Mitch was presented to his primary care veterinarian for evaluation of polyuria and polydipsia of six months' duration.
Hyperadrenocorticism affects many adult dogs. Whether the disease is pituitary-dependent (80% to 85% of spontaneous cases) or adrenal-dependent (15% to 20% of cases), the clinical and laboratory abnormalities associated with it result from chronic hypercortisolemia. Clinical signs of hyperadrenocorticism at the time of diagnosis can vary widely, and they develop so gradually that owners often mistake the signs for "normal" aging. Being aware of the more subtle signs of canine hyperadrenocorticism can be key to early diagnosis and initiation of therapy.
COMMON CLINICAL SIGNS OF CANINE HYPERADRENOCORTICISM
Whenever possible, pituitary-dependent hyperadrenocorticism and adrenal tumors should be differentiated to help guide therapy and patient monitoring. Early diagnosis and management of canine hyperadrenocorticism may not only improve the patient's clinical signs but may also keep the more severe consequences of Cushing's syndrome from developing.
CASE FILE: MITCH 12-year-old neutered male dachshund weighing 22 lb (10 kg)
Mitch was presented to his primary care veterinarian for evaluation of polyuria and polydipsia of six months' duration. The dog's urine specific gravity was 1.010 and a serum chemistry profile revealed an alkaline phosphatase activity of 1,240 IU/L (reference range 37 to 105 IU/L). The results of a complete blood count were within normal limits, and urine bacterial culture results were negative.
Adrenal function test results
The results of an adrenocorticotropic hormone (ACTH) stimulation test revealed a baseline cortisol concentration of 3.6 μg/dl (reference range = 1.4 to 5 μg/dl) and a one-hour post-ACTH cortisol concentration of 12.9 μg/dl (reference range = 5.5 to 20 μg/dl). Low-dose dexamethasone suppression (LDDS) test results revealed a resting cortisol concentration of 9.1 μg/dl (reference range 1.4 to 5 μg/dl) with four- and eight-hour post-dexamethasone cortisol concentrations of 5.6 μg/dl and 2.3 μg/dl (reference range < 1.4 μg/dl), respectively.
The abnormal LDDS eight-hour cortisol concentration, in combination with more than 50% suppression in cortisol concentration during the test, was diagnostic of pituitary-dependent hyperadrenocorticism (PDH). Mitch was referred to VCA West Los Angeles Animal Hospital to be evaluated for treatment.
Physical examination revealed mild hepatomegaly and mild bilaterally symmetrical alopecia involving the ventral abdomen and thighs. Surgical, radiation, and medical treatment options for PDH were discussed with the owners, who opted for medical management.
Treatment and follow-up
Treatment with VETORYL® Capsules (trilostane) was begun at a dose of 3 mg/kg, given orally once daily in the morning with food. The owner was instructed to monitor Mitch's water consumption, urination, appetite, and activity level and to observe the dog for vomiting or diarrhea. A recheck physical examination and an ACTH stimulation test with serum electrolyte measurements were scheduled for 10 days after the start of the treatment.
Initial follow-up visits
At the 10-day recheck visit, the owners reported a marked reduction in Mitch's polyuria and polydipsia. The dog's serum sodium and potassium concentrations were within normal limits. An ACTH stimulation test performed four hours after administration of the VETORYL Capsules dose revealed pre- and post-ACTH cortisol concentrations of 1.6 and 5.1 μg/dl, respectively, indicating adequate inhibition of glucocorticoid production.
Based on these results and the improvement in clinical signs, the initial VETORYL Capsules dosage was continued. Mitch was scheduled for a 30-day post-treatment recheck examination.
During the subsequent visit, the owners reported that Mitch was more active and exhibited normal water consumption and urination. A morning urine sample collected by the owner showed a specific gravity of 1.036. The dog's serum sodium and potassium concentrations were normal, and an ACTH stimulation test revealed pre- and post-ACTH cortisol concentrations of 2.8 and 5.1 μg/dl, respectively, indicating adequate inhibition of glucocorticoid production.
The initial VETORYL Capsules dosage was continued, and a 90-day post-treatment recheck examination was scheduled.
Mitch's long-term response
At his three and six month recheck visits, Mitch continued to be clinically normal, and his electrolyte concentrations remained within normal limits. The ACTH stimulation tests revealed post-ACTH cortisol concentrations of 5.2 μg/dl at three months and 5.9 μg/dl at six months of VETORYL Capsules treatment.
Mitch had three episodes of diarrhea 5.5 months after starting therapy, which resolved within 24 hours of the owners feeding the dog a bland diet. No adjustments were made in the VETORYL Capsules treatment protocol.
As illustrated by this case, polyuria and polydipsia may be the only clinical signs of hyperadrenocorticism in some patients. Although Mitch had mild bilaterally symmetrical endocrine alopecia, this abnormality was subtle. If the polyuria and polydipsia had not been identified, the alopecia may not have warranted a diagnostic workup.
This case also serves as a reminder that 15% to 20% of dogs with hyperadrenocorticism may have normal ACTH stimulation test results at initial evaluation.1 An LDDS test is the next diagnostic step for dogs that have clinical signs suggestive of hyperadrenocorticism but normal ACTH stimulation test results. However, up to 10% of dogs with hyperadrenocorticism will have a normal LDDS test result.1 So in direct contrast to Mitch's situation, if an LDDS test is used as the initial screening test and the result is normal, perform an ACTH stimulation test.
For dogs with hyperadrenocorticism being treated with VETORYL Capsules, the target post-ACTH serum cortisol concentration is 1.45 to 9.1 μg/dl, along with well-controlled clinical signs. Mitch obtained clinical and hormonal improvement with once-daily dosing of VETORYL Capsul
1. Gilor C, Graves TK. Interpretation of laboratory tests for canine Cushing's syndrome. Top Companion Anim Med 2011;26(2):98-108.
This case was solicited from the prescribing veterinarian and may represent an atypical case study. Similar results may not be obtained in every case.
* The dog in the photographs is not Mitch, the dog described in this article.
Dr. Bruyette is the medical director at VCA West Los Angeles Animal Hospital and a clinical professor in the Department of Radiation Oncology at UCLA.
David Bruyette, DVM, DACVIM
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• Diagnosing and treating canine hyperadrenocorticism
Presented by Audrey K. Cook, BVM&S, MRCVS, DACVIM, DECVIM, and David s. Bruyette, DVM, DACVIM
• Cushing's disease: Inside and out
Rhonda Schulman DVM, DACVIM, and John Angus, DVM, DACVD
• Diagnosing and treating feline hyperthyroidism
Presented by Andrew J. Rosenfeld, DVM, DABVP
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