Objective: Some growth hormone deficient adults (GHDAs) have an impaired quality of life, which may improve with growth hormone (GH) treatment. The objective of our study was to make an in-depth psychiatric evaluation of patients with adult-onset (AO) and childhood-onset (CO) GH deficiency (GHD), and to assess the time course of changes in their quality of life and symptoms of depression in response to GH treatment. Design: The study design was a 4-month, double-blind, cross-over, placebo-controlled trial of GH therapy. Methods: We used a detailed psychiatric interview to characterise 25 patients with proven GHD at baseline. They were reassessed at monthly intervals during treatment with GH or placebo, using the Nottingham Health Profile and two well-recognised depression rating scales. Results: 11/18 (61%) of the patients with AO-GHD, but 0/7 of the patients with CO-GHD, were found to have atypical depression at baseline. There were significant improvements in the depression rating scale scores after 2 months of GH therapy, with significant improvements in emotional reaction and social isolation scores from 1 month, and in energy levels and sleep disturbance from 2 and 3 months respectively. Conclusions:The results of our study confirm that a large proportion of GHDAs have unequivocal psychiatric morbidity, and suggest that a response to treatment can be seen after a short trial of GH therapy. We hypothesise that this rapid improvement of symptoms of atypical depression represents a direct central effect of GH therapy.European Journal of Endocrinology 151 325-332

GH deficiency (GHD) in adults is a well recognized clinical syndrome that results in significant metabolic and psychological morbidity. GH replacement therapy not only reverses these changes but improves the quality of life and results in a significant improvement in well being. There is no single simple and safe test to assess GHD. GHD in adults is diagnosed biochemically by provocative testing of GH secretion, and the insulin tolerance test (ITT) is accepted to be the test of choice. However, the ITT has many contraindications, needs multiple blood samples, and is potentially dangerous, requiring regular monitoring of patients in a specialized investigation unit. The aim of our study was to evaluate the GH-releasing effect of a combination of the hypothalamic secretagogue GHRH with a small dose of the synthetic peptide GHRP-2, to diagnose GHD. We have compared the GH response to ITT and GHRH/GHRP in a large group of adults with hypothalamic/pituitary disease (n = 36; 22 males and 14 females; age, 18 -59 yr) and in healthy volunteers (n = 30; 15 males and 15 females; age, 22-66 yr). The GHRH/GHRP test produces a measurable GH secretory response in normal, hypopituitary and GH-deficient patients. The test has no side effects. Using the ITT as our 'gold standard' with a GH response of 9 mU/L as our cut-off to define GHD, we compared the clinical efficacy of these two tests. Choosing an arbitrary cut-off of 17 mU/L to define GHD in the GHRH/GHRP test, this new test proved to have 78.6% sensitivity and 100% specificity even when we only used the 30-min datum point.

Development of acute neurological symptoms secondary to cerebral oedema is well described in diabetic ketoacidosis (DKA) and often has a poor prognosis. We present the clinical and radiological data of a 17-yr-old girl who developed cortical blindness, progressive encephalopathy, and seizures caused by posterior reversible encephalopathy syndrome (PRES) that developed after her DKA had resolved. Vasogenic oedema in PRES resolves if the underlying trigger is identified and eliminated. In this case, hypertension was identified as the likely precipitating factor and following treatment her vision and neurological symptoms rapidly improved. We suggest how recent DKA may have contributed to the development of PRES in this patient.

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