The most profound GH release is seen after insulin-induced hypoglycaemia. Glucagon appears to be more effective at inducing GH release than arginine. Clonidine at a dose of 100 or 200 micrograms is no more effective than placebo.

Our study suggests that all children who have received GH replacement therapy in childhood should undergo reassessment of GH status in young adult life. Between 40 and 60% of such patients merit consideration for GH therapy in adult life depending on the definition of severe GH deficiency in use. Patients with isolated GH deficiency should undergo two provocative tests of GH secretion, but those with additional anterior pituitary hormone deficiencies require only one test at reassessment.

GH secretion declines by 14% decade of adult life, leading to the suggestion that people over the age of 60 yr are functionally GH deficient. If this is the case, one might not be able to detect a difference in GH secretion between the elderly with documented hypothalamic-pituitary disease and an age-matched control group. We studied GH secretion in 24 patients with hypothalamic-pituitary disease and 24 controls matched for body mass index and age using 24-h GH profiles, arginine stimulation tests, and serum insulin-like growth factor I (IGF-I) levels. The median (range) area under the curve of the GH profile [< 9.6 (< 9.6-20) vs. 18.5 (10.7-74.4) micrograms/L.24 h; P < 0.0001], the median stimulated peak GH response to arginine [< 0.4 (< 0.4-7.7) vs. 8.0 (1.6-37.0) micrograms/L; P < 0.0001], and the median serum IGF-I concentration [102 (< 14-162) vs. 147 (65-255) ng/mL; P = 0.0002] were significantly lower in the patients than in the controls. Fifteen patients showed no evidence of spontaneous or stimulated GH secretion, whereas all controls had evidence of both. The area under the GH curve in the 33 subjects with demonstrable GH secretion correlated significantly with the peak GH response to arginine (r = 0.71; P < 0.0001), but not with serum IGF-I concentration. This study suggests that organic GH deficiency in the elderly is distinct from the decline in GH secretion associated with the aging process. These patients may benefit from GH replacement therapy.

SummaryContext and ObjectiveNonfunctioning pituitary adenomas (NFPAs) are the most common subtype of pituitary tumour. Hypopituitarism is observed in NFPAs due to tumour‐ or treatment‐related factors and may increase mortality risk. Here, we analysed the associations of hypopituitarism, hormone replacement and mortality in a large NFPA cohort derived from two large European centres.Design, Setting and ParticipantsCase note review of all patients treated for NFPA in University Hospitals Birmingham and Beaumont Hospital Dublin between 1999 and 2014 was performed.Main Outcome MeasuresClinical presentation, treatment strategies, pituitary function and vitality status were recorded in each patient. A multivariate Cox regression model was used to examine the association between hypopituitarism, hormone replacement and premature mortality.ResultsA total of 519 patients were included in the analysis. Median duration of follow‐up was 7·0 years (0·5–43). A total of 81 deaths were recorded (15·6%). On multivariate analysis, adrenocorticotropic hormone (ACTH) and gonadotropin (Gn) deficiencies were associated with an increased relative risk of death (OR 2·26, 95% CI 1·15–4·47, P = 0·01 and OR 2·56, 95% CI 1·10–5·96, P = 0·01, respectively). Increased hydrocortisone (HC) (P‐trend = 0·02) and lower levothyroxine (LT4) doses (P‐trend = 0·03) were associated with increased risk of death. Mortality increased with the degree of pituitary failure observed (P‐trend = 0·04).ConclusionACTH and gonadotropin‐deficient patients have higher mortality rates compared to those with intact hormonal axes. Excessive HC and suboptimal LT4 replacement may also increase risk of death. Complex associations between hormone deficiency and replacement underpin the increased mortality risk in NFPA patients.

GH secretion declines by 14% decade of adult life, leading to the suggestion that people over the age of 60 yr are functionally GH deficient. If this is the case, one might not be able to detect a difference in GH secretion between the elderly with documented hypothalamic-pituitary disease and an age-matched control group. We studied GH secretion in 24 patients with hypothalamic-pituitary disease and 24 controls matched for body mass index and age using 24-h GH profiles, arginine stimulation tests, and serum insulin-like growth factor I (IGF-I) levels. The median (range) area under the curve of the GH profile [< 9.6 (< 9.6-20) vs. 18.5 (10.7-74.4) micrograms/L.24 h; P < 0.0001], the median stimulated peak GH response to arginine [< 0.4 (< 0.4-7.7) vs. 8.0 (1.6-37.0) micrograms/L; P < 0.0001], and the median serum IGF-I concentration [102 (< 14-162) vs. 147 (65-255) ng/mL; P = 0.0002] were significantly lower in the patients than in the controls. Fifteen patients showed no evidence of spontaneous or stimulated GH secretion, whereas all controls had evidence of both. The area under the GH curve in the 33 subjects with demonstrable GH secretion correlated significantly with the peak GH response to arginine (r = 0.71; P < 0.0001), but not with serum IGF-I concentration. This study suggests that organic GH deficiency in the elderly is distinct from the decline in GH secretion associated with the aging process. These patients may benefit from GH replacement therapy.