CHAPTER 11 ATOPIC DISEASE 179
Dermatohistopathologic changes include superficial perivascular dermatitis with
lymphocytes, eosinophils and mast cells, mild to moderate acanthosis, foci of spon-
giosis with lymphocytes and histiocytes, and dilated sweat glands.
Eosinophilic epidermal micropustules suggest direct contact with aeroallergens.
THERAPEUTICS
Treatment of atopic disease in dogs and cats should be proactive rather than reactive.
Focus should be on the consistent and effective management of the disease rather
than “crisis management” during flare-ups.
Newer treatment modalities have expanded the ability to reduce pruritus but are not
replacements for diagnosis and resolution or control of the primary disease.
Treatment of AD should not be considered until other causes of pruritus have been
eliminated.
Previous treatment recommendations have focused more on management of the
immunologic causes of AD – the “inside-outside” model.
More recently, restoring the skin barrier function – the “outside-inside-outside”
model – has gained attention.
Skin Barrier Function
Mechanical action of bathing, regardless of product used, can reduce pruritus.
Topical therapies remove allergens, microbes, and inflammatory compounds from the
skin, help to restore the barrier function of the skin, and deliver medications directly
to areas of infection and inflammation.
Shampoos: medicated (e.g., oatmeal as an antipruritic, chlorhexidine as an antiseptic
to reduce bacterial colonization, ketoconazole to reduce yeast population); bathing
once to twice weekly; shampoo should be followed with a conditioner or emollient
to rehydrate the skin or to apply residual medications.
Ceramide, phytosphingosine, essential oil, or essential fatty acid-containing spot-on,
mousse, and spray products: improve barrier function of the skin and reduce transepi-
dermal water loss.
Topical corticosteroids: low-potency products (e.g., hydrocortisone aceponate)
applied twice weekly to pruritic areas decrease frequency of “flares”; high-potency
products (e.g. dexamethasone, fluocinolone) should be restricted to the short-term
treatment of acute lesions.
Essential fatty acid (specifically n-3 fatty acids) supplementation: high doses may
help repair skin barrier by providing structural components of the stratum corneum
deficient in AD; may reduce inflammation and pruritus by competitive inhibition and
displacement of proinflammatory phospholipids; may decrease need for antipruritic
medications; 40 mg/kg eicosapentaenoic acid.
Allergen-Specific Immunotherapy (ASIT)
The only intervention to resolve AD and to prevent recurrence of symptoms in sub-
sequent seasons.