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At least 343 records · Page 19Linked to original sources
PubMedDate not supplied

MR imaging of the adrenals: correlation with computed tomography.

The purpose of this study was to evaluate the role of magnetic resonance (MR) imaging in adrenal disease based on correlative imaging with CT. Fifty lesions in 36 patients with a variety of adrenal diseases were evaluated, at 0.5 T using spin echo (SE) multislice short repetition time (TR) and SE multislice multiecho long TR sequences. It is concluded that MR is capable of identifying most adrenal abnormalities previously detected by CT. The results suggest that MR has a greater specificity for mass lesions and might be useful to differentiate nonfunctioning adenomas from functioning adenomas, metastasis, pheochromocytomas, cysts, and intraadrenal hemorrhage. Magnetic resonance imaging also has the potential to detect aldosteronomas by increased signal intensity in addition to contour distortion using long TR/echo time sequences. The ability to perform multiplanar imaging and the presence of superior contrast as compared with CT are useful for the assessment of origin and extension of large lesions and the detection of pheochromocytomas in complex cases. Considering MR's limitations, we believe that at present its major role in evaluation of adrenal disease should be complementary to CT.

Adenoma↗
PubMed1983

Cushing's syndrome with bilateral multinodular adrenal hyperplasia. Ultrastructural, histochemical, and immunohistochemical study.

An unusual case of Cushing's syndrome of a 59-year-old man with bilateral multinodular adrenal hyperplasia and microadenoma of the pituitary gland is presented. Failure to suppress plasma cortisol with large doses of dexamethasone may suggest autonomous growth of hyperplastic nodules of the adrenals, which were at first induced by prolonged stimuli of ACTH from the microadenoma of the pituitary gland. ACTH could not be detected in the microadenoma cells on paraffin sections, while Crooke's cells were strongly positive for ACTH. The interrelation between bilateral multinodular adrenal hyperplasia and pituitary microadenoma is discussed.

3-Hydroxysteroid Dehydrogenases↗
PubMedDate not supplied

Changes in ultrasonographic appearance of adrenal glands in dogs with pituitary-dependent hyperadrenocorticism treated with trilostane.

Trilostane, a 3beta-hydroxysteroid dehydrogenase inhibitor, has been used successfully over the last few years for the treatment of canine pituitary-dependent hyperadrenocorticism. In a prospective study of 19 dogs with pituitary-dependent hyperadrenocorticism, the adrenal glands were measured before and at least 6 months after initiation of trilostane therapy. Right adrenal gland length and caudal pole thickness and left adrenal gland caudal pole thickness increased significantly (p < or = 0.05); there was no significant change in left adrenal gland length. Enlargement of adrenal glands during trilostane therapy may occur as a result of suppression of the negative feedback mechanism affecting cortisol production.

3-Hydroxysteroid Dehydrogenases↗
PubMed2001

Use of endogenous ACTH concentration and adrenal ultrasonography to distinguish the cause of canine hyperadrenocorticism.

Twenty-nine dogs were diagnosed with hyperadrenocorticism (HAC). A single determination of endogenous plasma adrenocorticotropic hormone (ACTH) and adrenal ultrasonography were used in a prospective study to differentiate between pituitary-dependent HAC (PDH) and adrenal-dependent HAC (ADH). In 27 out of the 29 dogs (93 per cent), both endogenous plasma ACTH concentrations and adrenal ultrasonography indicated the same cause of HAC. Twenty-one of the 29 cases (72 per cent) were shown to be pituitary-dependent; all had plasma ACTH concentrations of greater than 28 pg/ml (reference range 13 to 46 pg/ml) and both adrenal glands were ultrasonographically of similar size and of normal shape. All 21 cases responded well to mitotane therapy. Six cases (21 per cent) were shown to be adrenal-dependent; all had plasma ACTH concentrations below the limit of the assay (<5 pg/ml) and the presence of an adrenal mass on ultrasonography. The sensitivity and specificity of adrenal ultrasonography and endogenous ACTH determinations to identify the cause of HAC were demonstrated to be 100 per cent and 95 per cent, respectively, for ADH. These discriminatory tests are more accurate than published figures for dexamethasone suppression testing.

Adrenal Glands↗
PubMed1982

Functioning adrenocortical tumour in a dog.

Naturally-occurring hyperadrenocorticism was diagnosed in an 11-year-old female Dachshund with signs of polydipsia, polyuria, pendulous abdomen, weakness, depression and lethargy, and laboratory test abnormalities comprising lymphocytopaenia, eosinopaenia, hypercholesterolaemia and increased plasma alkaline phosphatase concentration. While awaiting hormonal test results, an adrenocorticolytic drug (o,p'-DDD) was administered for 14 days, during which the patient deteriorated. Hormonal assays suggested a functioning adrenocortical tumour, but the poor condition of the patient precluded adrenalectomy. An adrenocortical carcinoma with hepatic metastases was found at necropsy.

