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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.
While the acronyms are similar, reactive airway disease (RAD) and reactive airways dysfunction syndrome (RADS) are not the same. [1]Reactive airways dysfunction syndrome was first identified by Stuart M. Brooks and colleagues in 1985 as an asthma-like syndrome developing after a single exposure to high levels of an irritating vapor, fume, or smoke.
This specific condition, in the general population, can vary between 7 and 20 percent. This increases to around 80 percent in those with symptomatic asthma. In many cases, however, the constriction, even during or after strenuous exercise, is not clinically significant except in cases of severe to moderate emphysema.
Asthma. Chronic obstructive pulmonary disease (COPD) Smoking. Gastroesophageal reflux disease (GERD) Certain medications, like ACE inhibitors. Obstructive sleep apnea. Allergies.
Moderate to high intensity exercise Exercise-induced bronchoconstriction ( EIB ) occurs when the airways narrow as a result of exercise. This condition has been referred to as exercise-induced asthma ( EIA ); however, this term is no longer preferred. [ 1 ]
With the exception of formoterol, LABAs are not recommended for the treatment of acute asthma exacerbations because of their slower onset of action compared to salbutamol. Their long duration of action is due to the addition of a long lipophilic side-chain that binds to an exosite on adrenergic receptors.
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