Adrenocortical Function Tests in Dogs With Hyperfunctioning Adrenocortical Tumours

Meijer, J. C.; Lubberink, A. A. M. E.; Rijnberk, A.; Croughs, R. J. M.

doi:10.1677/joe.0.0800315

Cited by 28 publications

(19 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For 14 dogs with hyperadrenocorticism as diag nosed by pituitary-adrenocortical function tests [17,18] permission was obtained for autopsy and subsequent investigations. 8 dogs had PDH and 6 dogs had an adrenocortical tumor.…”

Section: Animalsmentioning

confidence: 99%

Hypothalamic Catecholamine Levels in Dogs with Spontaneous Hyperadrenocorticism

Meijer¹,

Croughs²,

Rijnberk³

et al. 1981

Neuroendocrinology

Self Cite

View full text Add to dashboard Cite

Hypothalamic norepinephrine (NE) and dopamine content was studied in dogs with spontaneous and iatrogenic hypercortisolism and in untreated normal dogs. The concentration of NE in the hypothalamus was subnormal in 4 of 8 dogs with pituitary-dependent hyperadrenocorticism (PDH), whereas long-term administration of corticotropin or cortisone acetate did not result in low hypothalamic NE content. In dogs with hyperadrenocorticism due to adrenocortical tumor subnormal as well as normal and high hypothalamic NE levels were found. Hypothalamic as well as striatal dopamine content did not differ among groups of dogs with PDH, adrenocortical tumor, corticotropin treatment, cortisone treatment and in untreated normal dogs. The subnormal hypothalamic NE levels in dogs with PDH may be involved in the hypersecretion of ACTH found in this disease. The normal hypothalamic dopamine levels in dogs with PDH are not consistent with a dopaminergic depletion as the cause of PDH.

show abstract

Section: Animalsmentioning

confidence: 99%

Hypothalamic Catecholamine Levels in Dogs with Spontaneous Hyperadrenocorticism

Meijer¹,

Croughs²,

Rijnberk³

et al. 1981

Neuroendocrinology

Self Cite

View full text Add to dashboard Cite

show abstract

“…The adrenal function of cat 1 was hardly be suppressed by high doses of dexamethasone and was slightly stimulated by synthetic ACTH in comparison with data for healty cats (24). This suggests an autonomous hyperadrenocorticism, which is indicative of the presence of an adrenal tumour (12,13,17). However other studies have demonstrated that dexamethasone resistance, as found in this cat, can also be caused by a dysfunctioning pituitary gland (2,21).…”

Section: Discussionmentioning

confidence: 99%

“…These findings are indicative of an adrenal tumour (12,13), and therefore a laparotomy was performed. However no abnormalities of the adrenal glands were observed.…”

Section: Clinical Data Catmentioning

confidence: 99%

Hyperadrenocorticism in four cats

Immink

Toor²,

Vos

et al. 1992

Veterinary Quarterly

Self Cite

View full text Add to dashboard Cite

SUMMARYThis paper describes four cats with hyperadrenocorticism. Cat I showed polydipsia and polyphagia. Diabetes mellitus was initially diagnosed As the animal appeared to be insulin resistant, pituitary and adrenocortical function tests were performed and the diagnosis of hyperadrenocoricism was made.Resistance to the high-dose dexamethasone suppression test was noticed in this cat. Pathological examination revealed a pituitary chromophobe adenoma Cat 2 presented with diabetes mellitus, which was treated with insulin. The animal had a pendulous abdomen and its coat was in a poor condition. The low-dose dexamenthasone suppression test demonstrated hyperadrenocorticism. Necropsy findings of pituitary tumour and hyperplasia of the adrenal cortex confirmed the diagnosis. Cat 3 showed clinical abnormalities indicative of hyperadrenocorticism, for instance, muscle weakness, alopecia, multiple abcesses. The diagnosis of hyperadrenocorticism was confirmed by the results of the lowe-dose dexamethasone suppression test.Pathological examination revealed an adrenocortical carcinoma. Cat 4 presented with polydipsia. The cause of this symptom was not found initially. One and a half years later additional symptoms, such as nephritis and polyphagia developed Hyperadrenocorticism was diagnosed because of a palpable mass cranial to the left kidney. The diagnosis was confirmed by the results of the lowe-dose dexamethasone suppression test and the necropsy findings.

show abstract

“…Peaks of normal dogs' cortisol levels overlap with those of hyperadrenocorticoid dogs and at least 50% of hyperadrenocorticoid dogs have resting cortisol concentrations in the normal range(2)(4)(5)(22)(4n)(47 (48). Stress, such as hospitalisation, handling, blood sampling and other factors, can also result in normocorticoid dogs having elevated basal cortisol levels(l )(4) (38).…”

Section: Resting Plasma Cortisolmentioning

confidence: 99%

Canine hyperadrenocorticism

Cayzer¹,

Jones

1993

New Zealand Veterinary Journal

View full text Add to dashboard Cite

Hyperadrenocorticism is a common endocrinopathy which results from the excessive production of cortisol by the adrenal cortex. In the majority of cases, this increased secretion of cortisol results from stimulation of the adrenal cortex by adrenocorticotrophic hormone secreted from the pituitary gland. In a smaller number of cases adrenal tumours are present. Clinical signs are variable but commonly include polydipsia and polyuria, polyphagia, obesity, a pendulous abdomen, hepatomegaly, alopecia, lethargy, weakness and anoestrus. Haematology, serum chemistry analysis and urinalysis should be performed on a dog with suspected hyperadrenocorticism. Finding a significant number of changes that are consistent with hyperadrenocorticism often allows a presumptive diagnosis to be made. Other tests can then be used to confirm the diagnosis and to help localise the cause, including liver biopsy, radiology, ultrasonography, gamma camera imaging, computed tomography, and measurement of blood and urine hormone levels. The ACTH stimulation test, low dose dexamethasone suppression test and measurement of the urine cortisol:creatinine ratio are used to assess whether hyperadrenocorticism is present. The high dose dexamethasone suppression test, measurement of plasma ACTH, corticotropin-releasing hormone stimulation test, and a modification of the urinary cortisol:creatinine ratio test are then implemented to determine the aetiology. The treatment of choice for adrenal neoplasia is surgical removal of the affected adrenal. On the other hand, pituitary hyperplasia or neoplasia may be treated either surgically, by bilateral adrenalectomy or hypophysectomy, or medically. The drug which is chosen most commonly for medical management is 1,1-dichloro-2(O-chlorophenyl)-2-(P-chlorophenyl) ethane (op'-DDD), which can be used to suppress adrenal function or to completely destroy the adrenal cortex. The antifungal agent ketoconazole also suppresses adrenal steroid synthesis and provides an alternative form of medical treatment for hyperadrenocorticoid dogs.

show abstract

Adrenocortical Function Tests in Dogs With Hyperfunctioning Adrenocortical Tumours

Cited by 28 publications

References 12 publications

Hypothalamic Catecholamine Levels in Dogs with Spontaneous Hyperadrenocorticism

Hypothalamic Catecholamine Levels in Dogs with Spontaneous Hyperadrenocorticism

Hyperadrenocorticism in four cats

Canine hyperadrenocorticism

Contact Info

Product

Resources

About