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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.
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 ...
Asthma phenotyping and endotyping is a novel approach to asthma classification inspired by precision medicine.It seeks to separate the clinical presentations or clusters of signs and symptoms of asthma, known as asthma phenotypes, from their underlying etiologies or causes, known as asthma endotypes.
Asthma triggers are factors or stimuli that provoke the exacerbation of asthma symptoms or increase the degree of airflow disruption, which can lead to an asthma attack. [1] An asthma attack is characterized by an obstruction of the airway , hypersecretion of mucus and bronchoconstriction due to the contraction of smooth muscles around the ...
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]
There is a strong association of C. pneumoniae with long-standing asthma among the non-atopic asthma in comparison to atopic asthma. [2] In fact, the severity of asthma can be determined by the elevated titres to C. pneumoniae, but not to other potential pathogens such as Mycoplasma pneumoniae, adenovirus, influenza A and B or parainfluenza ...
Airway remodelling is a multifaceted process involving multiple airway tissues. These include goblet cell hyperplasia, leading to increased mucus production, and airway smooth muscle hypertrophy (or smooth muscle cell hyperplasia), leading to the release of pro-inflammatory and pro-fibrotic messengers contributing to subepithelial fibrosis.
The role for eNO in other conditions is even less well established compared to asthma. Since asthma can be a cause of chronic coughing (it may even be the sole manifestation, such as in cough-variant asthma), studies have looked at whether eNO can be used in the diagnosis of chronic cough. [18] [19] [20] [21]