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 25-28 September, 2018 | Singapore
are actually deficient in aldosterone. Conversely some dogs may be hyponatremic with only glucocorticoid deficiency. Therefore, the lines have been blurred between primary and secondary hypoadrenocorticism in the absence of routine mineralocorticoid measurement. In order to fully determine aldosterone activity, it should be measured directly both before and after stimulation by ACTH remembering that pharmacologic doses of ACTH (such as CortrosynR doses used in a stimulation test) will stimulate aldosterone secretion.
So, what distinguishes full blown hypoadrenocorticism
and glucocorticoid-deficient hypoadrenocorticism? In the latter case, the dog will only be cortisol-deficient and will maintain mineralocorticoid activity. Clinical signs relate to glucocorticoid deficiency and will often be centered around gastrointestinal problems to include: vomiting, diarrhea, melena, hematemesis, hematochezia, weight loss, and generalized weakness. As with a full-blown Addisonian,
the clinical signs may wax and wane. The dogs are generally not polyuric and polydipsic since aldosterone concentrations are normal. Clinical pathology abnormalities may include a mild normocytic, nonregenerative anemia, reverse stress leukogram (lack of neutrophilia, eosinophilia, lymphocytosis), hypoglycemia. If significant blood loss
has occurred, the anemia may be severe. Sodium and potassium concentrations are generally normal.
WSV18-0132
SVA DERMATOLOGY (SIMULTANEOUS TRANSLATION INTO MANDARIN CHINESE)
UPDATE ON ALLERGIC DISEASE: ATOPY VS CONTACT ALLERGY
M. Burrows1
1Animal Dermatology Clinic Murdoch University Division of Veterinary and Biomedical Science Murdoch, Western Australia
CANINE ATOPIC DERMATITIS (CAD)
A definite diagnosis of atopic dermatitis is based on:
· A typical history
· Typical clinical signs
· Rule out of other pruritic dermatoses · Allergy investigations
HIreed:
There are strong breed and/or familial predispositions for CAD but predisposed breeds vary with geographical regions. Some breeds, such as West Highland White terriers, boxers and bulldogs seem predisposed in all regions; others such as German Shepherds, golden retrievers and Labradors seem to be predisposed for CAD only in some geographic regions. Breed-associated phenotypic variability of CAD has been reported.
Age of onset:
The typical age of onset is reported to be between 6 months and 3 years of age, but occasional dogs develop clinical signs after this age range. Food allergies can commence at any age.
CLINICAL:
The most prominent clinical sign in canine atopic dermatitis is pruritus. In the majority of cases, the pruritus has a characteristic distribution. The pruritus may be seasonal (with CAD) or more typically continuous. Approximately 80% of dogs with seasonal signs are symptomatic in spring or summer while other exhibit signs in autumn or winter.
Distribution
Generalised or limited to the face, ears, feet, and pinna, and axillae, inguinal region
Unilateral or bilateral otitis externa
  Glucocorticoid-deficient hypoadrenocorticism should
be diagnosed with an ACTH-stimulation test. Cortisol
and aldosterone should be measured since Na and K are only rough estimates of mineralocorticoid activity. If aldosterone levels are low or approaching the low end of the normal range, the dog should be monitored closely for emerging mineralocorticoid deficiency. Diagnosis
of glucocorticoid deficiency is based on resting cortisol levels lower than the normal range without a significant increase after ACTH-administration. Using resting cortisol levels of greater than 2 mcg/dL to rule out glucocorticoid- deficient hypoadrenocorticism has not been examined experimentally.
Treatment: Since mineralocorticoid activity is not
affected, only glucocorticoids need to be supplemented. Dexamethasone-SP may be used in an acute situation at a dose of 0.05-0.1 mg/kg. Dexamethasone has the advantage of being parenteral and also will not be read in the cortisol assay used for the ACTH-stimulation test. After stabilization, the dog may be transitioned to prednisone at 0.2-0.4 mg/kg once per day. Often dogs will need a dose increase during stress. The dose should be titrated to the lowest that will maintain good quality of life for the dog.
Follow-up: Glucocorticoid doses should be adjusted based on clinical signs. Sodium/potassium levels should be monitored so that conversion to mineralocorticoid deficiency will not be missed.
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43RD WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND 9TH FASAVA CONGRESS

































































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