Endocrine Abstracts (2008) 15 P200

Growth retardation in inflammatory bowel disease (IBD) is not universally associated with growth hormone resistance

SC Wong1, A Smyth1, E McNeill1, K Hassan2, P McGrogan2 & SF Ahmed1


1Bone and Endocrine Research Group and 2Department of Paediatric Gastroenterology, Hepatology and Nutrition, Royal Hospital for Sick Children Yorkhill, Glasgow, UK.


Background and aim: It is often proposed that growth retardation in IBD is associated with a state of growth hormone resistance but published data on the GH-IGF1 axis are scarce. We describe the results of routine clinical assessment of this axis in a group of such children.

Methods: A retrospective study of 24 children with IBD (22 CD, 2 UC) with growth retardation and/or pubertal delay who underwent insulin tolerance test (ITT) following referral to the endocrine clinic. Height velocity (HV) and IGF1 were converted to SDS; to account for delayed puberty for girls >11 years and boys >12 years, HV and IGF1 were adjusted for bone age. Results expressed as median (range).

Results: Seven children (29%) were on oral Prednisolone at point of ITT. Twenty-three (96%) were prepubertal at diagnosis and 11 (46%) at time of ITT. Median age at diagnosis and at time of ITT was 11 years (4.9, 13.9) and 14.6 years (7.7, 17.0) respectively. Median HtSDS at diagnosis and at time of ITT was −1.3 (−3.4, 0.4) and −2.0 (−3.6, −1.0) respectively. Median HVSDS over 12 months was −2.2 (−6.6, 2.8).

Peak GH<10 mU/lPeak GH≥10, <20 mU/lPeak GH≥20 mU/l
IGF1SDS<03/24 (12.5%)8/24 (33.3%)10/24 (41.7%)
IGF1SDS≥00/24 (0%)1/24 (4.2%)2/24 (8.3%)

In this cohort, 10 children (42%) were GH resistant, whilst 3 (12.5%) were GH insufficient. Two children (8%) had combined GH-IGF1 resistant. Peak GH showed no association with IGF1SDS (r=0.2, P=0.4). HVSDS showed no association with peak GH (r=0.2, P=0.4) and IGF1SDS (r=0.4, P=0.06). Similarly, HtSDS showed no association with peak GH (r=−0.3, P=0.1) and IGF1SDS (r=0.02, P=0.9).

Conclusion: In the largest cohort of children with IBD who have had evaluation of their GH axis, we demonstrate that poor growth is associated with a range of abnormalities in the GH-IGF1 axis. Biochemical evidence of systemic GH resistance is common but not universal. The lack of association between linear growth and systemic markers of GH-IGF1 may suggest a greater role of local growth factors associated with growth retardation in these children.

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