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The mechanisms behind allergic asthma—i.e., asthma resulting from an immune response to inhaled allergens—are the best understood of the causal factors. In both people with asthma and people who are free of the disease, inhaled allergens that find their way to the inner airways are ingested by a type of cell known as antigen-presenting ...
The American Academy of Allergy, Asthma, and Immunology (AAAAI) dates back to the 1920s through the founding of two professional organizations: The Society for the Study of Asthma and Allied Conditions and the American Association for the Study of Allergy. [5] In 1943, the two organizations united to create the American Academy of Allergy (AAA).
Asthma phenotyping and endotyping has emerged as a novel approach to asthma classification inspired by precision medicine which separates the clinical presentations of asthma, or asthma phenotypes, from their underlying causes, or asthma endotypes. The best-supported endotypic distinction is the type 2-high/type 2-low distinction.
Sensitizer-induced occupational asthma is an immunologic form of asthma which occurs due to inhalation of specific substances (i.e., high-molecular-weight proteins from plants and animal origins, or low-molecular-weight agents that include chemicals, metals and wood dusts) and occurs after a latency period of several weeks to years. [1]
Aspirin-exacerbated respiratory disease (AERD), also called NSAID-exacerbated respiratory disease (N-ERD) or historically aspirin-induced asthma and Samter's Triad, is a long-term disease defined by three simultaneous symptoms: asthma, chronic rhinosinusitis with nasal polyps, and intolerance of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs).
In 2000-2001 asthma prevalence was monitored at 6.5%; by 2010-2011 a 4.3% increase was shown, with asthma prevalence totaling 10.8% of Canada's population. [29] Furthermore, asthma prevalence varies among the provinces of Canada; the highest prevalence is Ontario at 12.1%, and the lowest is Nunavut at 3.8%. [29]