Preclinical Cushing’s Syndrome Resulting from Black Adrenal Adenoma

2004 ◽  
Vol 62 (2) ◽  
pp. 60-66 ◽  
Author(s):  
Hiroshi Tokunagaa ◽  
Nobuhiro Miyamura ◽  
Kazunari Sasaki ◽  
Kazuaki Yoshizato ◽  
Mina Itasaka ◽  
...  
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 62 (9) ◽  
pp. 466-469 ◽  
Author(s):  
Run Yu ◽  
Meng Wei ◽  
Xuemo Fan ◽  
Richard R. Ellis ◽  
Glenn D. Braunstein

2001 ◽  
Vol 24 (6) ◽  
pp. 723-726 ◽  
Author(s):  
Tadaaki HONDA ◽  
Tetsuya NAKAMURA ◽  
Yuichiro SAITO ◽  
Yoshio OHYAMA ◽  
Hiroyuki SUMINO ◽  
...  

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

1969 ◽  
Vol 60 (4) ◽  
pp. 645-656 ◽  
Author(s):  
Frances J. Thomas ◽  
A. W. Steinbeck

ABSTRACT Following β-glucuronidase hydrolysis, pregnanetriol, pregnanetriolone and tetrahydro S were extracted from urine, chromatographed on florosil and in two paper systems before semiquantitative estimation of pregnanetriol and pregnanetriolone with the phosphoric acid reaction and of tetrahydro S with blue tetrazolium. The chemical validity and reliability of the method were studied and excretions measured in normal subjects and endocrine disorders. Pregnanetriol excretions were compared with published values. Normal pregnanetriol excretions were found in »idiopathic« hirsutism, with Stein-Leventhal ovaries and in Cushing's syndrome due to adrenal adenoma and hyperplasia; increased excretions were found in congenital adrenal hyperplasia and Cushing's syndrome with adrenal carcinoma. Pregnanetriolone was detected only in congenital adrenal hyperplasia, Cushing's syndrome from hyperplasia and one carcinoma. Large amounts of tetrahydro S were found in Cushing's syndrome with adrenal carcinoma. The possible diagnostic significance of the findings is discussed.


1987 ◽  
Vol 114 (2) ◽  
pp. 166-170 ◽  
Author(s):  
D. Gordon ◽  
C. G. Semple ◽  
G. H. Beastall ◽  
J. A. Thomson

Abstract. The hypothalamic-pituitary-adrenal axis was investigated in all six patients requiring glucocorticoid replacement 2.5–11 years after unilateral adrenalectomy for adrenal adenomas causing Cushing's syndrome. The hypothalamic-pituitary-adrenal axis was assessed by insulin induced hypoglycaemia and CRF testing in each patient. Two patients showed normal cortisol and ACTH responses to hypoglycaemia. Two patients showed subnormal cortisol responses to hypoglycaemia in the presence of high or normal basal ACTH concentrations. ACTH concentrations increased with both hypoglycaemia and CRF. Two patients showed subnormal cortisol responses to hypoglycaemia and CRF. One of these patients showed an ACTH rise following hypoglycaemia but not CRF. Defects at either hypothalamic-pituitary or adrenal levels were demonstrated and recovery of the axis appears to commence at the hypothalamic-pituitary level.


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