title: Increased degradation of type I collagen in patients with inflammatory bowel disease.
abstract: To assess the mechanisms of osteopenia in inflammatory bowel disease (IBD), the serum markers of bone formation (osteocalcin and carboxyterminal propeptide of type I procollagen (PICP)) and bone degradation (carboxyterminal telopeptide of type I collagen (ICTP)), the bone mineral density (BMD) of the lumbar spine and the proximal femur and calcium intake of 150 unselected IBD patients and 73 healthy controls were investigated. The patients had higher ICTP values (3.69 (SD 1.40) microgram/l) than the healthy controls (3.25 (1.00) microgram/l, p = 0.035), but no differences in serum PICP and osteocalcin between these groups were detected. In the patients, the ICTP, PICP, and osteocalcin values did not have any significant correlation with BMD, but the patients with ICTP values above 3.6 microgram/l had significantly lower Z scores than those with lower ICTP. In the controls, however, a positive correlation between serum ICTP and BMD was found. The ulcerative colitis patients with total colitis had higher values of ICTP (3.96 (1.58) microgram/l) than those with a left sided disease (3.04 (0.86) micrograms/l, p = 0.009). The patients with a history of clinically active disease (n = 20) had higher ICTP (4.58 (1.55) microgram/l) and osteocalcin (12.56 (5.64) microgram/l) values than the patients (n = 130) with quiescent disease (ICTP 3.56 (1.33), p = 0.002, and osteocalcin 9.76 (3.62), p = 0.017). Increased serum osteocalcin, PICP, and ICTP concentrations and reduced BMD Z scores were found in a subgroup of Crohn's disease patients with a history of an active disease (n = 11). Raised serum ICTP and normal values of osteocalcin and PICP in IBD patients show increased breakdown of type I collagen without a compensatory increase in its synthesis suggesting an increased rate of bone degradation as a probable mechanism for osteopenia in IBD. Raised ICTP values are related to reduced bone mineral densities.
authors.affiliation: Department of Internal Medicine, University of Oulu, Finland.
authors.forename: J
authors.initials: J
authors.lastname: Silvennoinen
authors.forename: L
authors.initials: L
authors.lastname: Risteli
authors.forename: T
authors.initials: T
authors.lastname: Karttunen
authors.forename: J
authors.initials: J
authors.lastname: Risteli
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D015519:Bone Density; D001851:Bone Diseases, Metabolic / Q000097:blood* / Q000209:etiology; D016022:Case-Control Studies; D003094:Collagen / Q000097:blood*; D005260:Female; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000097:blood* / Q000150:complications; D008297:Male; D015675:Osteocalcin / Q000097:blood*; D011347:Procollagen / Q000097:blood*; D011897:Random Allocation
chemical_list: D015415:Biomarkers; D011347:Procollagen; D015675:Osteocalcin; D003094:Collagen