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At least 307 records · Page 17Linked to original sources
PubMed2002

[Incidental adrenal histoplasmosis].

An adrenal mass found in the course of abdominal ecographic or computed tomography (CT) techniques performed for other reasons is a new diagnostic challenge. The patient in this case was asymptomatic and without previous illness. An ecographic study revealed an enlarged right adrenal gland, 66 by 33 mm. CT showed bilateral irregular enlargement of both adrenal glands. Nonadrenal malignancies and hyperfunctioning tumors were ruled out. A CT-guided biopsy was performed, and the histopathologic study was consistent with the diagnosis of histoplasmosis. The patient lived in an area endemic for this disease, and had daily contact with bird droppings. Histoplasmosis is a rare unsuspected cause of bilateral adrenal masses in the asymptomatic immunocompetent host.

Adrenal Gland Diseases↗
PubMed1987

Acute, massive, haemorrhagic adrenal necrosis experimentally produced by the Shwartzman mechanism in rabbits.

Acute and severe haemorrhagic necrosis of the adrenal was produced experimentally in rabbits by means of intravenous injection of endotoxin after pretreatment by adrenocorticotropic hormone (ACTH) administration. The change occurred mainly in the zona fasciculata of the adrenal cortex, and its pathology was quite similar to that of the Shwartzman reaction. Numerous microthrombi were found in and around the lesion, but no marked changes were seen in other parts of the body. Heparin administration was very effective in preventing the necrosis. The pathogenesis of this lesion was postulated to be a univisceral Shwartzman mechanism in the adrenal. This seems to be a good experimental model for massive haemorrhagic necrosis of the adrenal in man, for example in the Waterhouse-Friderichsen syndrome, the pathogenesis of which has been assumed to involve intravascular clotting. It is suggested that hyperfunction of the adrenal cortex caused by ACTH administration could be a preparative condition for the Shwartzman reaction.

Acute Disease↗
PubMed1998

Multiple endocrine neoplasias in a dog: corticotrophic tumour, bilateral adrenocortical tumours, and pheochromocytoma.

In a 10-year-old ovariohysterectomized standard Schnauzer, the finding of dexamethasone-resistant hypersecretion of cortisol, the results of computed tomography, and elevated plasma concentrations of ACTH suggested the presence of both adrenocortical tumour and pituitary-dependent hyperadrenocorticism. The dog made an uneventful recovery after bilateral adrenalectomy and remained in good health for 31/2 years with substitution for the induced hypoadrenocorticism. Then the enlarged pituitary caused neurological signs and eventually euthanasia was performed. The surgically excised right adrenal contained a well-circumscribed tumour of differentiated adrenocortical tissue and in the left adrenal there were two adrenocortical tumours and a pheochromocytoma. The unaffected parts of the adrenal cortices were well developed and without regressive transformation. At necropsy there were no metastatic lesions. The cells of the pituitary tumour were immunopositive for ACTH and had characteristics of malignancy. The present combination of corticotrophic tumour, adrenocortical tumours, and pheochromocytoma may be called 'multiple endocrine neoplasia' (MEN), but does not correspond to the inherited combinations of diseases known in humans as the MEN-1 and the MEN-2 syndromes. It is suggested that the co-existence of hyperadrenocorticism and pheochromocytoma may be related to the vascular supply of the adrenals. Some chromaffin cells of the adrenal medulla are directly exposed to cortical venous blood, and intra-adrenal cortisol is known to stimulate catecholamine synthesis and may promote adrenal medullary hyperplasia or neoplasia.

Adrenal Cortex Neoplasms↗
PubMed1983

Ruder syndrome. Clinical and pathologic correlation.

Ruder syndrome is an unusual varient of adrenal hyperfunction characterized clinically by debilitating osteopenia, and pathologically by bilateral micronodular adrenal hyperplasia. A unique case resembling Ruder syndrome is described in which the dominant pathologic feature was unilateral adrenal adenomatosis.

Adenoma↗
PubMed1965

Adrenocortical hyperfunction associated with bronchogenic carcinoma: report of five cases.

Five patients with bronchogenic carcinoma associated with adrenocortical hyperfunction are described. The clinical features, laboratory studies and autopsy findings are discussed and compared with previously reported cases. Four patients presented most of the typical features of this disorder as previously described, whereas the fifth was atypical in some respects. Typical features included: acute onset of adrenocortical hyperfunction in a middle-aged male, rapid downhill course, slight or absent physical signs of Cushing's syndrome, frequently impaired glucose tolerance, markedly elevated plasma and urinary 17-hydroxycorticosteroids not suppressed by exogenous steroids, absent diurnal variation of plasma corticoids, hypokalemic alkalosis with normal aldosterone excretion, and tumour histology of the oat cell variety. The adrenal glands of two patients were of normal or slightly increased weight, and mean 17-ketosteroid excretion values were normal in three; this contrasts with the marked increase in adrenal weight and 17-ketosteroid excretion in most reported cases.

17-Ketosteroids↗
PubMedDate not supplied

State-of-the-art adrenal imaging.

The adrenal gland is a common site of disease, and detection of adrenal masses has increased with the expanding use of cross-sectional imaging. Radiology is playing a critical role in not only the detection of adrenal abnormalities but in characterizing them as benign or malignant. The purpose of the article is to illustrate and describe the appropriate radiologic work-up for diseases affecting the adrenal gland. The work-up of a suspected hyperfunctioning adrenal mass (pheochromocytoma and aldosteronoma) should start with appropriate biochemical screening tests followed by thin-collimation computed tomography (CT). If results of CT are not diagnostic, magnetic resonance (MR) and nuclear medicine imaging examinations should be performed. CT has become the study of choice to differentiate a benign adenoma from a metastasis in the oncology patient. If the attenuation of the adrenal gland is over 10 HU at nonenhanced CT, contrast material-enhanced CT should be performed and washout calculated. Over 50% washout of contrast material on a 10-minute delayed CT scan is diagnostic of an adenoma. For adrenal lesions that are indeterminate at CT in the oncology patient, chemical shift MR imaging or adrenal biopsy should be performed. Certain features can be used by the radiologist to establish a definitive diagnosis for most adrenal masses (including carcinoma, infections, and hemorrhage) based on imaging findings alone.

Adrenal Gland Diseases↗