[Reforms in professional education in nursing: (no) way out of the special program?].
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Biomedical subjects
Publications and source records attributed to Jutta Beier.
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BACKGROUND: In patients with allergic rhinitis, bronchial hyperresponsiveness (BHR) and airway inflammation may increase during pollen exposure. BHR can be assessed by adenosine-5'-monophosphate (AMP) or methacholine challenge. It has been suggested that BHR to AMP is more closely related to airway inflammation than BHR to methacholine. Seasonal allergic rhinitis offers a dynamic model to study changes in BHR and airway inflammation during natural allergen exposure. METHODS: We measured BHR [provocative concentration causing a 20% fall (PC(20)) in forced expiratory volume in 1 s (FEV(1))] to AMP and methacholine, and induced sputum cells in 16 rhinitis patients before and during the 2001 grass pollen season. RESULTS: There was a decrease in PC(20) methacholine during pollen exposure (geometric mean PC(20) from 3.22 to 1.73 mg/ml, p = 0.0023), whereas no reduction was observed for PC(20) AMP (p = 0.11). There was no increase in sputum eosinophils [pre: 0.69% (95% confidence interval 0.22-2.07); during: 1.85 (0.55- 5.6), p = 0.31]. Although the correlation of log PC(20) methacholine and log PC(20) AMP at baseline was good (r = 0.76, p = 0.001), individual seasonal changes (doubling concentrations) in PC(20) methacholine were not correlated with changes in PC(20) AMP (rho = 0.21, p = 0.44). There was no correlation between baseline log PC(20) methacholine or seasonal changes in PC(20) methacholine and sputum eosinophils (p > 0.12, all correlations). In contrast, there was a significant correlation between seasonal changes in PC(20) AMP and changes in sputum eosinophils (rho = -0.59, p = 0.025). CONCLUSIONS: These data show dissimilarity between seasonal changes in PC(20) AMP and methacholine in patients with seasonal allergic rhinitis. Moreover, PC(20) AMP seems to be more closely related to sputum eosinophils than PC(20) methacholine. The clinical significance of this discrepancy is unclear.
STUDY OBJECTIVES: Neutrophilic inflammation is a major feature of COPD. Induced sputum is increasingly used to monitor inflammatory airway diseases. Although short-term repeatability of selected sputum markers has been extensively studied in several populations, data on the long-term repeatability of induced sputum markers in stable COPD are scant. DESIGN: Sputum supernatant of 12 patients with stable COPD was analyzed on three separate occasions with 4-weekly intervals. Sputum cells and inflammatory markers interleukin (IL)-8 and soluble intercellular adhesion molecule (sICAM)-1 were measured in supernatant using enzyme-linked immunosorbent assay. Repeatability of sputum markers was expressed by intraclass correlation coefficients (Ri). MEASUREMENTS AND RESULTS: Sputum induction was safe in all patients. None of the sputum parameters analyzed changed significantly throughout the study. The repeatability for cell differential counts in stable COPD was as follows: total cells, Ri = 0.07; neutrophils, Ri = 0.66; macrophages, Ri = 0.47; eosinophils, Ri = 0.49; and lymphocytes, Ri = 0.58. The repeatability of soluble markers was as follows: IL-8, Ri = 0.50; and sICAM, Ri = 0.58. Sputum neutrophils were negatively correlated with lung function on each separate occasion, whereas soluble markers were not correlated with sputum cells (p > 0.16, all correlations) or lung function (p > 0.24, all correlations). CONCLUSIONS: Clinically stable, moderate COPD is associated with equally stable sputum inflammatory markers. Repeatability of induced-sputum markers of neutrophilic inflammation in stable COPD is satisfactory, even over extended periods of time. These data support the usefulness of serial monitoring of induced-sputum inflammatory markers in COPD.
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology. Biopsy and bronchoalveolar lavage studies have shown, that accumulation of inflammatory cells, particularily neutrophils, in the alveolar space is a relevant feature of the pathogenesis of IPF. This paper adresses the issue of whether the safe and non-invasive method of sputum induction is a suitable tool to study respiratory tract inflammation in IPF. METHODS: In a cross-sectional analysis, 15 IPF patients and 14 healthy, non-smoking subjects underwent sputum induction. Total sputum cell counts, differentials, and the amount of interleukin (IL)-8, granulocyte-macrophage-colony stimulating factor (GM-CSF), and soluble ICAM-1 (sICAM) in sputum supernatant were analyzed. RESULTS: IPF patients had increased sputum neutrophils (60 +/- 6 vs 22 +/- 3%, p = 0.0003), and supernatant concentrations of IL-8 (19 +/- 3 vs. 7 +/- 1 ng/ml, p = 0.0002), GM-CSF (205 +/- 43 vs. 122 +/- 36 pg/ml, p = 0.08) and sICAM (12 +/- 3 vs. 5 +/- 3 ng/ml, p = 0.01), when compared with healthy controls. Sputum IL-8 was correlated with sputum neutrophils (rho = 0.61, p = 0.0006) in all patients. The extent of sputum neutrophilia was also correlated with lung function impairment (vital capacity, % of predicted) in IPF patients (rho = -0.68, p = 0.007). CONCLUSION: These data confirm the established role of neutrophilic inflammation in the pathogenesis of IPF, and show the potential of induced sputum to directly study inflammatory processes and surrogate markers in interstitial lung diseases like IPF.
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