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.

ETHINYLOESTRADIOL IN THE PRE-OPERATIVE TREATMENT OF A SEVERE CASE OF CUSHING'S SYNDROME DUE TO ADRENOCORTICAL HYPERPLASIA

1963 ◽  
Vol 42 (2) ◽  
pp. 195-208 ◽  
Author(s):  
N. Norman ◽  
J. H. Vogt
Keyword(s):  
Cushing’S Syndrome ◽  
Clinical Remission ◽  
Severe Case ◽  
Cushing's Syndrome ◽  
Maximal Response ◽  
Oestrogen Treatment ◽  
Biochemical Characteristics ◽  
Adrenocortical Activity ◽  
Adrenocortical Hyperplasia ◽  
Response Capacity

ABSTRACT An extremely severe case of Cushing's syndrome due to adrenocortical hyperplasia is presented. The patient was treated with 0.5 mg of ethinyloestradiol four times daily for 106 days with short interruptions. The treatment caused a clinical remission with correction of the abnormal biochemical characteristics of the disease. The output of corticosteroids fell markedly, and the maximal response capacity of the adrenal cortex was reduced. Stressful stimuli continued to elicit an increase in corticosteroid excretion, and the pituitary-adrenal feed-back mechanism was preserved at the lower level of adrenocortical activity. It became evident, however, that the treatment in this patient did not provide a complete cure, and bilateral adrenalectomy was performed. Further trial with oestrogen treatment in this disease is recommended.

THE EXCRETION OF INDIVIDUAL 17-OXOSTEROIDS IN CUSHING'S SYNDROME

1961 ◽  
Vol 23 (2) ◽  
pp. 119-127 ◽  
Author(s):  
V. H. T. JAMES
Keyword(s):  
Urinary Excretion ◽  
Cushing’S Syndrome ◽  
Adrenal Adenoma ◽  
Cushing's Syndrome ◽  
High Ratio ◽  
Hepatic Enzymes ◽  
Normal Range ◽  
Adrenal Androgen ◽  
Adrenocortical Hyperplasia ◽  
Secretion Rates

SUMMARY The urinary excretion levels of individual 17-oxosteroids in eight patients with Cushing's syndrome have been determined quantitatively. Using these values approximate secretion rates of cortisol and 11β-hydroxyandrostenedione were calculated and found to be elevated above the normal range. The excretion values for 11-deoxy-17-oxosteroids were highly variable, being below normal, normal or elevated in different patients. The excretion patterns in adrenocortical hyperplasia and carcinoma showed no characteristic differences; however, the patients with adrenal adenoma showed steroid excretions which suggested that these tumours secreted cortisol almost exclusively, together with small quantities of 11β-hydroxyandrostenedione, and minimal amounts of 11-deoxy-C19-steroids. The majority of patients excreted aetiocholanolone and androsterone in an abnormally high ratio; this also occurred after administration of androst-4-ene-3:17-dione, and it is suggested that in Cushing's syndrome the hepatic enzymes preferentially reduce adrenal androgen to metabolites with the 5β configuration.

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

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

SKIN-FOLD THICKNESS IN NORMAL SUBJECTS AND IN PATIENTS WITH ACROMEGALY AND CUSHING'S SYNDROME

1969 ◽  
Vol 60 (4) ◽  
pp. 705-711 ◽  
Author(s):  
A. D. Wright ◽  
G. F. Joplin
Keyword(s):  
Cushing’S Syndrome ◽  
Normal Subjects ◽  
Cushing's Syndrome ◽  
Normal Range ◽  
Clinical Method ◽  
Skin Fold Thickness ◽  
Skin Fold ◽  
Normal Mean ◽  
The Mean ◽  
Age And Sex

ABSTRACT A simple clinical method of determining the skin-fold thickness on the dorsum of the hand has been described using the Harpendon spring-loaded caliper. A normal range for age and sex has been established in 258 normal subjects. The mean skin-fold thickness was greater in men than in women, and in both decreased with age, falling from 2.85 to 1.75 mm in men, and from 2.65 to 1.60 mm in women (aged 15–20 to 70–80). In 48 acromegalic patients, 71 % of the skin-fold measurements were abnormally thick. In 12 patients with Cushing's syndrome, although all measurements were below the normal mean, 42 % only were abnormally thin.

scholarly journals A ‘smart’ type of Cushing's syndrome

2007 ◽  
Vol 157 (6) ◽  
pp. 779-781 ◽  
Author(s):  
A J Razenberg ◽  
J W F Elte ◽  
A P Rietveld ◽  
H C T van Zaanen ◽  
M Castro Cabezas
Keyword(s):  
Body Weight ◽  
Cushing’S Syndrome ◽  
Ct Scanning ◽  
Cushing's Syndrome ◽  
Hydroxybutyric Acid ◽  
Normal Range ◽  
Free Cortisol ◽  
Suppression Test ◽  
Popular Party ◽  
Dexamethasone Suppression

Cushing's syndrome results from lengthy and inappropriate exposure to excessive concentrations of either endogenous or exogenous glucocorticoids. This case report describes a patient with a novel type of Cushing's syndrome due to the use of party drugs. A 35-year-old woman had gained 8 kg body weight in 5 months and complained of anxiety. She showed a Cushing-like appearance and mild hypertension (blood pressure, BP 150/95 mmHg). She reported daily use of increasing doses of γ-hydroxybutyric acid (GHB), a popular party drug. ACTH plasma levels were in the upper normal range (41 ng/l), with normal plasma cortisol (0.36 μmol/l). She showed an abnormal overnight 1 mg dexamethasone suppression test (cortisol 0.38 μmol/l). The urinary excretion of free cortisol in 24 h was also increased (0.47 μmol/24 h). CT scanning of the abdomen showed normal adrenals. After stopping GHB intake she lost 7 kg body weight and her BP normalized (BP 135/80 mmHg). GHB is a popular party drug in the Netherlands, but it is also used as a narcotic and for the treatment of narcolepsy. We hypothesize that GHB may bind to the pituitary gland γ-aminobutyric acid-B receptors leading to ACTH overproduction.

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

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