Mitotane treatment of 32 dogs with cortisol-secreting adrenocortical neoplasms

Peter P. Kintzer From the Departments of Environmental Studies and Medicine, School of Veterinary Medicine, Tufts University, North Grafton, MA 01536

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Mark E. Peterson Department of Medicine, The Animal Medical Center, 510 E 62nd St, New York, NY 10021.

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Summary

Thirty-two dogs with hyperadrenocorticism caused by cortisol-secreting adrenocortical neoplasia were treated with mitotane at an initial daily induction dosage of 27.5 to 75.0 mg/kg of body weight (mean, 46.3 mg/kg) for 10 to 14 days. All dogs received daily maintenance glucocorticoid supplementation during the induction period. After 2 weeks, the ACTH-stimulated serum cortisol concentration had decreased to within or below the reference range for baseline cortisol concentration in 18 (56.3%) of the 32 dogs; the remaining 14 (43.7%) still responded to ACTH administration with serum cortisol concentrations above the reference range. In these 14 dogs, mitotane was continued at a higher daily dosage (mean, 60.7 mg/kg) for an additional 1 to 9 weeks. Serum cortisol concentration subsequently fell within or below the reference range for baseline cortisol concentration in all but 1 dog. In 30 of the 32 dogs, mitotane was continued at an initial mean maintenance dosage of 101.6 mg/kg/wk, divided into 2 to 5 doses. Twenty-two dogs received prednisone daily (0.2 mg/kg) throughout the maintenance period. One or more relapses occurred in 19 (63%) of the 30 dogs. In dogs with relapse, the mean maintenance mitotane dosage was increased from 98.1 mg/kg/wk to a high of 212.4 mg/kg/wk. After a mean maintenance treatment time of 13.2 months, final mean maintenance dosage required in the 30 dogs ranged from 35.3 to 1,273 mg/kg/wk. Adverse effects were seen in 19 (59.4%) of the 32 dogs as a result of a drug toxicosis associated with high-dosage administration of mitotane, low serum cortisol concentration, or both. Complete glucocorticoid and mineralcorticoid deficiency (Addison's disease) developed in 3 dogs after mitotane treatment. Mean survival time of the 32 dogs was 16.4 months (range, 20 days to 5.1 years). Six dogs died or were euthanatized as a result of progression of adrenal carcinoma and 4 because of complications associated with hyperadrenocorticism. Results of this study revealed that mitotane is an effective and acceptable alternative to surgery in most dogs with cortisol-secreting adrenocortical tumors. Of the 32 dogs, 66% were considered to have a good to excellent response to treatment. In general, the response in dogs without evidence of metastatic disease was better than in those dogs with known metastatic disease.

Summary

Thirty-two dogs with hyperadrenocorticism caused by cortisol-secreting adrenocortical neoplasia were treated with mitotane at an initial daily induction dosage of 27.5 to 75.0 mg/kg of body weight (mean, 46.3 mg/kg) for 10 to 14 days. All dogs received daily maintenance glucocorticoid supplementation during the induction period. After 2 weeks, the ACTH-stimulated serum cortisol concentration had decreased to within or below the reference range for baseline cortisol concentration in 18 (56.3%) of the 32 dogs; the remaining 14 (43.7%) still responded to ACTH administration with serum cortisol concentrations above the reference range. In these 14 dogs, mitotane was continued at a higher daily dosage (mean, 60.7 mg/kg) for an additional 1 to 9 weeks. Serum cortisol concentration subsequently fell within or below the reference range for baseline cortisol concentration in all but 1 dog. In 30 of the 32 dogs, mitotane was continued at an initial mean maintenance dosage of 101.6 mg/kg/wk, divided into 2 to 5 doses. Twenty-two dogs received prednisone daily (0.2 mg/kg) throughout the maintenance period. One or more relapses occurred in 19 (63%) of the 30 dogs. In dogs with relapse, the mean maintenance mitotane dosage was increased from 98.1 mg/kg/wk to a high of 212.4 mg/kg/wk. After a mean maintenance treatment time of 13.2 months, final mean maintenance dosage required in the 30 dogs ranged from 35.3 to 1,273 mg/kg/wk. Adverse effects were seen in 19 (59.4%) of the 32 dogs as a result of a drug toxicosis associated with high-dosage administration of mitotane, low serum cortisol concentration, or both. Complete glucocorticoid and mineralcorticoid deficiency (Addison's disease) developed in 3 dogs after mitotane treatment. Mean survival time of the 32 dogs was 16.4 months (range, 20 days to 5.1 years). Six dogs died or were euthanatized as a result of progression of adrenal carcinoma and 4 because of complications associated with hyperadrenocorticism. Results of this study revealed that mitotane is an effective and acceptable alternative to surgery in most dogs with cortisol-secreting adrenocortical tumors. Of the 32 dogs, 66% were considered to have a good to excellent response to treatment. In general, the response in dogs without evidence of metastatic disease was better than in those dogs with known metastatic disease.

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