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Biomedical subjects

E H Bel

Publications and source records attributed to E H Bel.

At least 19 recordsLinked to original sources

Deficient alpha-1-antitrypsin phenotypes and persistent airflow limitation in severe asthma.

BACKGROUND: Persistent airflow limitation is common among patients with severe asthma, but its pathogenesis has not been fully clarified. Severe alpha-1-antitrypsin (AAT) deficiency is a risk factor of chronic airflow limitation and emphysema, and partially deficient phenotypes have been associated with an accelerated decline in lung function. We hypothesized that partial deficiency of AAT (non-PiM AAT phenotype) is a risk factor of persistent airflow limitation in asthma. METHODS: In 122 patients with severe asthma (86 females; age (median (range)): 44.0 yr (18-75)) postbronchodilator FEV1 and FEV1/VC were measured and the AAT phenotype was determined. Persistent airflow limitation was defined as postbronchodilator FEV1 or FEV1/VC < 75% pred. with TLC > 75% pred. RESULTS: Six patients (4.9%) had a non-PiM phenotype (1 MF, 3 MS, 1 MZ and 1 SZ). Of the 58 patients with persistent airflow limitation only 1 patient (1.7%) had a non-PiM phenotype vs. 7.8% among the patients without persistent airflow limitation (P = 0.21). Postbronchodilator FEV1/VC (% pred.) was higher in the non-PiM patients than in the PiM patients (P = 0.02), the other lung function parameters were not different. Linear regression analysis showed no association between AAT phenotype and FEV1% predicted (P = 0.26). CONCLUSIONS: AAT heterozygoty does not seem to be an important risk factor of persistent airflow limitation in patients with asthma. Although confirmation by longitudinal follow-up studies with larger sample sizes is needed, these results suggest that routine assessment of the AAT phenotype is not indicated in asthmatic patients even if they exhibit fixed airflow limitation.

Adolescent↗

Alveolar nitric oxide versus measures of peripheral airway dysfunction in severe asthma.

Alveolar nitric oxide (NO) is a measure of peripheral airway inflammation in asthma, potentially associated with disease severity. The relationship between alveolar NO and physiological tests of peripheral airway (dys)function has not been investigated. The present authors hypothesised that peripheral airway inflammation and dysfunction are inter-related and associated with asthma severity. Alveolar NO was compared between 17 patients with mild-to-moderate asthma and 14 patients with severe asthma and related to total lung capacity (TLC), residual volume (RV)/TLC, thoracic gas volume (FRC), slope of the single breath nitrogen washout curve (dN2), closing capacity (CC)/TLC and fall in forced vital capacity at the provocative concentration of methacholine causing a 20% fall in forced expiratory volume in one second. In patients with severe asthma, strong correlations were found between alveolar NO and RV/TLC % pred, FRC % pred, dN2, and CC/TLC. Patients with oral steroid-dependent asthma had higher alveolar NO levels (2.7 ppb) compared with the other patients with severe (0.6 ppb) and mild-to-moderate asthma (0.3 ppb). The present authors conclude that alveolar nitric oxide is closely related to parameters of peripheral airway dysfunction in patients with severe asthma, and that oral steroid-dependent asthmatics have more peripheral airway disease than nonsteroid-dependent asthmatics. This suggests that patients on chronic oral steroid treatment have more extensive disease and require additional anti-inflammatory treatment to better target the peripheral airways.

Adult↗

Risk factors of frequent exacerbations in difficult-to-treat asthma.

Recurrent exacerbations are a major cause of morbidity and medical expenditure in patients with asthma. Various exogenous and endogenous factors are thought to influence the level of asthma control, but systematical data on the involvement of these factors in the recurrence of asthma exacerbations are scarce. In this study, 13 clinical and environmental factors potentially associated with recurrent exacerbations were investigated in 136 patients with difficult-to-treat asthma. Patients with more than three severe exacerbations (n = 39) in the previous year were compared with those with only one exacerbation per year (n = 24). A systematic diagnostic protocol was used to assess 13 potential risk factors. Factors significantly associated with frequent exacerbations included: severe nasal sinus disease (adjusted odds ratio (OR) 3.7); gastro-oesophageal reflux (OR 4.9); recurrent respiratory infections (OR 6.9); psychological dysfunctioning (OR 10.8); and obstructive sleep apnoea (OR 3.4). Severe chronic sinus disease and psychological dysfunctioning were the only independently associated factors (adjusted OR 5.5 and 11.7, respectively). All patients with frequent exacerbations exhibited at least one of these five factors, whilst 52% showed three or more factors. In conclusion, the results show that recurrent exacerbations in asthma are associated with specific co-morbid factors that are easy to detect and that are treatable. Therapeutic interventions aimed at correcting these factors are likely to reduce morbidity and medical expenditure in these patients.

