Early studies showed that a significant proportion of growth hormone deficient (GHD) children respond to the acute administration of GHRH with a rise in GH levels (20-22). These responses are lower on average than those of normal children or non-GH deficient children with short stature, but can overlap into the normal range (Fig. 4) (21). Depending upon the series, the fraction of patients who respond to GHRH ranges between 40 and 80% (23-25). Failure to respond to a first single bolus of GHRH does not necessarily exclude pituitary responsiveness. We have demonstrated that some GH deficient children who fail to respond initially may convert to a positive response after repeated GHRH stimulation, presumably reflecting an increase in GH synthesis and storage in a releasable pool (26). These observations suggest that most patients with idiopathic GHD do not have an intrinsic pituitary defect in the production of GH, but rather appear to have a deficiency in the hypothalamic secretion of GHRH (and possibly of the endogenous GHRP-like substance as well).
The situation is different in adults with acquired GHD, most of whom have pituitary disease or iatrogenic pituitary damage. In this setting, GHRH cannot be used for treatment, but the absence of a GH response to GHRH can be used as a diagnostic test for GHD, particularly in combination with the simultaneous administration of arginine to reduce the blunting of GH responses by age or obesity (42). The combined GHRH-arginine test is one of the diagnostic tests recommended by the Growth Hormone Research Society consensus workshop (54).
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