Growth hormone deficiency in Down's syndrome children.
Growth-hormone shortage is common in Down syndrome and easy to miss with one-off tests.
01Research in Context
What this study did
Doctors tested 20 children with Down syndrome for growth-hormone problems. They gave two drug shots to trigger hormone release and also tracked hormone levels for 24 hours.
What they found
Seven kids had low peaks on both drug tests. The all-day test caught even more cases the single shots missed.
How this fits with other research
Gettinger (1993) ran the same checks one year later and saw the same blunted peaks, but found that the choice of drug matters. Clonidine gave the weakest signal, while growth-hormone-releasing hormone worked best.
Ghaziuddin et al. (1996) pooled many studies and listed hormone deficits as a common extra health issue in Down syndrome, so the 1992 finding is part of a bigger picture.
Flapper et al. (2013) later warned that we still lack clear long-term cognitive growth charts for these kids, so any medical or behavioral plan must stay flexible.
Why it matters
If you work with children with Down syndrome, know that about one in three may have an undetected hormone deficit that can slow growth and energy. Ask the family if endocrine testing has been done. A simple referral can boost the child’s stamina for learning and daily living skills.
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02At a glance
03Original abstract
Down's syndrome (DS) children have been reported to have severe postnatal growth arrest and microcephaly. To determine if growth hormone (GH) deficiency plays a role in growth retardation in DS, 20 children were studied. The subjects (13 boys, 7 girls) were aged between 15 months and 13.9 years, had a height SDS ranging from -1.19 to -5.48, weight SDS ranging from -0.21 to -4.58, head circumference SDS ranging from -0.40 to -6.6, and a skeletal age ranging from 0.9 to 4.6 SD below the mean for normal children of same age and sex. GH was evaluated by levodopa (125 mg up to 15 kg, and 250 mg between 15-30 kg), clonidine (0.15 mg m-2) stimulation tests and hGH secretory patterns by the integrated 24 h. GH concentration (IC-GH) using a constant withdrawal pump with continuous blood collection every 30 min. The serum concentrations were: TSH, 0.7-8.0 mIU ml-1 (0.2-5.5); T4, 6.6-14.3 micrograms dl-1 (5-12); T3, 95-254 ng dl-1 (85-185); LH, less than 2.0-8.3 mIU ml-1 (less than 3); FSH, less than 1.3-7.2 mIU ml-1 (less than 3); testosterone, less than 30 ng dl-1 (5-35); estradiol, less than 5 ng dl-1 (less than 5-25); prolactin, 35.7-2.9 (F: 5-25; m 5-15); and somatomedin-C (Sm-C), 0.14-1.98 U ml-1 (0.08-5.90) (normal values in brackets). Peak serum GH after levodopa and clonidine was found to be below 10 ng ml-1 for both stimulatory tests in seven out of the 20 children studied. Twelve children showed a disparity between levodopa and clonidine testing. Of the 12 children, peak serum GH after levodopa was found to be below 10 ng ml-1 in five children; and peak serum GH after clonidine was found to be below 10 ng ml-1 in six. One child had a clonidine peak increase in serum GH concentration exactly 10 ng ml-1, but had a 12 h IC-GH of 1.5 ng ml-1 (N greater than 3.2). Two children with peak GH after clonidine above 10 ng ml-1 had a 24 h IC-GH of 0.7 and 1.3 ng ml-1. A fourth child who had peak GH concentrations above 10 ng ml-1 with levodopa and clonidine had a 12 h IC-GH of 0.5 ng ml-1.(ABSTRACT TRUNCATED AT 400 WORDS)
Journal of intellectual disability research : JIDR, 1992 · doi:10.1111/j.1365-2788.1992.tb00469.x