Adolescent↗

Sputum induction in severe asthma by a standardized protocol: predictors of excessive bronchoconstriction.

Sputum induction is a noninvasive method to evaluate airway inflammation. We investigated whether it can be safely and successfully performed in patients with severe, difficult-to-control asthma, and whether the patients at risk can be identified. Ninety-three severe asthmatics were included, all symptomatic despite inhaled corticosteroids (> or = 1,600 microg/d) and long-acting beta(2)-agonists > 1 yr. Patients with a postbronchodilator FEV(1) < 1 L and < 50% predicted were excluded from participation. Sputum induction was performed according to a strict protocol, using 0.9%, 3.0%, and 4.5% NaCl inhalation. In 74% (CI: 64 to 83%) of patients an adequate sputum sample could be obtained. Twenty-two percent (CI: 14 to 33%) developed excessive bronchoconstriction (decrease in FEV(1) > 15% from baseline) despite the continuing use of long-acting bronchodilators and pretreatment with 400 microg salbutamol. The decrease in FEV(1) was associated with increased use of rescue short-acting beta(2)-agonists in the previous 2 d (r(s) = 0.51, p = 0.002), lower postbronchodilator FEV(1) (r(s) = -0.31, p = 0.004), and lower provocative concentration of histamine causing a 20% reduction in FEV(1) (PC(20)) (r(s) = -0.52, p < 0.001). Recent use of short-acting beta(2)-agonist increased the risk for excessive bronchoconstriction 10.2-fold (CI: 1.2 to 109.8). In conclusion, sputum induction can be safely and successfully performed in patients with severe, difficult-to-control asthma if a standardized protocol is used. However, severe bronchoconstriction may occur despite regular use of long-acting beta(2)-agonist and pretreatment with salbutamol 400 microg. In particular, patients who have used additional short-acting beta(2)-agonists as rescue medication during the days preceding the induction, are at high risk.

Asthma↗

Factors associated with persistent airflow limitation in severe asthma.

Persistent airflow limitation can develop in nonsmoking patients with asthma. However, the prevalence and risk factors for airways obstruction with incomplete reversibility in asthma are unknown. We assessed the prevalence of persistent airflow limitation (defined as postbronchodilator FEV(1) or FEV(1)/VC < 75% predicted) in 132 nonsmoking outpatients with severe asthma visiting chest physicians in general hospitals in The Netherlands. They had used inhaled corticosteroids (> or = 1,600 microg/d) and/or daily oral prednisone and long-acting bronchodilators for > 1 yr. In addition, we examined whether persistent airways obstruction in these patients was associated with specific clinical characteristics (age at onset, smoking history, atopic status, bronchodilator reversibility, provocative concentration of histamine causing a 20% decrease in FEV(1) [PC(20)histamine]) or markers of inflammation (exhaled nitric oxide [NO], blood eosinophils, total IgE; and eosinophilia or neutrophilia in induced sputum). Multiple logistic regression analyses were used to calculate adjusted odds ratios (OR). Persistent airflow limitation was observed in 49% of the patients in the study, and apart from older age and longer asthma duration, was strongly associated with a sputum eosinophils percent > or = 2% (OR = 7.7; confidence interval [CI]: 2.4 to 25), PC(20)histamine < or = 1.0 mg/ml (OR = 3.9; CI: 1.2 to 13), and adult onset (> or = 18 yr) of asthma (OR = 3.3; CI: 1.2 to 9). Only sputum eosinophilia appeared to be independently associated with persistent airflow limitation (OR = 8.9; CI: 1.3 to 59). In conclusion, persistent airflow limitation is common in adult patients with severe asthma, and is associated with adult onset of the disease, airway hyperresponsiveness, and most importantly, sputum eosinophilia. These findings suggest that eosinophilic airway inflammation contributes to persistent airflow limitation in severe asthma. Whether reduction of sputum eosinophils with more vigorous treatment leads to a better prognosis in severe asthma is still an open question.

