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Results for “Adrenocortical Hyperfunction”

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At least 1,063 records · Page 59Linked to original sources
PubMed1999

Concurrent pituitary and adrenal tumors in dogs with hyperadrenocorticism: 17 cases (1978-1995).

OBJECTIVE: To describe the clinicopathologic characteristics of dogs with hyperadrenocorticism and concurrent pituitary and adrenal tumors. DESIGN: Retrospective study. ANIMALS: 17 client-owned dogs. PROCEDURE: Signalment, response to treatment, and results of CBC, serum biochemical analysis, urinalysis, endocrine testing, and histologic examinations were obtained from medical records of dogs with hyperadrenocorticism and concurrent adrenal and chromophobe pituitary tumors. RESULTS: On the basis of results of adrenal function tests and histologic examination of tissue specimens collected during surgery and necropsy, concurrent pituitary and adrenal tumors were identified in 17 of approximately 1,500 dogs with hyperadrenocorticism. Twelve were neutered females, 5 were males (3 sexually intact, 2 neutered); and median age was 12 years (range, 7 to 16 years). Hyperadrenocorticism had been diagnosed by use of low-dose dexamethasone suppression tests and ACTH stimulation tests. During high-dose dexamethasone suppression testing of 16 dogs, serum cortisol concentrations remained high in 11 dogs but decreased in 5 dogs. Plasma concentrations of endogenous ACTH were either high or within the higher limits of the reference range (12/16 dogs), within the lower limits of the reference range (2/16), or low (2/16). Adrenal lesions identified by histologic examination included unilateral cortical adenoma with contralateral hyperplasia (10/17), bilateral cortical adenomas (4/17), and unilateral carcinoma with contralateral hyperplasia (3/17). Pituitary lesions included a chromophobe microadenoma (12/17), macroadenoma (4/17), and carcinoma (1/17). CLINICAL IMPLICATIONS: Pituitary and adrenal tumors can coexist in dogs with hyperadrenocorticism, resulting in a confusing mixture of test results that may complicate diagnosis and treatment of hyperadrenocorticism.

Adenoma↗
PubMed1976

Evaluation of a modified water-deprivation test for diagnosis of polyuric disorders in dogs.

A modified water-deprivation test was performed on 12 polyuric and 4 clinically normal dogs. Immediately after maximal urine osmolality had been achieved with water deprivation, antidiuretic hormone was injected to test further renal concentrating ability. The test provided accurate diagnosis of severe hypothalamic-neurohypophyseal diabetes insipidus in 3 dogs, partial diabetes insipidus in 2 dogs, and primary (psychogenic) polydipsia in 2 dogs. Five polyuric dogs with hyperadreno corticism had a response to the modified water-deprivation test similar to that of dogs with partial diabetes indipidus.

Adrenocortical Hyperfunction↗
PubMed1999

Evaluation of a low-dose synthetic adrenocorticotropic hormone stimulation test in clinically normal dogs and dogs with naturally developing hyperadrenocorticism.

OBJECTIVE: To determine whether low doses of synthetic ACTH could induce a maximal cortisol response in clinically normal dogs and to compare a low-dose ACTH stimulation protocol to a standard high-dose ACTH stimulation protocol in dogs with hyperadrenocorticism. DESIGN: Cohort study. ANIMALS: 6 clinically normal dogs and 7 dogs with hyperadrenocorticism. PROCEDURE: Each clinically normal dog was given 1 of 3 doses of cosyntropin (1, 5, or 10 micrograms/kg [0.45, 2.3, or 4.5 micrograms/lb] of body weight, i.v.) in random order at 2-week intervals. Samples for determination of plasma cortisol and ACTH concentrations were obtained before and 30, 60, 90, and 120 minutes after ACTH administration. Each dog with hyperadrenocorticism was given 2 doses of cosyntropin (5 micrograms/kg or 250 micrograms/dog) in random order at 2-week intervals. In these dogs, samples for determination of plasma cortisol concentrations were obtained before and 60 minutes after ACTH administration. RESULTS: In the clinically normal dogs, peak cortisol concentration and area under the plasma cortisol response curve did not differ significantly among the 3 doses. However, mean plasma cortisol concentration in dogs given 1 microgram/kg peaked at 60 minutes, whereas dogs given doses of 5 or 10 micrograms/kg had peak cortisol values at 90 minutes. In dogs with hyperadrenocorticism, significant differences were not detected between cortisol concentrations after administration of the low or high dose of cosyntropin. CLINICAL IMPLICATIONS: Administration of cosyntropin at a rate of 5 micrograms/kg resulted in maximal stimulation of the adrenal cortex in clinically normal dogs and dogs with hyperadrenocorticism.

Adrenal Cortex Function Tests↗
PubMed1976

[Transitory remission of hypercorticism by means of cyproheptadine in a patient with Cushing syndrome].

In patients with Cushing's syndrome of hypothalamischem Cushing-Syndrom wereden eine zentrale Störung und eine wichtige Rolle des Serotonins. Accordingly, in the present study a patient with hypothalamic-pituitary hypercorticism was treated with the seotonin antagonist cyproheptadine. Urinary free cortisol excretion was measured repeatedly before, during and after therapy. In addition, night-day rhythm of plasma cortisol was determined before and at the end of cyproheptadine medication. Within 2 months, therapy with 24 mg cyproheptadine resulted in a lowering of urinary cortisol excretion to normal values. Then, however, despite continuation of the therapy, urinary free cortisol excretion rates again rose to pathological levels. Due to the occurrence of severe psychosis, the drug had to be withdrawn. Before and under cyproheptadine no night-day rhythm of plasma cortisol could be observed.