Adrenal Cortex Neoplasms↗
PubMedDate not supplied

Ultrasonographic characteristics of the adrenal glands in dogs with pituitary-dependent hyperadrenocorticism: comparison with normal dogs.

Ultrasonographic evaluation of the adrenal glands was performed in 10 dogs with pituitary-dependent hyperadrenocorticism (PDH) and in 10 age- and weight-matched healthy control dogs. Thickness, shape, and echogenicity were determined for each adrenal gland. Adrenal thickness in dogs with PDH (median, 10 mm-left; 8.5 mm-right) was significantly greater than thickness in control dogs (median, 6 mm-left; 6 mm-right). Other ultrasonographic characteristics associated with PDH included bilaterally symmetrical adrenomegaly and maintenance of normal adrenal shape. Adrenal echogenicity was homogeneous and less than that of the adjacent renal cortex in 8 of 10 dogs with PDH and in 10 of 10 control dogs. Heterogenous echogenicity was present in 2 of 10 dogs with PDH, and was associated with nodular cortical hyperplasia in one of those dogs. Results of this study confirm the difference in sonographic appearance between PDH-induced bilateral cortical hyperplasia and functional adrenocortical neoplasia, and show a difference in sonographically determined adrenal size between healthy dogs and dogs with PDH.

Adrenal Glands↗
PubMed1995

Use of ACTH stimulation tests to monitor the treatment of canine hyperadrenocorticism.

The case histories of 60 dogs with hyperadrenocorticism were reviewed. Fifty-four of the dogs were treated with mitotane at a mean daily dose rate of 48.8 mg/kg (range 25.6 to 84 mg/kg) for between four and 21 days. The mean weekly maintenance dose of mitotane was 48.8 mg/kg. An adrenocorticotrophic hormone (ACTH) stimulation test was performed before the treatment began, and in 30 cases at the end of the induction course, and the response to ACTH was measured at regular intervals thereafter. Nine of the treated dogs developed complete hypoadrenocorticism during treatment and required permanent mineralocorticoid replacement therapy. Twelve of the dogs had normal responses to an ACTH stimulation test before treatment, and the diagnosis of hyperadrenocorticism was based on the result of a low-dose dexamethasone suppression test. These 12 dogs had consistently lower cortisol levels before and after stimulation with ACTH and four of them developed complete hypoadrenocorticism. In general the clinical signs were well controlled when the cortisol levels were less than 105 nmol/litre before and after the stimulation test. Dogs in which the clinical signs recurred had cortisol levels between 210 and 580 nmol/litre after the test, a level which is within the normal pretreatment range. Twenty-seven of the treated dogs died and six of these deaths were attributable directly to the disease or therapy. The median survival time of the 54 treated dogs was 30 months; eight dogs died during the first 16 weeks of treatment, and the dogs which survived this period had a median survival time of 39 months (mean 50 months).

Adrenal Cortex Function Tests↗
PubMed2000

Adrenocorticotropin-independent macronodular adrenal hyperplasia: an uncommon cause of primary adrenal hypercortisolism.

PURPOSE: To describe the imaging findings in the adrenal glands of 12 patients with adrenocorticotropin (ACTH)-independent macronodular adrenocortical hyperplasia (AIMAH). MATERIALS AND METHODS: Computed tomographic (CT) and magnetic resonance (MR) imaging findings in the adrenal glands were reviewed retrospectively in 12 patients (three men, nine women) with ACTH-independent Cushing syndrome and with bilateral nonpigmented multinodular adrenal hyperplasia. The results of pituitary MR imaging, adrenal scintigraphy, and petrosal sampling were available in nine, five, and six patients, respectively. Eleven patients underwent bilateral and one patient underwent unilateral adrenalectomy. RESULTS: Eleven patients had enlarged multinodular adrenal glands: Nodules were 0.1-5.5 cm. The combined weight of both adrenal specimens for the 11 bilateral adrenalectomy specimens was 28-297 g, with a mean weight of 122 g. Glands were hypointense compared with the liver on T1-weighted images and were hyperintense on T2-weighted images. Pituitary MR imaging findings were negative in nine of nine patients. Iodomethylnorcholesterol scintigraphy showed bilateral uptake in four of five patients. Petrosal sinus sampling revealed no petrosal-to-peripheral ACTH gradients before corticotropin-releasing hormone (CRH) stimulation in six of six patients, but three patients had gradients after CRH stimulation. After undergoing bilateral or unilateral adrenalectomy, all patients were cured. CONCLUSION: AIMAH is a rare cause of ACTH-independent Cushing syndrome, with characteristic CT findings of massively enlarged multinodular adrenal glands. Bilateral adrenalectomy is indicated on the basis of clinical and CT findings.

