Growth hormone response after administration of L-dopa, clonidine, and growth hormone releasing hormone in children with Down syndrome.
One normal growth-hormone test is not enough for kids with Down syndrome—clonidine often misses true deficiency.
01Research in Context
What this study did
Doctors gave three different drugs to the kids with Down syndrome.
Each child got L-dopa, clonidine, and growth-hormone-releasing hormone on separate days.
They measured how much growth hormone each child released after every drug.
What they found
Clonidine worked worst. Most kids made little or no growth hormone after it.
Growth-hormone-releasing hormone worked best. Every child made at least 10 ng/ml afterafter one of the drugs.
The same child could look normal on one test and low on another.
How this fits with other research
Jones et al. (1992) ran almost the same tests one year earlier. They also saw kids who passed one drug test but failed another.
Reza et al. (2013) later showed that weight-bearing exercise plus calcium can raise bone density in kids with Down syndrome. This links the weak hormone release to real bone health risks.
Geurts et al. (2008) and Waldron et al. (2023) found low bone mass in Down syndrome adults. The poor clonidine response seen here may help explain why.
Durand et al. (1990) used the same two drugs in autistic kids. Autistic children made normal amounts of growth hormone but at odd times. Down syndrome kids made less overall.
Why it matters
If you serve kids with Down syndrome, know that one normal hormone test does not rule out deficiency. Ask the pediatrician to repeat testing with different drugs before labeling a child as low-growth-hormone. This matters for height, bone health, and energy levels that affect learning and behavior programs.
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Join Free →Check the last growth-hormone test method in each Down-syndrome learner’s file—if it used clonidine alone, ask the doctor about re-testing with GHRH.
02At a glance
03Original abstract
We studied the response of growth hormone secretion after the administration of L-dopa, clonidine, and growth hormone releasing hormone in eight growth-retarded children with Down syndrome aged 1 to 6.5 years. After L-dopa administration, five children had low growth hormone secretion (M = 3.7 ng/ml, SD = 2.12 at 30 min) and three children had elevated growth hormone levels (> 30 ng/ml). After clonidine administration, six children had relatively low growth hormone levels (M = 3.15 ng/ml, SD = 2.53 at 60 min) and two children had high levels (38.3 ng/ml and 16.8 ng/ml, respectively). There was a better response after growth hormone releasing hormone administration; only one child had a growth hormone level of < 10 ng/ml. Most of the children had a modified response of growth hormone secretion subsequent to the various stimulation tests. All children, however, were able to secrete some growth hormone (> or = 10 ng/ml) at least during one of the stimulation tests. In comparison with peak growth hormone levels reported in normal children, our cohort had significantly lower growth hormone levels only after clonidine administration. It is postulated that children with Down syndrome have both anatomical and biochemical hypothalamic derangements that may result in decreased growth hormone secretion and reduced linear growth. In addition, other mechanisms that may be in part responsible for the observed growth retardation are discussed.
Research in developmental disabilities, 1993 · doi:10.1016/0891-4222(93)90023-d