Adrenalectomy↗
PubMedDate not supplied

[Adrenocortical tumors: mitotic index and nuclear size as criteria for differential diagnosis and prognosis].

A comparative study of the mitotic index (MI) and karyometric indices in 15 adrenocortical tumors with clinical syndrome of hypercorticism allowed to distinguish between adenomas and carcinomas. Carcinomas with hypercorticoidism symptoms have common features with inactive carcinomas but are different by lower expression of malignancy criteria (polymorphism, atypia, necrotic foci, capsule and vessel invasion), higher MI, increasing deficiency of cell division and larger nuclear size of tumor cells. Such tumors may be included into the prognostic group of risk.

Adenoma↗
PubMedDate not supplied

Primary aldosteronism and adrenal incidentaloma.

Adrenal incidentaloma are usually found during the assessment of non adrenal disease. In this paper we report the association between a bilateral adrenal hyperplasia and a macronodule of adrenal cortex (adrenal incidentaloma) which is a rare and misleading cause of primary aldosteronism. In the light of this association even if it is likely to remain rare and of those previously published, its existence is an additional reason for suggesting surgical treatment of primary aldosteronism only to patients who satisfy the following criteria: 1) satisfactory control with spironolactone; 2) poor spironolactone tolerance and poor control with other drugs; 3) accept to be operated on and the risk of a possible error.

Adrenal Cortex↗
PubMedDate not supplied

[Glucocorticoid-induced osteoporosis: recent findings].

The clinical features, pathogenesis and management of bone involvement in Cushing's syndrome are briefly reviewed. Personal data on bone mineral density and markers of bone turnover in Cushing's syndrome and adrenal incidentalomas are also reported. As long ago as 1932, Harvey Cushing recognized osteoporosis as a serious consequence of endogenous hypercortisolism. The introduction of cortisone in the therapy of autoimmune, rheumatic, allergic or dermatologic disorders was followed by several reports of detrimental effects on bone of patients who had undergone prolonged glucocorticoid treatment. Due to the rarity of Cushing's syndrome, most of the studies in the literature on glucocorticoid-induced osteoporosis refer to exogenous over-exposure to cortisone and its synthetic derivatives. Only a small number of works concern endogenous hypercortisolism, even if the characteristics of bone damage seem qualitatively the same. Finally, very few data are reported on the hypothetical detrimental effect on bone in the condition of the silent hypercortisolism of adrenal incidentalomas. Glucocorticoid-induced osteoporosis in Cushing's syndrome often results in vertebral fractures, and bone loss is more evident in trabecular than in cortical bone. Notwithstanding some distinctive features in osteoporosis induced by endogenous and exogenous glucocorticoid excess, the common eventual picture is notable bone damage that involves mainly the trabecular bone. Prompt and effective therapy is mandatory to reduce the risk of fractures. The present options include calcium and vitamin D supplementation, estrogen replacement therapy, bisphosphonates, either oral or parenteral. A novel approach to the clinical problem of glucocorticoid-induced osteoporosis might, in the future, be based on studies on selective glucocorticoid receptor modulators, a new class of synthetic glucocorticoids that exhibit significant anti-inflammatory and immunosuppressive activities, with reduced side effects on bone.

Adrenal Cortex Neoplasms↗
PubMed2000

Stress-level cortisol treatment impairs inhibitory control of behavior in monkeys.

Most studies of cortisol-induced cognitive impairments have focused on hippocampal-dependent memory. This study investigates a different aspect of cognition in a randomized placebo-controlled experiment with monkeys that were treated with cortisol according to a protocol that simulates a prolonged stress response. Young adult and older adult monkeys were assigned randomly to placebo or chronic treatment with cortisol in a 2 x 2 factorial design (n = 8 monkeys per condition). Inhibitory control of behavior was assessed with a test shown previously in primates to reflect prefrontal cortical dysfunction. Failure to inhibit a specific goal-directed response was evident more often in older adults. Treatment with cortisol increased this propensity in both older and young adult monkeys. Age-related differences in response inhibition were consistent across blocks of repeated test trials, but the treatment effects were clearly expressed only after prolonged exposure to cortisol. Aspects of performance that did not require inhibition were not altered by age or treatment with cortisol, which concurs with effects on response inhibition rather than nonspecific changes in behavior. These findings lend support to related reports that cortisol-induced disruptions in prefrontal dopamine neurotransmission may contribute to deficits in response inhibition and play a role in cognitive impairments associated with endogenous hypercortisolism in humans.

Adrenocortical Hyperfunction↗
PubMed1975

Bilateral adrenal medullary hyperplasia in multiple endocrine neoplasia, type 2: the precursor of bilateral pheochromocytoma.

An asymptomatic 12-year-old girl with multiple endocrine neoplasia, type 2, had high urinary levels of vanillylmandelic acid that suggested pheochromocytoma; she also had bilateral medullary thyroid carcinoma and hyperparathyroidism. Her mother and maternal aunt and uncle had bilateral pheochromocytoma (metastatic in the former two). Bilateral adrenalectomy was performed. Diffuse, non-nodular adrenal medullary hyperplasia was present. This hyperplasia was characterized by increased medullary mitotic activity, decreased corticomedullary ratio, increased total adrenal weight, and increased total catecholamine content (left adrenal). The results in this case suggest that diffuse hyperplasia of the adrenal medulla may be the precursor of pheochromocytoma in patients with this syndrome.

Adrenal Cortex↗