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At least 577 records · Page 32Linked to original sources
PubMed2001

[Adrenocortical macronodular hyperplasia with massive enlargement of the gland. A rare variant of autonomous hypercortisolism].

OBJECTIVE: To present a case of Cushing's syndrome due to massive adrenocortical macronodular hyperplasia that gave the gland the appearance of a pseudotumor. METHODS: In a review of the surgical pathology of the adrenal gland recently performed in our hospital, 82 adrenalectomy specimens obtained from 1978-1998 were found. Of these 82 surgical specimens, 44 (53.6%) were cortical pathologies and 10 of these (12.1%) were hyperplasia. There was only one with massive adrenocortical macronodular hyperplasia. A 53-year-old male, chronic alcoholic with cushingoid obesity and hypercortisolism is described. RESULTS: Ultrasound and CT assessment showed enlarged, asymmetrical adrenal glands and macronodules. The analytical and MRI study of the sella turcica showed primary adrenal hypercortisolism. Adrenalectomy of the dominant gland (the left adrenal whose activity was demonstrated on the 131Iodine scintiscan) was performed. The postoperative cortisol levels returned to normal and remain normal up to the present time, 18 months after surgery. The surgical specimen weighed 104 gms and was completely macronodular. CONCLUSIONS: Massive adrenocortical macronodular hyperplasia is a rare cause of pituitary-independent autonomous primary adrenal hypercortisolism. It is always bilateral. Adrenal weight is significantly increased (total weight of both adrenals 60-180 gms) and present yellow or golden, non-encapsulated nodules of a few millimeters to up to 4 cms, comprised of cells with scanty activity, therefore massive enlargement of the glands is necessary to produce Cushing's syndrome. The clinical, biochemical and surgical aspects can cause confusion and can be suggestive of an adrenocortical neoplasm. Treatment is by adrenalectomy.

Adrenal Cortex↗
PubMed1976

[Primary aldosteronism].

The syndrome of primary aldosteronism is caused either by an aldosterone-producing adenoma or by idiopathic bilateral adrenal hyperplasia. Hypokalemic hypertension is the leading symptome of the disease. Diagnosis is by the combination of abnormally high and non-suppressible aldosterone values with undetectable or low renin values unresponsive to postural changes or salt restriction. Patients with aldosterone-producing adenoma normally show a fall in plasma aldosterone in response to posture and ACTH-dependent circadian rhythm of aldosterone, whereas bilateral hyperplasia is characterized by postural increases in plasma aldosterone and an ACTH-independent diurnal aldosterone rhythm. These creteria serve to differentiate between adenoma and hyperplasia. An aldosterone-producing adenoma can be localized by veinography, determination of aldosterone concentration in both adrenal veins and by 131I-cholesterol scintigraphy. In our hands the determination of aldosterone in blood from both adrenal veins is the most efficient procedure. In interpreting the results, however, rhythmic and sudden changes in adrenal hormone secretion should be considered. In cases where no adrenal venous blood is obtained, 131I-cholesterol scintigraphy may be used to localize adenoma. In patients with aldosterone-producing adenomas unilateral adrenalectomy should be performed, whereas patients with idiopathic bilateral hyperplasia should receive antihypertensive therapy. As rare instances of primary aldosteronism, a case of aldosterone-producing carcinoma of the adrenal cortex and a case of presumably unilateral adrenal hyperplasia are reported.

Adenoma↗
PubMed1992

Comparison of mitotane treatment for adrenal tumor versus pituitary-dependent hyperadrenocorticism in dogs.

