A fundamental defect of adrenocortical control in Cushing's disease.
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An initial step of experimental myocardium hyperfunction, caused by coarctation of the subphrenic part of abdominal aorta, was accompanied by a distinct increase in content of corticosterone in rat blood and adrenal glands. Administration of ethanolamine at a dose of 10 mg/kg decreased the hormone content under conditions of heart hyperfunction. The data obtained suggest that adrenal gland cortex was activated in response to the myocardium pathology as well as that content of corticosterone in blood and adrenal glands might be regulated by administration of ethanolamine.
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Of the various entities producing adrenal hyperfunction, nodular adrenal hyperplasia is rarely described, however, recent reports have established it as a distinct cause of Cushing's syndrome. Although the etiology of this disease remains uncertain, two distinct forms are recognised, namely: macronodular hyperplasia and micronodular dysplasia. Establishing the diagnosis preoperatively is difficult but essential to ensure the correct treatment is performed. Two cases of macronodular hyperplasia are reported herein followed by a review of the available literature on this subject.
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The authors analyze the results of the surgical treatment of patients with progressive essential hypertension (PEN). The treatment involved cryodestruction (adrenalectomy) of the right adrenal and autotransplantation of the left adrenal on the vascular peduncle into the transverse mesentery. Before the operation the data on water-salt homeostasis, central and cerebral hemodynamics and on the renin-angiotensin-aldosterone system attested to PEH. 1 to 3 years after the operation natriuresis was revealed (210% of the initial value), as were a decrease of the total peripheral vascular resistance, amelioration of the cerebral blood flow and peripheral blood aldosterone lowering from 246 +/- 17 to 90 +/- 14 sh/ml.
We reviewed the records of 13 patients with adrenal masses operated on over a ten-year period to clarify clinical characteristics of adrenal tumors. Tumors were found incidentally in seven of nine patients with primary adrenal tumors (78%); however, three of these seven patients (43%) proved to have shown symptoms related to adrenal hyperfunction when re-evaluated. Other adrenal tumors (metastatic in three patients and inflammatory in one) were found without any symptoms referable to the tumors. In nine of 13 patients (69%), tumors were discovered by computerized tomography (CT). All patients with primary tumors have been gotten free of disease postoperatively. In contrast, although all three patients with metastatic adrenal tumors underwent resection of all known disease tissue, they died of the recurrence of malignancies within 10 months. This study suggests that a number of functional adrenal tumors are possibly left undiagnosed until found incidentally, and that CT is the most powerful tool to detect adrenal tumors. Our data did not support surgical intervention in cases of metastatic adrenal tumors.
An aldosterone-producing adenoma is the cause of primary aldosteronism in about 85%. Unilateral adrenalectomy cures the potassium wasting and normalizes the blood-pressure in more than 70%, independently of the severity or duration of the hypertension. The location of an aldosteronoma is best obtained by computerized tomography and selective venous catheterization with determination of the aldosterone/cortisol ratio. When the biochemical studies suggest hyperplasia, medical treatment is recommended. It is, however, our policy to remove an adrenal gland with hyperplasia, when catheterization demonstrates unilateral hyperfunction. At operation a posterior or a flank approach is preferably used.
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A method of gas chromatography on glass capillary columns (g. c. c. c.) is presented which allows the determination of 26 urinary C19 and C21 steroid metabolites in one procedure. Hundredthirtyseven normal individuals of both sexes from 6 months through 32 years of age were studied regarding their urinary steroid patterns. These were compared to the excretion patterns of patients with congenital adrenal hyperplasia before and during treatment and of a child with virilizing adrenal carcinoma. From the results it is concluded that g. c. c. c. may be considered a valuable tool in the study of steroid production and metabolism.
Compensatory hypertrophy of the remaining gland in unilaterally adrenalectomized rats was investigated by morphometric techniques. It was observed that compensatory adrenal growth occurred in both dexamethasone-treated and hypophysectomized rats, receiving maintenance doses of ACTH. However, it was only half that found in intact animals. These results support the view that activation of the hypothalamo-hypophyseal axis is not the unique mechanism underlying adrenal compensatory hypertrophy in the rat.
Functional dynamic studies of the adrenal in vivo employing 131I-19-cholesterol were carried out as a further screening test, according to the method previously described (Pavonia and Magrini, 1977), on seven patients in whom hyperadrenocorticism was suspected on the basis of clinical symptoms. The data obtained in basal conditions, under ACTH stimulation, and under dexamethasone suppression, compared with each other and supported by the results of conventional examinations, demonstrate that the quantitative information provided by this radioisotope test is correlated with the functional state of each adrenal, thus confirming the potential value of the method for diagnostic purposes. The functional dynamic test proposed does not require a higher dose of tracer than morphologic studies and the radiation risk (approximately 2.5 rad to the ovaries or gonads) seems acceptable in adult subjects.
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