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To further define the influence of methylphenidate on the growth hormone-somatomedin axis and prolactin secretion, serum growth hormone and prolactin concentrations were assessed over 24 hours and in response to provocative stimuli. The nine hyperactive subjects were all studied during methylphenidate therapy and after drug discontinuation, Diurnal patterns of growth hormone and prolactin concentrations were assessed using an ambulatory, continuous blood withdrawal procedure to ensure that activity, caloric intake, and sleep patterns mimicked normal schedules. No significant difference in integrated concentration of growth hormone, fasting somatomedin concentration, or prolactin integrated concentration was detected between subjects receiving or not receiving methylphenidate. There was a significant increase in peak growth hormone response to arginine stimulation among subjects receiving methylphenidate therapy; however, this appeared to correlate with acute methylphenidate administration. These data do not support the hypothesis that growth defects in hyperactive children treated with methylphenidate are caused by alteration in the hypothalamic-pituitary-somatomedin axis.
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F R Schultz, and
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F R Schultz, and
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