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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 27 (1997), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Aspirin-induced asthma (AIA) affects one in 10 individuals with adult-onset asthma. It is not known if aspirin sensitivity is due to immune mechanisms or to interference with biochemical pathways.Objective The study aimed to test for possible involvement of the genes of the Major Histocompatibility Complex (MHC) in AIA.Methods HLA-DPB1 and HLA-DRB1 genotyping was carried out by DNA methods in 59 patients with positive challenge tests for AIA and in 48 normal and 57 asthmatic controlsResults The DPB 1*0301 frequency was increased in AIA patients when compared with normal controls (19.5% vs 5.2%, Odds Ratio = 4.4, 95% Confidence Interval (CI) 1.6–12.1, P= 0.002), and compared with asthmatic controls (4.4%, OR = 5.3, 95%CI= 1.9–14.4, P= 0.0001). The frequency of DPB 1*0401 in AIA subjects was decreased when compared with normal controls (28.8% vs 49.0%, OR = 0.42, 95%CI = 0.24–0.74, P= 0.003) and asthmatic controls (45.6%, OR = 0.48, 95%CI = 0.28–0.83, P= 0.008). The results remained significant when corrected for multiple comparisons. There were no significant HLA-DRB 1 associations with AIA.Conclusion The presence of an HLA association suggests that immune recognition of an unknown antigen may be part of the aetiology of AIA.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 22 (1992), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have determined IgG subclass concentrations in 100 patients with aspirin-induced asthma and 80 healthy controls. Patients on chronic corticotherapy (n= 64) had significantly lower total IgG levels than patients not receiving steroids (n= 36) or controls. Corticotherapy was not associated with changes in the subclass distributions. In patients, the most striking finding was elevation of IgG4. It was not related to corticotherapy or serum IgE levels. The rise in IgG4 was accompanied by a modest, though statistically significant, depression of IgG1. No changes of IgG2 and IgG3 concentrations were observed. Thus, aspirin-induced asthma is characterized by a distinct pattern of distributions of IgG subclasses. It is suggested that in aspirin-induced asthma elevation of IgG4 might result from chronic antigenic stimulation, of viral origin, and that determination of IgG subclass distribution might be of clinical interest.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 21 (1991), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: There have been several reports on alterations of platelet function and raised plasma heparin levels in symptom-free atopic subjects. Either of these can affect formation of thrombin in vivo. In 25 symptom-free atopic patients and 32 healthy volunteers we studied the generation of thrombin in blood emerging from a standardized skin microvasculature injury, which also served to determine bleeding time. Generation of thrombin was delayed in atopies. They produced significantly less thrombin (P〈0.01) during the early and central phase of haemostasis. The amount of thrombin generated was inversely correlated to bleeding time, which in atopies was on average 50 sec longer than in controls (P= 0.055). Two hours after ingestion of 500 mg aspirin, this difference increased up to 150 sec, although the individual responses varied markedly (P= 0.08), while the generation of thrombin became strongly depressed in both groups. The possible clinical relevance of the delayed formation of thrombin in atopy awaits further studies.
    Type of Medium: Electronic Resource
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