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At least 505 records · Page 28Linked to original sources
PubMed1983

[Malignant adrenal cortex tumors responsible for primary hyperaldosteronism and biological hypercorticism. Remarks apropos of 2 surgically-treated cases].

Two cases of malignant adrenal cortex tumors revealed by primary hyperaldosteronism with hypertension, and associated with a biological hypercortisonism, are reported. Diagnosis of this very rare affection depends on the finding of marked biological hyperaldosteronism associated with a large adrenal tumor. The outcome appears to be rapidly fatal for tumors exceeding 5 cm in diameter and associated with lymph node invasion. This raises the problem of the utility of surgery in these cases, operative intervention apparently accelerating progression of the lesion. In practice, however, a laparotomy is always justifiable, the most rational biopsy being excision of the tumor.

Adrenal Cortex Neoplasms↗
PubMed1995

Altered adrenal steroid metabolism underlying hypercortisolism in female endurance athletes.

OBJECTIVE: To explore possible changes in adrenal steroid metabolism and androgenic-anabolic status in female endurance athletes as a mechanism for their hypercortisolism. DESIGN: Adrenal steroids and androgenic-anabolic factors were studied during basal conditions and in response to ACTH stimulation related to menstrual status. SETTING: Department of Obstetrics and Gynecology, Karolinska Hospital, Stockholm, Sweden. PARTICIPANTS: Thirteen female elite middle to long distance runners (six eumenorrheic, seven oligoamenorrheic) and seven regularly menstruating controls. INTERVENTIONS: Blood samples were collected before and after an injection of 250 micrograms IV synthetic ACTH 1-24. Body weight, height, and body fat were measured. MAIN OUTCOME MEASURES: Basal serum concentrations of cortisol, androstenedione (A), DHEA, DHEAS, 17 alpha-hydroxyprogesterone (17-OHP), T, steroid-binding proteins, and insulin-like growth factor I and ACTH-induced response (area under the curve) of cortisol, DHEA, and 17-OHP. RESULTS: Oligoamenorrheic athletes had higher basal cortisol and A concentrations compared with healthy controls, whereas basal levels of DHEA and DHEAS were normal. Important findings in the oligoamenorrheic athletes were a significantly lower ratio between the ACTH-induced increments of DHEA and 17-OHP and an increased ratio between basal A and DHEAS. Insulin-like growth factor I was correlated negatively to sex hormone-binding globulin and to the amount of body fat in the combined material. CONCLUSIONS: The results indicate a redistribution of adrenal steroid metabolism in favor of glucocorticoid production in female endurance athletes. We suggest that hypercortisolism in female endurance athletes is a physiological adaptation to maintain adequate blood glucose levels during a condition of energy deficiency.

17-alpha-Hydroxyprogesterone↗
PubMedDate not supplied

[The coupling of the contrariwise changes in the steroid-secreting activity of the adrenals and the steroid-metabolizing activity of the liver in rats after x-ray irradiation].

The rat adrenal cortex activation is accompanied by inhibition of steroid metabolism in liver and vice versa at acute radiation disease caused by X-ray irradiation. A coupling of contrary changes of corticosteroid secretion and metabolism evidences that there is common regulation of these functions. The possible ACTH participation in coupling of adrenals and liver functions and the liver role in radiation hypercorticism genesis are discussed.

11-Hydroxycorticosteroids↗
PubMed1994

Mitotane treatment of 32 dogs with cortisol-secreting adrenocortical neoplasms.

Thirty-two dogs with hyperadrenocorticism caused by cortisol-secreting adrenocortical neoplasia were treated with mitotane at an initial daily induction dosage of 27.5 to 75.0 mg/kg of body weight (mean, 46.3 mg/kg) for 10 to 14 days. All dogs received daily maintenance glucocorticoid supplementation during the induction period. After 2 weeks, the ACTH-stimulated serum cortisol concentration had decreased to within or below the reference range for baseline cortisol concentration in 18 (56.3%) of the 32 dogs; the remaining 14 (43.7%) still responded to ACTH administration with serum cortisol concentrations above the reference range. In these 14 dogs, mitotane was continued at a higher daily dosage (mean, 60.7 mg/kg) for an additional 1 to 9 weeks. Serum cortisol concentration subsequently fell within or below the reference range for baseline cortisol concentration in all but 1 dog. In 30 of the 32 dogs, mitotane was continued at an initial mean maintenance dosage of 101.6 mg/kg/wk, divided into 2 to 5 doses. Twenty-two dogs received prednisone daily (0.2 mg/kg) throughout the maintenance period. One or more relapses occurred in 19 (63%) of the 30 dogs. In dogs with relapse, the mean maintenance mitotane dosage was increased from 98.1 mg/kg/wk to a high of 212.4 mg/kg/wk. After a mean maintenance treatment time of 13.2 months, final mean maintenance dosage required in the 30 dogs ranged from 35.3 to 1,273 mg/kg/wk. Adverse effects were seen in 19 (59.4%) of the 32 dogs as a result of a drug toxicosis associated with high-dosage administration of mitotane, low serum cortisol concentration, or both.(ABSTRACT TRUNCATED AT 250 WORDS)

Addison Disease↗
PubMed1994

Prognosis for treatment of adult-onset demodicosis in dogs: 34 cases (1979-1990).

