SFEBES2009 Poster Presentations Growth and development (8 abstracts)
Delayed puberty in children with inflammatory bowel disease may be associated with gonadotrophin resistance
Jarod Wong 1 , Avril Mason 1 , Richard Russell 2 , Paraic McGrogan 2 , Jonathan Bishop 2 & Faisal Ahmed 1
1Bone and Endocrine Research Group, Royal Hospital for Sick Children Glasgow, Glasgow, UK; 2Department of Paediatric Gastroenterology, Hepatology and Nutrition, Royal Hospital for Sick Children Glasgow, Glasgow, UK.
Background: The aetiology of delayed puberty in children with inflammatory bowel disease (IBD) is unclear.
Methods: Retrospective analysis of 27 children with IBD with growth retardation and/or pubertal delay, who had basal LH and FSH (27) and LHRH stimulation test as part of clinical evaluation (25). Height velocity was converted to SDS for bone age for girls >11 years and boys >12 years to adjust for delayed puberty. Data expressed as median (range).
Results: Twenty-seven children (five females), with IBD (25 Crohn’s disease; two ulcerative colitis), median age 14.5 years (7.7, 17.0); median height (Ht) SDS −1.9 (−3.6, −0.9); median HV SDS −2.4 (−7.7, 2.8); and median bone age delay 1.7 years (−0.6, 2.9) are described.
| M:F | Age (years) | BA delay (years) | Basal FSH (U/l) | Peak FSH (U/l) | Basal LH (U/l) | Peak LH (U/l) | |
| Tanner 1 <12 years (n,7) | 5:2 | 10.4 (7.7, 11.3) | 1.1 (0.7, 2.9) | 0.7 (0.3, 2.9) | 5.4 (2.9, 11.1) | 0.1 (0.1,0.3) | 2.3 (0.9,8.3) |
| Tanner 1 ≥12 years (n, 6) | 6:0 | 14.1 (12.3, 15.3) | 2.2 (−0.6, 2.8) | 1.1 (0.2, 3.5) | 3.9 (0.7, 7.0) | 0.2 (0.1, 1.8) | 17.9 (6.2, 31.1) |
| Tanner 2 (n, 8) | 6:2 | 14.9 (11.3, 15.7) | 1.7 (0.7, 2.5) | 1.8 (0.3, 6.1) | 4.2 (2.3, 30.1) | 0.8 (0.1, 2.5) | 17.3 (1.2, 73.7) |
| Tanner 3 (n, 6) | 5:1 | 15.1 (14, 17) | 1.8 (0.3, 2.9) | 3.1 (1.4, 11.4) | 2.7 (2.2, 5.8) | 2.8 (0.6, 20) | 13.5 (8.5, 18.5) |
| P value | – | <0.0001 | 0.98 | 0.08 | 0.56 | 0.03 | 0.08 |
All children ≥12 years of age, and one boy aged 10.9 years, who were pre pubertal had peak LH >5 U/l and LH dominance to an LHRH stimulation test. Two children who were tanner stage two had a pre pubertal response.
Conclusion: The LHRH stimulation test correlates poorly with clinical stages of puberty in children with IBD. A sub-group of children who had biochemical evidence of activation of the gonadotrophin axis were clinically prepubertal, raising the possibility of inadequate negative feedback on LH secretion or resistance to LH action.
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