Adrenal Glands↗
PubMed1991

Inappropriate elevation of the aldosterone/plasma renin activity ratio in hypertensive patients with increases of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone: a subtype of essential hypertension?

Among 436 patients with hypertension unrelated to any renal lesion, renovascular damage, pheochromocytoma, Cushing's syndrome or hyperthyroidism, 15 patients had low plasma renin activity (PRA) and elevated plasma aldosterone concentrations in the upright position and resultant high aldosterone/PRA ratios: 8 with aldosterone-producing adenoma (APA; group 1) and 7 with idiopathic hyperaldosteronism (IHA; group 2). Thirty-nine patients had suppressed PRA in the presence of normal plasma aldosterone levels and moderately elevated aldosterone/PRA ratios (group 3). Thirty of them had elevated plasma 11-deoxycorticosterone (DOC) and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) concentrations (group 3a) and 9 of them had normal levels of those mineralocorticoids (group 3b). The rest of them (382 patients) had low aldosterone/PRA ratios (group 4). Adrenal scintigraphy with dexamethasone pretreatment revealed [13I]-cholesterol accumulation not only in patients with APA (unilateral) or IHA (bilateral), but also in patients of group 3a (bilateral). In patients in groups 3a and 3b adrenal size (especially thickness), as measured by computed tomography (CT scan), was enlarged, as in patients with IHA (group 2), and was significantly greater than in patients of group 4 (p less than 0.001). Spironolactone reduced blood pressure in all tested patients of group 3a, and the removal of adrenal tumor or hyperplastic tissue normalized blood pressure in patients of groups 1, 2 and 3a. Excised adrenal glands exhibited cortical hyperplasia with or without nodular hyperplasia in patients of group 3a. Good agreement was found between the actual size of the excised tissue and the measurement obtained by CT scan. Since beta-endorphin and beta-lipotropin were depressed in patients of group 3a, it is suggested that an unknown pituitary substance stimulates the adrenal cortex to release too large amounts of DOC and 18-OH-DOC and inappropriate secretion of aldosterone.

18-Hydroxydesoxycorticosterone↗
PubMed1976

Arterial lesions in repeatedly bred spontaneously hypertensive rats.

Repeatedly bred male and female rats of many strains develop hyperglycemia, hyperlipidemia, hypertension, and arteriosclerosis spontaneously. The intensity of their arterial disease and related metabolic derangements appear to be related to their reproductive activity. Repeatedly bred spontaneously hypertensive rats (SHR) were found to have severe hypertension, hyperglycemia, hyperlipidemia, elevated creatine phosphokinase (CPK), serum glutamic oxaloacetic and glutamic pyruvic transaminase (SGOT, SGPT), and lactic dehydrogenase (LDH), as well as high circulating corticosterone levels. Despite these atherogenic metabolic derangements and their severe hypertension, the breeder SHR did not develop the severe, generalized arteriosclerosis found in other strains of breeder rats. Instead, the arterial lesions, consisting of intimal hyalinization and fibrosis, medial hypertrophy, and occlusion of the lumen, were found only in male breeder SHR and were confined to the intratubular arteries of the testes. It is suggested that the severe hypertension, genetic influences, or differences in hypothalamic-pituitary-adrenal-gonadal function in breeder SHR may not have been conducive to the development of arteriosclerosis in this particular strain of rats.

Adrenal Glands↗
PubMed1977

Urinary free 11-hydroxycorticosteroid/creatinine ratios in early morning urine samples as an index of adrenal function.

Urinary free 11-hydroxycorticosteroid/creatinine ratios were determined in early morning urine samples from 113 females (age range 20-45 years) and 65 males (age range 22-45 years). Basal values in normal subjects fluctuated between 5 and 55 mumol/mol creatinine. In four patients in whom Cushing's syndrome was diagnosed, urinary free 11-hydroxycorticosteroid/creatinine ratios were greater than 85 mumol/mol creatinine. Administration of dexamethasone (0.5 mg/q.i.d.) to nine normal laboratory staff for two days resulted in a suppression of the urinary free 11-hydroxycorticosteroid/creatinine ratio to less than 50% of the mean basal value in all cases. This degree of suppression did not occur in two cases of Cushing's syndrome due to adrenal tumours.

11-Hydroxycorticosteroids↗