Effect of ophthalmic prednisolone acetate on the canine adrenal gland and hepatic function.

Iatrogenic hypothalamic-hypophysis-adrenal axis suppression occurred in 5 small dogs as a result of ophthalmic instillation of 1% prednisolone acetate. An ophthalmic suspension was applied 4 times a day to each eye, such that 4 mg/day was delivered for 2 weeks followed by 2.67 mg/day for 2 weeks. After treatment week 2, serum cortisol decreased from base-line mean values of 17.66 ng/ml (before ACTH) and 139.16 ng/ml (60 minutes after ACTH) to 3.22 ng/ml (before ACTH) and 13.58 ng/ml (60 minutes after ACTH). After treatment week 4, serum cortisol values decreased to a mean of 1.76 ng/ml (before ACTH) and 4.82 ng/ml (60 minutes after ACTH). Before ACTH cortisol values returned to base line 2 weeks after discontinuing treatment. Values after ACTH administration remained 26% lower than base line (P = 0.0132), although within a normal response range. Hepatic carbohydrate metabolism was altered, allowing marked glycogen accumulation. Marked increases in the blood glucose values after glucagon stimulation testing occurred at 3, 5, 15, 30, and 60 minutes after glucagon administration. The greatest increase corresponded to the 30-minute sample with a mean glucose increase of 112.40 mg/dl from base-line values (P = 0.0022) as a result of the ophthalmic corticosteroid applied. Seemingly, topical ophthalmic corticosteroids have the potential for causing adrenocortical suppression and hepatic metabolic changes. The dosage level of treatment was low enough to avoid major hematologic changes. The exaggerated response to the glucagon tolerance test indicates that this test can be used in detecting hyperglucocorticism.