scholarly journals A CASE OF A TOTAL BILATERAL ADRENALECTOMY FOR CUSHING'S SYNDROME DUE TO BILATERAL NODULAR ADRENOCORTICAL HYPERPLASIA

1983 ◽  
Vol 44 (2) ◽  
pp. 183-190
Author(s):  
Masao KAWAMURA ◽  
Sei SHIRAHA ◽  
Takaaki SUDO ◽  
Masahiko TAKEMOTO ◽  
Kenji ISHIYAMA ◽  
...  
Keyword(s):  
Cushing’S Syndrome ◽  
Cushing's Syndrome ◽  
Bilateral Adrenalectomy ◽  
Adrenocortical Hyperplasia

OESTROGEN TREATMENT IN CUSHING'S SYNDROME

1969 ◽  
Vol 61 (2) ◽  
pp. 320-322
Author(s):  
N. Norman ◽  
J. H. Vogt
Keyword(s):  
Blood Plasma ◽  
Cushing’S Syndrome ◽  
Left Lung ◽  
Cushing's Syndrome ◽  
Bilateral Adrenalectomy ◽  
Normal Range ◽  
Oestrogen Treatment ◽  
Adrenocortical Hyperplasia ◽  
Striking Effect

ABSTRACT In 1963 we reported the case of a female, 32 years of age, with Cushing's syndrome due to bilateral adrenocortical hyperplasia, and successfully treated with large doses of ethinyloestradiol and subsequent total bilateral adrenalectomy. A round shadow which had been present in her left lung was still unchanged since first observed in 1956. A tumour consisting of closely packed cells, with partly granulated cytoplasm, and apparently nonmalignant, was removed from this lung in January 1967, 5 years after adrenalectomy. After this operation the pigmentation of the patient's skin was reduced. Six months after the operation, while on 5 mg prednisolone administered daily in the morning, her blood plasma contained ACTH in the lower normal range, and β-MSH was not significantly raised. If the tumour was ACTH producing, and was the cause of her Cushing's syndrome, this might explain the unusual and striking effect of the oestrogen treatment observed before adrenalectomy.

ACTH-lndependent Bilateral Macronodular Adrenocortical Hyperplasia Caused Cushing’s Syndrome

1997 ◽  
Vol 58 (4) ◽  
pp. 259-262 ◽  
Author(s):  
Akira Miyajima ◽  
Jun Nakashima ◽  
Masaaki Tachibana ◽  
Shim Baba ◽  
Kaoru Nakamura ◽  
...  
Keyword(s):  
Cushing’S Syndrome ◽  
Cushing's Syndrome ◽  
Adrenocortical Hyperplasia

ACTH-independent massive bilateral adrenal disease (AIMBAD): A subtype of Cushing's syndrome with major diagnostic and therapeutic implications

1994 ◽  
Vol 131 (1) ◽  
pp. 67-73 ◽  
Author(s):  
Steven A Lieberman ◽  
T Ross Eccleshall ◽  
David Feldman
Keyword(s):  
Cushing’S Syndrome ◽  
Adrenal Glands ◽  
Medical Center ◽  
Serum Cortisol ◽  
Cushing's Syndrome ◽  
Bilateral Adrenalectomy ◽  
Preoperative Treatment ◽  
Therapeutic Implications ◽  
Adrenal Imaging ◽  
Adrenal Disease

