Six patients with primary
aldosteronism (PA), one with idiopathic
hyperaldosteronism (IHA), one with
glucocorticoid responsible
hyperaldosteronism (GRHA) and eight with
essential hypertension (EH) were treated with
trilostane (MWD-1822) (4 alpha, 5-epoxy-17 beta-hydroxy-3-oxo-5 alpha-androstane-2 alpha-carbonitrile), an inhibitor of adrenal
steroid biosynthesis, for 9-47 days with a daily dose of 30-960 mg. Blood pressure decreased slightly and gradually from 30 min. to 360 min, plasma
aldosterone (PAC) and
cortisol concentration (F) decreased, and plasma
dehydroepiandrosterone concentration (
DHEA) increased 120 min. after the administration of a single dose of 120 mg of
trilostane. In the patients with PA, IHA and GRHA on long term
therapy with
trilostane, blood pressure decreased, PAC and F were depleted, serum improved within normal limits and
DHEA increased, but plasma
progesterone concentration (Prog.) changed variously and plasma
renin activity (PRA) remained suppressed. In the patients with EH, systolic pressure decreased in 5 out of 8 (under - 20 mmHg), and diastolic pressure decreased in 3 out of 8 (under - 10 mmHg),
DHEA increased in all, but the changes in serum
potassium, PAC, F, Prog. and PRA were various. There was no remarkable reaction after the administration of
trilostane. It is concluded that
trilostane is an effective inhibitor of 3-hydroxysteroid
dehydrogenase in vivo and that it is useful in the treatment of primary
aldosteronism and other
hypertension due to hyperproduction of
aldosterone.