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At least 469 records · Page 26Linked to original sources
PubMed1984

[Cushing's disease caused by adrenocortical nodular hyperplasia--diagnosis and surgical treatment].

Six cases of Cushing's disease, in which perplex diagnostic problem was encountered, were reported. In the endocrinological examination two cases were not suppressed by a high dose of dexamethasone (8 mg), and the other four cases showed complicated clinical findings due to adrenocortical nodular hyperplasia. Among those four cases with adrenocortical nodular hyperplasia two of them were of functionally autonomic and showed different attitude in responding endocrine assay. When the serum cortisol is not suppressed by a high dose of dexamethasone, differential diagnosis from other causes, such as Cushing's syndrome due to adrenocortical macronodular hyperplasia, becomes quite important for surgical treatment. Usually plasma ACTH in the case of Cushing's disease is slightly increased over the normal range and, on the other hand, it is lower than normal value in the case of Cushing's syndrome due to autonomic adrenocortical nodular hyperplasia because of negative feed back phenomenon. However, in some cases of Cushing's disease plasma ACTH is within normal range or even lower than normal level, and, furthermore, it is not extremely unusual to find a case of adrenocortical macronodular hyperplasia with slightly increased plasma ACTH level over normal range. Those cases offer particularly complex problem in making diagnosis and therapeutic indication. According to our clinical experiences with those six cases, selective venous sampling is found quite useful in differentiating Cushing's disease from other causes and ACTH value in selective venous sampling from inferior petrosal vein is remarkably increased in the cases due to pituitary ACTH secreting adenoma. Cushing's disease with adrenocortical nodular hyperplasia reduces the ACTH value in the sampling to the lower normal range as the adrenocortical nodular hyperplasia progresses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMedDate not supplied

[Lipolysis in fatty tissue of patients with adrenohypercorticism].

Lipolytic activity was studied in subcutaneous and peripheric adipose tissue of patients with adrenohypercorticism (25 patients with Itsenko-Cushing disease and 4 patients with Cushing syndrome caused by corticosteroma of adrenal gland) and in 11 persons without this pathology. The lipolytic activity of the both adipose tissues in the patients with Itsenko-Cushing disease was similar to that of healthy persons and decreased in the patients with Cushing syndrome. The receptor-enzymatic system, responsible for lipolysis in adipose tissue, was not impaired in Itsenko-Cushing disease; differences found in lipolytic effects of corticotropin and somatotropin were caused by deteriorations in secretion of endogenous hormones in the disease. This system was inhibited in Cushing syndrome. Antilipolytic effect of insulin (especially in presence of glucose) was more distinct in subcutaneous adipose tissue of patients with Itsenko-Cushing disease as compared with controls.

Adipose Tissue↗
PubMed1983

[Modification of the renotrophic action of adrenal hypercorticism by nutritional factors in uninephrectomized rats].

In the rat renal compensatory hypertrophy (RCH) was enhanced by hyperadrenocorticism induced by the administration of a long acting ACTH at a dose of 18 Y/100 g body weight/d. for 7 d. after uninephrectomy (UN). In the present experiments we compared the differences delta between the weight, the content in protein, RNA and DNA of the left solitary kidney and the same determinations done on the right kidney excised at UN 7 d. earlier. The rats drank freely a isotonic solution of NaCl (G1) or KCl (G2) or glucose (G3, G4). The rats of group G1, G2 and G3 received a standard solid food; the G4 rats ate a K poor diet. About half of the animals were treated with ACTH. RCH occurred in all the rats even when they lost body weight. The gain in weight of the solitary kidney was enhanced in all the rats treated with ACTH but not in the G2 rats loaded with KCl. This renotropic action of hyperadrenocorticism was most prominent in the K depleted G4 rats. The protein/DNA ratio, a marker of cellular hypertrophy, was increased by hyperadrenocorticism in the G1 and D2 rats drinking respectively the NaCl or the KCl solutions. This ratio did not change in the ACTH treated G3 and G4 rats drinking the glucose solution suggesting that, in this experimental condition, cellular hyperplasia and hypertrophy occurred at the same extent. These experiments suggest that, in the uninephrectomized rat, the renotrophic action of ACTH is modulated by nutritional factors. The enhancement of RCH by ACTH may be related to hyperglycemia, hyperinsulinism or altered handling of Na and K by the nephron.

Adrenal Glands↗
PubMed1981

[Computerized tomography in adrenal diseases with excessive production of hormones].

