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Results for “Adrenocortical Hyperfunction”

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PubMedDate not supplied

[Magnetic resonance tomography of the adrenals in the diagnosis of total and partial hypercorticism].

The paper is devoted to the use of a new method of nuclear magnetic resonance tomography (MR tomography) in the diagnosis of diseases of the adrenal glands developing with the syndrome of total and partial hypercorticism. A MR tomograph with resistive magnet (0.234 T) was employed. Altogether 25 patients were examined (21 with Itsenko-Cushing disease of various degrees of severity, 2 patients with Itsenko-Cushing syndrome and 2 patients with aldosteronoma). MR tomography was shown to possess a high informative value permitting the assessment of a type of adrenal changes without irradiation of a patient. In combination with routine methods of examination (hormonal investigation, retropneumoperitoneum, x-ray computerized tomography) MR tomography makes it possible to improve considerably the diagnosis of Itsenko-Cushing disease and to specify tumor sizes and tumor growth type.

11-Hydroxycorticosteroids↗
PubMedDate not supplied

[The function of the hypothalamo-hypophyseal-adrenal system in Itsenko-Cushing syndrome].

Altogether 28 patients with adrenocortical tumors (corticosteromas and corticoandrosteromas) were examined using a radioimmunoassay to determine the concentration of corticotropin, cortisol, blood cyclic nucleotides, the circadian rhythm and time course of corticotropin and cortisol levels against a background of insulin hypoglycemia. In patients with Itsenko-Cushing's syndrome the basel level of cortisol was notably raised, that of corticotropin was sharply decreased. The circadian rhythm of the levels of corticotropin and cortisol was disturbed, a response of the hypophyseal-adrenal system to a stressor was suppressed. The concentration of blood cyclic nucleotides was increased, and these changes were dependent on the nature of adrenal pathology.

Adrenal Cortex Neoplasms↗
PubMed1989

[An assay for aldosterone precursors: a tool for clinical diagnosis and adrenal physiopathology].

After their contribution to the study of 18 hydroxycorticosterone as an intermediate in aldosterone biosynthesis the authors present here a new series of assays for the measurement of plasma aldosterone precursors as a pertinent tool in the extensive study and clinical evaluation of the mineralocorticoid function of the adrenal. These radioimmunoassays must be undertaken under strict technical conditions: time of blood withdrawal and also posture. Their use is irrelevant in any other clinical feature but the salt loss syndrome and hyper mineralo-corticism together with or without high plasma aldosterone.

18-Hydroxycorticosterone↗
PubMed1989

[Hyperandrogenism originating from the adrenal gland. Current observations on a clinical case].

Recent reported data on hyperandrogenisms of suprarenal origin are presented and the case of a 26-year-old woman suffering from hirsutism and secondary amenorrhoea reported. Preoperative hormonal measurement showed very high Dehydroepiandrosterone (DHEA) levels (8,000 ng/ml) and a less dramatic increase in Androstenedione (A) and Testosterone (T), of 3.5 and 1.17 ng/ml respectively. Androgens were uniformly increased following administration of ACTH (250 micrograms for 3h for 2 days) and inhibited by intake of Desamethazone (8 mg/die for 3 days per os). ACTH values were low and failed to increase after insulin-induced hypoglycaemic stimulus. Pelvic echography and laparoscopy showed normal ovaries. A suprarenal scan revealed slight bilateral hyperplasia with irregular trace distribution on the left. CT showed a slight anomaly of the left gland which appeared spherical with convex margins. Unilateral suprarenectomy was carried out and the controlateral gland explored. The removed gland presented a histological picture of "micronodular focal hyperplasia". Treatment was begun with Prednisone and temporary remission of the clinical and biochemical pictures was achieved but one year after the operation androgen concentration was found again to be abnormally increased. The final diagnosis was "Bilateral suprarenal hyperplasia" with initial unilateral involvement. To conclude, this particular hyperandrogenism with ACTH levels at the lower limits of normal and with underlying primary suprarenal hyperplasia may be included among the better known suprarenal hyperplasia syndromes responsible for the Cushing and Conn syndromes.

Adrenal Glands↗
PubMed1989

Primary pigmented nodular adrenocortical disease. A light and electron microscopic study of eight cases.

Primary pigmented nodular adrenocortical disease (PPNAD) is a rare cause of Cushing's syndrome, which is adrenocorticotropic hormone-independent and involves both adrenal glands. The characteristic pathological features include multiple pigmented cortical nodules and atrophy of the internodular cortex. The adrenal size ranges from small to normal or slightly enlarged. Review of the gross, light microscopic, and ultrastructural features of eight cases seen at the National Institutes of Health revealed several very unusual findings. We observed the following in our patients: macronodules up to 3.0 cm; microscopic foci of necrosis; mitoses; cortical hyperplasia rather than internodular atrophy; focal confluence of nodules giving a diffuse pattern of cortical involvement, and a focal trabecular growth pattern. The nodules were composed primarily of eosinophilic, lipid-poor cells similar to those of the zona reticularis. However, lipid-rich cells similar to those of the zona fasciculata were also demonstrated in the nodules by both light and electron microscopy. This suggests that the adrenal cortical nodules of PPNAD may be derived from not only the zona reticularis, but also the zona fasciculata.

Adolescent↗
PubMed1989

[Diagnosis of extrarenal, secondary forms of hypertension].

