Veterinary Medicine - February 2008 - (Page 113) abnormalities are evident (hyponatremia, hyperkalemia), and the patient may appear dehydrated and weak. Once again, discontinuing therapy should be curative, but any patient showing substantial compromise may need uid support. Rarely, trilostane has been associated with acute adrenal gland necrosis.16,17 The mechanism for this is not understood, as the drug is not expected to be cytotoxic. It is possible that complete shutdown of steroid hormone synthesis is somehow injurious to cell metabolism. This rare event does not appear to be dosedependent because it may occur when therapy is rst started or after several months.16,17 It is essential to promptly identify this syndrome and start appropriate treatment ( uid therapy, glucocorticoids, and mineralocorticoids). This complication is permanent and irreversible, and lifelong supplementation of both mineralocorticoids and glucocorticoids will be necessary. TABLE 6 Dosage Recommendations for Starting Trilostane Therapy Body Weight < 3 kg ≥ 3 kg and < 10 kg ≥ 10 kg and < 20 kg ≥ 20 kg and < 40 kg ≥ 40 kg Starting Dose 10 mg 30 mg 60 mg 120 mg 120–240 mg Switching from another therapy If a patient receiving mitotane, ketoconazole, or selegiline is poorly controlled or adverse effects are noted, a switch to trilostane is appropriate. To minimize complications, I recommend stopping the previous medication for two weeks, so that clinical signs of hyperadrenocorticism are evident before starting trilostane. In addition, an ACTH stimulation test should be done to con rm exaggerated adrenal gland function. ated with deregulation of both growth hormone and adrenal androgen synthesis.23 In classic cases, nonpruritic truncal alopecia occurs; no other signs or changes are noted. Many of these dogs have elevated concentrations of the precursors to cortisol, particularly 17-hydroxyprogesterone. A recent study evaluating trilostane’s effectiveness in 24 affected dogs (Pomeranians and miniature poodles) reported a 90% response rate within eight weeks.24 Trilostane was given once or twice daily, with a mean dose of 10.85 mg/kg/day. Treating adrenocortical tumors Historically, functional adrenal tumors are resistant to medical therapy.18 High doses of mitotane may be required to reduce hypercortisolemia, and some patients show no response at all.18 It should be noted, however, that mitotane may have a direct cytotoxic effect on neoplastic adrenal tissue, independent of its ability to effectively control cortisol production.19 Ketoconazole may control clinical signs in up to 30% of dogs, but side effects are commonly reported.20 In contrast, trilostane has been demonstrated to control the clinical signs of hyperadrenocorticism in dogs with adrenocortical tumors, even in dogs with distant metastases.21,22 The drug will not slow tumor growth, but it can control clinical signs and improve patient well-being.21,22 In dogs with operable adrenal tumors, surgical morbidity from infection and thromboembolism may be mitigated by pretreatment with trilostane, although this has not been evaluated systematically.10 I recommend a two-week course at the standard dose, with an ACTH stimulation test performed at day 10. I also recommend that trilostane be discontinued 24 hours before surgery, at which time the usual perioperative management for anticipated hypocortisolemia becomes necessary. Treating alopecia-X Alopecia-X is a dermatologic disorder usually described in Pomeranian, poodle, and husky breeds. It is related to an arrest in the normal hair growth cycle and has been associVETERINARY MEDICINE February 2008 113 http://healthcare.goarmy.com/info/vclpra http://healthcare.goarmy.com/info/vclpra
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