By Stephen T. Holgate MD DSc FRCP FRCPE MRC, Martin K. Church MPHARM PhD DSc, Fernando D Martinez MD, Lawrence M. Lichtenstein MD PhD
This complete, clinically orientated full-color source provide you with a wealth of certain info at the analysis, therapy, and administration of allergic diseases—from bronchial asthma to urticaria. completely up to date to mirror modern wisdom, this third version gains all the newest advancements in hypersensitive reaction and immunology. Plus, a constant, logical association places very important info at your fingertips.
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Holgate ST, Chuchalin AG, Hebert J, et al. Efficacy and safety of recombinant anti-immunoglobulin E antibody (omalizumab) in severe allergic asthma. Clin Exp Allergy 2004; 34:632–638. Wark PA, Johnston SL, Bucchieri F, et al. Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus. J Exp Med 2005; 201:937–947. Barbers R. Asthma. Curr Opin Pulm Med 2000; 6:1–89. 3 Chapter Definition: Extrinsic allergic alveolitis (synonym: hypersensitivity pneumonitis) describes an interstitial and bronchioloalveolar disease of the lungs caused by an immunemediated hypersensitivity response.
The development of symptoms 4–8 hours after exposure (reminiscent of the Arthus reaction), the presence of high levels of precipitating antibodies against the offending etiologic agents, and the detection of immunoglobulin and complement deposits in BAL fluid and lung lesions are among the arguments in favor of this hypothesis. The acute lung inflammation model, pioneered by Ward, is triggered by the intrapulmonary deposition of IgG immune complexes, and has been used to study the roles of chemokines, cytokines, and complement in the early processes of disease.
Macrophages and directly activating the alternative and lectinbinding pathways of complement. This provides the necessary mediator stimuli for increasing vascular permeability and promoting chemotactic migration of neutrophils and other cells into the lung. Organic dusts commonly contain toxic substances, many of which have enzymatic activities, while other agents produce scavenger receptor-mediated macrophage enzyme release and non-specific lymphocyte blastogenesis. The inflammatory consequences of these direct effects, and of those modulated by complement and macrophages, are important factors in the pathogenesis of EAA.
Allergy by Stephen T. Holgate MD DSc FRCP FRCPE MRC, Martin K. Church MPHARM PhD DSc, Fernando D Martinez MD, Lawrence M. Lichtenstein MD PhD