Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 21 P295

SFEBES2009 Poster Presentations Pituitary (65 abstracts)

Effects on insulin action of dehydroepiandrosterone sulphate replacement in hypopituitary females

Claire McHenry 1 , Patrick Bell 1 , Steven Hunter 1 , Christopher Thompson 2 , Hamish Courtney 1 , Cieran Ennis 3 , Brian Sheridan 3 , David McCance 1 , Karen Mullan 1 & Brew Atkinson 1


1Regional Centre for Endocrinology and Diabetes, Royal Victoria Hospital, Belfast, UK; 2Department of Endocrinology and Diabetes, Beaumont Hospital, Dublin, Ireland; 3Regional Endocrine Laboratory, Royal Victoria Hospital, Belfast, UK.


Hypopituitary patients are at increased vascular risk. This may be partly attributable to changes in insulin action. It has been suggested that the addition of dehydroepiandrosterone sulphate (DHEAS), which is low in patients with secondary hypoadrenalism, to routine replacement may have beneficial effects on glucose metabolism. Previously, patient populations and techniques used to assess insulin action varied and overall results have been conflicting.

We assessed effects on insulin action of DHEAS replacement in female patients with hypopituitarism on stable replacement therapy using the hyperinsulinaemic–euglycaemic clamp. A randomised double blind placebo control crossover design was used. Fourteen patients were assigned to either DHEAS 50 mg daily or placebo for 12 weeks with 4 weeks washout between treatments. Insulin action was assessed at the end of each treatment period.

Thirteen patients completed the study. DHEAS (DHEAS 5.4±0.8 versus placebo <0.8±0.0 μmol/l; P<0.001) and androstenedione (DHEAS 4.1±0.8 versus placebo 1.3±0.2 nmol/l) levels rose to within the normal range after DHEAS. There were no differences between treatments in testosterone, SHBG or IGF1 concentrations. There were no differences between treatments in fasting glucose, serum insulin concentrations or HbA1c. Triglyceride concentrations were lower following DHEAS (DHEA 1.24±0.18 versus placebo 1.41±0.19 mmol/l; P<0.05) but other lipid parameters were the same. Following treatment with DHEAS, there was no statistical difference in glucose infusion rates required to maintain euglycaemia when compared with placebo (DHEAS 21.9±2.5 versus placebo 24.5±2.1 μmol/kg per min; P=0.4).

In summary, there were no differences in insulin action following DHEAS replacement therapy across 12 weeks. These results do not provide any evidence for a positive effect on insulin action or support the addition of DHEAS for this purpose to routine hypopituitary replacement therapy.

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