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The insulin-like growth factor axis in children with inflammatory bowel disease
Mark R Corkins1, Ajay D Gohil, Joseph F Fitzgerald
1Division of Pediatric Gastroenterology, Hepatology and Nutrition, James Whitcomb Riley Hospital for Children, Indiana University School of Medicine, 702 Barnhill Drive, Room ROC 4210, Indianapolis, IN 46202-5225, USA. MRCorkin@pol.net
Background:
The insulin-like growth factor (IGF) axis consists of two IGFs and six IGF-binding proteins (IGFBPs) that regulate proliferation and differentiation of many cell types. Malnutrition and inflammation alter the IGF axis. The authors evaluated circulating IGFs and IGFBPs in patients with inflammatory bowel disease (IBD) at the time of presentation and compared them with values obtained during remission.
Methods:
Seventeen newly diagnosed pediatric IBD patients were studied on presentation and during remission. Nutritional status was assessed by body mass index (BMI) and serum protein assay. The Lloyd-Still and Green IBD clinical scoring system was used. IGF-I and IGF-II levels were measured by radioimmunoassay, and IGFBP-3 levels were measured by immunoradiometric assay. IGFBPs were quantified on ligand blots with a PhosphorImager.
Results:
Body mass index and IBD clinical scores improved after treatment: 18.7 +/- 3.0 versus 21.3 +/- 3.0 kg/m (P = 0.023) and 74.6 +/- 16.7 versus 93.1 +/- 7.4 (P< 0.001), respectively. Protein changes were insignificant. IGFBP-3 levels increased from time of first evaluation to remission: 3,470 +/- 850 versus 4,700 +/- 473 ng/mL (P< 0.001). The ratio of IGFBP-3 to IGFBP-2 increased from first evaluation to remission: 1.7 +/- 1.9 versus 3.9 +/- 1.9 (P= 0.003). IGF-I and IGF-II levels also increased: 139 +/- 167 versus 223 +/- 118 ng/mL (P= 0.011) and 307 +/- 111 versus 386 +/- 73 ng/mL (P= 0.007), respectively.
Conclusions:
Circulating IGFBP-3 levels were low during active IBD and increased at remission in parallel with the IGF-I levels. The IGFBP-3 to IGFBP-2 ratio was altered in the presence of active disease in a manner that would reduce IGF-I action. This abnormality improved after treatment.