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Results for “Adrenocortical Hyperfunction”

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At least 685 records · Page 38Linked to original sources
PubMed2004

Trilostane treatment of bilateral adrenal enlargement and excessive sex steroid hormone production in a cat.

A 14-year-old neutered female cat was presented for the investigation of aggression and male-type behaviour. Bilateral adrenal enlargement together with elevated plasma concentrations of oestradiol and testosterone were identified, with no evidence of hypercortisolaemia. These findings are similar to the syndrome of hyperadrenocorticism recognised most commonly in ferrets. The cat was treated for six months with the enzyme inhibitor drug, trilostane, and showed a moderate improvement in clinical signs.

3-Hydroxysteroid Dehydrogenases↗
PubMed2004

Adrenal necrosis in a dog receiving trilostane for the treatment of hyperadrenocorticism.

Clinical and biochemical changes suggestive of hypoadrenocorticism were observed in a 10-year-old male neutered Staffordshire bull terrier shortly after beginning therapy with trilostane for the treatment of hyperadrenocorticism. The dog's condition was stabilised with intravenous fluids, fludrocortisone and prednisolone. An exploratory laparotomy and excisional biopsy of the left adrenal gland were performed. Histopathological analysis showed adrenal cortical necrosis with reactive inflammation and fibrosis. Trilostane is a reversible inhibitor of steroid synthesis and this complication has not been reported previously. Clinicians should be aware that trilostane therapy may result in adrenal necrosis but that prompt treatment might correct a life-threatening situation.

3-Hydroxysteroid Dehydrogenases↗
PubMed2005

Hyperparathyroidism in dogs with hyperadrenocorticism.

OBJECTIVES: To assess the effect of canine hyperadrenocorticism (HAC) on parathyroid hormone (PTH), phosphate and calcium concentrations. METHODS: PTH concentrations and routine biochemical parameters were measured in 68 dogs with HAC. Ionised calcium was measured in 28 of these dogs. The results obtained were compared with an age- and weight-matched group of 20 hospital patients that did not show signs of HAC. RESULTS: There were significant differences between the PTH, phosphate, alkaline phosphatase, creatinine and albumin concentrations between the two groups. Total and ionised calcium concentrations were not significantly different. Most of the dogs (92 per cent) with HAC had PTH concentrations that were greater than the reference range (10 to 60 pg/ml), and in 23 dogs they were greater than 180 pg/ml. There were significant positive correlations between the PTH and basal cortisol, post-adrenocorticotropic hormone (ACTH) cortisol and alkaline phosphatase concentrations, and also the phosphate and post-ACTH cortisol concentrations. CLINICAL SIGNIFICANCE: Adrenal secondary hyperparathyroidism is a cause of increased PTH concentrations and may be associated with abnormalities in calcium and phosphate metabolism in dogs with HAC. The findings of this study could explain why canine HAC may cause clinical signs such as calcinosis cutis that are associated with altered calcium metabolism.

Adrenocortical Hyperfunction↗
PubMed2005

Canine hyperadrenocorticism: effects of trilostane on parathyroid hormone, calcium and phosphate concentrations.

OBJECTIVES: To determine the effects of treating canine hyperadrenocorticism (HAC) on parathyroid hormone (PTH), calcium and phosphate concentrations in dogs. METHODS: Serum calcium, phosphate and PTH concentrations were analysed in 22 dogs with HAC before treatment with trilostane and at a median of 210 days after commencing treatment. Pretreatment data were compared with data from an age- and weight-matched group of hospitalised patients, and post-treatment data were compared with pretreatment data. RESULTS: PTH and phosphate concentrations were significantly higher in dogs with HAC compared with control dogs. PTH concentrations reduced significantly with treatment, such that there was no longer a difference between the HAC and control groups. Phosphate concentrations also reduced significantly with treatment but there was still a significant difference between those in dogs with HAC and control dogs. Despite no significant difference between calcium concentrations in the pretreatment HAC and control groups, calcium concentrations increased significantly with treatment. CLINICAL SIGNIFICANCE: These results show that adrenal secondary hyperparathyroidism resolves with treatment and suggest that increased calcium and phosphate levels have a role in its pathogenesis.

3-Hydroxysteroid Dehydrogenases↗
PubMed2002

Familial/sporadic glucocorticoid resistance syndrome and hypertension.

