Short-term dehydroepiandrosterone treatment increases platelet cGMP production in elderly male subjects

Summary Objective Several clinical and population‐based studies suggest that dehydroepiandrosterone (DHEA) and its sulphate (DHEA‐S) play a protective role against atherosclerosis and coronary artery disease in human. However, the mechanisms underlying this action are still unknown. It has recently been suggested that DHEA‐S could delay atheroma formation through an increase in nitric oxide (NO) production. Study design and methods Twenty‐four aged male subjects [age (mean ± SEM): 65·4 ± 0·7 year; range: 58·2–67·6 years] underwent a blinded placebo controlled study receiving DHEA (50 mg p.o. daily at bedtime) or placebo for 2 months. Platelet cyclic guanosine‐monophosphate (cGMP) concentration (as marker of NO production) and serum levels of DHEA‐S, DHEA, IGF‐I, insulin, glucose, oestradiol (E2), testosterone, plasminogen activator inhibitor (PAI)‐1 antigen (PAI‐1 Ag), homocysteine and lipid profile were evaluated before and after the 2‐month treatment with DHEA or placebo. Results At the baseline, all variables in the two groups were overlapping. All parameters were unchanged after treatment with placebo. Conversely, treatment with DHEA (a) increased (P