In 41 patients with adrenal diseases and hormonal excess (pheochromocytoma n = 9, Cushing's syndrome n = 6, primary aldosteronism n = 26) computer tomography was performed for localization and classification of the adrenal lesion(s). In all patients diagnosis was confirmed by surgery. In all patients with pheochromocytoma a tumor was detected. 8 patients had unilateral adrenal pheochromocytoma, whereas in one female patient the pheochromocytoma was multilocular. 4 of the 6 patients with hypothalamic-pituitary Cushing's syndrome had enlargement of the adrenals. In the 26 patients with primary aldosteronism, computed tomography showed normal adrenal glands in 2 of the 17 patients with unilateral adenoma (with a diameter of 8 mm in both of the 2 patients) and in 6 of the 9 patients with bilateral hyperplasia. In the remaining patients adenoma or hyperplasia was detected. The results document that in patients with pheochromocytoma, with Cushing's syndrome, and in those with primary aldosteronism, computed tomography is a simple and valid method for localization and classification of the adrenal lesion(s). In primary aldosteronism with a normal adrenal computed tomography, however, differentiation between a small unilateral adrenal adenoma and bilateral adrenal hyperplasia remains problematic.

Adrenal Gland Neoplasms↗
PubMed1995

Ultrasonographic evaluation of the adrenal glands in dogs.

OBJECTIVE: To determine normal adrenal gland size by means of ultrasonography in dogs and to determine the value of ultrasonography in the diagnosis of pituitary-dependent hyperadrenocorticism (PDH) in dogs. DESIGN: Prospective observational study. ANIMALS: 62 dogs: 20 healthy dogs, 20 dogs with non-endocrine disease, and 22 dogs with untreated PDH. PROCEDURE: Length and maximum and minimum diameter of the adrenal glands were measured ultrasonographically. Multiple regression and correlation analyses were used to determine whether body weight, kidney length, aortic diameter, or age was related to adrenal gland size. Two-tailed t-tests and multiple linear regression analysis were used to compare values between groups. Sensitivity and specificity of using ultrasonographic measurement of adrenal gland size as a diagnostic test for PDH were determined. RESULTS: There was a significant linear relationship between adrenal gland length, but not maximum and minimum diameters, and body weight, aortic diameter, and kidney length in healthy dogs and in dogs with nonendocrine diseases. Length, maximum diameter, and minimum diameter of the right adrenal gland and maximum and minimum diameters of the left adrenal gland were significantly greater in dogs with PDH than in healthy dogs and dogs with nonendocrine diseases. As a diagnostic test for PDH, ultrasonographic measurement of maximum or minimum diameter of the left adrenal gland gave the best combination of sensitivity and specificity. For maximum diameter of the left adrenal gland, sensitivity was 77% and specificity was 80%. For minimum diameter of the left adrenal gland, sensitivity was 73% and specificity was 85%. CLINICAL IMPLICATION: Ultrasonography of the adrenal glands is a valuable diagnostic procedure in dogs suspected of having pituitary-dependent hyperadrenocorticism.

Adrenal Glands↗
PubMed1996

Evidence for heterogeneous etiologies of adrenal dysfunction in polycystic ovary syndrome.

OBJECTIVE: To examine the hypothesis that, in polycystic ovary syndrome (PCOS), ovarian steroids induce adrenal enzyme dysfunction or adrenal androgen hyperresponsiveness to ACTH. DESIGN: Prospective controlled clinical study. SETTING: Reproductive endocrinology unit of an academic medical center. PATIENTS: Twelve women with PCOS who had adrenal androgen excess were compared with five weight-matched ovulatory women. In half of the women with PCOS, prestudy screening was suggestive of mild 3 beta-hydroxysteroid dehydrogenase (HSD) deficiency. INTERVENTIONS: Basal and adrenal dynamic blood sampling before and after GnRH agonist (GnRH-a) administration for 6 months. MAIN OUTCOME MEASURES: Basal E2 and androgen levels as well as dexamethasone-suppressed, ACTH-stimulated 17 alpha-hydroxyprogesterone, 17 alpha-hydroxypregnenolone, and androgen levels before and after ovarian suppression. RESULTS: Although none of the subjects with PCOS proved to have mild 3 beta-HSD deficiency, the majority of them (58%) met the criteria for 17,20 lyase hyperactivity before and after GnRH-a therapy. As a group, the remaining subjects with PCOS exhibited an elevated DHEAS response to ACTH before GnRH-a treatment, which may have normalized after GnRH-a treatment. CONCLUSION: Adrenal androgen excess in PCOS may be heterogeneous in etiology, whereas 17,20 lyase hyperactivity appears to be an intrinsic adrenal disorder, adrenal androgen hyperresponsiveness to ACTH may be ovarian induced. Reliance on historical controls may lead to overdiagnosis of mild 3 beta-HSD deficiency.

17-alpha-Hydroxypregnenolone↗