Recent developments in canine Cushing’s syndrome

Abstract

Cushing’s syndrome or hypercortisolism is in most of the cases ACTH-dependent due to ACTH hypersecretion by a pituitary corticotroph adenoma, however, the ectopic ACTH secretion has been now described in a dog as well. In the remaining cases, hypercortisolism is ACTH-independent and results from hypersecretion of glucocorticoids by an adrenocortical tumour. A food-dependent hypercortisolism has been reported in one dog.

Research about the pathogenesis of cortisol-secreting adrenocortical tumors in dogs revealed that hypercortisolism is not the result of a larger quantity of steroidogenic enzymes responsible for the production of cortisol. Also, the malignant adrenocortical tumours contain significantly lower amount of ACTH receptors than are found in benign tumours. This knowledge may eventually lead to techniques for diagnosing adrenocortical tumours as either malignant or benign.

Lately, trilostane has become the favorable medical treatment of hypercortisolism. Its effect on the hypothalamic-pituitary-adrenal axis, but also on the renin-aldosterone system has been demonstrated.