This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

We evaluated the growth hormone (GH) response to an acute clonidine test (0.15 mg/m2 po) in 30 normal prepubertal children (stature between the 3rd and 97th centile), in 29 short children (stature < 3rd centile for age) with height velocity (HV) > 10th centile and in 20 short children with HV < 10th centile. The three groups had comparable chronological ages. After clonidine administration mean peak GH levels were similar in the three groups (19.4 +/- 9.8, 17.7 +/- 8.8 and 14.6 +/- 8.9 micrograms/l, mean +/- SD, respectively). By choosing 10 micrograms/l as the limit for a normal response we found that stimulated GH levels had a sensitivity of 50% and a specificity of 83% in identifying children with suspected GHD (short children with subnormal HV). The diagnostic accuracy was almost superimposable, for cut-off values of 10 and 12 micrograms/l. Eight of the 10 children with subnormal HV and a GH peak < 10 micrograms/l had a GH peak < 10 micrograms/l also after a second stimulation test. Six of the 29 short children with normal HV had a GH peak < 10 micrograms/l. Only one of them had a GH peak < 10 micrograms/l after a second stimulation test. Five of the normal children had peak GH levels < 10 micrograms/l. These results indicate that HV is a useful variable to predict the GH response to an acute GH stimulus, since the great majority of children with a normal growth rate had a normal GH response to at least one stimulation test.

The effect of treatment with oxandrolone, an anabolic steroid, on GH response to GH-releasing hormone (GHRH) has been evaluated in children with constitutional growth delay. Five subjects, four males and one female, aged 11.0-17.1 years were given oxandrolone 0.1 mg/kg p.o. daily for 2 months, and underwent acute administration of GHRH (GRF 1-40, 1 microgram/kg i.v.) before and after withdrawal of oxandrolone therapy. GHRH administration induced a much greater GH response, evaluated either as a peak plasma GH levels or plasma GH integrated area, after than it did before oxandrolone treatment. These findings indicate that in children with constitutional growth delay oxandrolone increases the sensitivity of somatotrophs to exogenous GHRH and, likely, to the endogenously-released neurohormone.

No abstract

No abstract