scholarly journals Combined Primary Aldosteronism and Preclinical Cushing's Syndrome: An Unusual Case Presentation of Adrenal Adenoma.

2001 ◽  
Vol 24 (6) ◽  
pp. 723-726 ◽  
Author(s):  
Tadaaki HONDA ◽  
Tetsuya NAKAMURA ◽  
Yuichiro SAITO ◽  
Yoshio OHYAMA ◽  
Hiroyuki SUMINO ◽  
...  
2017 ◽  
Vol 55 (1) ◽  
pp. 61-63
Author(s):  
Muzaffer İlhan ◽  
Özcan Karaman ◽  
İrem Yasin Çetin ◽  
Nur Büyükpınarbaşılı ◽  
Jamshid Hamdard ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yoshiro Fushimi ◽  
Fuminori Tatsumi ◽  
Junpei Sanada ◽  
Masashi Shimoda ◽  
Shinji Kamei ◽  
...  

Abstract Background Various adrenal disorders including primary aldosteronism and Cushing’s syndrome lead to the cause of hypertension. Although primary aldosteronism is sometimes complicated with preclinical Cushing’s syndrome, concurrence of overt Cushing’s syndrome and primary aldosteronism is very rare. In addition, it has been drawing attention recently that primary aldosteronism is brought about by the presence of aldosterone-producing cell cluster in adjacent adrenal cortex rather than the presence of aldosterone-producing adenoma. Case presentation A 67-year-old Japanese female was referred to our institution due to moon face and central obesity. Based on various clinical findings and data, we diagnosed this subject as overt Cushing’s syndrome and primary aldosteronism. Furthermore, in immunostaining for cytochrome P450 (CYP) 11B1, a cortisol-producing enzyme, diffuse staining was observed in tumorous lesion. Also, in immunostaining for CYP11B2, an aldosterone-producing enzyme, CYP11B2 expression was not observed in tumorous lesion, but strong CYP11B2 expression was observed in adjacent adrenal cortex, indicating the presence of aldosterone-producing cell cluster. Conclusions We should bear in mind the possibility that concurrence of overt Cushing’s syndrome and primary aldosteronism is accompanied by aldosterone-producing cell cluster in adjacent adrenal cortex.


1985 ◽  
Vol 110 (3) ◽  
pp. 302-307 ◽  
Author(s):  
Hajime Watanobe ◽  
Takahiko Kawagishi ◽  
Yuichi Hirai ◽  
Tatsuro Sato ◽  
Masahiro Tsutsui ◽  
...  

Abstract. A very unusual case of Cushing's syndrome is presented. Most of the preoperative biochemical and radiological examinations were compatible with Cushing's syndrome owing to a right adrenal adenoma. Exceptional findings include normal concentrations of adrenocorticotrophin (ACTH) in plasma as well as a disturbance of its circadian rhythmicity and a significant adrenocortical responsiveness to exogenous ACTH. Secretory patterns of ACTH did not change even after right adrenalectomy. Studies in vitro revealed that the adenoma itself, but not the surrounding normal adrenal, was the source of cortisol secreted in response to ACTH. Post mortem examinations disclosed unexpectedly a hormonally inactive left adrenal adenoma and a focal hyperplastic lesion of the anterior pituitary with an ACTH concentration 53 times higher than that of the remaining tissue of the gland. It is a possibility that this case may have represented a transition between pituitary-dependent adrenocortical hyperplasia and adrenal adenoma to this date reported in only one similar case.


2015 ◽  
Vol 62 (9) ◽  
pp. 466-469
Author(s):  
Run Yu ◽  
Meng Wei ◽  
Xuemo Fan ◽  
Richard R. Ellis ◽  
Glenn D. Braunstein

2020 ◽  
Vol 4 (1) ◽  
pp. 56-58
Author(s):  
Shoko Uketa ◽  
Yousuke Shimizu ◽  
Kosuke Ogawa ◽  
Noriaki Utsunomiya ◽  
Satsuki Asai ◽  
...  

2015 ◽  
Vol 173 (4) ◽  
pp. M99-M106 ◽  
Author(s):  
Davide Calebiro ◽  
Guido Di Dalmazi ◽  
Kerstin Bathon ◽  
Cristina L Ronchi ◽  
Felix Beuschlein

The cAMP signaling pathway is one of the major players in the regulation of growth and hormonal secretion in adrenocortical cells. Although its role in the pathogenesis of adrenocortical hyperplasia associated with Cushing's syndrome has been clarified, a clear involvement of the cAMP signaling pathway and of one of its major downstream effectors, the protein kinase A (PKA), in sporadic adrenocortical adenomas remained elusive until recently. During the last year, a report by our group and three additional independent groups showed that somatic mutations of PRKACA, the gene coding for the catalytic subunit α of PKA, are a common genetic alteration in patients with Cushing's syndrome due to adrenal adenomas, occurring in 35–65% of the patients. In vitro studies revealed that those mutations are able to disrupt the association between catalytic and regulatory subunits of PKA, leading to a cAMP-independent activity of the enzyme. Despite somatic PRKACA mutations being a common finding in patients with clinically manifest Cushing's syndrome, the pathogenesis of adrenocortical adenomas associated with subclinical hypercortisolism seems to rely on a different molecular background. In this review, the role of cAMP/PKA signaling in the regulation of adrenocortical cell function and its alterations in cortisol-producing adrenocortical adenomas will be summarized, with particular focus on recent developments.


2003 ◽  
Vol 29 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Ilias Vrezas ◽  
Paul Wentworth ◽  
Stefan R. Bornstein

2011 ◽  
Vol 58 (7) ◽  
pp. 543-551 ◽  
Author(s):  
Kiichiro Hiraishi ◽  
Takanobu Yoshimoto ◽  
Kyoichiro Tsuchiya ◽  
Isao Minami ◽  
Masaru Doi ◽  
...  

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