Abstract
Background: In dogs, spontaneous Cushing’s syndrome is most often pituitary-dependent and caused by hypersecretion of adrenocorticotropic hormone (ACTH), resulting in increased adrenocortical glucocorticoid secretion similar to horses. In horses with Cushing’s syndrome (or pituitary pars intermedia dysfunction [PPID]) a thyrotropin-releasing hormone (TRH) stimulation test can be used for diagnosis, as TRH administration results in increased circulating ACTH and cortisol concentrations in affected horses.Objective: The aim of this study was to investigate the effect of TRH administration on the circulating ACTH and cortisol concentrations in dogs with pituitary-dependent hypercortisolism (PDH).Methods: Ten clinically normal control dogs and 10 dogs with PDH, all client owned, underwent a TRH stimulation test with measurement of plasma concentrations of ACTH and cortisol, before and after intravenous administration of 10 μg TRH/kg bodyweight.Results: Plasma ACTH concentration did not rise significantly after TRH stimulation, neither in PDH dogs nor in clinically normal dogs. In contrast, the plasma cortisol concentration did increase significantly after TRH stimulation in both groups (p = .003 in PDH and p < .001 in control). Immunohistochemistry of normal adrenal glands demonstrated the presence of TRH receptors in the whole adrenal cortex.Conclusions: The results of this study demonstrate that the TRH stimulation test should be rejected as a tool to diagnose PDH in dogs. The observed TRH-induced increase in plasma cortisol concentration without a significant rise in plasma ACTH concentration may be explained by a direct effect of TRH on adrenocortical cells mediated by adrenocortical TRH receptors.
Highlights
Spontaneous hypercortisolism or Cushing’s syndrome is one of the most common endocrinopathies in dogs, with a reported incidence of 1–2 per 1000 dogs per year (Willeberg and Priester 1982)
75–80% of dogs with pituitarydependent hypercortisolism (PDH) have an adrenocorticotropic hormone (ACTH) producing adenoma located in the anterior lobe (AL) of the pituitary gland; in the other 20–25% the adenoma arises from the pars intermedia (PI) (Peterson et al 1982; Peterson et al 1986)
This study investigated the effect of thyrotropin-releasing hormone (TRH) administration on circulating concentrations of ACTH and cortisol, in both clinically normal control dogs and dogs with pituitary-dependent hypercortisolism (PDH), in order to evaluate whether a TRH stimulation test may be used to diagnose hypercortisolism in dogs
Summary
Spontaneous hypercortisolism or Cushing’s syndrome is one of the most common endocrinopathies in dogs, with a reported incidence of 1–2 per 1000 dogs per year (Willeberg and Priester 1982). In the other 80–85% of cases, canine hypercortisolism is pituitary-dependent and caused by hypersecretion of adrenocorticotropic hormone (ACTH), resulting in increased glucocorticoid secretion by the adrenals (Owens and Drucker 1977). Spontaneous Cushing’s syndrome is most often pituitary-dependent and caused by hypersecretion of adrenocorticotropic hormone (ACTH), resulting in increased adrenocortical glucocorticoid secretion similar to horses. In horses with Cushing’s syndrome (or pituitary pars intermedia dysfunction [PPID]) a thyrotropin-releasing hormone (TRH) stimulation test can be used for diagnosis, as TRH administration results in increased circulating ACTH and cortisol concentrations in affected horses. Objective: The aim of this study was to investigate the effect of TRH administration on the circulating ACTH and cortisol concentrations in dogs with pituitary-dependent hypercortisolism (PDH). The observed TRH-induced increase in plasma cortisol concentration without a significant rise in plasma ACTH concentration may be explained by a direct effect of TRH on adrenocortical cells mediated by adrenocortical TRH receptors
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