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Growth hormone deficiency in Down's syndrome children
Author(s) -
CASTELLS S.,
TORRADO C.,
BASTIAN W.,
WISNIEWSKI K. E.
Publication year - 1992
Publication title -
journal of intellectual disability research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.941
H-Index - 104
eISSN - 1365-2788
pISSN - 0964-2633
DOI - 10.1111/j.1365-2788.1992.tb00469.x
Subject(s) - medicine , endocrinology , prolactin , testosterone (patch) , growth hormone deficiency , growth hormone , microcephaly , hormone , psychiatry
. 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); T 4 , 6.6–14.3 μg dl −1 (5–12); T 3 , 95–254 ng dl −1 (85–185); LH, <2.0–8.3 mlU ml −1 (<3); FSH, <1.3–7.2 mIU ml −1 (<3); testosterone, <30 ng dl −1 (5–35); estradiol, <5 ng dl −1 (<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<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 . These data suggest that DS children have marked growth retardation, associated with a reduced serum GH response to levodopa and clonidine stimulation tests, or disparity in responses to the stimulatory tests and low 24 h IC‐GH.