Introduction

Clinical and Diagnostic Aspects

Hyperadrenocorticism (HAC) can either be pituitary dependent (PDH) due to hyperse­cretion of corticotropin (ACTH) by the pituitary gland, adrenal dependent (ADH) due to functional adrenocortical tumors, or iatrogenic from the administration of corti­costeroids.

In dogs, the most common clinical signs are polyuria and polydipsia, polyphagia, alo­pecia, pendulous abdomen, hepatomegaly, panting, and muscular atrophy (Arenas, Melian, and Perez-Alenza 2013). In cats, the clinical signs are less obvious since HAC is associated with diabetes mellitus in 90% of cases (Mellett, Bruyette, and Stanley 2013); the most characteristic abnormality is thin­ning and extreme skin fragility (Figure 12.1). Systemic hypertension is more frequent in dogs than cats.

The initial approach to an animal sus­pected with HAC includes complete blood count, serum biochemistry, and urinalysis. The most common findings are stress leuko- gram (dogs), moderate thrombocytosis (dogs), variable increase in ALP (dogs and cats), ALT (dogs and cats), cholesterol, and triglycerides (dogs and cats), hyperglycemia (more common in cats), frequent isosthenu­ria or hyposthenuria (dogs), and proteinuria (dogs and cats). In both species, diagnosis of naturally acquired HAC will be confirmed through dexamethasone suppression and/or ACTH stimulation test; the latter is also use­ful to diagnose the iatrogenic form and mon­itor treatment. The urine cortisol:creatinine ratio may not be helpful as a screening test for HAC because of its variable sensitivity and low specificity. Ultrasound evaluation of the adrenal glands and endogenous ACTH measurement are useful for distin­guishing PDH from ADH, and CT and MRI can be used to characterize the pituitary gland.