[Allergic diseases of the nose, ears and throat].
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Biomedical subjects
Publications and source records attributed to G Loewe.
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A retrospective case-control study was conducted in 1042 arbitrarily selected bronchial asthma patients (197 patients with AIA and 845 controls with normal analgesic tolerance). Two thirds of all AIA patients reported one or more diseases in the region of the upper airways. Quite different from the control group, highly significant coincidence of AIA with nasal polyposis (42.6%), paranasal sinus diseases (39%), and chronic rhinitis (42,1%) was recorded in the AIA patients. AIA was characterized by stronger inclination to recurrence of nasal polyps and more frequent negative impact of polypectomy upon the course of asthma. The classical triad of "intrinsic asthma - nasal polyps - analgesic intolerance" was established in 39% of the AIA patients. The pathogenetic factors causing the association of asthma with polyps and the even more strongly association of AIA with polyps are still unknown. The presumed pathogenetic relationship between chronic hyperplastic alterations in the upper airways and the phenomenon of AIA might be caused by disorders in phospholid metabolism (liberation of arachidonic acid, lipoxygenase products, radical mechanisms).
In a retrospective investigation 469 pseudoallergic reactions (analgesics asthma reactions) that emerged in 197 patients with analgesics intolerance have been analysed. Besides mostly severe asthma-attacks 26.5% of the reactions were sneeze-attacks and in 37.5% nasal secretion was found. 86% of the reactions emerged within a maximum of 45 minutes after oral application of the analgesic. About a third of the analgesics-asthma reactions occurs together with reactions of the nose mucous membrane. So the connection of analgesics-asthma and chronic hyperplastical changes of the mucous membrane of the upper respiratory tract is also reflected in the course of the pseudoallergic intolerance reaction.
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The sensitization of lymphocytes from patients with different tumors was tested against a 3 M KCl-extract of fetal tissue (3.--6. month) by the leukocyte adherence inhibition assay (LAI) and by the leukocyte migration inhibition assay (LMI). Sensitization was compared with the reactivity of controls without any detectable tumor. In the LAI assay the leukocytes of 13/15 patients and 2/12 controls showed an inhibition of the adherence. In the LMI-assay 11/17 tumor-bearing patients and 6/18 controls reacted positive in the presence of the antigen preparation. The two methods demonstrated that patients bearing tumors of different histology are sensitized to fetal antigens.
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