What are histologic findings characteristic of hyperaldosteronism?

Updated: Sep 08, 2020
  • Author: George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London); Chief Editor: Robert P Hoffman, MD  more...
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Unlike cortisol-producing adrenocortical tumors, in which the remaining ipsilateral and contralateral glands are commonly atrophic, APAs may show hyperplasia of the zona glomerulosa in the nontumorous cortex, either forming a broad zone locally or thickening the entire cortex, with tongues of glomerulosa like cortex extending inward from the subcapsular region.

This appearance has been reported in as many as one third of patients with APAs and suggests that the tumor has arisen from within an area that was hyperplastic, though to date, neither an external stimulus nor an intrinsic defect has been found.

IHA is a disease of the zona glomerulosa with a variable macroscopic appearance that can range from hyperplasia with micronodules and macronodules to hyperplasia without nodules to normal-appearing zona glomerulosa with micronodules. The glands may be normal in weight or heavy.

The normal microscopic appearance of the zona glomerulosa is of small discontinuous subcapsular nests of cells. In hyperplasia, the zona glomerulosa may contain continuous bands of cells that may be visibly thickened, either forming a continuous sheet or focally extending as tongues into the adjacent cortex. This process may be focal or diffuse and may vary from one part of the gland to another, requiring multiple sections.

GRA, or familial hyperaldosteronism (FH) type I (FH-I), results from the formation of a hybrid gene that leads to ACTH-mediated mineralocorticoid synthesis by the zona fasciculata. Histologically, evidence suggests hyperplasia of this zone in addition to the zona glomerulosa.

FH type II (FH-II) has been linked to a locus on chromosome 7p22. Histologically, evidence suggests adrenocortical hyperplasia or hypertrophy and the presence of adenomas.

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