Canine Addison’s Disease
By Donna Patterson
I didn’t start out with a plan to do an article on Addison’s Disease.In fact, I’d barely even heard of Addison’s until Luba (Ch Ebonies Pride Moya Lubov, CGC, RN), my almost 4 year old female, was diagnosed with Typical Addison’s Disease on December 16, 2008.
The diagnosis came after a three week health crisis where, for a time, I was not sure that she would survive.
Her appetite started to wane on our return from the 2008 Nationals.Luba normally will clean her bowl then proceed over to Zil’s to see if he left anything.But she started not finishing all of her food.She’s a big girl with a normal weight of 100 pounds, so I really don’t worry about a few missed meals.We got home on November 19th,and I fed her some raw ground beef to try to get her to eat.Well she did eat, but
during the night she vomited.I still wasn’t overly concerned, because she seemed normal otherwise.However over that weekend, not eating turned into very, very sick; first with nonstop vomiting and then refusing to drink even a small amount of liquid. I knew then that I needed to take her to the emergency clinic in Hattiesburg.
After running blood work, and doing x-rays to rule out blockage, she was diagnosed with pancreatitis. But the blood work was terrible, with elevated liver enzymes,and poor kidney function. So she had to stay at the hospital, and stay, and stay, and stay. Five days total. During this time she was receiving IV fluids, antibiotics, anti-nausea drugs, and steroids (the importance of the steroids will come into play later). Her blood work was returning to normal by the fifth day, so she was allowed to come home.By this time she had lost almost 20 pounds. Even after coming home, she didn’t have much of an appetite and never really seemed to feel great.She would eat only if I sat there and hand fed her, and only if it was something that she really liked. Since we thought that she had pancreatitis and that fat in her diet would be an issue, they sent me home with a case of Science ID cans. She laughed at me when I tried to feed her a can of that stuff! Instead I was cooking chicken breast and mixing with rice, draining cooked ground steak and she would just eat a small amount, so we were feeding her 4 or 5 times a day.We went along like this for about 2 weeks with her just eating enough to keep her going, but not enough to gain back any of the weight that she lost.
By December 15, she had quit eating again. This time I took her to my local vet, partly because of the huge vet bill that I had just two weeks ago, and I figured that I could just take her in and tell her about the pancreatitis. When Dr Miller came out with the blood test in her hand she said, “Donna, she doesn’t have pancreatitis, she is in acute renal failure.” Luba’s BUN was 98 (normal range 7-25), her creatin was 5.4 (normal range .0.3-1.4) and her potassium was elevated at 6.9 (normal range 3.7-5.8). She was very sick and once again placed on IV fluids. This went on for 2 more days, only this time I would bring her in the morning for the fluids then pick her up when they closed because Luba is always happier at home with me.
The reality of the situation was that this crisis started a few weeks ago, but over the past two years there had been changes in Luba which only now can we relate to the onset of Addison’s. She was crate trained as a puppy and never had a problem with her crate, but had started drooling, and panting when in her crate, getting progressively worse until it got to the point where I would take her out of her crate and she would have drooled so much that her entire front and the crate were soaking wet. She had never been thunderstorm phobic, but around 2 years old she started getting upset at thunder and had gotten to the point where just the sound of rain would put her in a panic.When we went outside at night, she would be jumping back at every shadow that she saw. These phobias had gotten so bad that back in July I’d asked the vet about putting her on Prozac. She responded well to the Prozac and seemed much calmer.
There were two more troubling sign in the prior months. First was that her eyes were in terrible condition.Not the normal crud in the corner of the eye.Luba’s eyes were bloodshot and runny and infected looking. We had been using ointment for months and it never seemed to get better. Second was increasingly bad breath.
Fast forward five months and I’m thinking how could a dog not yet four years old all of a sudden develop renal failure. I remembered a conversation that I had with someone who had a female develop Addison’s Disease after taking Clomicalm for the same stress-like symptoms that Luba had. So I came home and started looking at Addison’s Disease on the internet.And the symptoms were exactly what Luba
started off with; nausea, loss of appetite, lethargy, depression.Symptoms can also include: collapse, shaking and shivering, excessive urination with or without excessive thirst, fluctuating symptoms, pain or sensitivity in the abdomen, fatigue or exercise intolerance.So I called Dr. Miller back and said, “Linda, would you look at Addison’s Disease as a possibility?” She told me that she was already a step ahead of me and had called the emergency clinic where Luba was back in November and asked them for copies of all of her blood work. It turns out that all of the blood work from the very beginning had been consistent with an Addison’s diagnosis.
The only definitive test for Addison’s is called ACTH (adrenocorticotropic hormone) stimulation test. The patent receives a dose of ACTH, the pituitary hormone responsible for the release of corticosteroids by the adrenal glands in times of stress. In a dog with Addison’s, the before and after numbers are almost the same because the body cannot produce the needed hormones to process stress in the body. But because Luba was in such bad condition we decided not to wait for the test results, but to administer the initial treatment for Addison’s disease, which is a shot of Percorten-V and prednisone, a steroid.We didn’t have much to lose by doing it.
Typical Addison’s Disease (also called Hypoadrenocorticism) is a deficiency of the adrenal glands, which are located just forward of the kidneys, in which they either completely are unable to produce, or barely produce, the corticosteroids, two primary hormones that the body requires, Glucocorticoids and Mineralocorticoids.
