title: Therapeutic outcome of primary aldosteronism: adrenalectomy versus enucleation of aldosterone-producing adenoma.
abstract: Our followup study of 48 patients with primary aldosteronism concerns the results of 2 different operative methods. After preoperative localization of the unilateral solitary tumor 22 patients underwent unilateral adrenalectomy and 26 underwent enucleation of aldosterone-producing adenoma. Both operative methods improved hypertension, hypokalemia, the low urinary sodium-to-potassium ratio, suppressed plasma renin activity, high plasma aldosterone concentration, high urinary aldosterone excretion and high urinary kallikrein excretion in similar orders of magnitude for 5 years. Levels of plasma cortisol and plasma adrenocorticotropic hormone following respective operations were also identical. Five years postoperatively, ambulation and furosemide administration under low sodium diet stimuli remarkably enhanced plasma renin activity and plasma aldosterone concentration in the aldosterone-producing adenoma enucleation group (p < 0.001), almost similar to that of normal subjects but increment magnitudes were slight (p < 0.05 to < 0.01) in the adrenalectomy group. Preoperatively, angiotensin II infusion failed to increase plasma aldosterone concentration in patients with primary aldosteronism. After respective operations, responses of plasma aldosterone concentration to angiotensin II infusion and of plasma cortisol to adrenocorticotropic hormone administration in the aldosterone-producing adenoma enucleation group were more sensitive than those in the adrenalectomy group. There was no remission of recurrent hyperaldosteronism in either group throughout the study. These results suggest that angiotensin II induces aldosterone release by an activation of tumor uninvolved cortical cells and that the enucleation of aldosterone-producing adenoma is more preferable than unilateral adrenalectomy.
authors.affiliation: Department of Urology, Yamagata University, School of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nakada
authors.forename: Y
authors.initials: Y
authors.lastname: Kubota
authors.forename: I
authors.initials: I
authors.lastname: Sasagawa
authors.forename: T
authors.initials: T
authors.lastname: Yagisawa
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: M
authors.initials: M
authors.lastname: Ishigooka
mesh_terms: D000306:Adrenal Cortex Neoplasms / Q000097:blood / Q000150:complications / Q000378:metabolism / Q000601:surgery*; D000315:Adrenalectomy; D018246:Adrenocortical Adenoma / Q000097:blood / Q000150:complications / Q000378:metabolism / Q000601:surgery*; D000328:Adult; D000450:Aldosterone / Q000097:blood / Q000378:metabolism; D000804:Angiotensin II / Q000627:therapeutic use; D005260:Female; D005500:Follow-Up Studies; D005665:Furosemide / Q000627:therapeutic use; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006929:Hyperaldosteronism / Q000097:blood / Q000209:etiology / Q000601:surgery*; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000097:blood; D012189:Retrospective Studies; D016896:Treatment Outcome
chemical_list: D000804:Angiotensin II; D000450:Aldosterone; D005665:Furosemide; D012083:Renin; D006854:Hydrocortisone