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In a man of 48 who had suffered for a long time from a high arterial blood pressure, the autopsy revealed corticosteroma of the left and diffuse-nodular hyperplasia of the right adrenal glands. Both adrenals also had tumours of the sympathetic nervous system considered to be a gangliocytoneurilemmoma (angliocytic neurilemmoma) on the left and gangliocytoma on the right. The combination of morphological lesions, clinical data and laboratory examinations permit to state a combination of hypercorticism and hypercatecholaminemia.
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The adenylate cyclase activity and cyclic nucleotide content in excised human adrenal tumours (Icenko-Cushing syndrome) were determined. The experimental data were compared to those obtained for hyperplastic adrenals. All adrenal tumours under study revealed a decreased cAMP level, an increased cGMP level and a resulting decrease of the cAMP/cGMP ratio. In malignant adrenal tumours the adenylate cyclase activity was sharply increased in comparison with that in hyperplastic adrenals. In the majority of malignant tumours the adenylate cyclase response to ACTH was either altogether absent or sharply decreased. In benign adrenal tumours the basal activity of the enzyme was unchanged and the enzyme response to ACTH was essentially normal. The decrease of adenylate cyclase response to ACTH in malignant tumours is apparently not due to the impaired catalytic activity of the enzyme, since its response to stimulation by sodium fluoride remains unaffected. In some tumours (one malignant and two benign ones) a non-specific stimulation of adenylate cyclase by hormones, which are not natural activators of the enzyme was observed. It was assumed that these changes are due to the damage of hormonal receptors in adrenal tumours.
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A study was made of the effect of adrenalectomy (10 days after operation), administration of hydrocortisone to adrenalectomized rats (1 mg per 100 g bw a day for 10 days, starting from the 1st day after operation), and hydrocortisone-induced hypercorticoidism (5 mg per 100 g bw a day for 14 days) on the parameters of insulin receptors of liver plasma membranes. Depiction of the obtained data in the form of the Sketchard-Meites-Rose dependencies has shown that adrenalectomy increases the concentration and affinity of the receptors for the hormone. Administration of hydrocortisone to adrenalectomized rats reduces the concentration of the receptors, while hypercorticoidism decreases their affinity without affecting the concentration. The data obtained suggest an indirect action of glucocorticoids on the insulin receptors in liver plasma membranes.
An equally lowered insulin specific binding in the fatty cell plasmic membranes was found in patients with glucocorticoid, somatotropin and catecholamine hyperproduction during diabetes mellitus and/or its absence. This fall is due exclusively to a reduced amount of binding sites in patients with hypercorticism and acromegaly, accompanied or not by diabetes, and in persons with diabetes-aggravated pheochromocytoma. The above decrease is caused by a lowered binding site number and augmented negative cooperativity in patients suffering from pheochromocytoma without diabetes. The results obtained allow a conclusion that inhibited expression of insulin receptors in the presence of counter-insulin hormone hyperproduction promotes diabetes arising.
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The dynamics of five plasma steroids were studied by CPB and RIA in twenty patients with Cushing's syndrome of differing etiologies: pituitary induced adrenal hyperplasia (10), recurrence after adrenal surgery or pituitary irradiation (4), adrenal carcinoma (4) and adrenal adenoma (2). Basal mean values of plasma steroids, showed increase of cortisol in hyperplasia and cancer groups, increase of 17-hydroxyprogesterone (17-OH-P) in recurrence and cancer groups and decrease of testosterone in male patients. In hyperplasia, the changes in 11-desoxycortisol and 17-OH-P (respectively by CPB assay and RIA after LH-20-Sephadex separation) were the reverse of those for cortisol 2 h and 24 h after metyrapone administration. Adrenalectomy determined in all but one patients, significant decrease of cortisol and in male patients, parallel gradual increase of testosterone.
The value of the urine tests: free aldosterone, aldosterone-18-glucuronide, tetrahydroaldosterone 18-hydroxycorticosterone and 18-hydroxydeoxycorticosterone in distinguishing primary aldosteronism from essential hypertension was studied in patients with typical and atypical primary aldosteronism and in patients with essential hypertension. The discriminating function of the tetrahydroaldosterone determination was the best, followed by 18-hydroxycorticosterone, free aldosterone and aldosterone-18-glucuronide. The measurement of 18-hydroxydeoxycorticosterone was without distinguishing value. Three cases with hypertension, adrenal adenoma, elevated 18-hydroxycorticosterone but normal aldosterone values were observed. In longitudinal studies the excretions of aldosterone, aldosterone metabolites and possible precursors periodically varied independently of each other. Determinations of urine aldosterone, aldosterone metabolites, 18-hydroxycorticosterone and 18-hydroxydeoxycorticosterone were not applicable for differential diagnosis of the adenoma and hyperplasia forms of primary aldosteronism.