Scientific Journal

Scientific Journal of the Hellenic Companion Animal Veterinary Society (HCAVS)

 

Iatrogenic hypoaldosteronism following treatment with trilostane for hyperadrenocorticism in a dog


Pozoukidou E. DVM, Medicine Unit, Companion Animals Clinic, School of Veterinary Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki
Papadimas K. DVM, Medicine Unit, Companion Animals Clinic, School of Veterinary Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki
Konstantinidis A.O. DVM, Medicine Unit, Companion Animals Clinic, School of Veterinary Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki
Soumpasis N. DVM, Medicine Unit, Companion Animals Clinic, School of Veterinary Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki

Introduction

Trilostane is currently the medical treatment of choice for hyperadrenocorticism in dogs. Iatrogenic hypoadrenocorticism is considered infrequent. Mineralocorticoid concentrations remain normal in most dogs, and the glucocorticoid deficiency is usually transient. This presentation describes a case of iatrogenic hypoaldosteronism in a dog on maintenance trilostane therapy for hyperadrenocorticism.

Clinical Case

A 6.5-year-old, female spayed Cocker Spaniel was presented due to anorexia. The dog had been treated with trilostane for the last 2.5 years since it was diagnosed with hyperadrenocorticism. Clinical examination revealed no abnormal findings. Serum biochemistry showed hyponatremia and normal potassium, with a reduced Na+/K+ ratio of 23. Basal and post-ACTH cortisol concentrations were within normal values for a dog with hyperadrenocorticism receiving trilostane. In contrast, serum basal and post-ACTH aldosterone concentrations were extremely low.

Results

Based on history, clinical and laboratory findings, including basal and post-ACTH cortisol and aldosterone concentrations, iatrogenic hypoaldosteronism was diagnosed. Trilostane was discontinued, desoxycorticosterone pivalate (DOCP) was prescribed and the dog responded well to therapy.

Conclusion

Aldosterone deficiency may occur in dogs receiving trilostane. This is the first case describing complete aldosterone deficiency without cortisol deficiency in a dog. Iatrogenic hypoaldosteronism should be considered as a differential in dogs receiving trilostane, especially when presented with diarrhea, anorexia and vomiting.

References

  • Griebsch C, Lehnert C, Williams GJ, Failing K, Neiger R (2014) Effect of trilostane on hormone and serum electrolyte concentrations in dogs with pituitary-dependent hyperadrenocorticism. J Vet Intern Med 28(1).
  • Wenger M, Sieber-Ruckstuhl NS, Müller C, Reusch CE (2004) Effect of trilostane on serum concentrations of aldosterone, cortisol, and potassium in dogs with pituitarydependent hyperadrenocorticism. Am J Vet Res 65(9).
  • Reid LE, Behrend EN, Martin LG, Kemppainen RJ, Ward CR, Lurye JC, Donovan TC, Lee HP (2014) Effect of trilostane and mitotane on aldosterone secretory reserve in dogs with pituitary-dependent hyperadrenocorticism. J Vet Intern Med 28(2).
  • Galac S, Buijtels JJCWM, Mol JA, Kooistra HS (2010) Effects of trilostane on the pituitary-adrenocortical and renin-aldosterone axis in dogs with pituitary-dependent hypercortisolism. Vet J 183(1).

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