11 research outputs found

    Urinary leukotriene levels are increased during exacerbation of atopic eczema/dermatitis syndrome. Relation to clinical status

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    Background:  Leukotrienes are potent mediators of allergic inflammation and their role in the pathogenesis of allergic disorders, particularly asthma, is well established. Their importance in the pathogenesis of atopic eczema/dermatitis syndrome (AEDS) is still unclear. We aimed to compare urinary cysteinyl leukotriene (Cys-LT) levels during exacerbation and remission of AEDS in relation to clinical status, IgE levels, and eosinophil counts. Methods:  Urinary Cys-LTs were measured by direct enzyme immunoassay in 17 adult patients with AEDS and in 17 healthy controls in whom atopy had been excluded. Cys-LTs were compared during exacerbation and remission of AEDS in relation to the clinical status measured by SCORAD. Total IgE levels were measured by enzyme-linked immunoassay (ELISA). Results:  Mean clinical score during the exacerbation was 64.3 ± 3.1 and during remission 22.4 ± 4 ( P < 0.01). Cys-LTs levels were significantly higher during the exacerbation of AEDS than in the control group (230.9 ± 20.8 vs 123.2 ± 9.9 pg/mg creatinine; P < 0.005). During the remission, the difference between AEDS patients and the control group was not significant (96.3 ± 8.7 vs 123.2 ± 9.9 pg/mg creatinine; P = 0.8). During AEDS exacerbation Cys-LTs levels were significantly correlated with the clinical status ( rS = 0.73, P < 0.01) and with eosinophil counts ( r = 0.86; P < 0.01) but not with the duration of the disease, age of patients, or IgE levels. Conclusions:  Our results point to enhanced biosynthesis of Cys-LTs during the AEDS exacerbations. Inflammatory cells, e.g. eosinophils are the most probable source of Cys-LTs. A strong correlation between Cys-LT levels and clinical status may in part explain preliminary clinical observations of efficacy of leukotriene antagonists in alleviating symptoms of AEDS

    [Selected parameters of the cellular and humoral immunity in atopic dermatitis. Relationship to the severity of the disease]

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    Despite the great progress, our understanding of the pathogenesis of atopic dermatitis (AD) is still incomplete. In particular, the clinical importance of various changes of the immune system parameters is unclear. Accordingly we have undertaken the study to compare selected parameters of cellular and humoral immunity between AD subjects (n = 26) and healthy controls (n = 10). These parameters included immunoglobulin levels (IgE in particular), neutrophil respiratory, oxygen burst, peripheral blood lymphocyte phenotype and response to mitogens. We also analysed the relationship between these parameters and clinical severity of skin lesions. RESULTS Mean total immunoglobulin E levels were very significantly increased in the AD group (1563 +/- 459 vs 35.5 +/- 12.1 IU/ml; p = 0.001). Simultaneously total serum IgE levels varied extensively between individual subjects with AD and were significantly correlated to clinical severity of the disease (Rs = 0.44; p = 0.02). Atopic dermatitis was also associated with the increase in the number of CD4+ and simultaneous decrease in the CD8+ lymphocytes causing statistically significant difference in CD4:CD8 ratio compared to the control group. We also observed changes of proliferation indices to phytohaemagglutinin (decrease) and increase of responses to anti CD3 mAb (OKT-3) and staphylococcal enterotoxin B. None of these immune parameters however, appeared to be statistically correlated to clinical status. CONCLUSIONS We find that atopic dermatitis is associated with significant changes of several important indices of cellular and humoral immunity including increased IgE levels and altered peripheral lymphocyte proliferation capacity and phenotype. Change of total IgE levels appears to be the most important from clinical point of view

    [Selected parameters of the cellular and humoral immunity in atopic dermatitis. Relationship to the severity of the disease]

    No full text
    Despite the great progress, our understanding of the pathogenesis of atopic dermatitis (AD) is still incomplete. In particular, the clinical importance of various changes of the immune system parameters is unclear. Accordingly we have undertaken the study to compare selected parameters of cellular and humoral immunity between AD subjects (n = 26) and healthy controls (n = 10). These parameters included immunoglobulin levels (IgE in particular), neutrophil respiratory, oxygen burst, peripheral blood lymphocyte phenotype and response to mitogens. We also analysed the relationship between these parameters and clinical severity of skin lesions. RESULTS Mean total immunoglobulin E levels were very significantly increased in the AD group (1563 +/- 459 vs 35.5 +/- 12.1 IU/ml; p = 0.001). Simultaneously total serum IgE levels varied extensively between individual subjects with AD and were significantly correlated to clinical severity of the disease (Rs = 0.44; p = 0.02). Atopic dermatitis was also associated with the increase in the number of CD4+ and simultaneous decrease in the CD8+ lymphocytes causing statistically significant difference in CD4:CD8 ratio compared to the control group. We also observed changes of proliferation indices to phytohaemagglutinin (decrease) and increase of responses to anti CD3 mAb (OKT-3) and staphylococcal enterotoxin B. None of these immune parameters however, appeared to be statistically correlated to clinical status. CONCLUSIONS We find that atopic dermatitis is associated with significant changes of several important indices of cellular and humoral immunity including increased IgE levels and altered peripheral lymphocyte proliferation capacity and phenotype. Change of total IgE levels appears to be the most important from clinical point of view

    Persistent skin colonization with Staphylococcus aureus in atopic dermatitis: relationship to clinical and immunological parameters

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    Background: Staphylococcus aureus has important implications for the pathogenesis of atopic dermatitis (AD). In some patients S. aureus can be eradicated from the skin during anti-inflammatory treatment, while in others bacterial colonization is persistent. Potential mechanisms and features of these two distinct groups of patients are not known. Objective: Accordingly, we studied relationships between the ability to eliminate S. aureus during an anti-inflammatory treatment and selected clinical and immunological features. Methods: Quantitative assessment of S. aureus on the skin, in nasal vestibule and throat, serum IgE levels, CD4/CD8 T-cell ratio, lymphocyte proliferation and phagocyte oxidative burst were determined during the exacerbation and after 4 and 12 weeks of the treatment using topical steroid and oral antihistamine in 34 patients with AD. Results: S. aureus was found on the skin of all 34 patients during exacerbation. Disease severity scoring of atopic dermatitis (SCORAD) correlated with the density of bacteria. Treatment with oral antihistamine and topical steroid resulted in a significant alleviation of symptoms, which correlated with the elimination of S. aureus from the skin in 70% of patients. In the remaining 30% of patients, dense (more than 1010/cm2) S. aureus skin colonization, persisted despite the treatment. Patients with persistent S. aureus presented with higher serum IgE levels, lower lymphocyte proliferation in response to staphylococcal enterotoxin B, phytohaemagluttinin and anti-CD3. Persistence of S. aureus was more common in men. Conclusions: Patients with AD differ in the ability to clear S. aureus from the skin during anti-inflammatory treatment, which appears to be related to the abnormalities in immunological parameters. Local antibiotic therapy should be considered only in patients with persistent S. aureus colonization
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