Lieberman SA, Eccleshall TR, Feldman D. ACTH-independent massive bilateral adrenal disease (AIMBAD): a subtype of Cushing's syndrome with major diagnostic and therapeutic implications. Eur J Endocrinol 1994:131:67–73. ISSN 0804–4643 A 49-year-old man with classic manifestations of Cushing's syndrome had undetectable levels of ACTH, lack of suppression of hypercortisolism with dexamethasone in doses of 2, 8, or 16 mg per day, bilaterally enlarged adrenal glands on MRI, and bilateral adrenal uptake of iodocholesterol. Preoperative treatment with ketoconazole lowered blood pressure and serum cortisol and produced symptoms of steroid withdrawal. Bilateral adrenalectomy revealed massively enlarged adrenal glands (left: 199 g, right: 93 g). Sequencing of the gene encoding the stimulatory G protein, Gsα, did not show either of two activating mutations previously reported in patients with McCune–Albright syndrome or acromegaly. Twenty-three previous cases of Cushing's syndrome due to ACTH-independent massive bilateral adrenal disease (AIMBAD) have been reported. AIMBAD may cause confusion in the differential diagnosis of Cushing's syndrome as endocrine testing suggests a unilateral, ACTHindependent process while adrenal imaging demonstrates bilateral abnormalities. Bilateral adrenalectomy is curative and appears to carry little risk of Nelson's syndrome. The pathogenesis of AIMBAD appears to be heterogeneous, as recent reports have demonstrated GIP-mediated hypercortisolism and familial AIMBAD. Transition from Cushing's disease to ACTH-independence is not supported by the available data. Future cases of AIMBAD should be investigated carefully to further elucidate the pathogenesis of this disorder. David Feldman, Division of Endocrinology, Dept. of Medicine, Room S-005, Stanford University Medical Center, Stanford, CA 94305, USA

scholarly journals Transsphenoidal Surgery for Cushing's Disease

1986 ◽  
Vol 79 (5) ◽  
pp. 262-269 ◽  
Author(s):  
R Fahlbusch ◽  
M Buchfelder ◽  
O A Müller
Keyword(s):  
Cushing’S Syndrome ◽  
Cushing’S Disease ◽  
Transsphenoidal Surgery ◽  
Dynamic Testing ◽  
Remission Rate ◽  
Cushing's Syndrome ◽  
Bilateral Adrenalectomy ◽  
Pituitary Function ◽  
Cushing's Disease ◽  
Mortality And Morbidity

A series of 101 patients with Cushing's disease underwent transsphenoidal surgery. Diagnosis was fundamentally based on dynamic testing, mainly on the dosage-dependent suppression of cortisol after dexamethasone. The effect of surgery was monitored by intraoperative ACTH measurements. In 96 out of 101 patients a microadenoma of the pituitary was identified and removed selectively. In 74% of patients there was a clinical and endocrinological remission of Cushing's disease. Four ‘operative failures’ after selective adenomectomy underwent hypophysectomy in a second operation and each remitted. Thus the overall remission rate was 77%. In general, bilateral adrenalectomy was performed in patients who had failed to remit after selective adenomectomy. Although there is a considerable mortality and morbidity in patients with Cushing's syndrome, complications attributed to surgery were low. Two patients died postoperatively. In general, an improvement of disturbed pituitary function was noted after selective adenomectomy.

scholarly journals Cortisol responsiveness to insulin-induced hypoglycemia in Cushing's syndrome with huge nodular adrenocortical hyperplasia.

1986 ◽  
Vol 33 (4) ◽  
pp. 479-487 ◽  
Author(s):  
KOZO HASHIMOTO ◽  
YOSHIRO KAWADA ◽  
KAZUHARU MURAKAMI ◽  
TERUHIKO HATTORI ◽  
SHUSO SUEMARU ◽  
...  
Keyword(s):  
Cushing’S Syndrome ◽  
Cushing's Syndrome ◽  
Adrenocortical Hyperplasia

Properties of partially purified thymidine kinase in adrenal tissue of hyperplasia, adenomatous hyperplasia, adenoma and carcinoma of patients with Cushing's syndrome.

1980 ◽  
Vol 93 (2) ◽  
pp. 208-215 ◽  
Author(s):  
Hajime Nawata ◽  
Ken-ichi Kato ◽  
Hiroshi Ibayashi
Keyword(s):  
Adrenal Gland ◽  
Thymidine Kinase ◽  
Cushing’S Syndrome ◽  
Adrenocortical Carcinoma ◽  
Catalytic Properties ◽  
Deae Cellulose ◽  
Cushing's Syndrome ◽  
Adrenocortical Adenoma ◽  
Adenomatous Hyperplasia ◽  
Adrenocortical Hyperplasia

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.

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