This is the most common type of asthma and is a classic example of type I IgE–mediated hypersensitivity reaction (Chapter 5). It usually begins in childhood. A positive family history of atopy and/or asthma is common, and the onset of asthmatic attacks is often preceded by allergic rhinitis, urticaria, or eczema. Attacks may be triggered by allergens in dust, pollen, animal dander, or food, or by infections. A skin test with the offending antigen results in an immediate wheal-and-flare reaction. Atopic asthma also can be diagnosed based on serum radioallergosorbent tests (RASTs) that identify the presence of IgEs that recognize specific allergens.
Patients with nonatopic forms of asthma do not have evidence of allergen sensitization, and skin test results usually are negative. A positive family history of asthma is less common. Respiratory infections due to viruses (e.g., rhino-virus, parainfluenza virus) and inhaled air pollutants (e.g., sulfur dioxide, ozone, nitrogen dioxide) are common triggers. It is thought that virus-induced inflammation of the respiratory mucosa lowers the threshold of the subepithelial vagal receptors to irritants. Although the connections are not well understood, the ultimate humoral and cellular mediators of airway obstruction (e.g., eosinophils) are common to both atopic and nonatopic variants of asthma, so they are treated in a similar way.
Several pharmacologic agents provoke asthma, aspirin being the most striking example. Patients with aspirin sensitivity present with recurrent rhinitis, nasal polyps, urticaria, and bronchospasm. The precise pathogenesis is unknown but is likely to involve some abnormality in prostaglandin metabolism stemming from inhibition of cyclooxygenase by aspirin.
Occupational asthma may be triggered by fumes (epoxy resins, plastics), organic and chemical dusts (wood, cotton, platinum), gases (toluene), and other chemicals. Asthma attacks usually develop after repeated exposure to the inciting antigen(s).
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Release of granules and mediators
Fig.13.10 (AandB)Comparisonofanormalairwayandanairwayinvolvedbyasthma.Theasthmaticairwayismarkedbyaccumulationofmucusinthe bronchiallumensecondarytoanincreaseinthenumberofmucus-secretinggobletcellsinthemucosaandhypertrophyofsubmucosalglands;intensechronic inflammationduetorecruitmentofeosinophils,macrophages,andotherinflammatorycells;thickenedbasementmembrane;andhypertrophyandhyperplasia ofsmoothmusclecells.(C)Inhaledallergens(antigen)elicitaTH2-dominatedresponsefavoringIgEproductionandeosinophilrecruitment.(D)Onreexposure toantigen(Ag),theimmediatereactionistriggeredbyAg-inducedcross-linkingofIgEboundtoFcreceptorsonmastcells.Thesecellsreleasepreformed mediatorsthatdirectlyandvianeuronalreflexesinducebronchospasm,increasedvascularpermeability,mucusproduction,andrecruitmentofleukocytes. (E) Leukocytes recruited to the site of reaction (neutrophils, eosinophils, and basophils; lymphocytes and monocytes) release additional mediators that initiatethelatephaseofasthma.Severalfactorsreleasedfromeosinophils(e.g.,majorbasicprotein,eosinophilcationicprotein)alsocausedamagetothe epithelium.