The purpose of this study was to determine the sensitivity of dogs with hyperadrenocorticism to treatment with the adrenocorticolytic agent mitotane. Specifically, we looked for differences in response to treatment using this drug in dogs with adrenocortical tumors (adrenal tumor hyperadrenocorticism, ATH) vs those with pituitary-dependent hyperadrenocorticism (PDH). For inclusion in this study, each dog must have had clinical signs, data base laboratory abnormalities, and endocrine screening test results consistent with the diagnosis of hyperadrenocorticism. Further, each dog had to have been treated for at least 6 months with mitotane and have histologic evidence for adrenocortical or pituitary neoplasia (all dogs were necropsied). Thirteen dogs with ATH (8 carcinomas, 5 adenomas) were identified. The ages and body weights of these 13 dogs were computer-matched to 13 dogs with PDH. All dogs were initially treated with approximately 50 mg of mitotane/kg/d of body weight. Reexaminations were performed after 7, 30, 90, and 180 days of treatment. Individual dosages varied widely after the initial 5 to 12 days of treatment. The mean (+/- SD) dose of mitotane (mg/kg/d) for the first 7 days of treatment was 47.5 +/- 9.4 for dogs with ATH vs 45.7 +/- 11.9 for dogs with PDH. The mean plasma cortisol concentrations 1 hour after ACTH administration at the 7-day recheck were significantly higher in dogs with ATH (502 +/- 386 nmol/L) than in dogs with PDH (88 +/- 94 nmol/L).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1961

Cushing's syndrome.

Sixteen cases of verified Cushing's syndrome, and twelve cases of probable Cushing's syndrome were reviewed and data on them were compared with various reports on Cushing's syndrome in the literature. The diagnosis hinges upon a high index of suspicion, and one or several of the major criteria may be lacking. Ultimate establishment of correct diagnosis should be based largely on the clinical features, although stimulation and suppression tests may help to confirm a clinical diagnosis. In well-established clinical cases, with borderline laboratory confirmation, exploration may be justified, especially if tests fail to identify a specific cause. In cases of adrenal cortical tumor, all pathological tissue should be removed if possible, with great care to support and stimulate the remaining atrophic adrenal gland during and following operation. In cases of bilateral adrenal cortical hyperplasia, the problem is one of how much to remove. At present most investigators advocate radical subtotal resection, leaving less than 10 per cent of one side.

Adrenal Cortex Neoplasms↗
PubMed1950

Adrenocortical tumors.

Hormonally active tumors of the adrenal cortex are either benign adenomas or adenocarcinomas. They may be located within the adrenal gland or as adrenal rests along the Wolffian tract. Hyperplastic cortical tissue without actual neoplastic formation is also capable of elaborating excessive cortical secretions.AT THE PRESENT STATE OF KNOWLEDGE, ANY ONE OR A COMBINATION OF THE FOLLOWING COMPOUNDS MAY BE ELABORATED IN A GIVEN CASE: the electrolytic, glucogenic, androgenic, or estrogenic corticosteroids. Whether or not Cushing's syndrome is primarily pituitary or adrenal in origin is still a matter of conjecture.

Adenoma↗
PubMed1990

[The diagnosis of adrenal cortical function in animals using hormone analysis].

This paper describes the use of hormone analysis in the diagnosis of adrenal cortex dysfunction in the dog, cat and horse. Analytical problems concerning the determination of corticosteroid levels are discussed and the pathology of adrenal dysfunction is briefly presented. The paper focuses on the problems in establishing physiological norms for adrenal function based on the established assays. Own experiences and other reported data are referred to.

Adrenal Cortex Diseases↗
PubMed1985

Effect of o,p'DDD therapy on endogenous ACTH concentrations in dogs with hypophysis-dependent hyperadrenocorticism.

The effect of o,p'DDD therapy on the endogenous plasma ACTH concentration was evaluated in 15 dogs with hypophysis-dependent hyperadrenocorticism. Adequate control of hyperadrenocorticism with o,p'DDD was based on the reduction of water consumption to within the normal range, disappearance of clinical signs of lethargy, weakness, alopecia, thin skin, or pendulous abdomen, and an increase in blood cortisol below the normal range after exogenous ACTH administration. Endogenous ACTH concentrations were determined for each dog after the disease was controlled and while they were given o,p'DDD on a maintenance schedule. Endogenous ACTH concentrations increased in 14 of 15 dogs after o,p'DDD therapy, indicating a lack of suppressive effects of o,p'DDD on hypophysis ACTH secreting cells.

Adrenal Cortex Function Tests↗