Addisonian Crisis due to Metastatic Adenocarcinoma in a Pygmy Goat

A 15-year-old Pygmy doe was evaluated for acute onset of lethargy, anorexia, and weakness. Adrenal insufficiency was diagnosed based on physical exam findings, blood work abnormalities (hyponatremia, hyperkalemia, azotemia, and hypoglycemia), and lack of cortisol response to the ACTH stimulation test. Abdominal ultrasound exam revealed an intact urinary tract and multiple bilateral peri-renal masses. The doe was treated with intravenous fluid therapy aimed at correcting the electrolyte abnormalities and intravenous corticosteroids. She responded favorably to medical therapy in 24 hours, with dramatic improvement in attitude and appetite. Fluid therapy was discontinued, and the doe was discharged from the hospital on steroid supplementation. She deteriorated rapidly and died at home 36 hours after discharge. Necropsy results revealed metastatic adenocarcinoma originating from the uterus that infiltrated the urinary bladder, the region of the adrenal glands, the left and right renal lymph nodes, the left kidney, the caudal vena cava, the submandibular lymph nodes, the diaphragm, the lungs, and the omentum. Addison’s syndrome in ruminants should be considered as an uncommon sequel of intra-abdominal neoplastic processes. 1. Introduction To the authors’ knowledge, this is the first clinical report of Addison’s syndrome in a goat. Addison’s syndrome describes a clinical phenomenon when the adrenal cortex is unable to produce steroid hormones, in particular the corticosteroid cortisol and the mineralocorticoid aldosterone. Cortisol is produced by the zona fasciculata of the adrenal cortex, and its primary functions are in the maintenance of blood pressure, cardiovascular function, and physiologic glucose levels as well as the regulation of protein, carbohydrate, and fat metabolism. Aldosterone is produced by the zona glomerulosa of the adrenal cortex and acts on the collecting ducts and the distal convoluted tubules in the kidneys. It is responsible for conservation of sodium, water retention, maintenance of blood pressure, and secretion of potassium？？[1]. Addison’s disease is a well-described clinical syndrome in dogs, characterized by diarrhea, vomiting, lethargy, anorexia, muscle weakness, hyperkalemia, hyponatremia, hypoglycemia, and lack of corticosteroid-induced stress leukogram despite illness？？[2]. The doe in this case report presented with similar, nonspecific clinical signs and, along with the characteristic serum electrolyte and biochemical abnormalities, raised the clinician’s suspicion for primary hypoadrenocorticism. 2. Case Presentation A