Cushing's syndrome due to a black adenoma of the adrenal gland: Lack of tumour visualization by radiocholesterol scintigraphy

1994 ◽  
Vol 21 (12) ◽  
pp. 1367-1368 ◽  
Author(s):  
B. Ambrosi ◽  
P. Colombo ◽  
G. Faglia
1997 ◽  
Vol 46 (2) ◽  
pp. 227-234 ◽  
Author(s):  
Fumitoshi Satoh ◽  
Osamu Murakami ◽  
Kazuhiro Takahashi ◽  
Junji Ueno ◽  
Tetsuo Nishikawa ◽  
...  

1951 ◽  
Vol 27 (3) ◽  
pp. 82-82
Author(s):  
Shigeo OKINAKA ◽  
Michiyoshi HARASAWA ◽  
Mitsuo NISHIKAWA

1980 ◽  
Vol 93 (2) ◽  
pp. 208-215 ◽  
Author(s):  
Hajime Nawata ◽  
Ken-ichi Kato ◽  
Hiroshi Ibayashi

Abstract. Thymidine kinase (TK) was partially purified from adrenal tissues with adrenocortical hyperplasia, adenomatous hyperplasia, adenoma and carcinoma from patients with Cushing's syndrome and from normal adrenal glands. Adrenocortical carcinoma, adenoma, hyperplasia and nodule and hyperplastic portion of adenomatous hyperplasia contained higher concentration of TK than normal adrenal gland. By DEAE-cellulose column chromatography, adrenocortical carcinoma gave two peaks (Peak I and Peak II) of TK, while in other adrenal tissues the second peak (Peak II) was only slightly detected or hardly detected. TK in all these tissues was identical with respect to pH optimum, metal requirement and inhibition by dTTP. dCTP inhibited TK activities of normal adrenal gland and the hyperplastic portion of adenomatous hyperplasia by 55%, respectively, but hardly affected the activity of the nodule of adenomatous hyperplasia, adenoma, hyperplasia and carcinoma. TK from hyperplastic portion of adenomatous hyperplasia showed the intermediate heat stability between the heat-stable enzyme from normal adrenal gland and the heat-labile enzyme from adrenocortical carcinoma, adenoma, hyperplasia and the nodule of adenomatous hyperplasia. The apparent Km for thymidine from adenocortical carcinoma (Peak I and Peak II) was 5.0 and 11.1; adenoma, 4.8; hyperplasia, 5.5; adenomatous hyperplasia (nodule, 5.0 and hyperplastic portion, 19.8) and normal adrenal gland, 25.0 μm. These observations indicated that TK with different catalytic properties existed in various human adrenal tissues. They also demonstrated that TK isolated from the nodule of adrenocortical adenomatous hyperplasia had similar properties as adrenocortical adenoma, while TK from the hyperplastic portion had the intermediate catalytic properties between normal adrenal gland and adrenocortical hyperplasia.


2009 ◽  
Vol 94 (3) ◽  
pp. 746-747 ◽  
Author(s):  
Takashi Kimura ◽  
Takeshi Usui ◽  
Susumu Inamoto ◽  
Sachiko Minamiguchi ◽  
Hiroshi Okuno ◽  
...  

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Emma Punni ◽  
Jonea Lim

Abstract Introduction: Adrenocortical carcinoma (ACC) is a rare malignancy with poor prognosis. Most ACC cases are hormonally functional. Commonly produced hormones are cortisol, followed by adrenal androgens. Aldosterone secretion is quite rare (< 2%) (1). Co-secretion of multiple hormones is further rare. Case Presentation: A 59 year old female presented with progressive worsening hypertension. Initial biochemical evaluation confirmed primary hyperaldosteronism. Her potassium was low at 2.9 mEq/L (N: 3.5-5.3 meq/L). Aldosterone level was elevated at 23 ng/dL (N: < or = 28 ng/mL), renin value was 0.90 ng/mL/h (N: 0.25-5.82 ng/mL/h). Aldosterone Renin Ratio was 25. CT abdomen with and without contrast showed 2 lesions within the right adrenal gland. The larger nodule was 3.7 x 2.7 x 4.9 cm with an absolute washout of 61%. A smaller nodule was 2.3x1.8 cm with an absolute washout of approximately 64%. Left adrenal gland was unremarkable. Further biochemical workup showed plasma catecholamines and metanephrines were normal. A random cortisol value was 22.8 mcg/dL (N: 3.0-16.0 mcg/dL) with a low ACTH level of 3.3 pg/mL (N: 7.2 - 63.3 pg/mL). Given suspicion for adrenal Cushing’s syndrome, we further obtained a 24 hour free urinary cortisol which was elevated at 84.1 mcg/24 h (N: 4-50 mcg/24 h). 8 am Cortisol after an overnight 1 mg Dexamethasone failed to suppress at 17.5 mcg/dL (n<1.8 mcg/dL). DHEAS level was low at 14.1 ug/dL (N: 29.4-220.5 ug/dL). The patient eventually underwent a right adrenalectomy. Post-operatively, her cortisol was suppressed at 1.9 mcg/dL (8 am ref range: 4-22 mcg/dL), and Hydrocortisone replacement dose was initiated. Surgical pathology report was consistent with adrenocortical carcinoma. The patient continues to follow-up with the endocrinology and oncology department for treatment. Conclusion: This case is particularly interesting given the co-secretion of both aldosterone and cortisol by an adrenocortical carcinoma which has been reported in only a few cases in literature. The case highlights the importance of completing a comprehensive biochemical workup pre-operatively in patients with suspicious adrenal mass. There should especially be a low threshold for initiating workup for cortisol hypersecretion as early intervention can help avoid an adrenal crisis in the post-operative period for such patients. A low DHEAS level should raise suspicion for cortisol hypersecretion in a patient with adrenal lesions. As ACTH is the primary stimulant of DHEA, the suppression of ACTH secretion in the setting of adrenal Cushing’s syndrome can contribute to a low DHEAS level. Reference 1.Else, T et al. Adrenocortical Carcinoma. Endocr Rev. 2014; 35(2):282-326.


PEDIATRICS ◽  
1964 ◽  
Vol 33 (2) ◽  
pp. 239-244
Author(s):  
J. Bar-Hay ◽  
A. Benderly ◽  
G. Rumney

A case of a nontumorous Cushing's syndrome in a 10-year-old girl is presented. The diagnosis was based on the clinical picture, the high levels of urinary steroids and plasma 17-OH corticosteroids, the results of ACTH stimulation tests, and finally by the histology of the left adrenal. Therapy with o,p'DDD had a dramatic effect on the patient's condition. The typical signs of Cushing's syndrome disappeared, and the girl is developing normally. The urinary steroids and the plasma 17-OH corticosteroids returned to normal levels. The ACTH stimulation tests gave results indicative of a normally functioning adrenal gland.


1985 ◽  
Vol 108 (2) ◽  
pp. 245-254 ◽  
Author(s):  
Naonori Mimou ◽  
Schun-ichi Sakato ◽  
Hajime Nakabayashi ◽  
Zenzo Saito ◽  
Ryoyu Takeda ◽  
...  

Abstract. The fifth case of Cushing's syndrome with bilateral adrenocortical tumours is described. By the hormonal dynamic studies both tumours have been shown to be autonomous in the secretion of cortisol. Histopathologically, both tumours were identified as benign adrenocortical adenomas without nodules, and the right one was a so-called black adenoma. A high concentration of cortisol was obtained from both tumour tissue extracts. The differential diagnosis of Cushing's syndrome due to bilateral adrenocortical adenomas from primary adrenocortical nodular dysplasia is briefly discussed.


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