Monday, April 18, 2011

Treating Dogs with Hypoadrenocorticism (Addison's Disease)

Addison's disease, the common name for hypoadrenocorticism or adrenal insufficiency, as I have discussed in my last two blog posts, is a disease with vague clinical features that are common in many other ailments, making diagnosis difficult in many cases. But once Addison's disease is correctly diagnosed, a properly treated dog can live a normal and happy active life.

The missing adrenal hormones
The adrenal, one on each kidney, is made up of two layers, the cortex and the medulla. The inner medulla secretes epinephrine (adrenaline) and is not affected by Addison's disease. The outer cortex layer secretes two corticosteroid hormones, cortisol and aldosterone, both of which are deficient in Addison's disease.

Aldosterone is a corticosteroid hormone (more specifically, a mineralocorticoid — think minerals: salt, sodium, potassium) responsible for maintaining normal circulating electrolyte levels. Once secreted, aldosterone acts on the kidney to conserve sodium, excrete potassium, and retain needed water.

Cortisol is also a corticosteroid hormone (in this case, a glucocorticoid — think glucose, sugar, energy) that is essential for life. It supports a variety of important cardiovascular, metabolic, immunologic, and stress functions.

Not all forms of hypoadrenocorticism are treated the same
There are three forms of hypoadrenocorticism: primary, secondary and atypical Addison's disease.
  1. Primary Addison's disease is most commonly is the result of immune-mediated damage to the glands.
  2. Atypical Addison's disease is a poorly understood disorder, thought to generally be an early stage of primary Addison's disease.
  3. Secondary hypoadrenocorticism results from a deficiency of the pituitary hormone, adrenocorticotropic hormone (ACTH). Without circulating ACTH, cortisol cannot be secreted by the adrenal glands.
It is important which form of hypoadrenocorticism is present in order to provide the correct treatment. In primary hypoadrenocorticism, both cortisol and aldosterone are deficiency and must be replaced for life. In atypical and secondary hypoadrenocorticism, on the other hand, only the glucocorticoids need to be replaced, at least initially.

Treating the acute adrenal crisis: A true medical emergency
Untreated, hypoadrenocorticism (especially primary Addison's disease) can lead to an adrenal crisis. An adrenal crisis is a medical emergency that requires intravenous fluids and glucocorticoids to restore the body’s levels of fluids, salt, and sugar to normal.

Once stabilized, the dog can then be treated with glucocorticoid and mineralocorticoid replacement therapy at home.

Treating chronic hypoadrenocorticism: A lifelong disease
Depending of the subtype of hypoadrenocorticism, synthetic corticosteroid drugs that act like mineralocorticoid or glucocorticoids used for hormone replacement therapy.

Mineralocorticoid treatment
For mineralocorticoid (aldosterone) replacement, either an oral medication called fludrocortisone acetate (Florinef™) or the injectable desoxycorticosterone pivalate (DOCP; Percorten-V™) is used.

We typically institute treatment with DOCP (Percorten-V) at a dosage of 2.2 mg/kg, subcutaneously or intramuscularly, every 25 to 30 days. Side effects associated with DOCP therapy are rare. This dosage interval is effective in almost all dogs, and most are well controlled with a DOCP injection every 4 weeks.

Initially, serum kidney and electrolyte concentrations should be monitored at approximately 2-weeks intervals in order to determine the drug’s peak effect and to help make necessary dosage adjustments. Once stabilized, serum electrolyte and creatinine concentrations are checked every 3 to 6 months. Because DOCP is a pure mineralocorticoid and has no glucocorticoid activity, it is essential that dogs receive concurrent glucocorticoid supplementation (see below).

Fludrocortisone is a synthetic corticosteroid that possesses moderate glucocorticoid activity as well as having marked mineralocorticoid potency. By comparison, fludrocortisone has 10 times the glucocorticoid activity and 125 times the mineralocorticoid activity of cortisol. In this regard, fludrocortisone is very different than DOCP, which possess no glucocorticoid activity.

If fludrocortisone acetate is employed as mineralocorticoid supplementation, we recommend an initial oral dosage of approximately 0.02 mg/kg/day.

After initiation of fludrocortisone therapy, serum electrolyte and creatinine concentration should be monitored weekly, with the dosage adjusted by 0.05-0.1 mg/day increments until values have stabilized within the reference range. Once this is achieved, the dogs should be reevaluated monthly for the first 3 to 6 months of therapy, then every 3 to 6 months thereafter.

