Growth Hormone Secretion in Prader‐Willi Syndrome

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Abstract
Integrated 12-hour growth hormone secretion studies, peak growth hormone response to clonidine provocation. Somatomedin-C levels, T-4 and TSH levels were studied in six growth-retarded children with the Prader-Willi syndrome, of whom five had a 15 q - karyotype. Only one of the subjects was obese. All showed abnormally low growth hormone secretion. None achieved a nocturnal peak above 10 .mu.g/l, none had a mean noctural level over 1.8, and none showed a level above 8 .mu.g/l after clonidine provocation. These findings contrasted with normal TSH in all and normal T-4 in five. These findings suggest that the poor linear growth in the Prader-Willi syndrome is caused by a true deficiency of growth hormone secretion, and that the low growth hormone levels observed in such cases are not an artifact of obesity.