Atopic Dermatitis Flashcards
Pruritic think…
Allergies!
Atopic Dermatitis
Background
Genetically predisposed inflammatory and pruritic skin disease; pruritis is a must
Tendency to develop IgE-mediated allergy vs. environmental allergens
Strong hereditary tendencies
Usually a food allergy
More exposure = more reactive
Atopic Dermatitis
Multifactorial components
Genetic
Barrier Function
Immunologic Factors
Allergens
Atopic Dermatitis
Cycle
Allergen
Langerhans cell stimulates T-cell
T-cell releases cytokines that stimulate sensory nerve fibers –> itch
Get local inflammation (mast cell degranulation, stimulation of other T-cells, more cytokines) –> itch
Local inflammation can also stimulate Dendritic cells which will release their own cytokines and end up contributing to inflammation
Atopic Dermatitis
Genetic Factors
Veterinary studies still needed
Suggested to be seen in West Highland Terriers
Atopic Dermatitis
Barrier Function
Compromise; allergens can enter, water evaporates, dry skin (may cause pruritis)
Major lipids of SC
Cholesterol
FFA’s
Ceramides (holds everything together!)
Atopic Dermatitis
Immunologic Factors
Helper T Lymphocytes release cytokines and stimulate may ILs
Important one:
IL-4 with T-helper 2 cells
IL-4, IL-5, IL-13, IL-31
IL-31 has a targeted therapy
Atopic Dermatitis
Presentation
1-3 years
Seasonal pruritus
Breeds: Terriers, Boxers, Labs
Sites: Ventral hairless areas Face Feet Peri-anal (licks under tail)
Atopic Dermatitis
Diagnosis
No definitive test! Signalment History (seasonality?) Clinical Signs Diagnosis of exclusion (rule out: ectoparasites, infections, allergies) Must address secondary infection(s)
Allergy test in animals is not useful; can appear to have allergens to all things but what is important is what is causing the pruritis
Atopic Dermatitis
Treatment
Symptomatic Rx
Antihistamines
Glucocorticoids
Free Fatty Acids
Topical therapy
Atopic Dermatitis
Treatment
Specifc Rx
Immunotherapy (shot, sublingual)
Atopica
Apoquel
Cytopoint
Antihistamines
What is the problem with these?
Does not target T-helper 2 cells which are the problem cells
Targets mast cells which do contribute to increased inflammation though
Therefore do not see a significant benefit
Antihistamines
Examples
First generation:
Hydroxyzine (Benadryl)
Second generation:
Cetirizine (non-sedating)
Can give as a prevenative
Glucocorticoids
Commonly used
Very effective (especially for environmental allergens)
Acts at multiple sites along atopic dermatitis cycle
Potent anti-inflammatory effects
Should NOT be used life long
Glucocorticoids
Atopic Dermatitis Cycle
Acts on: T-helper 2 cells Reduces cytokines released Mast cells Neutrophils Monocytes Eosinophils
Reduces inflammation