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Sex differences in statural growth impairment in Crohn's disease: Role of IGF-1

Gupta, Neera MD, MAS1,*; Lustig, Robert H. MD1; Kohn, Michael A. MD, MPP2; McCracken, Marjorie MD, PhD3; Vittinghoff, Eric MPhil, MPH, PhD2

doi: 10.1002/ibd.21617
Original Article: Original Clinical Articles

Background: Growth impairment in Crohn's disease (CD) is more common in males than females for unknown reasons. Since insulin-like growth factor-1 (IGF-1) is important for statural growth, we hypothesized that IGF-1 levels are lower in males with CD.

Methods: Sex differences in hormone Z-scores based on chronological age (CA-Z) and bone age (BA-Z) were examined in a cross-sectional study of 82 CD patients <21 years of age (43% female).

Results: IGF-1 CA-Z and BA-Z-scores were 0.50 units (P = 0.04) and 1.24 units (P = 0.003) lower in males. Mean bone age (12.2 years) was lower than chronological age (13.1 years) (P < 0.0001). Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and albumin did not differ by sex (P ≥ 0.08), but were associated with IGF-1 CA-Z and BA-Z-scores (P ≤ 0.02). Insulin-like growth factor binding protein-3 (IGFBP-3) CA-Z and BA-Z-scores were 0.71 units (P = 0.004) and 1.26 units (P < 0.001) lower in males. Inflammatory markers were correlated with sex hormone CA-Z and BA-Z and pituitary hormone BA-Z-scores in males (P ≤ 0.03), but not females (P ≥ 0.25). IGF-1 BA-Z-scores were positively associated with height BA-Z-scores (P = 0.03). Mean height BA-Z-scores were lower in males (P = 0.03).

Conclusions: Lower IGF-1 levels in males may explain sex differences in growth impairment in CD. Inflammation appears to more adversely affect hormone levels and statural growth in males. Prospective longitudinal studies are needed to further clarify the role of IGF-1 in sex differences in statural growth impairment in pediatric CD. (Inflamm Bowel Dis 2011;)

1Department of Pediatrics, University of California, San Francisco, San Francisco, California

2Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, California

3Department of Pediatrics, Pediatric Gastroenterology Associates, San Jose, California.

*Reprints: Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of California, San Francisco, 500 Parnassus Ave., MU-407 East, Box 0136, San Francisco, CA 94143

Email: ng719@yahoo.com

Received 29 November 2010; Accepted 2 December 2010

Published online 1 February 2011 in Wiley Online Library (wileyonlinelibrary.com).

Grant sponsor: NIH grant DK077734 (to N.G.); Grant sponsor: Children's Digestive Health and Nutrition Foundation/Crohn's and Colitis Foundation of America (CCFA) Award for New Investigators (to N.G.); Grant sponsor: CCFA Career Development Award (to N.G.); Grant sponsor: UCSF Department of Pediatrics PCRC Clinical Research Pilot Funding Award (to N.G); Grant sponsor: NIH/NCRR UCSF-CTSI; Grant Number: UL1 RR024131.

© Crohn's & Colitis Foundation of America, Inc.
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