What question did this study set out to answer?

To determine whether short stature in children with Prader-Willi syndrome is driven by true growth hormone deficiency rather than obesity-induced endocrine suppression.

November 1, 1990Acta Paediatrica

Growth Hormone Secretion in Prader‐Willi Syndrome

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Authors

HCHanan CosteffTel Aviv University VHVanja A. HolmMadigan Army Medical Center RRRogelio H.A. RuvalcabaMadigan Army Medical Center

Discussion

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Implication

Observational study demonstrates severe growth hormone deficiency in children with Prader-Willi syndrome, indicating growth failure occurs independently of obesity.

Key Points

To determine whether short stature in children with Prader-Willi syndrome is driven by true growth hormone deficiency rather than obesity-induced endocrine suppression.
Evaluated integrated 12-hour nocturnal growth hormone secretion and peak growth hormone responses to clonidine provocation in six growth-retarded children with Prader-Willi syndrome (five with a 15q- karyotype; one obese).
Measured circulating levels of somatomedin-C, thyroxine (T-4), and thyroid-stimulating hormone (TSH) across all subjects.
All six subjects exhibited markedly suppressed growth hormone secretion, with nocturnal peaks below 10 μg/L, mean nocturnal concentrations below 1.8 μg/L, and clonidine-stimulated peaks below 8 μg/L.
Thyroid function remained largely intact, evidenced by normal TSH levels in all six children and normal T-4 levels in five children.

Cite This Study

Costeff et al. (1990) studied this question.

synapsesocial.com/papers/6a938f99c71ca0043637ce2c https://doi.org/10.1111/j.1651-2227.1990.tb11383.x

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November 1, 1990Acta Paediatrica

Growth Hormone Secretion in Prader‐Willi Syndrome

View Full Paper

Ask AI

Bookmark

Authors

HCHanan CosteffTel Aviv University VHVanja A. HolmMadigan Army Medical Center RRRogelio H.A. RuvalcabaMadigan Army Medical Center

Discussion

Member takes

Implication

Observational study demonstrates severe growth hormone deficiency in children with Prader-Willi syndrome, indicating growth failure occurs independently of obesity.

Key Points

To determine whether short stature in children with Prader-Willi syndrome is driven by true growth hormone deficiency rather than obesity-induced endocrine suppression.
Evaluated integrated 12-hour nocturnal growth hormone secretion and peak growth hormone responses to clonidine provocation in six growth-retarded children with Prader-Willi syndrome (five with a 15q- karyotype; one obese).
Measured circulating levels of somatomedin-C, thyroxine (T-4), and thyroid-stimulating hormone (TSH) across all subjects.
All six subjects exhibited markedly suppressed growth hormone secretion, with nocturnal peaks below 10 μg/L, mean nocturnal concentrations below 1.8 μg/L, and clonidine-stimulated peaks below 8 μg/L.
Thyroid function remained largely intact, evidenced by normal TSH levels in all six children and normal T-4 levels in five children.

Cite This Study

Costeff et al. (1990) studied this question.

synapsesocial.com/papers/6a938f99c71ca0043637ce2c https://doi.org/10.1111/j.1651-2227.1990.tb11383.x

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