Endocrine Abstracts

In adults, the absence of a biological marker equivalent to height in children, means the diagnosis of GHD relies exclusively on biochemical tests. Confirmation of GHD when suspected involves use of GH stimulation tests, serum levels of GH-dependent peptides, and 24 h GH profiles.

GH stimulation tests have become the mainstay for diagnosis of adult GHD, which superficially appears to be relatively simple. GHD in the adult is accepted as a peak GH response of <3 μg/l to the ITT. This value provides good separation of GHD adults from normal subjects, however, is arbitrary. The peak GH response to all GH stimulation tests is significantly impaired by increases in fat mass. A gender dichotomy further complicates interpretation of GH stimulation tests; the peak response to the ITT is greater in males, whereas the peak GH response to the GST is greater in females.

A number of clinical scenarios present a further degree of complexity to the diagnosis of GH status. Given the effect of fat mass on the peak response to stimulation tests, how does one diagnose GHD in obese individuals who have received a putative insult to the hypothalamo-pituitary axis? In patients who have received cranial irradiation for tumours distant to the h-p axis a differential response to the ITT and GHRH-arginine test/AST is observed. Which of these tests is the more reliable in defining GH status of these individuals? In patients with GH-secreting tumours, GHD is most likely to occur in those who have received XRT. In these individuals the relationship between GH and IGF1 is perturbed, with IGF1 levels being relatively more preserved than predicted from prevailing GH levels. Is a patient with treated acromegaly GHD if there is failure to respond to stimulation tests, but IGF1 SDS is in the upper half of the normative range?