The Glucocorticoids are the hormones that enable us to adapt physiologically to stress.They act on the mechanics of sugar, fat and protein metabolism the regulation of the body’s immune systems, and gear the metabolism towards the preparation of burning (rather than storing) fuel so that the body is ready for a “fight or flight” situation.The lack of this hormone explains why Luba had, over a period of time, no longer been able to tolerate the stress ofbeing in a crate or the sound of thunderstorms, things that had hardly seemed to bother her before because her body compensated by releasing additional hormones to help her with these situations.
The Mineralocorticoids influence the body’s electrolytes:sodium and potassium. As a general biological rule, where there is sodium, there is water. When the Mineralocorticoids circulate as part of the “fight or flight” reaction, sodium is conserved in anticipation of blood loss so that there will be extra fluid in the vasculatory system (spare blood). When sodium is conserved, potassium is lost as part of the biological balance.The process is too complicated to go into here, but the bottom line is that corticosteroid hormones are needed to adapt to stressful situations and without these hormones, even small stresses (like crating) can lead to physiologic disaster because the body’s electrolytes are so out of balance. Luba was in physiological disaster.
In Luba’s first stay at the hospital as a course of her treatment for pancreatitis she was given IV fluids, and dexamethasone, a steroid. This is exactly what an Addisonian dog needs, so she improved, came home, the steroids in her system diminished and she crashed again.She never had pancreatitis, it was an Addisonian crash.
I know that the first reaction is to say that steroids will shorten a dog’s life span and should not be used. But the body produces and requires steroids and in the case of an Addison’s dog the prednisone is what will keep them alive.
Low daily dose of prednisone will replace the Glucocorticoids that her body will no longer produce.And a shot every 25-30 days of Percorten-V is what I have chosen at this time to replace the Mineralocorticoids.
That sounds so simple when you say it, but in reality it will be an awful lot of blood testing until we come up with the optimal dose of Percorten-V to suit Luba.The goal is to be on the lowest dose of prednisone that will keep her eating, drinking and “happy”, and the lowest dose of Percorten that will keep her electrolytes in balance.We started out at 7mg of prednisone daily and have worked our way down to 2.5mg daily and will probably go lower still because she still seems a little too hungry.You can’t test for the amount of prednisone required, so that dose will be trial and error by observation, and will have to be modified based on her appetite, her overall mood and activity level. Also during times of stress (travel, crating, or whatever else is stressful to her), her dose will have to be increased slightly to compensate for the extra stress since her body cannot do iton its own.
For the next 5 or 6 months we will be testing her sodium and potassium levels before administering another dose of Percorten-V., until we determine the optimal dose. I am fortunate in that my vet has experience treating Addisonian dogs. Fortunate for me, but unfortunate for her, her Standard Poodle also has Addison’s Disease.
Addison’s is an autosomal recessive autoimmune disease that is genetic/hereditary in nature. The most commonly affected breeds are Bearded Collie, West Highland White Terrier, Rottweiler, Standard Poodle, Leonberger, and Portuguese Water Dog. The genetic marker is not known yet. In all breeds but the Standard Poodle, the ratio of female to male development of the disease is approximately
75/25 (with more females developing Addison’s), with the average of manifestation between 4 and 5 years of age.In the Standard Poodle it is approximately 50/50. In an autoimmune disease the body begins to reject its own tissue as foreign and destroy the tissue. Within the genetic line a range of autoimmune diseases can occur, with some dogs developing Addison’s, some hemolytic anemia, thrombocytopenia (a blood clotting disorder, autoimmune skin disorders, lupus, polyarthritis and hypothyroidism, or the inability to fight off reoccurring infection. There is no predictive test to identify carriers of Addison’s and until one is found the best course of action until this marker is located would be not to breedthe affected dog, the sire, dam or siblings.
Because Addison’s Disease has so many different symptoms, diagnosis can be difficult unless the vet will specifically look for it., and will initially be diagnosed as many other ailments, with the most frequent being acute renal failure.
University of California Davis currently has a study of the Bearded Collie, Poodle, Leonberger, PWD and Great Dane to attempt to characterize the mode of inheritance and identify the genetic marker.
Untreated Addison’s disease is 100% fatal.With proper medication and monitoring Luba can be expected to have a relatively normal life, although this first period hasn’t been easy. Since November, besides the Addison’s crisis she has had a nasty abscess, sporadic limping, a UTI, and now occasional incontinence. Hopefully things will get better as her body recovers from this near-fatal illness.
The main problem with Addison’s is the ongoing cost of treatment in a large dog, with her treatment and blood work running approximately the current cost of a new BRT puppy annually. We’ll have to cut other things from our budget.
Of course, there is no replacing Luba.
Since this article was written, Luba is now stabilized on 1mg of prednisone per day and a 1.8mg shot of Percorten V every 30 days. She has regained the weight she lost, and has had no more episodes of abcesses. The incontenance has been controlled by reducing the amount of prednisone to the current level, which I believe is the lowest dose we can use and still keep her eating and "happy". Stress is still an ongoing concern, since her body cannot adapt to it. I've found that she seems less stressed out being borded rather than the unknown of traveling. She doesn't like strange places and strange situations, and does well staying at the vet's office when we leave town. I feel better with her there knowing that if she were to start with a crisis, Dr Miller will know what she needs immediately to prevent a crash. Luba is now 8 1/2 years old and has lived with Addison's for 4 years.