Dexamethasone suppression adrenal scintiscans were performed on 37 patients referred for evaluation of primary
aldosteronism (PA). Twenty-one had
aldosterone-secreting adrenal
adenoma (AA) and 16 had bilateral adrenal
hyperplasia (BAH). The diagnosis of either AA or BAH was confirmed by
adrenalectomy in 19 of 21 subjects with AA and by adrenal venous sampling in 15 of 16 patients with BAH. Biochemical parameters of PA were found in each patient while on both high (150 meq Na) and low
salt (10 meq Na) intakes. Urinary
aldosterone excretion values were 49.7 +/- 10.2 (+/- SEM) micrograms/day (range, 11.2-103.9) and 44.2 +/- 12.1 micrograms/day (range, 14.3-128.0) in AA patients on high and low
salt intakes, respectively. In BAH patients, urinary
aldosterone values were 29.1 +/- 2.6 micrograms/day (range, 10.0-55.0) and 47.7 +/- 9.0 micrograms/day (range, 23.0-102.0) on high and low
salt intakes, respectively. A semioperator-independent computer algorithm was used to calculate adrenal gland uptake of [131I]
6 beta-iodomethyl-19-norcholesterol (NP-59) in PA patients and in 7 patients with
essential hypertension.
NP-59 adrenal uptake values were 0.20 +/- 0.02%/dose (range, 0.03-0.72), 0.28 +/- 0.04% (range, 0.10-0.65), and 0.14 +/- 0.02%/dose (range, 0.08-0.30) in AA, BAH, and
essential hypertension, respectively. A significant correlation was found between adrenal gland uptake of
NP-59 and urinary
aldosterone excretion in AA (r = 0.93; P less than 0.001) and BAH (r = 0.6; P less than 0.01) patients. These data confirm that adrenal gland accumulation of
NP-59 while on
dexamethasone suppression can be used to characterize abnormal zona glomerulosa function in PA, in addition to localizing AA and differentiating AA from BAH.