Glucocorticoid-suppressible hyperaldosteronism. Ultrastructural observation of a case.
A 56-year-old woman presented with intracranial hemorrhage. Laboratory examinations revealed severe hypertension, hypokalemia, elevated aldosterone excretion, and suppressed plasma renin activity. Left adrenocortical tumor was suspected and adrenalectomy was performed. The laboratory data after operation, however, showed no significant difference from the preoperative data. On the basis of further examinations, dexamethasone was administered and returned blood pressure to normal, and also normalized serum potassium, plasma aldosterone, and renin activity. The patient's illness was diagnosed as glucocorticoid-suppressible hyperaldosteronism. Light microscopically, the zona glomerulosa was hypertrophic and the outer zona fasciculata decreased in lipid droplets and was centrifugally arranged in small alveoli. Electronmicroscopically, the cells of the outer zona fasciculata had several lipid droplets and well-developed sER. Mitochondria were round to oval with lamellar or lamellovesicular cristae. These findings were evidence of hyperfunction. The cytoplasm of the cells also contained spironolactone bodies. Therefore, it is assumed that the aldosterone, which induced the disorder, was produced mainly in the outer zona fasciculata.
D000302:Adrenal Cortex / Q000378:metabolism / Q000648:ultrastructure*; D000450:Aldosterone / Q000096:biosynthesis; D003907:Dexamethasone / Q000627:therapeutic use; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D005260:Female; D006801:Humans; D006929:Hyperaldosteronism / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D006984:Hypertrophy; D008875:Middle Aged; D011956:Receptors, Cell Surface / Q000502:physiology; D018043:Receptors, Corticotropin; D012084:Renin-Angiotensin System; D013148:Spironolactone / Q000032:analysis
D011956:Receptors, Cell Surface; D018043:Receptors, Corticotropin; D013148:Spironolactone; D000450:Aldosterone; D003907:Dexamethasone