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.

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.

METABOLIC CHANGES RESULTING FROM 90YT IRRADIATION OF THE PITUITARY IN A PATIENT WITH CUSHING'S SYNDROME

1959 ◽  
Vol 19 (4) ◽  
pp. 366-376 ◽  
Author(s):  
R. V. BROOKS ◽  
R. R. McSWINEY ◽  
D. MATTINGLY ◽  
F. T. G. PRUNTY
Keyword(s):  
Cushing’S Syndrome ◽  
Plasma Corticosterone ◽  
Cushing's Syndrome ◽  
The Body ◽  
Fatty Tissue ◽  
Thyroid Activity ◽  
Adrenocortical Activity ◽  
Adrenocortical Hyperplasia ◽  
Positive Urine ◽  
Low Levels

SUMMARY A detailed metabolic study has been made of a 48-year-old woman with Cushing's syndrome associated with presumed adrenocortical hyperplasia. The patient was shown to be secreting excessive amounts of cortisol. The urine contained low levels of aldosterone, but there was a hypokalaemic alkalosis. Plasma corticosterone was not raised. Destruction of the pituitary by insertion of 90Yt seeds produced clinical improvement and amelioration of hypertension. The adrenocortical activity promptly subsided to below normal levels. Negative nitrogen and calcium balances became positive, urine calcium fell and hyperglycaemia disappeared. The condition of hypokalaemic alkalosis was restored to normal and aldosterone excretion increased. The decline in thyroid activity was slower than that of adrenocortical activity. Calculation of the distribution of muscular and fatty tissue in the body showed that treatment produced an improvement. The significance of some of these changes is discussed.

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

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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