Discordance between growth hormone responses after growth hormone-releasing hormone (GHRH) and insulin hypoglycemia in ectopic GHRH syndrome.

Dynamic studies of growth hormone (GH) secretion were performed in two patients with ectopic GHRH syndrome. Patient 1 (female, 33 years old) had a growth hormone releasing hormone (GHRH) producing carcinoid of the lung with clinical features of acromegaly while patient 2 (50 years old male) had small cell carcinoma of the lung without acromegaly. Insulin hypoglycemia stimulated GH secretion in both patients (i.e. from a basal level of 10 mU/l to 48 mU/l in patient 1, while the respective values in patient 2 were 5 mU/l and 61 mU/l), TRH acutely stimulated GH in both patients. Synthetic GHRH 1-29 (KABI) i.v. bolus 100 micrograms did not stimulate GH release in either patient (i.e. basal GH 14 mU/l and peak 18 mU/l (patient 1); basal GH 4.6 mU/l and peak 8.8 mU/l (patient 2). It is concluded that: 1. prolonged pituitary exposure to GHRH is associated with chronic GH hypersecretion with or without clinical acromegaly; 2. GH response to TRH may be mediated at the pituitary level and results from prolonged exposure to GHRH; 3. the discordant response of GH after GHRH and insulin induced hypoglycemia might suggest the involvement (at least partially) of somatostatin in the mechanism of GH release after hypoglycemia and after GHRH.