Medical records of 41 dogs with adult-onset generalized demodicosis diagnosed between 1979 and 1990 were reviewed. Of the 41 dogs, 8 had hyperadrenocorticism, 5 were suspected or confirmed to have hypothyroidism, 10 had allergic disease and had been treated with corticosteroids, and 6 were receiving chemotherapy because of a neoplastic or immune-mediated condition. In the remaining 12, a concurrent underlying condition was not identified. Thirty-four of the dogs were treated with amitraz dips: 7 were cured, 22 were clinically improved but still had Demodex canis mites in skin scrapings and needed amitraz dips on a maintenance basis, and 5 did not improve with treatment and were euthanatized. Of the 13 dogs with a definitively treatable underlying disease (hyperadrenocorticism or hypothyroidism), 9 were treated for the underlying disease and for demodicosis: 4 were cured, 3 were improved but still had D canis mites in skin scrapings and required maintenance amitraz dips, and 2 did not improve and were euthanatized. Of the 16 dogs that were receiving chemotherapy or had allergic disease, 15 were treated for the demodicosis while still receiving treatment for their underlying disease: 1 was cured, 13 were improved but needed maintenance amitraz dips, and 1 did not improve and was euthanatized. Of the 12 dogs without an identifiable underlying problem, 10 were treated: 2 were cured, 6 improved, but needed maintenance amitraz dips, and 2 did not improve and were euthanatized.

Administration, Topical↗
PubMed1994

A Chinese lady with Carney's complex.

A young Chinese lady with ACTH-independent Cushing's Syndrome was reported. Her clinical features was compatible with the recently described Carney's complex. Bilateral adrenalectomy was then performed. The diagnosis of bilateral pigmented nodular adrenocortical dysplasia was microscopically confirmed.

Adrenal Cortex↗
PubMed1993

Hyperadrenocorticism caused by bilateral adrenocortical neoplasia in dogs: four cases (1983-1988).

Hyperadrenocorticism caused by bilateral adrenocortical neoplasia was diagnosed in 4 dogs. Three dogs had bilateral adrenocortical adenomas, and 1 dog had bilateral adrenocortical carcinomas. The history, physical findings, clinicopathologic abnormalities, and results of ACTH stimulation and low-dose dexamethasone suppression tests were compatible with diagnosis of hyperadrenocorticism. Adrenocortical neoplasia was differentiated from pituitary-dependent hyperadrenocorticism on the basis of a combination of test results, including lack of suppression of plasma cortisol after being given a high dose dexamethasone (n = 4), undetectable (< 20 pg/ml) plasma endogenous ACTH concentration (n = 4), identification of a single mineralized adrenal mass by abdominal radiography (n = 2) and abdominal ultrasonography (n = 1), and identification of bilateral nonmineralized adrenal masses by ultrasonography (n = 1). A left adrenal mass was excised from 1 dog. Clinical signs persisted and administration of mitotane was initiated. One dog was treated only with mitotane. Treatment with ketoconazole was attempted in 2 dogs. All dogs died or were euthanatized because of persistent hyperadrenocorticism. Necropsy and histologic evaluation of the pituitary and adrenal tissue confirmed bilateral adrenocortical neoplasia in all dogs. Bilateral adrenocortical neoplasia should be considered as an uncommon, but possible, cause of bilaterally large adrenal glands in dogs with hyperadrenocorticism.

Adenoma↗
PubMed1977

[The renin-angiotensin-aldosterone system in hypertensive patients. II. Diagnosis of primary hyperaldosteronism].

Twenty patients suffering from primary hyperaldosteronism were studied. Sixteen had a single adenoma of the adrenal and four had bilateral hyperplasia affecting both adrenals. Cases of primary hyperaldosteronism due to a tumour were characterised by a higher degree of hypermineralocorticism than was seen in the patients with hyperplasia. Plasma aldosterone, after acute volaemic expansion, did not fall below 13 ng/100 ml in the adenoma patients whilst it was lower in the case of hyperplasia. Adrenal phlebography is a useful tool in preoperative diagnosis.

Adenoma↗
PubMed1997

Glycosylated hemoglobin concentrations in the blood of healthy dogs and dogs with naturally developing diabetes mellitus, pancreatic beta-cell neoplasia, hyperadrenocorticism, and anemia.