Adolescent↗

Similar psychological characteristics in mild and severe asthma.

OBJECTIVE: Psychological factors have been implicated as potentially contributing to asthma severity. In the present study, we investigated whether patients with mild and severe asthma differ with regard to several psychological characteristics. METHODS: Ninety outpatients with severe asthma (74% female, mean [S.D.] age: 46.5 [13.7] years) and 37 outpatients with mild asthma (73% female, age: 39.4 [13.9] years) were compared with respect to general psychological health, anxiety sensitivity, hyperventilation symptoms, personality, and locus-of-control orientation, all measured by well-validated self-report questionnaires. Analysis of (co)variance (ANCOVA) was used to assess between-groups differences. RESULTS: No significant differences in psychological characteristics were found between patients with mild and severe asthma. Only on the subscale for external locus-of-control orientation, severe asthmatic patients differed from those with mild disease (P=.005) in showing less trust in physicians and medication with regard to influencing their asthma. CONCLUSION: The results suggest that mild and severe asthmatic patients cannot be differentiated on the basis of psychopathology or personality. Whether or not the observed lack of confidence in the influence of physicians or medication on asthma course is cause or consequence of disease severity, remains to be established.

Adult↗

Persistent airflow limitation in adult-onset nonatopic asthma is associated with serologic evidence of Chlamydia pneumoniae infection.

BACKGROUND: Persistent airflow limitation may develop in patients with asthma, particularly in adults with nonatopic (intrinsic) disease. Although the underlying mechanisms are still unknown, respiratory infections might be involved. OBJECTIVE: We investigated the annual loss of lung function in relation to seropositivity to Chlamydia pneumoniae in different subgroups of patients with severe asthma according to age at onset of asthma and atopic status. METHODS: One hundred one nonsmoking outpatients with a pulmonologist's diagnosis of severe asthma (32 men and 69 women; mean age, 46.0 years; range, 18-75 years) were included in a cross-sectional study. C pneumoniae-specific serum IgG and IgA were measured by means of ELISA. The estimated decline in lung function was calculated from the relationship between postbronchodilator FEV(1)/vital capacity (percent predicted) and the duration of asthma and expressed as the slope of the regression line. RESULTS: Patients with adult-onset nonatopic asthma and positive IgG antibodies to C pneumoniae had a significantly steeper slope of the regression line compared with the other subgroups of asthmatic patients (P =.001), being indicative of a 4-fold greater estimated decline in postbronchodilator FEV(1)/vital capacity (2.3% vs 0.5% predicted per year of asthma duration). CONCLUSION: These results suggest that C pneumoniae infection might promote the development of persistent airflow limitation in patients with nonatopic adult-onset asthma. It remains to be established whether viable pathogens that are accessible for therapeutic intervention are still present in the lower airways.

Adolescent↗

Psychopathology in patients with severe asthma is associated with increased health care utilization.

Severe asthma accounts for the majority of health costs for this disease, which is mainly related to the treatment of failed control. Several psychosocial factors have been associated with poor asthma control, but the question remains whether psychiatric disorder in patients with severe asthma predisposes for increased health care utilization. In the present study we compared outpatients with severe asthma with and without psychological dysfunctioning with respect to health care utilization. All patients used high dose inhaled corticosteroids and long-acting bronchodilators for more than 1 yr, and had difficult-to-control asthma, requiring one or more courses of corticosteroids during the past year or maintenance therapy with prednisone. Medical history was taken and health care utilization questionnaires were completed. The General Health Questionnaire (GHQ) was used to identify psychiatric cases (GHQ-12 score of > or = 6). There were no differences between the psychiatric cases (n = 21) and the noncases (n = 77) with respect to demographic and objective disease characteristics. However, the psychiatric cases had increased odds ratios (OR) for frequent visits to GP (OR = 5.9), frequent emergency visits (OR = 5.3), frequent exacerbations (OR = 12.4), and frequent hospitalizations (OR = 4.8) as compared with the nonpsychiatric patients. The present findings suggest that the morbidity and costs of asthma might be related to the level of psychological dysfunctioning in patients with severe asthma rather than to asthma severity per se, thereby identifying an area of potential intervention.

