Hypersensitivity process

Abstract: The lung is the site of a variety of complex inflammatory reactions. In many instances the inflammation is a normal reaction against various infectious agents, such as bacteria and viruses, or is a response to necrotic tissue, such as infarcted lung parenchyma or degenerating tumor. In extrinsic allergic alveolitis, the inflammatory reaction characteristic of this condition is thought to represent a hypersensitivity process mediated by immunoglobulins, lymphokines, and immune effector cells. Although the four immunologic responses described by Gell and Coombs1 (Fig. 18-1) are often used in characterizing various inflammatory reactions in the lungs, the immunopathogenesis of extrinsic allergic alveolitis remains poorly understood. Extrinsic allergic alveolitis, also referred to as hypersensitivity pneumonitis or microgranulomatous hypersensitivity reaction, is a predominantly chronic inflammatory disease of the peripheral gas-exchanging portion of the lung resulting from sensitization and subsequent exposure to a variety of organic dusts. The condition was first described in 1932 in farmers exposed to moldy hay.2 Initially it was considered a mycotic process.3,4 Pepys and colleagues5,6 elucidated some of the initial immunologic mechanisms though to be operative in the disease. Williams7,8 demonstrated that the disease could be produced in sensitized farmers by the inhalation of extracts of moldy hay. Farmer’s lung disease was found to result from a hypersensitivity reaction against a species of thermophilic actinomyces, Thermoactinomyces vulgarus, that proliferated as the hay became overheated in the process of becoming moldy.9,10 Numerous organic antigens have now been recognized as causing hypersensitivity reactions in the lung, and these are usually named after the occupation in which the patient was exposed to the organic antigen. The term extrinsic allergic alveolitis was coined by Pepys11 to refer to the entire group of similar reactions to organic dusts.

Abstract: Background: The presence of allergic mucin in allergic fungal sinusitis (AFS) is a manifestation that identifies it as a hypersensitivity process. AFS has a phenomenon of cross-reactivity to IgE-bound proteins having at least two shared epitopes. Case report: A 13-year-old male with nasal obstructive symptoms of three years of evolution. An obstructive mass was identified in the sinuses through physical examination and CT. In endoscopic surgery, the left nostril polyp was identified with the macroscopic appearance of allergic mucin; the polyp was resected. Final histopathological examination using periodic acid-Schiff and Grocott’s methenamine silver staining indicated Aspergillus. Two weeks after surgery, percutaneous tests showed sensitization to Alternaria, Helminthosporium sativum, and Deramatophagoides farianae with negativity to Aspergillus fumigatus. Conclusions: The absence of significant titers of specific IgE antibodies to Aspergillus fumigatus was the evidence that the hypersensitivity response was triggered by a pathogen other than that isolated in histopathological study, which coupled with positive tests for other fungi may be explained by the cross-reactivity phenomenon in a phenomenon of likely hypersensitivity.

Abstract: The appearance of eosinophilia in maintenance hemodialysis patients (ED) is a relatively frequent clinical fact. (1) Some of the latest studies carried out point towards a hypersensitivity phenomenon as the cause of ED.(2). Ethylene oxide (ETO) has been mentioned as one of the foreign substances used during hemodialysis which could trigger this hypersensitivity process.