II. Epidemiology
- Much more common in children than adults
- Age Onset under 40 years old
III. Pathophysiology
- IgE mediated response to allergens
- Immediate Allergic Reaction
- Late-phase Allergic Reaction
IV. Types: T2 High Phenotypes
- Early Onset Allergic Asthma (Atopic Asthma)
- Classic Asthma presentation, allergic sensitization and steroid responsiveness
- Late Onset Eosinophilic Asthma
- Often steroid refractory, and typically severe from onset with frequent exacerbations
- Associated with Staphylococcus aureusEnterotoxins
-
Aspirin Exacerbated Respiratory Disease (Samter's Triad)
- Associated with disordered Arachidonic Acid metabolism (cyclooxygenase mediated to inflammatory agents)
- Typically severe from onset with frequent exacerbations
- Associated with increased urinary LTE4 > 166 pg/mgCr
V. Causes: Triggers
- Indoor allergens (perennial allergens)
- Outdoor allergens (seasonal allergens)
- Tree, grass or weed pollens
- Mold Spores
-
Aspirin Exacerbated Respiratory Disease (Samter's Triad)
- Aspirin or NSAID sensitivity
- Nasal Polyps
- Asthma
VI. Findings: Symptoms and Signs
VII. Labs: Markers
-
Eosinophilia
- Induced Sputum with >3% Eosinophils
- Complete Blood Count with increased Eosinophils
- Fractional Excretion of Nitric Oxide (FeNO)
- FeNO > 50 ppb in adults (>35 ppb in children) is associated with Eosinophilic airway inflammation
- Positive values are associated with steroid responsiveness
- Serum Total IgE
-
Serum Periostin
- Elevated in Type 2, Eosinophilic Asthma
VIII. Management
- See Environmental Allergen
- See Asthma Management
- See Asthma Exacerbation
- Consider Immunotherapy for those with persistent Allergic Rhinitis and Asthma
- Allergic, refractory Severe Asthma may be treated with Biologic Agents