Hypoadrenocorticism following therapy with o,p-DDD for hyperadrenocorticism in four dogs.
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.
D000224:Addison Disease / Q000139:chemically induced / Q000662:veterinary*; D000818:Animals; D003480:Cushing Syndrome / Q000150:complications / Q000188:drug therapy / Q000662:veterinary*; D004283:Dog Diseases / Q000139:chemically induced / Q000188:drug therapy; D004285:Dogs; D005260:Female; D008297:Male; D008939:Mitotane / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use
D008939:Mitotane