Page 110 - WSAVA2018
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 25-28 September, 2018 | Singapore
or if clinical signs consistent with HAC persist with insulin therapy.5 Other reasons for insulin resistance should
be considered to include improper insulin injection technique, outdated insulin, or incorrect syringes. The practitioner should also check for other concurrent diseases such as urinary tract infections. If HAC is still suspected, adrenal function testing should be initiated. Do not test for HAC if the dog is clinically unstable. There should be loose control of diabetes mellitus with the blood sugar ideally ranging from 100-350 mg/dl for most of the day. Do not test for HAC if the dog is ketotic, hypoglycemic, or hyperosmolar. Three screening tests FOR HAC are available.6 The urine cortisol:creatinine ratio is very sensitive (100%) although not specific.
A second screening test for HAC is the low dose dexamethasone suppression test. This should be to go to test unless there is significant concurrent disease such as diabetes mellitus. A third screening test for HAC is
the ACTH Stimulation Test. It is more specific in animals with concurrent disease and recommended for use in dogs with concurrent diabetes mellitus to decrease the possibility of a false positive response. The practitioner measures cortisol before and 60 min after injection of
5 ug/kg synthetic ACTH (cortrosyn). In diabetic patients, the owner should feed and administer insulin as usual.
A simultaneous glucose curve should be performed in conjuction with the ACTH-stimulation test to ensure that the animal has blood glucose within the optimal range during testing. If ACTH-stimulation testing supports
HAC, then treatment should be initiated. If HAC is still suspected but is not supported by the ACTH-stimulation test, then the test can be repeated 2-4 weeks later.
Medical treatment of HAC includes trilostane (VetorylR) and mitotane (LysodrenR). Ketoconazole and deprenyl (AniprilR) have also been advocated, but are substantially less effective than trilostane or lysodren. Surgical options include adrenalectomy and hypophysectomy. Trilostane is a competitive 3B-OH steroid dehydrogenase
inhibitor that inhibits the conversion of pregnenolone
to progesterone in the adrenal gland. This blocks the formation of the end products of progesterone including cortisol and aldosterone. Trilostane can be compounded but a manufactured product is available (Vetoryl R, Dechra Pharmaceuticals). VetorylR is FDA approved
for veterinary use so that the veterinarian is legally protected. VetrorylR is much more consistent in active ingredients than compounded trilostane and should
be used when possible. The drug must be given daily twice daily. The recommended dose is 1.5-3 mg/kg, with the lower dose given bid considered safer and more efficacious.7Trilostane therapy should be monitored 10-14 days after initiation. An ACTH-stimulation test measuring cortisol is performed 4-6 hours after the morning dose of trilostane is given.. A sodium/potassium level should be measured as well. This often decreases with trilostane treatment because of increasing K+ due to loss of
aldosterone function.8
Mitotane is a DDT derivative. It kills adrenocortical cells with a preference for the cortisol producing ones (zonae fasciculata and reticularis). The induction phase consists of administering 35 (big dog)-50 (little dog) mg/kg PO q.d. x 5-7 d. The maintenance phase is 35-50 mg/kg
PO divided twice per week. Which therapy should the practitioner choose to treat HAC. In comparing trilostane and mitotane, both are as efficacious in controlling clinical signs and in the longevity of the treated animals. 9,10 We recommend starting with trilostane therapy as it is easier for owners to manage while simultaneously giving insulin injections. If the response to trilostane is not optimal, then lysodren therapy can be initiated.
Treatment for HAC in the patient with concurrent diabetes mellitus should be approached cautiously.
11 Removal of excess glucocorticoids will lessen the concurrent insulin resistance and result in more profound glucose-lowering activity by the usual insulin dose. The current insulin dose should be decreased by 25% upon initiation of treatment of HAC. Owners should be sent home with ketodiastix and instructed to measure urine
at least once per day approximately 6 hours after insulin is given (if given twice per day). If ketones are detected or the absence of urine glucose is detected more than twice in a row, the owner should be instructed to inform the veterinarian. Lack of urine glucose may indicate hypoglycemia that may necessitate therapy. Alternately, if owners are able to collect blood glucoses at home, they should perform spot checks 4-8 hours after the insulin is given. Severe hyperglycemia or hypoglycemia should be reported to the veterinarian.
A glucose curve should be performed at every recheck to monitor HAC treatment. After the HAC is controlled, tight control of glucose with insulin can be attempted

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