Adrenomedullary Hyperplasia Associated with Cortisol Producing Adenoma.

Yoshioka, Mitsuaki; Saito, Hideaki; Kawakami, Yoshiaki; Mineyama, Hirotada; Sekiya, Masao

doi:10.1507/endocrj.40.467

Cited by 9 publications

(5 citation statements)

References 16 publications

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“…The histological association of adrenal medullar hyperplasia with either functioning or non-functioning adenomas originating from the reticulata or glomerulosa, as presented by our patients, has been communicated in a few reports (27)(28)(29)(30)(31).…”

Section: Morpho-functional Interactions Between Adrenal Cortex and Mesupporting

confidence: 53%

Association of adrenal medullar and cortical nodular hyperplasia

Valdés

Roessler

Salazar

et al. 2006

Endocr

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Arterial hypertension of adrenal etiology is mainly attributed to primary hyperaldosteronism. However, subtle expressions of hyperadrenergic or glucocorticoid excess can also generate arterial hypertension. The present report describes two hypertensive patients cataloged as resistant essential hypertensives, in whom adrenal masses were found incidentally, who highlight the need to recognize these tenuous clinical or laboratory presentations. Case 1 was a 50-yr-old female with hyperadrenergic hypertension associated to a left adrenal node, normal cortisol and aldosterone:renin ratio, marginally increased urinary normetanephrine, and a positive 131I MIBG radioisotope scan. Adrenalectomy normalized blood pressure and urinary metanephrines. Pathology showed a hyperplastic adrenal medulla associated to a multinodular cortical hyperplasia. Case 2 was a 62- yr-old female with progressive hypertension, a slight Cushing phenotype, non-suppressible hypercortisolism, normal urinary metanephrines, and bilateral adrenal nodes. Bilateral adrenalectomy and subsequent replacement normalized blood pressure and phenotypic stigmata. Pathology demonstrated bilateral cortical multinodular hyperplasia and medullary hyperplasia. The clinical study in both patients was negative for MEN. The apparently rare association of cortical and medullary lesions presented by both patients is probably overlooked in routine pathology exams, but should be meticulously searched since the crosstalk between the adrenal cortex and medulla may prompt dual abnormalities.

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Section: Morpho-functional Interactions Between Adrenal Cortex and Mesupporting

confidence: 53%

Association of adrenal medullar and cortical nodular hyperplasia

Valdés

Roessler

Salazar

et al. 2006

Endocr

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“…Nevertheless, this mechanism may not be exclusive. In fact, hyperplasia of the adrenal cortex adjacent to pheochromocytoma has also been observed, indicating that ACTH originating from the pheochromocytoma tissue can stimulate adrenocortical cells in a paracrine manner ( 11 , 77 – 80 ). Such a histological pattern is close to what is observed in corticomedullary mixed tumors that are composed of intermingled adrenocortical and pheochromocytoma tissues ( 81 – 84 ).…”

Section: Paracrine Control Of Adrenal Steroidogenesis By Intraadrenalmentioning

confidence: 99%

Role of ACTH in the Interactive/Paracrine Regulation of Adrenal Steroid Secretion in Physiological and Pathophysiological Conditions

et al. 2016

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In the normal human adrenal gland, steroid secretion is regulated by a complex network of autocrine/paracrine interactions involving bioactive signals released by endothelial cells, nerve terminals, chromaffin cells, immunocompetent cells, and adrenocortical cells themselves. ACTH can be locally produced by medullary chromaffin cells and is, therefore, a major mediator of the corticomedullary functional interplay. Plasma ACTH also triggers the release of angiogenic and vasoactive agents from adrenocortical cells and adrenal mast cells and, thus, indirectly regulates steroid production through modulation of the adrenal blood flow. Adrenocortical neoplasms associated with steroid hypersecretion exhibit molecular and cellular defects that tend to reinforce the influence of paracrine regulatory loops on corticosteroidogenesis. Especially, ACTH has been found to be abnormally synthesized in bilateral macronodular adrenal hyperplasia responsible for hypercortisolism. In these tissues, ACTH is detected in a subpopulation of adrenocortical cells that express gonadal markers. This observation suggests that ectopic production of ACTH may result from impaired embryogenesis leading to abnormal maturation of the adrenogonadal primordium. Globally, the current literature indicates that ACTH is a major player in the autocrine/paracrine processes occurring in the adrenal gland in both physiological and pathological conditions.

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“…Although we are aware that adrenal medullary hyperplasia may be diffuse, nodular or both, the presence of only a few medullary cells mixed with cortical cells in the neighbourhood of the tumour capsule was not considered to be sufficient to explain the described clinical and chemical features. Thus there is no evidence for the presence of adrenomedullary hyperplasia in combination with a cortisol producing adenoma as has been described (Yoshioka et al, 1993). Moreover, a glucocorticoid-producing adrenal cortical tumour would not exhibit the neuroendocrine differentiation present in this patient.…”

Section: Discussionmentioning

confidence: 56%

Adrenal Cortical Phaeochromocytoma: A Case Report of a Rare Entity

Simon

Tötsch²,

Schmidlin³

et al. 2003

Exp Clin Endocrinol Diabetes

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Adrenal cortical phaeochromocytomas (pseudo-phaeochromocytomas) are a very rare entity and a diagnostic challenge. Of the few cases previously reported, most have incomplete data or lack clinical and biochemical follow-up documenting the cure of the excess secretion of catecholamines after resection of the tumour. We report herein a 62-year-old patient with clinical and biochemical findings diagnostic of a phaeochromocytoma associated with a 2-cm adrenal mass on CT scan. Surgery revealed the presence of an adrenal cortical adenoma with positive staining for the neuroendocrine marker synaptophysin, but negative for chromogranin, as has been previously reported for these rare cortical phaeochromocytomas. After removal of the tumour the clinical symptoms resolved and biochemical markers normalized, demonstrating the causal relationship between the cortical tumour and the excess production of catecholamines.

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Adrenomedullary Hyperplasia Associated with Cortisol Producing Adenoma.

Cited by 9 publications

References 16 publications

Association of adrenal medullar and cortical nodular hyperplasia

Association of adrenal medullar and cortical nodular hyperplasia

Role of ACTH in the Interactive/Paracrine Regulation of Adrenal Steroid Secretion in Physiological and Pathophysiological Conditions

Adrenal Cortical Phaeochromocytoma: A Case Report of a Rare Entity

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