000188:drug therapy* / Q000503:physiopathology; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000097:blood* / Q000187:drug effects*; D007334:Insulin-Like Growth Factor I / Q000032:analysis* / Q000187:drug effects*; D008297:Male; D011239:Prednisolone / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*
chemical_list: D000893:Anti-Inflammatory Agents; D018972:Insulin-Like Growth Factor Binding Protein 3; D007334:Insulin-Like Growth Factor I; D011239:Prednisolone; D010450:Endopeptidases