Urinary corticoids in the diagnosis of canine hyperadrenocorticism

Background: The adrenocorticotropic hormone (ACTH) stimulation test is used to evaluate trilostane treatment in dogs with hypercortisolism.Hypothesis: The urinary corticoid : creatinine ratio (UCCR) is a good alternative to the ACTH stimulation test to determine optimal trilostane dose.Animals: Eighteen dogs with pituitary-dependent hypercortisolism.Methods: In this prospective study, the dose of trilostane was judged to be optimal on the basis of resolution of clinical signs of hypercortisolism and results of an ACTH stimulation test. The owners collected urine for determination of UCCR at 2-week intervals for at least 8 weeks after achieving the optimal trilostane dose.Results: The UCCRs were significantly higher before treatment (11.5-202.0 Â 10

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“…The urinary creatinine concentration was determined by the Jaffé kinetic method (initial rate reaction). From these, the UCCR was calculated 14 …”

Section: Methodsmentioning

confidence: 99%

Urinary Corticoid : Creatinine Ratios in Dogs with Pituitary‐Dependent Hypercortisolism during Trilostane Treatment

Galac¹,

Buijtels²,

Kooistra³

2009

Veterinary Internal Medicne

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“…In these animals the diagnosis of hyperadrenocorticism was based upon elevated corticoid/creatinine (C/C) ratios (>10xl0-6) in two consecutive morning urine samples collected at home (Stolp et al 1983, Rijnberk et al 1988a. After the collection of the second urine sample the dogs received three doses of OT mg dexamethasone per kg body weight orally at 8-h intervals.…”

Section: Animals and Testsmentioning

confidence: 99%

“…The interassay coefficient of variation was 10% and the sensitivity was 1 nmol/1. The urinary corticoid concentration was related to the urinary creatinine concentration (Jaffé kinetic method, initial rate reaction) and C/C ratios were calculated (Stolp et al 1983, Rijnberk et al 1988a.…”

Section: Hormone Determinationmentioning

confidence: 99%

Correlation between impairment of glucocorticoid feedback and the size of the pituitary gland in dogs with pituitary-dependent hyperadrenocorticism

Kooistra¹,

Voorhout²,

Mol³

et al. 1997

Journal of Endocrinology

127

145

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Under the assumption that the impaired inhibitory effect of glucocorticoids on cell division is an important determinant in the progression of corticotrophic adenomas, it is postulated that the magnitude of proliferation and the resistance to glucocorticoids are correlated. To test this hypothesis, 67 dogs with pituitary-dependent hyperadrenocorticism were studied to determine whether a correlation could be demonstrated between the effect of dexamethasone administration on the activity of the pituitary-adrenocortical axis and the size of the pituitary gland as estimated by computed tomography. The volumes of the pituitary glands as calculated from summations of subsequent images of pituitary areas, ranged from 11.8 to 3238.6 mm3. Among the three dimensions, the height of the pituitary was the most sensitive indicator of enlargement. Calculation of the pituitary height/brain area ratio (P/B ratio) allowed correction for the size of the dog. The P/B ratio had the highest discriminatory power in distinguishing enlarged (n = 41) from non-enlarged (n = 26) pituitaries. The effects of dexamethasone (0.1 mg/kg) on the plasma concentrations of cortisol and ACTH and on the urinary corticoid/creatinine (C/C) ratios were expressed as percentage changes from the initial values. For ACTH, cortisol and C/C ratios these figures for resistance to dexamethasone were significantly correlated with the dimensions of the pituitary, particularly the height, volume and P/B ratio. It is concluded that the magnitude of the expansion of pituitary corticotrophic adenomas is dependent upon the loss of restraint by glucocorticoids, i.e. the degree of insensitivity to glucocorticoid feedback.

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“…The biochemical diagnosis was based on the findings of plasma concentrations of cortisol greater than 40 nmol/1 at 8 h after intravenous administra¬ tion of 001 mg dexamethasone/kg (Meijer, De Bruijne, Rijnberk & Croughs, 1978) and/or meas¬ urements of urinary corticoids (Stolp, Rijnberk, Meijer & Croughs, 1983). The ability of dexameth¬ asone to suppress glucocorticoid secretion was studied by measuring urinary corticoid : creatinine ratios before and after three oral doses of 0-1 mg dexa¬ methasone (Oradexon; Organon, Oss, The Netherlands) per kg body weight at 8-h intervals (Rijnberk, Van Wees & Mol, 1988Ò).…”

Section: Diagnosismentioning

confidence: 99%

Pituitary-dependent hyperadrenocorticism in a family of Dandie Dinmont terriers

Scholten-Sloof

Knol²,

Rijnberk³

et al. 1992

Journal of Endocrinology

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Adrenocortical function studies were performed in seven Dandie Dinmont terriers with pituitary-dependent hyperadrenocorticism. The ability of dexamethasone at a dose rate of 0.1 mg/kg body weight to suppress cortisol secretion was only moderate in four out of the six dogs tested. Concentrations of alpha-melanocyte-stimulating hormone in plasma were highly increased. Responses to stimulation with corticotrophin-releasing hormone and the dopamine-antagonist haloperidol, examined in three animals, were moderate or absent. These results indicate that adrenocortical stimulation, i.e. hyperadrenocorticotrophism, was caused by pituitary lesions which were functioning autonomously. In six of the seven animals there was a very close familial relationship and the coefficients of relationship and the coefficients of inbreeding were significantly higher than in a representative control population. It was concluded that these seven related terriers with hyperadrenocorticotrophism had the biochemical characteristics of de-novo neoplasms of proopiomelanocortin-producing cells, and there was evidence for a genetic involvement in tumorigenesis.

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Urinary corticoids in the diagnosis of canine hyperadrenocorticism

Cited by 74 publications

References 10 publications

Urinary Corticoid : Creatinine Ratios in Dogs with Pituitary‐Dependent Hypercortisolism during Trilostane Treatment

Urinary Corticoid : Creatinine Ratios in Dogs with Pituitary‐Dependent Hypercortisolism during Trilostane Treatment

Correlation between impairment of glucocorticoid feedback and the size of the pituitary gland in dogs with pituitary-dependent hyperadrenocorticism

Pituitary-dependent hyperadrenocorticism in a family of Dandie Dinmont terriers

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