OBJECTIVE: To characterize glycosylated hemoglobin (GHb) concentrations in the blood of dogs with disorders that may affect serum glucose or blood GHb concentrations, and to determine whether changes in GHb concentration correlate with changes in control of diabetes in dogs. DESIGN: Prospective study. ANIMALS: 63 healthy dogs, 9 dogs with anemia, 24 dogs with untreated hyperadrenocorticism, 12 dogs with pancreatic beta-cell neoplasia, 23 dogs with newly diagnosed diabetes mellitus, and 77 diabetic dogs treated with insulin. PROCEDURE: Control of diabetes in dogs treated with insulin was classified as good or poor on the basis of history, physical examination findings, changes in body weight, and measurement of serum glucose concentrations Sequential evaluations of control were performed and GHb concentration in blood was measured, by means of affinity chromatography, for 5 untreated diabetic dogs before and after initiating insulin treatment, for 10 poorly controlled diabetic dogs before and after increasing insulin dosage, and for 5 diabetic dogs before and after pancreatic islet cell transplantation. RESULTS: Mean (+/-SD) GHb concentration was 3.3 +/- 0.8% in the blood of healthy dogs. Compared with results from healthy dogs, mean GHb concentration was significantly lower in the blood of dogs with anemia and pancreatic beta-cell neoplasia and significantly higher in the blood of untreated diabetic dogs. Mean GHb concentration was significantly higher in the blood of 46 poorly controlled diabetic dogs, compared with 31 well-controlled diabetic dogs (7.3 +/- 1.8 vs 5.7 +/- 1.7%, respectively). Mean GHb concentration in blood decreased significantly in 5 untreated diabetic dogs after treatment (8.7 +/- 1.9 vs 5.3 +/- 1.9%). Mean GHb concentration in blood also decreased significantly in 10 poorly controlled diabetic dogs after control was improved and in 5 diabetic dogs after they had received a pancreatic islet cell transplant. CLINICAL IMPLICATIONS: Measurement of GHb concentration in blood may assist in monitoring control of diabetes in dogs.

Adrenal Cortex Diseases↗
PubMed1997

DNA topoisomerase II alpha and Ki-67 in human adrenocortical neoplasms: a possible marker of differentiation between adenomas and carcinomas.

Cell kinetic information is valuable in evaluating the diagnosis and/or biologic behavior of various human neoplasms. Monoclonal antibody Ki-67 recognizes the cells other than G0 of the cell cycle. A cell cycle-related intranuclear protein, topoisomerase II alpha (topoII alpha), separates chromosomes at the end of mitosis. Its expression is mostly limited to the S to G2/M phases of the cell cycle. We studied cell proliferative activity in adrenocortical adenomas (n = 28), carcinomas (n = 17), and normal adrenal glands (n = 6) by immunohistochemical analysis of Ki-67 and topoII alpha to evaluate their value in the diagnosis of adrenocortical malignancy. We detected Ki-67 and topoII alpha immunohistoreactivity in the nuclei of each case we examined. There was a significant positive correlation (r = 0.927) between the Ki-67 and topoII alpha labeling indexes (LIs), the percentage of positive cells. In normal adrenal cortex and adenoma, the LIs for Ki-67 and topoII alpha were 0.48 +/- 0.16 and 0.44 +/- 0.15 for normal and 0.64 +/- 0.11 and 0.72 +/- 0.12 for adenoma, respectively, with no significant differences in the LIs of adenomas and normal adrenals. The Ki-67 and topoII alpha LIs in the carcinomas were 5.84 +/- 1.33 and 6.13 +/0 1.65, respectively; these LIs were significantly higher than the LIs of adenomas. Eleven of 17 carcinomas demonstrated topoII alpha and Ki-67 LIs of more than 2.5, whereas none of the adenomas did. The topoII alpha and Ki-67 LIs in carcinomas with metastasis (11.21 +/- 3.15 and 9.75 +/- 2.31 respectively; n = 7) were significantly higher than in those without metastasis (2.58 +/- 0.61 and 3.12 +/- 0.90, respectively; n = 10). This indicates that immunohistochemical analysis of Ki-67 and topoII alpha could help to differentiate carcinoma from adenoma in resected adrenocortical neoplasms and might predict aggressive biologic behavior in carcinomas.

Adenoma↗
PubMed1988

Computed tomography in the diagnosis of canine hyperadrenocorticism not suppressible by dexamethasone.

Computed tomography (CT) was performed in 10 dogs with hyperadrenocorticism not suppressible by dexamethasone. In 6 of these dogs, a unilateral adrenal mass was found on CT images. Specimens of the masses were obtained via retroperitoneal laparotomy; histologic examination revealed 4 carcinomas, 1 adenoma, and 1 nodular hyperplasia. In the 4 other dogs, CT revealed symmetric bilateral adrenal gland enlargement. In 2 of these dogs, contrast-enhanced CT revealed a mass in the pituitary fossa, which could be identified at necropsy as a pituitary tumor. The other 2 dogs were successfully treated with mitotane.

Adrenal Cortex Function Tests↗