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Asymptomatic hypopituitary adults (especially women) on conventional replacement therapy have increased stiffness of the common carotid arteries. These findings provide additional evidence for a process leading to premature atherosclerosis in this group of patients.

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The objective of this study was to evaluate whether the degree of suppression of ovarian volume effected by a gonadotropin releasing hormone (GnRH) agonist in patients with polycystic ovary syndrome (PCOS) correlated with basal insulin secretion and insulin secretion provoked by a glucose challenge. Eighteen PCOS patients received the GnRH agonist D-tryptophan-6-LHRH (Decapeptyl, 3.75 mg monthly i.m.) for 6 months and had blood glucose and insulin measured during a 75 g oral glucose tolerance test (OGTT) prior to and at the end of therapy. According to ovarian volume suppression after GnRH agonist therapy, two groups were defined: in group A (n = 10; mean body mass index (BMI) +/- SEM, 25.6 +/- 1.6 kg/m2) ovarian volume regressed from 17.9 +/- 1.6 to 6.7 +/- 0.3 ml (full responders) and in group B (n = 8; mean BMI +/- SEM, 28.1 +/- 2.3 kg/m2) from 21.5 +/- 1.1 to 15.1 +/- 1.0 ml (partial responders). Results showed that GnRH agonist therapy did not affect significantly BMI or fasting levels and area under the curve (AUC) for glucose and insulin in the respective groups. Fasting insulin levels correlated positively with ovarian volume prior to (r = 0.56, p < 0.05) and after 6 months of GnRH agonist therapy (r = 0.80, p < 0.005). The suppressibility of ovarian volume with GnRH agonist therapy correlated negatively with the difference between maximal and basal levels (r = -0.68), the area under the curve (r = -0.62) and maximal levels (r = -0.72) for insulin during the OGTT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adults with hypopituitarism die prematurely, and the excess mortality is from vascular disease. On echocardiography we have demonstrated abnormalities of myocardial diastolic function in hypopituitary adults, indicating possible early ischaemic change. Peripheral arterial disease is evident on ultrasonography. Vascular risk factors have also been examined. Impaired glucose tolerance and unrecognized diabetes are common in hypopituitary adults. Total cholesterol levels are elevated, particularly in hypopituitary women. The role of growth hormone (GH) deficiency in the vascular disease and in the vascular-risk-factor abnormalities is unknown at present. Prolonged GH therapy causes a decrease in the levels of fasting total cholesterol, without any adverse effects on glucose homeostasis. GH therapy trials in adults will clarify the role of GH in the excess vascular risk of hypopituitarism. Prolonged GH therapy will be necessary for the vascular effects to be defined.