Glucocorticoids regulate diverse functions important for the maintenance of central nervous system, cardiovascular, metabolic, and immune homeostasis. The actions of these hormones are mediated by the specific intracellular glucocorticoid receptors (GRs). Pathologic conditions associated with changes of tissue sensitivity to these hormones have been described. The syndrome of familial/sporadic glucocorticoid resistance is characterized by hypercortisolism without Cushing syndrome stigmata. Many of the patients present with hypertension, with or without hypokalemic alkalosis, as a result of elevated concentrations of cortisol and other salt-retaining steroids. The molecular defects of 4 kindreds and one sporadic case have been elucidated as inactivating mutations in the ligand-binding domain of the GR. In two patients in whom the GR was mutated at amino acid isoleucine 559 to aspartic acid (GRalphaI559N) and isoleucine 747 to methionine (GRalphaI747M), respectively, glucocorticoid resistance developed at the heterozygous state, with transdominant negative activity of each of the mutant receptors upon the wild-type protein. Retention of the wild-type receptor in the cytoplasm by the mutant receptor was found in the former, while inappropriate accumulation of p160-type coactivators on the promoter region of glucocorticoid-responsive genes, because of a defective interaction between the AF2 region of the mutant receptor and the LXXLL motif of the coactivators, was determined in the latter. These results suggest that the pathologic mechanisms of glucocorticoid resistance is quite broad, and this is reflected in the wide variability of the clinical picture in patients with the syndrome.

Adrenocortical Hyperfunction↗
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↗
PubMed1985

Pituitary tumour causing multiple endocrinopathies in a dog.

A 9-year-old male Boxer with signs of lethargy, weight gain, polyuria, polydipsia, eosinopaenia and lymphopaenia was diagnosed as having hyperadrenocorticism. Concurrent central diabetes insipidus was diagnosed using a water deprivation test and antidiuretic hormone response test. A contrast radiographic technique was used to outline a pituitary mass. A chromophobe adenoma and secondary hypothyroidism were found on post-mortem examination.

Adenoma, Chromophobe↗
PubMed1987

Glucose metabolism in a pony mare with a tumour of the pituitary gland pars intermedia.

A case of pituitary dependent hyperadrenocorticism in a horse is reported. Clinical signs included hirsutism, polydipsia and general debility. The horse was persistently hyperglycaemic and glucose values were unchanged following subcutaneous administration of insulin. Resting cortisol values were normal, but dexamethasone suppression of cortisol concentration was shorter than normal. Plasma glucose, cortisol, insulin and glucagon concentrations were measured as part of an intravenous glucose tolerance test. The patient responses were different from those in a control pony.

Adrenocortical Hyperfunction↗
PubMed1998

Myotonia associated with hyperadrenocorticism in two dogs.

Two dogs developed a disabling gait abnormality characterised by stiffness. The abnormality was consistent with a diagnosis of myotonia secondary to hyperadrenocorticism. The first dog had iatrogenic hyperadrenocorticism, and its signs improved substantially after corticosteroid administration was gradually withdrawn. The second had pituitary-dependent hyperadrenocorticism, but myotonic signs progressed despite effective mitotane therapy. Procainamide administration reduced the myotonic stiffness in the second case.

Adrenocortical Hyperfunction↗
PubMed1998

Mitotane (o,p'-DDD) resistance in a dog with pituitary-dependent hyperadrenocorticism and phaeochromocytoma.

A dog was presented with a 2 year history of polyuria and polydipsia due to pituitary-dependent hyperadrenocorticism. A low-dose dexamethasone suppression test and measurement of plasma ACTH concentration confirmed the diagnosis. Treatment was instituted with mitotane at 44 mg/kg/day and then 88 mg/kg/d without complete resolution of signs. The dog collapsed with signs consistent with liver disease and was euthanased. Necropsy revealed a phaeochromocytoma of the left adrenal medulla with extensive metastases to the liver. A chromophobe adenoma of the pars intermedia of the pituitary was found.

Adrenal Cortex Function Tests↗
PubMed1999

Hepatic carcinoid, hypercortisolism and hypokalaemia in a dog.

A German Shepherd dog was diagnosed with periodic myopathy secondary to persistent hypokalaemia. Hormone analysis revealed excess cortisol secretion. A neuroendocrine carcinoma, thought to be a primary hepatic carcinoid, was detected in the liver. Ectopic adrenocorticotrophin hormone secretion was suspected as the cause of hypercortisolism and hypokalaemia, although this could not be confirmed by immunohistochemical staining.

Adrenocortical Hyperfunction↗
PubMed1999

Plasma cortisol concentrations following cortisone infusion in dogs before and after treatment with cortisone acetate.

OBJECTIVE: To evaluate effects of iatrogenic hyperadrenocorticism on plasma cortisol concentrations produced by an infusion of hydrocortisone in dogs. PROCEDURE: Plasma cortisol concentrations were measured regularly during a 6 h infusion of hydrocortisone sodium succinate at two dose rates. The infusions were performed before and after treatment for 30 d with oral cortisone acetate at 10 mg/kg/24 h, divided thrice daily. Adrenal activity during the experimental period was assessed by weekly ACTH stimulation tests. RESULTS: Both infusion rates produced lower plasma cortisol concentrations after treatment for 30 d with cortisone. CONCLUSION: Prior exposure to high concentrations of glucocorticoids may result in accelerated metabolism of glucocorticoids administered subsequently. This may necessitate increased dosages when using glucocorticoids to support inadequate adrenal function.

Administration, Oral↗