Search Results

You are looking at 1 - 2 of 2 items for

  • Author or Editor: Peter P. Kintzer x
  • Refine by Access: All Content x
Clear All Modify Search

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.

Free access
in Journal of the American Veterinary Medical Association

Objective

To evaluate clinical and laboratory findings in 225 dogs with naturally occurring hypoadrenocorticism diagnosed over a 14-year period.

Design

Retrospective case series.

Animals

220 dogs with primary hypoadrenocorticism and 5 dogs with secondary hypoadrenocorticism (primary ACTH deficiency).

Procedure

We reviewed medical records of all dogs with naturally occurring hypoadrenocorticism examined at The Animal Medical Center between 1979 and 1993 or at Tufts University, Foster Hospital for Small Animals, between 1987 and 1993.

Results

Dogs ranged from 4 months to 14 years old. Most (71%) were female, and female dogs had a significantly higher relative risk of developing hypoadrenocorticism than did males. Great Danes, Portuguese Water Dogs, Rottweilers, Standard Poodles, West Highland White Terriers, and Wheaton Terriers had a significantly higher relative risk of developing hypoadrenocorticism than did dogs of other breeds. Common owner complaints included lethargy, poor appetite, and vomiting, whereas lethargy, weakness, and dehydration were common abnormalities detected on physical examination. Serum biochemical testing at the time of diagnosis revealed moderate-to-severe azotemia and hyperphosphatemia in most dogs. In 99 of 172 (57.6%) dogs that had a pretreatment urinalysis performed, urine specific gravity was < 1.030 even though dogs were azotemic. Serum electrolyte changes included hyperkalemia (n = 215), hyponatremia (183), hypochloremia (94), and hypercalcemia (69). Five of the 220 dogs with primary hypoadrenocorticism and the 5 dogs with secondary hypoadrenocorticism did not have hyperkalemia at time of diagnosis. In all dogs, ACTH stimulation testing revealed a low to low-normal baseline serum cortisol concentration with little to no rise after ACTH administration. Endogenous plasma ACTH concentration measured in 35 dogs with primary hypoadrenocorticism was markedly high; whereas ACTH concentration was undetectable to low in the 5 dogs with secondary hypoadrenocorticism.

Clinical Implications

Hypoadrenocorticism is a rare disease in dogs, most commonly affecting young to middle-aged females; some breeds are at greater risk of developing the disease than others. In general, clinical signs are nonspecific and similar to manifestations of more common diseases. Serum electrolyte disturbances of hyperkalemia and hyponatremia are characteristic in dogs with primary hypoadrenocorticism, but concentrations may be normal in dogs with early or mild primary or secondary hypoadrenocorticism. Diagnosis of hypoadrenocorticism is best confirmed by demonstration of a low baseline serum cortisol concentration with a subnormal or negligible response to ACTH administration. Determination of endogenous plasma ACTH concentrations is valuable in differentiating primary from secondary hypoadrenocorticism, particularly in dogs with normal serum electrolyte concentrations.

Free access
in Journal of the American Veterinary Medical Association