Takeda Y, Miyamori I, Iki K, Takeda R, Vecsei P
Second Department of Internal Medicine, School of Medicine, Kanazawa University, Japan.
Acta Endocrinol (Copenh). 1992 Jun;126(6):484-8. doi: 10.1530/acta.0.1260484.
Urinary excretion of 19-noraldosterone, 18. 19-dihydroxycorticosterone (18, 19(OH)2-B), 18-hydroxy-19-norcorticosterone (18-OH-19-nor-B), 18-hydroxycorticosterone (18-OH-B), 18-hydroxycortisol (18-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 +/- 51 pmol/day), 18, 19(OH)2-B (21 +/- 4.2 nmol/day) and 18-OH-19-nor-B (879 +/- 213 pmol/day) levels were lower but not significantly different from 19-noraldosterone (263 +/- 56 pmol/day), 18, 19(OH)2-B (40 +/- 8.7 nmol/day) and 18-OH-19-nor-B (1322 +/- 267 pmol/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 +/- 5.2 nmol/day, 1660 +/- 318 nmol/day, respectively) compared with patients with idiopathic hyperaldosteronism (19 +/- 3.3 nmol/day, 541 +/- 93 nmol/day, respectively) (p less than 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-noraldosterone, 18, 19(OH)2-B and 18-OH-19-nor-B, could not be used to distinguish the two subsets of primary aldosteronism.