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Somatomedin and growth hormone in psychosocial dwarfism
Insights
Psychosocial dwarfism (PSD) growth rates fluctuated significantly due to emotional stress, not nutrition or hormones. Somatomedin levels in untreated PSD can be low, normalizing with recovery.
Area of Science:
- Pediatric Endocrinology
- Child Psychology
- Growth Disorders
Background:
- Psychosocial dwarfism (PSD) is a condition characterized by growth failure linked to emotional deprivation.
- Diagnosis and management of PSD require careful assessment of growth patterns and psychosocial factors.
Observation:
- A 7-year-old boy diagnosed with PSD exhibited variable growth rates correlating with emotional state and caregiver relationships.
- Growth hormone and somatomedin activity showed fluctuations, but did not consistently explain the observed growth velocity changes.
- Caloric intake varied but did not directly correlate with catch-up growth phases.
Findings:
- Serum somatomedin levels in untreated PSD can present in the hypopituitary range.
- Markedly fluctuating growth rates in this PSD patient were not attributable to caloric intake, growth hormone, or somatomedin activity.
- An unidentified factor related to emotional stress appears to significantly influence growth velocity during recovery in PSD.
Implications:
- This case highlights the complex interplay between emotional well-being and physical growth in children.
- Further research is needed to identify the specific mechanisms underlying emotional stress-induced growth modulation.
- Understanding these factors is crucial for comprehensive treatment strategies for children with psychosocial dwarfism.
Abstract:
The diagnosis of psychosocial dwarfism (PSD) was made in a 7 year old boy upon admission to the hospital. In the period following admission, he grew at a slightly accelerated rate of 0.6 cm in 24 days (extrapolated growth rate--9.1 cm/yr); his caloric intake was 1663 calories/day (147 cal/kg/day), stimulable growth hormone was 5.9 ng/ml and somatomedin activity was in the hypopituitary range (0.24, 0.05 U/ml). In the following period of marked catch-up growth of 8.6 cm in 102 days (extrapolated growth rate 30.8 cm/yr), his caloric intake decreased significantly to 1514 cal/day (106 cal/kg/day, 0.005 less than p less than 0.01), stimulable growth hormone in this period was 13.6 ng/ml and somatomedin activity normalized (0.98 U/ml). While under continued observation, with separation from his favorite nurse, his growth velocity dropped significantly to the rate immediately following admission, but there was no change in his stimulable growth hormone or in somatomedin activity. With the return of his favorite nurse, he resumed his previous rapid catch-up growth with no change in caloric intake (p equals not significant), growth hormone level, or somatomedin activity. Upon transient return to his depriving home, his growth rate decreased to 1.4 cm in 70 days (extrapolated growth rate 7.2 cm/yr); growth hormone remained in the normal range. Somatomedin activity was in the low normal range (0.57 U/ml) and rose to high normal activity (1.31 U/ml) as rapid catch-up growth resumed after he had been readmitted. We conclude from these data that: 1. Serum somatomedin in longstanding untreated PSD may be in the hypopituitary range. 2. Markedly fluctuating growth rates during recovery in this patient with PSD were not due to changes in caloric nutrition, growth hormone release or somatomedin activity, but to an as yet unidentified factor affecting growth during emotional stress.