Willard M D, Schall W D, Nachreiner R F, Shelton D G
J Am Vet Med Assoc. 1982 Mar 15;180(6):638-41.
Hypoadrenocorticism developed in 4 of 26 dogs treated with mitotane (o,p-DDD) for hyperadrenocorticism. Evidence of the hypoadrenocorticism was detected from 2-8 weeks after the beginning of weekly or bimonthly maintenance o,p-DDD therapy. The adversely affected dogs had hyponatremia plus hyperkalemia, and 3 of the 4 had severely diminished plasma cortisol concentrations at rest or after stimulation with ACTH given IM. One dog did not have detectable plasma aldosterone concentrations before or after ACTH administration. Clinically, 3 of the 4 dogs responded well to mineralocorticoid replacement. Electrolyte determinations after replacement therapy in 1 dog documented normal serum sodium and potassium concentrations. One dog died despite therapy and was determined to have adrenocortical destruction.