Suboptimal linear growth despite entry into puberty in children with inflammatory bowel disease

SC Wong; A Mason; RK Russell; P McGrogan; SF Ahmed

Background: Growth retardation and pubertal delay is frequently encountered in children with inflammatory bowel disease (IBD). There are currently no published data on sitting height (SH), subischial leg length (SILL)and growth rates in relation to pubertal status in these children.

Objective: To assess skeletal disproportion and growth rates in children with IBD.

Methods: Retrospective study of 40 children (32M):35 Crohn’s disease, 4 ulcerative colitis and 1 indeterminate colitis. Height (ht), SH, SILL were obtained from 1st endocrine clinic. Height velocity (HV) over the prior 12 months was converted to SDS according to chronological age (CA), pubertal age (≥12 years) (PA) and bone age (BA). Results expressed as median (range).

Results: Overall at 1st endocrine assessment, median CA was 13.6 years (7.2, 16.3), HtSDS −1.8 (−3.2, 1.9), SHSDS −2.3 (−4.4, 0.1), SILLSDS −1.0(−3.0, 3.5), HV 4.6 cm/year (0.0, 9.7), HVSDS(CA) −1.6(−6.5, 17.1), HVSDS(PA) −1.2(−6.4, 3.9) and HVSDS(BA) −1.1(−7.7, 5.1).


		≥12 years
	<12 years Tanner Stage 1 (n, 11)	TS1 (n, 14)	TS2 (n, 9)	TS3-5 (n, 6)	P value
CA	10.2 (7.2, 11.3)	13.9 (12.6, 16.3)	15.0 (12.0, 15.4)	14.7 (13.6, 16.0)	<0.0001
HtSDS	−2.2 (−3.0, −1.2)	−1.4 (−3.0, 1.9)	−1.7 (−2.9, −0.7)	−1.5 (−1.8, −0.6)	0.53
SHSDS-SILLSDS	−0.9 (−2.0, 1.9)	−1.4 (−3.8, 0.5)	−1.5 (−4.4,−0.5)	−1.0 (−1.5, 0.9)	0.10
HV (cm/years)	4.8 (0.0, 8.0)	3.7 (1.2, 6.2)	4.8 (3.4, 6.9)	5.5 (3.0, 9.7)	0.15
HVSDS (CA)	−1.2 (−3.8, 3.5)	−3.1 (−6.5, 5.2)	−1.0 (−5.4, 17.1)	−1.4 (−4.4, 9.6)	0.16
HVSDS (PA)	Not applicable	−2.6 (−6.4, 1.8)	−0.4 (−2.8, 3.4)	−1.7 (−3.2, 3.9)	0.42
HVSDS (BA)	−1.2 (−7.7, 2.1)	−2.0 (−5.1, 0.3)	−2.1 (−4.1, 5.1)	−0.2 (−3.0, 3.6)	0.44

Conclusion: We have demonstrated for the first time that skeletal disproportion occurs in children with inflammatory bowel disease regardless of stage of puberty and that linear growth remained poor in the group in puberty even after accounting for delayed puberty. We hypothesise that abnormal growth hormone/insulin like growth factor secretion and action maybe the underlying aetiology of poor pubertal growth in these children but further translational studies are needed to test this.

Endocrine Abstracts

P6