Effects on the urinalysis

A common occurrence with glucocorticoid use in dogs is a rapid onset of PU/PD accompanied by a decrease in the urine specific gravity. In multiple studies, glucocorticoids have caused no significant changes in feline urine specific gravity.^11,15,18,24 Increases in water intake and urine output can occur in glucocorticoid-treated cats, but longer treatment courses and higher glucocorticoid doses seem to be necessary to generate these signs than in dogs.^15,24 Consequently, interference with the release or action of antidiuretic hormone does not appear to be a major factor in the onset of glucocorticoid-induced PU/PD, as is proposed for dogs.

Glucocorticoid-induced glucosuria has been documented in cats, and osmotic diuresis may be involved in the PU/PD seen in some cases.^18,24-26 In other cases, PU/PD has been seen in the absence of concurrent glucosuria, suggesting additional mechanisms may be involved.^18,25 Other urinalysis changes were seen in a study of five cats that received 2.2 mg/kg once a day of prednisolone for two weeks; these included a significant decrease in urine pH, as well as significant increases in the urinary excretion of creatinine, magnesium, phosphate, and potassium.²⁷

Glucocorticoids can antagonize the effects of insulin and promote increased circulating blood glucose concentrations. These effects are mediated through various pathways, including increased hepatic glucose production and decreased glucose uptake by the peripheral tissues.²⁸ Glucocorticoids decrease insulin sensitivity and glucose tolerance measurements in cats.^25,29 This induced insulin-resistance can, in some cases, lead to overt diabetes mellitus similar to type II diabetes in people. Some authors think that cats are particularly susceptible to this adverse effect and that glucocorticoids are more potent hyperglycemic agents in cats than in other species.^9,24 Combined and controlled studies relative to other species would be required to confirm this theory.

However, weak support of the theory exists when comparing separate studies that showed no changes in blood glucose or glucose-tolerance measurements in dogs after 28 days of prednisone therapy at a dose of 1.1 mg/kg once a day with studies that revealed cats treated with similar doses of prednisolone (2 mg/kg once a day) developed hyperglycemia and impaired glucose tolerance after only eight days.^29,30 Drug withdrawal should resolve the glucocorticoid-induced hyperglycemia and glucosuria in otherwise healthy cats. However, in cats with pre-existing subclinical diabetes mellitus, glucocorticoid therapy may be enough to "push" the patient into a clinical diabetic state that requires insulin therapy.

Effects on the liver

Cats do not possess the glucocorticoid-induced isoenzyme of ALP, which is present in dogs.³¹ Consequently, a glucocorticoid-induced increase in ALP activity, while common in dogs, is rare in cats, though it may occasionally be seen in individual cases.^15,32 Additionally, palpable enlargement of the liver is not a common feature of glucocorticoid use in cats as it is in dogs. Glucocorticoid-induced hepatomegaly in dogs is caused by a vacuolar hepatopathy from glycogen deposition. These changes have been termed a corticosteroid hepatopathy, which has been said to be unique to dogs.⁹ However, several studies have examined liver biopsy specimens of cats either with natural hyperadrenocorticism or after glucocorticoid treatment, and each consistently has shown excessive glycogen deposition in a typical vacuolar pattern that is characteristic of the corticosteroid hepatopathy.^{15,18,24,32,33}

Thus, corticosteroid hepatopathy occurs in cats, but it may be difficult to detect without invasive tests such as liver biopsies. Even abdominal ultrasonography may fail to identify typical hepatic changes in affected cats.¹⁵