Trilostane treatment of 78 dogs with pituitary‐dependent hyperadrenocorticism

Neiger, Reto; Ramsey, Ian; O'Connor, J. R.; Hurley, Karyl J.; Mooney, Carmel T.

doi:10.1136/vr.150.26.799

Cited by 143 publications

(194 citation statements)

References 19 publications

(38 reference statements)

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“…Trilostane is a competitive inhibitor of the 3β-hydroxysteroid dehydrogenase enzyme system and interferes with synthesis of glucocorticoids at the level of the adrenal glands. Trilostane has been shown to reduce the circulating concentrations of cortisol leading to substantial improvement of clinical signs in 70 to 96% of cases (Ruckstuhl et al, 2002;Braddock et al, 2003;Neiger et al, 2003). Since its first use in veterinary medicine, the recommended daily dose has been adjusted several times.…”

Section: Introductionmentioning

confidence: 99%

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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: Introductionmentioning

confidence: 99%

“…Treatment response is monitored by assessing improvement or resolution of clinical signs and by measuring the adrenocortical reserve capacity with an ACTH-stimulation test (Ruckstuhl et al, 2002;Neiger et al, 2003). However, this test is time consuming and expensive.…”

Section: Introductionmentioning

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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“…The clinical use of trilostane in canine HAC, and in particular PDH, has now been evaluated in several published clinical studies from centres across the world [18][19][20][21][22][23]. In addition unpublished studies have been conducted for regulatory purposes (Dechra Veterinary Products; data on file).…”

Section: Use In Canine Pituitary Dependent Hyperadrenocorticismmentioning

confidence: 99%

Trilostane in Dogs

Ramsey

2010

Veterinary Clinics of North America: Small Animal Practice

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SynopsisOver the last 10 years trilostane, a competitive inhibitor of steroid synthesis, has become widely used for the treatment of canine hyperadrenocorticism. Trilostane causes a significant but reversible decrease in cortisol production and a concomitant improvement in clinical signs in most dogs with this common condition. Side effects, though infrequent, can be serious: dogs treated with this drug require regular monitoring. This review summarises current knowledge of the use of this drug with particular emphasis on its efficacy, safety, adverse reactions and effects on endocrine parameters. Brief mention is made of its other uses in dogs and other species.

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“…Trilostane is prescribed as a treatment for PDH, and is reported to suppress cortisol and aldosterone secretion [7,9]. One report has discussed its prescription for functional adrenocortical neoplasm [3].…”

mentioning

confidence: 99%

“…After a discussion with the owner, medication rather than surgery was selected, and trilostane administration was initiated (60 mg/head, orally at 7 a.m., once daily). The dose of trilostane administration was based on previous reports [3,4,7,9].…”

mentioning

confidence: 99%

Aldosterone-, Corticosterone- and Cortisol-Secreting Adrenocortical Carcinoma in a Dog: Case Report

Machida

Uchida

Matsuda

et al. 2008

The Journal of Veterinary Medical Science

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ABSTRACT. A 12-year-old, intact female beagle exhibited symptoms of polyuria-polydipsia and hyperorexia for two months. Blood tests showed elevated asparate aminotransferase, alanine aminotransferase, alkaline phosphatase and creatine kinase levels, as well as marked hypokalemia. The results of adrenocorticotropic hormone stimulation test showed elevated cortisol, aldosterone and corticosterone concentrations. Abdominal ultrasonography confirmed a mass in the left adrenal gland. Masses were also seen in the liver and caudal vena cava. Diagnosis was a tumor of the adrenal cortex with metastases. Trilostane administration was initiated. The dog initially showed improved demeanor as a result of regulating hormone secretion. However, after 88 days, the dog weakened rapidly, before dying on the 117th day. Pathological findings confirmed a diagnosis of adrenocortical carcinoma. KEY WORDS: adrenocortical carcinoma, aldosterone, canine.

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Trilostane treatment of 78 dogs with pituitary‐dependent hyperadrenocorticism

Cited by 143 publications

References 19 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

Trilostane in Dogs

Aldosterone-, Corticosterone- and Cortisol-Secreting Adrenocortical Carcinoma in a Dog: Case Report

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