The secondary, nonrenal forms of hypertension principally include pheochromocytoma, hyperaldosteronism, hypercortisolism, iatrogenic hypertension following medication, and hypertension related to overindulgence. Other very rare secondary forms of hypertension will not be considered here. Pheochromocytoma is the most dangerous of all the forms of hypertension. Diagnosis of the underlying cause of endocrine-derived hypertension is achieved by hormone analysis. Due to the small size of endocrine tumors, their exact localization can often not be established by sonography, such that CT or MR are the examinations of choice. Scintigrams are only necessary in special cases. For tumor localization in Cushing's disease, hormone measurements from the petrosal sinus are occasionally required. Medication, and above all, continual alcohol consumption, play an increasing role in the etiology of hypertension.

Adrenal Gland Neoplasms↗
PubMed1978

Multi-column chromatography of urinary steriods and adrenocortical dysfunction.

The potential of the multi-column assay for urinary neutral steroids in work with samples from patients with adrenocortical pathology is demonstrated through analyses performed on urine samples from Cushing and congenital adrenal hyperplasia cases, after modification of the routine methodology to include the quantitation of additional steroids of particular importance for pathological samples.

Adrenocortical Hyperfunction↗
PubMed1989

Pituitary macroadenomas and macroadenocarcinomas in dogs treated with mitotane for pituitary-dependent hyperadrenocorticism: 13 cases (1981-1986).

Pituitary macroadenoma/macroadenocarcinoma (PMA; tumor size greater than or equal to 1 cm in diameter) was diagnosed in 13 dogs after 0.5 to 24 months of mitotane treatment for pituitary-dependent hyperadrenocorticism (PDH). The diagnosis of PDH was established on the basis of results of common tests of the pituitary-adrenocortical axis in conjunction with results of x-ray computed tomography or necropsy. Initial clinical findings and clinicopathologic test results were typical of PDH. Signs referable to the CNS developed in 7 of the 13 dogs. The most common neurologic sign was stupor. Pituitary macroadenoma/macroadenocarcinoma was an unexpected finding in the other 6 dogs, because none had clinical signs of disease referable to the CNS at the time that pituitary tumor was documented. In the 13 dogs, strong correlation existed between tumor volume, compression/invasion of the surrounding nervous tissue, and development of neurologic signs, ie, neurologic signs were most frequently associated with larger tumors. The size of the tumor, however, was not always an indication of whether neurologic signs would be observed. All 7 dogs with neurologic signs were euthanatized because of the deleterious effects of the PMA. Of the 6 dogs without neurologic signs, 2 died of unrelated cause. Alternative treatment (ie, hypophysectomy, 60Co-teletherapy) was used successfully in 2 other dogs. Alternative treatment would seem indicated if PMA is documented in a dog with PDH. However, identification of PMA is dependent on evaluation of x-ray computed tomographic images. Signalment, history, physical examination, and alterations in routine clinicopathologic findings in these 13 dogs of our study were similar to previously reported findings in dogs with PDH but apparently without large pituitary tumors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1989

[Clinical observation on hypercortisolism treated with amino-glutethimide].

We reported the clinical results in 13 cases of hypercortisolism treated with amino-glutethimide (AG), which was developed by Tiantsin Research Institute of Medical Industry. Of the thirteen cases nine were confirmed by surgery and histology, and the others were diagnosed clinically. Clinical improvements have been achieved in ten of the thirteen cases over a therapeutic course of 8 to 12 wk with a daily dosage of 1.0 to 2.0 g of AG. Plasma and urinary corticosteroids, as well as plasma testosterone levels were significantly decreased after one-month treatment followed, however, by somewhat return and fluctuation. The high levels of blood glucose and serum insulin were declined after therapy consistent with the decrement of corticoids. Serum potassium levels in hypokalemic patients returned to normal after one month of therapy. Radial bone mineral contents in patients with low bone density returned or closed to normal after three-month treatment. The main side effects of AG are anorexia, nausea, drowsy, tierdness, skin rashes, etc, which are mild and transient. Adrenal hypofunction was seen in one case after treatment.

Adolescent↗
PubMed1988

Hyperadrenocorticism in cats: seven cases (1978-1987).

Hyperadrenocorticism was diagnosed in 7 cats with concurrent diabetes mellitus. Four cats had pituitary adenoma with bilateral adrenocortical hyperplasia, 1 cat had pituitary carcinoma with bilateral adrenocortical hyperplasia, 1 cat had adrenocortical carcinoma, and 1 cat had adrenocortical adenoma of the left adrenal gland. One year later, adrenocortical adenoma involving the right adrenal gland also was diagnosed in this cat. Clinical signs included polyuria and polydipsia (n = 7), development of pot-bellied appearance (n = 5), dermatologic alterations (n = 5), lethargy (n = 3), weight loss (n = 3), dyspnea/panting (n = 2), and recurrent bacterial infections (n = 2). In 6 cats, the diagnosis of hyperadrenocorticism was established before death on the basis of results of the ACTH stimulation test (n = 3) and the dexamethasone screening test (n = 5). Pituitary-dependent hyperadrenocorticism was differentiated from adrenocortical neoplasia on the basis of results of the dexamethasone suppression test (n = 4), endogenous ACTH concentration (n = 3), results of abdominal radiography and ultrasonography (n = 3), and exploratory celiotomy (n = 1). Four cats died or were euthanatized without treatment attempts. Treatment with mitotane followed by 60Co teletherapy was ineffective in one cat with pituitary adenoma. One cat with pituitary carcinoma died one week after bilateral adrenalectomy. Bilateral adrenocortical adenomas were removed surgically in the affected cat.

Adenoma↗