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

Galac, Sara; Buijtels, J.J.C.W.M.; Kooistra, Hans S.

doi:10.1111/j.1939-1676.2009.0374.x

Cited by 28 publications

(30 citation statements)

References 29 publications

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“…Although the ACTH-stimulation test certainly can be discussed as a gold standard in monitoring trilostane therapy, it has been proven to objectively assess the therapeutic response. Treatment monitoring with the use of the ACTH-stimulation test is very often successful and helpful in identifying excessively-controlled dogs (Sieber- Galac et al, 2009;Burkhardt et al, 2013). Again, the problem could be the subjectivity of owner questionnaires, which may even increase when owners are not able to look back at their answers on previous questionnaires.…”

Section: Discussionmentioning

confidence: 99%

Lack of association between clinical signs and laboratory parameters in dogs with hyperadrenocorticism before and during trilostane treatment

Boretti¹,

Holzthüm²,

Reusch³

et al. 2016

SAT

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INTRODUCTION Trilostane therapy, the treatment of choice for pituitary-dependent hyperadrenocorticism (HAC) in dogs, is monitored by assessing resolution of clinical signs and measuring adrenocortical reserve capacity with an ACTH-stimulation test. The aim of this prospective study was to evaluate agreement between clinical signs reported by owners and cortisol or ACTH concentrations before and during trilostane therapy (starting dose 1-2 mg/kg once daily). A questionnaire on signs of HAC was used and a clinical score calculated as the sum of the 9 questions. Eighteen questionnaires at diagnosis and 97 during therapy were filled out by owners of 32 dogs. An ACTH-stimulation test was performed at each reevaluation. There were weak correlations between abdominal girth, appetite or weight gain and cortisol concentrations during therapy. However, the clinical score did not correlate with cortisol or cACTH values. In 50% of dogs, trilostane application had to be changed from once daily to twice daily during the study. Clinical signs reported by owners matched poorly with cortisol or cACTH concentrations at any time point. If low-dose trilostane is used, treatment frequency often has to be increased. SummaryTrilostane therapy, the treatment of choice for pituitary-dependent hyperadrenocorticism (HAC) in dogs, is monitored by assessing resolution of clinical signs and measuring adrenocortical reserve capacity with an ACTH-stimulation test. The aim of this prospective study was to evaluate agreement between clinical signs reported by owners and cortisol or ACTH concentrations before and during trilostane therapy (starting dose 1-2 mg/kg once daily). A questionnaire on signs of HAC was used and a clinical score calculated as the sum of the 9 questions. Eighteen questionnaires at diagnosis and 97 during therapy were filled out by owners of 32 dogs. An ACTH-stimulation test was performed at each reevaluation. There were weak correlations between abdominal girth, appetite or weight gain and cortisol concentrations during therapy. However, the clinical score did not correlate with cortisol or cACTH values. In 50% of dogs, trilostane application had to be changed from once daily to twice daily during the study. Clinical signs reported by owners matched poorly with cortisol or cACTH concentrations at any time point. If low-dose trilostane is used, treatment frequency often has to be increased.

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Section: Discussionmentioning

confidence: 99%

Lack of association between clinical signs and laboratory parameters in dogs with hyperadrenocorticism before and during trilostane treatment

Boretti¹,

Holzthüm²,

Reusch³

et al. 2016

SAT

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“…A diagnosis of PDH was made if a dog had at least 2 of the following 3 diagnostic test results: an LDDst result indicative of PDH (transient suppression of serum cortisol concentration), ultrasonographic evidence of 2 relatively equal‐sized adrenal glands with no evidence of an adrenal gland tumor, or plasma concentration of endogenous ACTH >45 pg/mL 6, 17, 18. A diagnosis of ATH was made if all of the following were present: a LDDst result consistent with ATH, ultrasonographic evidence of an adrenal mass, and, after trilostane control of NOH, histologic confirmation of an adrenocortical tumor (adenoma or carcinoma) 6, 17, 18, 19…”

Section: Methodsmentioning

confidence: 99%

“…A diagnosis of ATH was made if all of the following were present: a LDDst result consistent with ATH, ultrasonographic evidence of an adrenal mass, and, after trilostane control of NOH, histologic confirmation of an adrenocortical tumor (adenoma or carcinoma) 6, 17, 18, 19…”

Section: Methodsmentioning

confidence: 99%

“…Trilostane treatment, at appropriate doses and frequency of administration, may control many of the clinical and biochemical abnormalities associated with canine NOH 3, 4, 5, 6, 7. However, there is uncertainty in the literature regarding what test might serve as an objective, specific, and sensitive means of assessing therapeutic response to trilostane 6, 7, 8. Results from such a test (if it fulfills these criteria) should complement the more subjective information determined from the owner history and physical examination.…”

mentioning

confidence: 99%

“…This test has also been adopted for the assessment of therapeutic response to trilostane. Since trilostane began to be used as a medical treatment for dogs with NOH approximately 15 years ago, no other test has been widely accepted as a more objective, specific, and sensitive means of assessing therapeutic response 6, 7, 8. If ACTHst results are utilized to aid in assessing trilostane dose, frequency of administration, or both, there is a question of when the test should be started relative to time of trilostane administration.…”

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confidence: 99%

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Comparison of Adrenocorticotropic Hormone Stimulation Test Results Started 2 versus 4 Hours after Trilostane Administration in Dogs with Naturally Occurring Hyperadrenocorticism

Bonadio

Feldman

Cohen

et al. 2014

Veterinary Internal Medicne

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BackgroundTrilostane medical treatment of naturally occurring hyperadrenocorticism (NOH) in dogs is common, as is use of the adrenocorticotropic hormone (ACTH) stimulation test (ACTHst) in monitoring response to treatment. There is uncertainty regarding when the ACTHst should be started relative to time of trilostane administration.ObjectiveTo compare ACTHst results in dogs being treated for NOH with trilostane when the test is begun 2 versus 4 hours after trilostane administration.AnimalsTwenty‐one privately owned dogs with NOH, each treated with trilostane for at least 30 days.MethodsEach dog had 2 ACTHst completed, 1 started 2 hours and the other 4 hours after trilostane administration. The second test was started no sooner than 46 hours and no later than 74 hours after the first.ResultsFor all 21 dogs, the mean post‐ACTH serum cortisol concentration from tests started 2 hours after trilostane administration (5.4 ± 3.7 μg/dL) was significantly lower (P = .03) as compared with results from the tests started 4 hours after administration (6.5 ± 4.5 μg/dL).ConclusionsResults of ACTHst started at different times yield significantly different results. Dogs with NOH, treated with trilostane, and monitored with ACTHst results should have all of their subsequent ACTHst tests begun at or about the same time after trilostane administration.

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Canine Hyperadrenocorticism

Behrend¹

2015

Canine and Feline Endocrinology

111

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

Cited by 28 publications

References 29 publications

Lack of association between clinical signs and laboratory parameters in dogs with hyperadrenocorticism before and during trilostane treatment

Lack of association between clinical signs and laboratory parameters in dogs with hyperadrenocorticism before and during trilostane treatment

Comparison of Adrenocorticotropic Hormone Stimulation Test Results Started 2 versus 4 Hours after Trilostane Administration in Dogs with Naturally Occurring Hyperadrenocorticism

Canine Hyperadrenocorticism

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