I guess for myself, I would still question whether she might have atypical Addisons. My husband is an atypical Addisonian....he showed none of the normal blood work abnormalities of a normal Addisonian....hence he went undiagnosed and getting worse while in the hospital for 28 days.
I would be curious to know if your girl has a CK that is elevated? Could you please get back with me on that? Jaimee has an elevated CK, don't know if that is common in a dog with ITP or not....my vets can't figure out why it is so high and yes, she had trembling and muscle (back end) weakkness during her ITP, and at times when her CK is continuing to go up.
Here is some info on atypical Addisons in dogs. As you notice it says "most" showed signs of inappetence, weakness, or vomiting...not all....and their conclusion is that definite diagnosis is only made with an ACTH test. Atypical Addisonians only need prednisone or some form of cortisone/prednisone to maintain them, they do not need Florinef or DOCP. Hence, your girl could be Addisonian, not be showing electrolyte imbalance and be maintained on the prednisone for life...unless at some point she would switch over to primary Addisons where she would need electrolyte replacement. I guess as long as the vet is willing to maintain her on prednisone her entire life it is a moot point as to whether she is really an Addisonian or not. However, if she is an Addisonian....the stressors in life will affect how much pred she will need. Having said all of this....you do know that her platelets are crashing when reducing the prednisone dose, so you know that ITP is definitely a factor you are dealing with. Whether or not Addisons might be causing that or not I don't know....and, I don't think you could do the testing with her being on the prednisone....so, you are rather at a catch 22. But, I certainly believe that you could be dealing with both.
I wonder how much your vet has dealth with auto-immune disease? Have you chatted with her about what she has seen in SPs, or other breeds, when it comes to their recovery from ITP? How many have recovered using prednisone alone and how many were able to get off it completely? How many required chlorambucil to stabilize them and is there an advantage to using this and will it bring about a permanent stabilization. Just some questions to ask about other options if there might be a way to bring her into a state where she can eventually get off the meds.
Here is a good site on ITP with a case story and many great links for more info on ITP.
http://www.cloudnet.com/~jdickson/midnight.htm>>Atypical Addison's disease in the dog: a retrospective survey of 14 cases
D Sadek and M Schaer
http://www.jaaha.org/cgi/content/abstract/32/2/159Fourteen dogs diagnosed with Addison's disease and having atypical serum electrolyte levels are described. Seventy-eight percent were female, and most showed signs of inappetence, weakness, or vomiting. Ninety-three percent of the cases had either hyponatremia without hyperkalemia or normal serum electrolyte concentrations. Hemogram features were variable and were not useful in suggesting a diagnosis of hypoadrenocorticism. The results of this study show that normal or mild serum electrolyte changes in a dog with clinical signs compatible with Addison's disease should not exclude this diagnosis from consideration. Definitive diagnosis depends on the demonstration of inadequate adrenocortical response to adrenocorticotropic hormone (ACTH) stimulation.
Here is a much easier article on atypical Addisons to read, it is a website by an owner who has an atypical Addisonian St Poodle.
http://www.k9addisons.com/faqs/atypical.htmland one more vet article about Atypical Addisons in dogs.
http://www.veterinarypartner.com/Content.plx?P=A&A=608What is "Atypical Addison's Disease?"
Approximately one dog in 42 will have a special form of Addison's disease. Most dogs get Addison's disease when all three layers of the adrenal gland are destroyed and no corticosteroid hormones can be produced. With atypical Addison's disease, the problem is not with the adrenal gland itself but with the pituitary gland, which islocated at the base of the brain. The normal pituitary gland secretes ACTH adrenocorticotropic hormone), which stimulates the zona fasciculata and zona reticularis to produce glucocorticoids. Without this hormone, these two areas of the adrenal gland atrophy but the zona glomerulosa remains normal. This yields a patient who cannot regulate blood sugar normally but who is not at risk for an Addisonian crisis. Diagnosis is still by ACTH stimulation test and an endogenous ACTH level. Treatment is supplementation of glucocorticoid hormones, such as prednisone. It should be noted that often these patients progress to the more typical Addison's disease complete with electrolyte imbalance.
Making The Diagnosis
Veterinarians are classically presented with a young animal in shock. There is usually no history of trauma or toxic exposure so general treatment for shock is initiated. This consists of rapid administration of fluids (usually lactated ringers solution, which has little potassium and a moderate amount of sodium) plus some glucocorticoids. By coincidence, this also happens to be similar to the specific treatment for Addison's disease so that often the patient simply recovers without the veterinarian really knowing why.
The blood panel will come back showing elevations in the renal parameters (BUN and Creatinine) and thus with the elevated potassium is suggestive of acute renal failure, a condition with an extremely poor prognosis. The veterinarian may become suspicious of another diagnosis as the patient will respond well to fluid administration and most renal failure patients do not respond as well.
Addison's disease may present in more unusual ways. Inability to maintain normal sugar levels (ultimately manifesting as a seizure disorder) may be strongly suggestive of an insulin-secreting pancreatic tumor but before a major abdominal surgery is planned, it is important to test for Addison's disease.
Similarly unexpected, regurgitation of undigested food due to abnormal nerve function in the esophagus (a condition called Megaesophagus) can be caused ultimately by Addison's disease.
Because of the numerous symptoms Addison's disease can be present with, Addison's disease has earned the medical nickname "the Great Imitator." The only definitive test for Addison's disease is the ACTH stimulation test. The patient receives a dose of ACTH, the pituitary hormone responsible for the release of corticosteroids in times of stress. A normal animal will show an elevation in cortisol in response to ACTH while an Addisonian has no corticosteroids to respond with. This lack of response is diagnostic for Addison's disease; however, a false positive may be obtained if corticosteroids have been used in the treatment of the crisis prior to the test. Only dexamethasone does not interfere with the assay for cortisol; if any other steroid has been used, the test will not be valid for at least a couple of days.
Barb
