Primary aldosteronism: inability to differentiate unilateral from bilateral adrenal lesions by various routine clinical and laboratory data and by peripheral plasma aldosterone.
In 31 patients with primary aldosteronism routine clinical and laboratory data, the effect of orthostasis on plasma aldosterone (PA), plasma renin activity (PRA) and cortisol (PC), effect of fludrocortisone or high sodium intake on basal PA and night-day fluctuations of basal PA and PC with and without suppression of pituitary ACTH by dexamethasone were determined to differentiate patients with a unilateral aldosterone producing tumour (adenoma, APA, n=20; carcinoma, CA, n=1) from those with idiopathic bilateral adrenal hyperplasia (IAH, n=10). Mean systolic and diastolic blood pressure, age, serum potassium and urinary excretion of sodium and potassium were not significantly different in both groups of patients. Normokalaemic primary aldosteronism occurred both in patients with APA (n=2) and in patients with IAH (n=1). Mean basal PA and mean urinary excretion rate of aldosterone-18-glucuronide were higher though not significantly different in patients with APA or CA than in those with IAH. A substantial number of the patients with APA (n=5) and with IAH (n=3) showed urinary excretion rates of aldosterone-18-glucuronide less than 13 microgram/24 h. Mean PA and PRA significantly increased (P less than 0.025) in patients with IAH in response to posture. However, these changes also occurred at times in some patients with APA. Both fludrocortisone and high sodium intake produced a variable and no group-specific effect on basal PA. Night-day variations in PA were positively correlated with those in PC in all patients with APA (n=12) and in 5 of 8 patients with IAH. A dissociation of PA and PC, however, was only observed in patients with IAH. Finally, the effect of dexamethasone on plasma aldosterone curves was variable in both groups of patients. Our results indicate that under the described conditions analysis of routine clinical and laboratory data and of peripheral PA, PRA and PC are of limited value in differentiating patients with APA or CA from those with IAH.
D000236:Adenoma / Q000175:diagnosis* / Q000378:metabolism; D000302:Adrenal Cortex / Q000378:metabolism / Q000473:pathology; D000306:Adrenal Cortex Neoplasms / Q000175:diagnosis* / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000328:Adult; D000450:Aldosterone / Q000097:blood*; D002277:Carcinoma / Q000175:diagnosis* / Q000378:metabolism; D002940:Circadian Rhythm; D003907:Dexamethasone / Q000494:pharmacology; D003937:Diagnosis, Differential; D005260:Female; D005438:Fludrocortisone / Q000494:pharmacology; D005965:Glucuronates / Q000652:urine; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006929:Hyperaldosteronism / Q000175:diagnosis* / Q000209:etiology / Q000378:metabolism; D006965:Hyperplasia; D008297:Male; D008875:Middle Aged; D011187:Posture; D011188:Potassium / Q000378:metabolism; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism; D012965:Sodium Chloride / Q000494:pharmacology
D005965:Glucuronates; D012965:Sodium Chloride; D000450:Aldosterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D012964:Sodium; D012083:Renin; D011188:Potassium; D005438:Fludrocortisone; D006854:Hydrocortisone