8-OH-F) and aldosterone were measured in 25 patients with primary aldosteronism, 16 with an aldosterone-producing adenoma and 9 with idiopathic hyperaldosteronism. In patients with idiopathic hyperaldosteronism, urinary 19-noraldosterone (207\m=+-\51pmol/day), 18, 19(OH)2-B (21 \ m=+-\ 4.2 nmol/day) and 18-OH-19-nor-B (879 \ m=+-\ 21 3 pmol/day) levels were lower but not significantly different from 19-noraldosterone (263\m=+-\56pmol/day), 18, 19(OH)2-B (40\m=+-\8.7nmol/day) and 18-OH-19-nor-B (1322\m=+-\267pmol/day) seen in patients with aldosterone-producing adenoma. Urinary aldosterone did not differ significantly between patients with idiopathic hyperaldosteronism and those with aldosterone-producing adenoma. Both urinary 18-OH-B and 18-OH-F excretion were significantly higher in aldosterone-producing adenoma (39\m=+-\5.2nmol/day, 1660\m=+-\318nmol/day, respectively) compared with patients with idiopathic hyperaldosteronism (19\m=+-\3.3nmol/day, 541 \m=+-\93 nmol/day. respectively) (p<0.05). Though urinary 18-OH-F and 18-OH-B concentrations were useful markers, the mineralocorticoid steroids which we can only now measure, 19\ x=req-\ noraldosterone, 18, 19(OH)2-B and 18-OH-19-nor-B, could not be used to distinguish the two subsets of primary aldosteronism.