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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 52 (1997), S. 0 
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Bronchial hyperreactivity (BHR) is found in Sjögren's syndrome, as in a number of other conditions such as asthma. BHR associated with asthma can be effectively treated with corticosteroids or sodium cromoglycate. We treated 19 Sjögren's syndrome patients with BHR with inhaled budesonide and inhaled cromoglycate for 6 weeks each. None of the treatments had any significant effect on symptoms of hyperreactivity or lung function. There was no effect on BHR measured as methacholine reactivity. Primary Sjögren's syndrome is a disease with inflammation not only in the salivary and lacrimal glands but also in the pulmonary alveoli and the bronchi. The main inflammatory cell is the lymphocyte, whereas, in the bronchi in asthma, the eosinophil granulocyte is the characteristic inflammatory cell. The cause of the discrepancy with regard to treatability of BHR in asthma and in Sjögren's syndrome is not known. Possibly not all BHR is caused by inflammation. There is not a perfect correlation between inflammation and hyperreactivity even in asthma. Even if the bronchial inflammation and the asthma symptoms are easy to treat with anti-inflammatory medicines, a considerable component of BHR usually still remains, as measured with methacholine or histamine.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The question of whether there is a preferential use of certain V genes in T cells entering an inflamed joint has hitherto been studied mainly using unfractionated cells from synovial fluid and tissue respectively, and no clear answer to the question has yet been provided. Concomitantly. evidence has been provided that the use of V genes may differ considerably between CD4+ and CD8+ T cells, and consequently that detection of biased V-gene expression within an inflammatory lesion may require separate analysis of the two T-cell subsets.In this paper we have therefore studied T-cell receptor V-gene expression in rheumatoid arthritis by means of double stainings of synovial fluid and blood for available anti-TCR monoclonal antibodies and antibodies to CD4 and CD8. respectively. Double stainings were also performed with anti-TCR antibodies and antibodies to activation markers HLA-DR and 1L-2R. A certain bias towards the preferential use of certain V genes was seen particularly in the synovial fluid samples within both the CD4+ and CD8+ T-cell populations, but no uniform pattern was evident among the 35 patients investigated.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: Different mechanisms may underlie bronchial hyperresponsiveness (BHR) in different diseases. The aim of this study was to investigate the bronchial responsiveness profile produced by three different challenge tests, methacholine, a direct simulus, and two indirect stimuli, adenosine 5′-monophosphate (AMP) and cold air, in subjects with asthma and patients with Sjögren's syndrome. Methods: The study population comprised 40 adult patients with asthma, 18 subjects with Sjögren's syndrome, and 20 controls. Blood samples were collected before each challenge for measurements of serum eosinophil peroxidase (S-EPO) and eosinophil cationic protein (S-ECP). The investigated subjects recorded peak expiratory flow and kept a symptom diary. Results: Atopic subjects with asthma were significantly more hyperresponsive to AMP than nonatopic subjects with asthma (P=0.01) and subjects with Sjögren's syndrome (P=0.02). No difference was seen between atopic and nonatopic subjects with asthma in the case of challenges with methacholine or cold air. In atopic subjects with asthma, a significant correlation was found between challenges with methacholine and AMP (r=0.91, P=0.0001) and methacholine and cold air (r=0.83, P=0.004), but, in nonatopic subjects with asthma, no significant correlation was seen between methacholine and AMP or cold air challenges. In atopic subjects with asthma, the dose-response slope for AMP was correlated to S-EPO (r=−0.56; P=0.01) and S-ECP (r=−0.51, P=0.02), while no correlation between BHR and inflammation markers was found in the two other patient groups. Conclusions: The results of this study suggest that patients with asthma and subjects with Sjögren's syndrome display different bronchial responsiveness profiles for different challenge agents. Atopic subjects with asthma are more hyperresponsive to AMP than nonatopic subjects and patients with Sjögren's syndrome. More than one challenge may be required to detect different aspects of bronchial responsiveness.
    Type of Medium: Electronic Resource
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