Adrenal disease in cats (Proceedings) - Veterinary Healthcare
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Adrenal disease in cats (Proceedings)


CVC IN BALTIMORE PROCEEDINGS


Radiation therapy

Because approximately 85% of cats with HAC have PDH, radiation therapy is another treatment option for many patients; however, radiation therapy is expensive and time-consuming. Radiation therapy is an effective method of treatment in cats associated with low morbidity, but signs of PDH may take several months to subside in treated animals. The major advantage of pituitary irradiation is that the primary disorder, a pituitary tumor, has been addressed. Cats with FCS that undergo bilateral adrenalectomy followed by pituitary irradiation have the best prognosis and many will live a normal life (with resolution of the DM) following these procedures.

Feline hyperaldosteronism

Feline hyperaldosteronism may be caused by a unilateral aldosterone-secreting adrenal tumor or bilateral adrenal hyperplasia. Tumors of the adrenal are usually benign; however, reports of an adrenocortical carcinoma secreting aldosterone have been described. Over secretion of aldosterone results in the classic electrolyte changes of hypokalemia, hypernatremia, and metabolic alkalosis (opposite of Addison's disease). However, primary hyperaldosteronism and secondary hyperaldosteronism caused by renal disease may be difficult to differentiate.

Hyperaldosteronism is associated with clinical signs resulting from systemic hypertension caused by expansion of blood volume or by polymyopathy resulting from hypokalemia. There is no breed predilection; however, reported cases tend to occur in older cats. In a report of 13 cases of primary hyperaldosteronism in cats, the most common clinical sign was hypokalemic polymyopathy, presenting as ventroflexion of the neck, paresis and hind limb weakness in cats. Less commonly, hypertension, fundic changes, blindness, polydipsia and polyuria, and polyphagia were observed.

The most common laboratory findings were moderate to severe hypokalemia in all cats; elevations in serum creatine kinase were observed in the majority. Only one cat exhibited hypernatremia and no cats showed metabolic alkalosis (a characteristic of hyperaldosteronism in human beings). Also surprising was the low incidence of azotemia in these cats with only two cases showing elevations of both serum creatinine and BUN. Urine-specific gravity was normal in most of the cats; however, two cats did show isosthenuria. Elevated plasma aldosterone concentrations were measured in all cases.

Plasma renin activity (PRA) was not measured in any of the cases. Abdominal ultrasonography revealed unilateral adrenal enlargement (1-3.5 cm) with an adrenal mass in almost all cases, all of which were biopsied and diagnosed as adrenal adenomas (seven cats) or carcinomas (six cats); two cats had bilateral adrenal enlargement with adenomas on postmortem examination.

Treatment of cats with primary hyperaldosteronism resulting from a unilateral adrenal tumor consists of potassium supplementation, an aldosterone blocker such as spironolactone, and amlodipine. None of the reported cases showed a normalization of serum potassium with supplementation; however, all cats showed resolution of the clinical signs of hypokalemia. Most hypertensive cats became normotensive on calcium channel therapy. Three cats were treated medically and eventually euthanatized due to chronic progressive renal failure. Surgical removal of the adrenal mass has been considered the treatment of choice in most cases.

In cats with primary hyperaldosteronism caused by benign bilateral adrenal hyperplasia; hypertension, blindness, and renal failure are more common than signs of hypokalemia (i.e., muscle weakness, cervical ventroflexion, and paresis). In a study of 11 cats with primary hyperaldosteronism, the cats were more likely to be older and have higher systolic blood pressure than the cats with adrenal tumors. Many of the affected cats exhibited ocular signs of hypertension such as retinal hemorrhage, hyphema, retinal detachments, and blindness; in contrast, only two cats with adrenal tumors exhibited blindness as a clinical sign.

Classic laboratory abnormalities observed in primary aldosteronism such as hypokalemia, elevated CK, and metabolic alkalosis are less commonly observed in cats with bilateral adrenal hyperplasia. Hypernatremia was not observed in cats with bilateral adrenal hyperplasia. Azotemia was observed in most of the cats. In the case of bilateral adrenal hyperplasia, diagnosis was achieved by documentation of increased plasma aldosterone, low to undetectable PRA, and/or increased plasma aldosterone concentration (PAC) to PRA ratios. In contrast to the previous study of adrenal tumors producing aldosterone, only four cats with bilateral adrenal hyperplasia had elevated PAC. PRA was measured in all cats in this study and was found to be abnormally low in most of cats. However, all cats showed a high PAC: PRA ratio.

Because idiopathic adrenal hyperplasia resulting in hyperaldosteronism is a bilateral disease, medical treatment is the only option available. Treatment of cats with primary hyperaldosteronism resulting from a bilateral adrenal hyperplasia consists of potassium supplementation, an aldosterone blocker such as spironlolactone, and antihypertensive therapy such as amlodipine or beta-blockers (atenelol). Most of the cats with bilateral adrenal hyperplasia eventually succumb to progressive renal insufficiency.

References available on request


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Source: CVC IN BALTIMORE PROCEEDINGS,
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