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Treatment
The treatment of canine Addison’s disease can be vari- able depending on which form of the disease the dog has and how severe it is on presentation. Dogs that are only glucocorticoid deficient because of atypical dis- ease only need supplementation with oral prednisone. Conversely, dogs in an adrenal crisis will need emer- gency intensive care to save them. They will need shock level IV fluid therapy and emergency administration of steroid medications. Dexamethasone sodium phosphate is the drug of choice as it will not interfere with the ACTH stimulation test. Treatment measures to combat intestinal bleeding and ulceration may also be needed. In general, mineralocorticoid replacement therapy is not started in crisis dogs until they are stable.
Treatment for stable dogs with primary Addison’s disease involves lifelong supplementation with miner- alocorticoid medication. Two options currently exist for mineralocorticoid replacement therapy, oral and injectable. While some dogs do fine only on mineralo- corticoid replacement, some will also need concurrent glucocorticoid therapy. All Addison’s dogs will require additional glucocorticoid in times of stress (e.g. illness, elective surgery) because they have no adrenal gland reserve. They could easily crash without additional supplementation.
Oral medication with Florinef ® (fludrocortisone ace- tate) is a common choice for treating canine Addison’s disease. Fludrocortisone is very successful at controlling Addison’s disease in dogs. The drug has both glucocor- ticoid and mineralocorticoid effects, so approximately 50 percent of treated dogs will not need additional cortisone (unless stressed). However, despite its suc- cess and efficacy, there are some drawbacks to the use of fludrocortisone. First, dogs generally require higher doses than people do, with some being quite resistant. Second, many dogs develop bothersome side effects at doses required to maintain normal electrolyte balance. Typically these include increased thirst, increased uri- nation and incontinence. These adverse effects were occurring often enough to inspire researchers to look for alternative treatment methods.
In 1998 veterinarians found the alternative they were looking for when the FDA approved Percorten-V ® injectable (Desoxycorticosterone pivalate, or DOCP) for dogs. In actuality, this a reintroduction of an old drug that had been used to treat human Addison’s patients before Florinef became available. In dogs, DOCP pro- vides about 25 days of mineralocorticoid replacement. However, it does not provide any glucocorticoid activ- ity. Thus, treated dogs will need some degree of addi- tional glucocorticoid therapy. Still, DOCP injections are a more economical option for larger dogs than oral therapy with a large number of pills. In fact one recent study indicated that fewer than 20 percent of treated dogs required the full label dosing. So if cost is a con- cern, it is possible to wean the DOCP dose down once control has been established.
Monitoring schedules for dogs with Addison’s disease depends on the treatment protocols used. Generally,
dogs on oral fludrocortisone therapy should have their serum electrolytes checked every week until they become normal. Subsequent rechecks are then sched- uled for every 1–2 months until the dog’s condition is stable. After that, twice yearly rechecks are usually suf- ficient. Dogs receiving DOCP injections need a different monitoring schedule. These dogs need to have their electrolyte levels rechecked every three weeks until the proper dose and injection interval is established. Once the proper dose and interval are known, rechecks can be more spaced out until control is defined. After that, twice yearly monitoring should be adequate.
Summary
Addison’s disease may not be the most common dis- ease seen in dogs, but it can be a devastating one. That it is why it must be kept in mind for all cases of uniden- tified illness in the dog. Without lifelong therapy, dogs with Addison’s disease will die. But with proper treat- ment and monitoring, most dogs with Addison’s can survive to lead a normal life.
References
1. Feldman, E.C. Current Concepts on the Diagnosis and Management of Hypoadrenocorticism in Dogs. Western Veterinary Conference Proceedings, 2004.http://www.vin.com/Members/Proceedings
2. Greco, D.S. Hypoadrenocorticism in Small Animals. Atlantic Coast Veterinary Conference Proceedings, 2002 http://www.vin.com/Members/Proceedings 3. Lorenz, MD and Melendez L. Hypoadrenocorticism. Western Veterinary Conference Proceedings 2002. http://www.vin.com/Members/Proceedings 4. Kelch W.J., et al. Canine Hypoadrenocorticism (Addison’s Disease). Comp.
Cont. Ed. Pract. Vet. Vol. 20, no. 8, pp 921-934. August 1998
5. Cunningham J.G. Chapter 33: Endocrin Glands and Their Function. In: Textbook Of Veterinary Physiology, pp. 396-404. W.B. Saunders, Philadelphia,
1992
6. Canine Genetic Analysis Project Website: http://cgap.ucdavis.edu/Default.
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7. Reusch C.E. Hypoadrenocorticism. In: Textbook of Veterinary Internal
Medicine 5th Edition. Volume 2, pp 1488-1499. Ettinger, S.J., and Feldman E.C., ed. W.B. Saunders, Philadelphia 2000.
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