Hyperaldosteronism and Hyperprogesteronism in a Cat with an Adrenal Cortical Carcinoma

Abstract

A 12-year-old castrated male, domestic long-haired cat weighing 4.93 kg was evaluated for weight loss and an abdominal mass. The cat had a 3-month history of diabetes mellitus treated with 2 units of ultralente insulin a twice daily. Hypokalemia, mild azotemia, mild hyperglycemia, and glucosuria were noted on recent laboratory evaluations.Physical examination findings included a thin, greasy haircoat, dermal and epidermal atrophy, cutaneous fragility, a III/VI left peristernal systolic heart murmur, and a cranial abdominal mass. Clinicopathologic abnormalities included hyperglycemia (460 mg/dL, reference range 52-153 mg/ dL), azotemia (blood urea nitrogen 76 mg/dL, reference range 17-35 mg/dL; creatinine 3.1 mg/dL, reference range 0.50-2.20 mg/dL), hypokalemia (2.5 mmol/L, reference range 3.0-4.0 mmol/L), hypochloremia (110 mmol/L, reference range 114-122 mmol/L), hyperphosphatemia (6.1 mmol/L, reference range 2.0-5.3 mmol/L), increased total CO 2 (27 mmol/L, reference range 11-22 mmol/L), and glucosuria. Venous blood gas analysis was consistent with a metabolic alkalosis (pH 7.38, HCO 3 ϭ 28.2 mmol/L) with respiratory compensation (partial pressure of carbon dioxide [PCO 2 ] ϭ 48.7). Serum total thyroxine (T 4 ) concentration, magnesium concentration, creatine phosphokinase activity, and CBC were within reference ranges. A mass cranial to the right kidney (Fig 1) and mild cardiomegaly were noted on abdominal and thoracic radiographs, respectively. The mass, measuring 2 ϫ 2.5 cm by ultrasound, was identified as the right adrenal gland (Fig 2). Echocardiography was unremarkable. Mild hypertension was identified on an initial reading (blood pressure 170 mm Hg, systolic). However, considering the fractious nature of this cat during blood pressure measurement and a lack of ocular manifestations of hypertension, therapy was deemed unnecessary at the time.Endocrinologic testing was performed to investigate functionality of the adrenal tumor. Surgical exploration and tumor removal was planned. Potassium gluconate e supplementation was initiated (2 mEq q24h PO) and insulin therapy continued pending surgery. Serum potassium concentrations did not normalize before surgery despite supplementation. At surgery, the right adrenal gland contained a 1.5 ϫ 2.0-cm mass that appeared encapsulated but closely associated with the vena cava. Extension of tumor thrombi was evident into the phenicoabdominal vein but not into the vena cava. The phenicoabdominal vein was ligated at the level of the vena cava and tumor excision was accomplished with a combination of blunt dissection and the use of hemoclips. The left adrenal gland was grossly normal, and no evidence was found of gross metastasis to any abdominal organ. Histopathology of the right adrenal gland (Fig 3) was consistent with a cortical adrenal gland carcinoma.Initial postoperative treatment included insulin, dexamethasone f (0.25 mg/kg q24h IV), and a balanced electrolyte solution g with potassium supplementation (20 mEq/L IV). Insulin administration was discontinued after ...

Adrenal gland

“…4,5 In these cases the signs of hyperprogesteronism usually predominate, resulting in very similar clinical signs to those encountered with hypercortisolemia ( Fig. 35-2).…”

Excessive production of sex hormones in a cat with an adrenocortical tumor

“…6,8,11,12 In 3 of these reports, 6,8,12 cats had increased serum concentrations of progesterone and typical clinical signs of hyperadrenocorticism. In the fourth report, 11 the cat had bilaterally enlarged adrenal glands, increased serum concentrations of testosterone, and similar physical and behavior changes to that of the cat reported here.…”

Serum aldosterone and cortisol concentrations before and after suppression with fludrocortisone in cats

“…Two cats were reported to have concurrent hyperprogesteronism in addition to hyperaldosteronism. 2,4 To our knowledge, there are no reports of cats having concurrent hyperaldosteronism and hypercortisolism, but this is possible in theory. In such a case, fludrocortisone is unlikely to affect cortisol concentrations because cortisol secretion would presumably be autonomous.…”

“…15,23 In contrast, in cats, suspicion of PHA arises with identification of hypokalemia, hypertension, and elevated plasma aldosterone concentration; diagnosis ultimately relies on identification of a discrete tumor within the adrenal glands. 1,2,4,[7][8][9]14,17,[19][20][21] However, in the absence of a discrete tumor, such as in cats with adrenocortical nodular hyperplasia, minimal or no adrenal gland changes may be detected via ultrasound. 10 In fact, in humans, following a diagnosis of PHA, further testing such as a computed tomography scan and adrenal vein blood sampling is conducted to differentiate between unilateral and bilateral hyperplasia, adenoma or adenocarcinoma.…”