Addison's Disease (Hypoadrenocorticism)

Addison's disease is essentially the opposite of Cushing's disease, that is hypoadrenocorticism as opposed to hyperadrenocorticism. Primary hypoadrenocorticism (Addison's disease) results from a deficient production of glucocorticoid, mineralocorticoid or both due to bilateral destruction of all of the layers of the adrenal cortex.

Most cases of Addison's disease are thought to be idiopathic (unknown cause) but are probably immune mediated. Destruction of the adrenal cortex can also occur secondary to infections, tumors, ischemic necrosis, and the drug o,p'-DDD (used as treatment for Cushing's disease). There is no current evidence of a hereditary basis for primary hypoadrenocorticism (Addison's disease).

Secondary hypoadrenocorticism is associated with inadequate levels of circulating ACTH which results in a decreased level of adrenal glucocorticoids. Mineralocorticoids are not significantly affected. This is most commonly seen after abrupt withdrawal of long-term or high-dose corticosteriod therapy, but any lesion of the hypothalmus or the pituitary gland can cause decreased ACTH production.

Both types of hypoadrenocorticism are relatively uncommon in dogs with the highest incidence seen in young to middle age females. According to my current available references no breed predilection exists.

Early diagnosis is difficult since most of the clinical signs are present intermittently such as during stressful episodes. In the primary disease, as tissue destruction in the adrenal glands proceed the initial relative deficiency gives way to an absolute decrease in circulating cortisol level. Similarly in the secondary disease an early relative lack of ACTH becomes an absolute deficiency as the disease process progresses.

A presumptive diagnosis of hypoadrenocorticism can be made utilizing the following; history, physical examination, red cell counts and morphology, measures of kidney function (including urea nitrogen level, creatinine, urine specific gravity, and serum electrolyte levels), radiographic studies and electrocardiogram.

ACTH stimulation test is used in the definitive diagnosis of hypoadrenocorticism. While numerous protocols for ACTH stimulation tests have been published the following is in wide use:
  • Patient fasted for 12 hours overnight in the hospital.
  • Plasma sample for cortisol assay to determine basal level.
  • ACTH injection
  • Plasma sample taken 2 hours post-injection for cortisol assay.



Patients with either primary or secondary disease will show a sub-normal response to the ACTH administration. In most the resting or basal concentration of cortisol will be well below normal and the post injection value will be the same as or only slightly elevated from the basal level. In patients with primary disease there is no response due to lack of functional adrenal cortical tissue. In cases of secondary disease due to lack of ACTH there is no or minimal response since chronic ACTH deficiency results in atrophy of the adrenal cortex and the atrophied cells are not capable of responding to a single injection of ACTH.

Differentiation between primary and secondary disease can be done by either ACTH assays or repeating the ACTH stimulation test after several days of repeated ACTH injections. Most patients with primary disease will have significantly elevated ACTH level due to lack of negative feedback on the pituitary and continued unrestrained production of ACTH. ACTH determinations are somewhat difficult owing to rapid degradation in fresh whole blood samples. ACTH treatment over several days followed by another ACTH stimulation test can differentiate primary from secondary since the patient with primary disease will show the same pattern of response as with the initial test(low or minimal cortisol production) whereas the patient with secondary disease should be capable of responding to the ACTH injection after the atrophied cells have been stimulated into production by the repeated ACTH injections.

Since it is not particularly useful to specify a normal range of values for the ACTH stimulation test it is more relevant to test the response of the patient in terms of reference to the patients own baseline or resting values. The use of the test as a screening tool may have some value but would be subject to interpretation or the results, since subclinical disease may demonstrate a pretial or subnormal rels in cortisol levels that might well ball within what would be considered "normal".

The majority of dogs examined by researchers showed evidence for an immune mediated component to the primary disease, that is on histopathologic evaluation of the adrenal glands at necropsy, adrenal cortical tissue was found to be infiltrated by plasma cells, lymphocytes and replaced by fibrous connective tissue. This immune mediated atrophy was the most frequently observed lesion. This type of immune mediated disease process might in fact be genetically based but at present there is no evidence supporting this.

 

Dog Owner's Home Veterinary Handbook (Howell reference books) Dog Owner's Home Veterinary Handbook (Howell reference books)
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Comments on Addison's Disease (Hypoadrenocorticism)

By donna to Living with Canine Epilepsy on 13 Feb, 2010 - 10:25:02
it was very moving your article about ollie ,i have just lost my dogue de bordeaux duke to the disease age 6 this new years eve. absolutely devastating he was our best friend . he had so many fits he never recovered and just died. this is the second dog we have had and lost to this disease. your story highlighted exactly how are family felt and dealt with him and all the emotions you go through is so hard.r.i.p. duke 31.01.10

By Ken to Living with Canine Epilepsy on 13 Feb, 2010 - 10:24:46
Your article is excellent - it effectively captures both the joys and heartbreaks of owning an animal afflicted with this troubling disease.

With treatment epileptic dogs can live long and otherwise healthy lives. They are as lovable and as loving as any pet can be; perhaps more so.

I am currently the owner and best friend of a Pomeranian that was rescued from a shelter that later turned out to be epileptic. This is the second dog I have owned with this disease - it has to be one of the hardest things an owner can endure. But every day he makes it worthwhile.

Thank you for your article.

By Clare Askew to Living with Canine Epilepsy on 13 Feb, 2010 - 10:24:20
Thank you for your moving story about Ollie. Although it brought both my mum and myself to tears to gave me hope for my dog Buddy. Buddy beautiful crooss lab collie is 8 years old . He had his first fit last week and has now had 4 already every emotion you had written about your little Ollie we have witnessed with our Buddy.

By Janet Ashworth to Living with Canine Epilepsy on 13 Feb, 2010 - 10:24:03
Shelley has now now set up a fund in Ollies memory called "Ollies Fund" and together with the help and support of the Animal Health Trust are researching this cruel disease.

By Gail Jackson to Living with Canine Epilepsy on 13 Feb, 2010 - 10:19:28
This article reduces me to tears each time I read it. Having lived with my epileptic Staffordshire Bull TerrierBareny for the last 8 years, the article is all the more real. I too live this life through my epileptic dog and the way this article is written puts across exactly how I feel. No-one can understand the raw feelings that you fo through when your dog has each fit, and you never come to terms with it, you just live through each one and love your dog a little bit more than before.
I have saved this article and have let friends and family read it. Mostly they have no idea what Bareny and I go through when he is endless pounding the walss after his fits. People do assume that he 'shakes a bit' and then it is all over. This is not how it is at all, the actual fit is just the beginning.
Well done on a fantastic post. Your love for Ollie shines through and I'm sure, as any epileptic dog owner knows, Ollie knew just how muchyou lovedhim and appreciated you for it.

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