For dogs that have atypical or secondary Addison’s, mineralocorticoid replacement therapy with DOCP or fludrocortisone aren't needed because the production of aldosterone isn’t effected and the serum electrolytes remain in balance.

Glucocorticoid treatment
In addition to replacing deficient mineralocorticoids in dogs with Addison's disease, the missing glucocorticoids must also be replaced. This is typically done with an oral form of the synthetic glucocorticoids prednisone, prednisolone, or hydrocortisone. With atypical Addison's and secondary forms of hypoadrenocorticism, glucocorticoid replacement is all that is needed, at least initially, since these dogs do not have serum electrolyte abnormalities.


 The correct dose of the supplemented glucocorticoids, such as prednisone, cannot be measured with a blood test. Rather it's determined by your observations: the lowest dose that keeps your dog symptom free, happy and eating! The most common side effect of overdosage is an increase in thirst and urination, which can be intense in some dogs.

Prognosis of Addison's disease
With proper treatment, the long-term prognosis is excellent. While your dog with Addison’s disease will need medications and monitoring for the rest of his life, most dogs with Addison’s can return to their favorite activities. You will help your dog lead a normal, active and fun-filled life.

207 comments:

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Dr. Mark E. Peterson said...

The dose is fine, as I describe in this blog post.

oneros777 said...

Greetings Dr Peterson. We are having great difficulty in our country getting hold of prednisolone or prednisone tablets for that matter. My dog has been on prednisolone 3mg for 2 years now and very stable.The only alternative available to our vet for now is the prednisolone sodium phosphate in liquid form.
Would this be OK to use and just swap over? And would we still give him the equivalent dose of 3mg but in ml conversion?
Your input would be greatly appreciated
Kind regards

Amanda Taks said...

Pouring over your comments to other posters has been incredibly helpful. Our dog was just diagnosed 5 days ago. Electrolytes were fine but ACTH test confirmed Addison's. Our vet prescribed her 20mg Prednisone for 1 week, then 10mg for 1 week and finally reducing to 5mg. After doing some research and noticing PU/PD symptoms, I called him to ask if we should reduce. He gave me the okay to reduce to 15mg for 2 days and then down to 5mg. A day and a half into the reduction to 15mg and she has severe diarrhea. Could this be a symptom of too much Prednisone? She's eating and drinking but energy is a bit low. We are scheduled to go back to the vet tomorrow but I have lost a bit of confidence after researching and seeing that the dose prescribed was likely way too high. Does it sound like I should seek a second opinion? Thank you for your help.

Dr. Mark E. Peterson said...

Diarrhea could be due to prednisone. No reason to start so high, especially with atypical Addison's. The dose should be based on body weight and no more than 0.2 mg/kg per day for most dogs. Many dogs do well on 0.1 mg/kg per day or even a bit less. Another opinion may be needed.

If you don't know, divide the weight in lbs by 2.2 to get weight in kg. But no dog needs a maintenance dose more than 5 mg, which is the human dose.

Amanda Taks said...

Thank you for your reply. It's very kind of you to take the time to reply to all of these questions.

Susan Miller said...

Hello, my dog was diagnosed during a crisis with Addison's disease on June 8, 2017. She is a 6 year old, 55 lb. Labrador retriever. ACTH test was used. 2 weeks later, after receiving Percorten injection on June 9, 2017, she was rushed back to emergency, this time with pulmonary edema. She was diagnosed with congestive heart failure, which they believe was brought on by Percorten shot with an underlying undiagnosed heart valve condition. Now she takes 10 mg. Pimodendan, 60 mg Lasix (furosemide) and 2.5 mg prednisone daily. We have had several blood tests, but her electrolyte levels have remained steady and not a level for concern (sorry I don't have the numbers). Internal medicine vet wants us to test blood weekly to keep checking electrolytes so we know when to introduce Florinef (they do not want to use Percorten on her again) but honestly, I can't afford to keep doing that. Our local vet said "wait a month" but that seems kind of long and we don't want her getting sick again. She seems to be doing quite well right now. My question is, if we wait on next blood test, are their symptoms we should be looking for that may indicate a change in her electrolyte levels? She never did vomit when in crisis, but was lethargic (and had been for a while leading up to crisis) and during crisis stopped eating...we just don't want to wait too long for a blood test till she is sick, but can't really afford to do them weekly either. Thank you.

Dr. Mark E. Peterson said...

Never heard of Percorten inducing heart disease. If this were my dog, I'd start a low dose of Florinef now (0. 4 mg or so per day). Then you can raise the dose in a month or two as needed. Have you seen a cardiologist -- that's what you need to help figure this out.

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