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Controlled Clinical Trial
. 2017 Sep 4;13(1):279.
doi: 10.1186/s12917-017-1187-0.

Effects of Trilostane on urinary Catecholamines and their metabolites in dogs with Hypercortisolism

Affiliations
Controlled Clinical Trial

Effects of Trilostane on urinary Catecholamines and their metabolites in dogs with Hypercortisolism

Nadja Sieber-Ruckstuhl et al. BMC Vet Res. .

Abstract

Background: Glucocorticoids influence the synthesis and metabolism of catecholamines (epinephrine and norepinephrine) and metanephrines (metanephrine and normetanephrine). The aim of this study was to measure urinary catecholamines and metanephrines in dogs with hypercortisolism before and during trilostane therapy. Urine samples were collected during initial work up and during therapy with trilostane in 14 dogs with hypercortisolism and in 25 healthy dogs. Epinephrine, norepinephrine, metanephrine and normetanephrine were measured using high-pressure liquid chromatography and expressed as ratios to urinary creatinine concentration.

Results: Untreated dogs with hypercortisolism had significantly higher epinephrine, norepinephrine, and normetanephrine:creatinine ratios compared to healthy dogs. During trilostane therapy, urinary catecholamines and their metabolites did not decrease significantly. However, dogs with low post-ACTH cortisol concentrations during trilostane therapy had less increased epinephrine, norepinephrine and normetanephrine:creatinine ratios compared to healthy dogs. There was no correlation of urinary catecholamines and their metabolites with baseline or post-ACTH cortisol or endogenous ACTH concentrations during trilostane therapy.

Conclusion: Influences between steroid hormones and catecholamines seem to occur, as dogs with hypercortisolism have significantly higher urinary epinephrine, norepinephrine, and normetanephrine:creatinine ratios. Once-daily trilostane therapy does not lead to a significant decrease in catecholamines and their metabolites. Trilostane-treated dogs still have increased urinary epinephrine, norepinephrine and normetanephrine:creatinine ratios during trilostane therapy.

Keywords: ACTH; Canine; Metanephrines; Pheochromocytoma; Trilostane therapy.

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Conflict of interest statement

Ethics approval

The use of the dogs was approved by the veterinary office of the canton of Zurich and was in accordance with the guidelines and directives established by the Animal Welfare Act of Switzerland (TVB 199/2004). Informed consent of all pet owners was obtained before including the dogs in the study.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
Urinary epinephrine (a), norepinephrine (b), metanephrine (c) and normetanephrine:creatinine (d) in dogs with hypercortisolism before (open circles) and during (closed circles) trilostane therapy and in healthy dogs (squares). The horizontal bars represent the median of each group. The shaded area indicates the preliminary reference interval
Fig. 2
Fig. 2
Urinary epinephrine (a), norepinephrine (b), metanephrine (c) and normetanephrine:creatinine (d) in dogs with hypercortisolism during trilostane therapy according to their post-ACTH cortisol concentration (41-138 nmol/L or <41 nmol/L). The horizontal bars represent the median of each group. The shaded area indicates the preliminary reference interval

References

    1. Rosol TJ, Yarrington JT, Latendresse J, Capen CC. Adrenal gland: structure, function, and mechanisms of toxicity. Tox Pathol. 2001;29:41–18. doi: 10.1080/019262301301418847. - DOI - PubMed
    1. Eisenhofer G, Kopin IJ, Goldstein DS. Catecholamine metabolism: a contemporary view with implications for physiology and medicine. Pharmacol Rev. 2004;56:331–349. doi: 10.1124/pr.56.3.1. - DOI - PubMed
    1. Goodman R, Edgar D, Thoenen H, Wechsler W, Herschman H. Glucocorticoid induction of tyrosine hydroxylase in a continuous cell line of rat pheochromocytoma. J Cell Biol. 1978;78:R1–R7. doi: 10.1083/jcb.78.1.R1. - DOI - PMC - PubMed
    1. Tai TC, Claycomb R, Her S, Bloom AK, Wong DL. Glucocorticoid responsiveness of the rat phenylethanolamine N-methyltransferase gene. Mol Pharmacol. 2002;61:1385–1392. doi: 10.1124/mol.61.6.1385. - DOI - PubMed
    1. Yoshida-Hiroi M, Bradbury MJ, Eisenhofer G, Hiroi N, Vale WW, Novotny GE, Hartwig HG, Scherbaum WA, et al. Chromaffin cell function and structure is impaired in corticotropin-releasing hormone receptor type 1-null mice. Mol Psychiatry. 2002;7:967–974. doi: 10.1038/sj.mp.4001143. - DOI - PubMed

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