Adult↗

Recurrent exacerbations in severe asthma are associated with enhanced airway closure during stable episodes.

Excessive airway narrowing is a cardinal feature of asthma, and results in closure of airways. Therefore, asthmatic patients in whom airway closure occurs relatively early during expiration might be prone to severe asthma attacks. To test this hypothesis, we compared closing volume (CV) and closing capacity (CC) in a group of asthmatic patients with recurrent exacerbations (more than two exacerbations in the previous year; difficult-to-control asthma), consisting of 11 males and two females, aged 20 to 51 yr, with those in a group of equally severely asthmatic controls without recurrent exacerbations (stable asthma) consisting of 13 males and two females aged 18 to 52 yr. Both groups used equivalent doses of inhaled corticosteroids and were matched for sex, age, atopy, postbronchodilator FEV(1), and provocative concentration of methacholine causing a 20% decrease in FEV(1). They were studied during a clinically stable period of their disease. The patients inhaled 400 microg salbutamol via a spacer device, after which TLC and RV were measured by multibreath helium equilibration, together with the slope of Phase 3 (dN(2)), CV, and CC, by single-breath nitrogen washout. CV and CC were expressed as ratios of VC and TLC, respectively, and all data are presented as % predicted (mean +/- SEM). There was no difference in TLC in patients with difficult-to-control asthma and those with stable asthma (106.7 +/- 4.0% predicted versus 101.7 +/- 4.3% predicted, p = 0.40), RV (113.1 +/- 7.8% predicted versus 100.9 +/- 7.1% predicted, p = 0.26), or dN(2) (142.7 +/- 16.3% predicted versus 116.0 +/- 20.2% predicted, p = 0.23). In contrast, CV and CC were increased in the patients with difficult-to-control asthma as compared with the group with stable asthma (CV: 159.5 +/- 26.8% predicted versus 98.8 +/- 12.5% predicted, p = 0.024; CC: 114.0 +/- 6.4% predicted versus 99.9 +/- 3. 6% predicted, p = 0.030). These findings show that asthmatic individuals with recurrent exacerbations have increased CV and CC as compared with equally severely asthmatic but stable controls, even after bronchodilation during well-controlled episodes. The findings imply that airway closure at relatively high lung volumes under clinically stable conditions might be a risk factor for severe exacerbations in asthmatic patients.

Adolescent↗

Flow-dependency of exhaled nitric oxide in children with asthma and cystic fibrosis.

The concentration of nitric oxide in exhaled air, a marker of airway inflammation, depends critically on the flow of exhalation. Therefore, the aim of this study was to determine the effect of varying the flow on end-expiratory NO concentration and NO output in children with asthma or cystic fibrosis (CF) and in healthy children. Nineteen children with stable asthma, 10 with CF, and 20 healthy children exhaled from TLC while controlling expiratory flow by means of a biofeedback signal at approximately 2, 5, 10 and 20% of their vital capacity per second. NO was measured in exhaled air with a chemiluminescence analyser. Comparisons between the three groups were made by analysing the NO concentration at the endexpiratory plateau and by calculating NO output at different flows. Exhaled NO decreased with increasing flow in all children. Children with asthma had significantly higher NO concentrations than healthy children, but only at the lowest flows. Asthmatics using inhaled steroids (n=13) tended to have lower median exhaled NO than those without steroids. The slope of linearized (log-log transformed) NO/flow plots was significantly steeper in asthmatics than in healthy controls. CF patients had a significantly lower NO concentration and output over the entire flow range studied, compared to asthmatic and control subjects, with a similar NO/flow slope as control subjects. In conclusion, the nitric oxide concentration in exhaled air is highly flow-dependent, and the nitric oxide-flow relationship differs between asthmatics versus cystic fibrosis patients and control subjects. Assessment of the nitric oxide/flow relationship may help in separating asthmatics from normal children.

Asthma↗

Effect of inhaled steroids on airway hyperresponsiveness, sputum eosinophils, and exhaled nitric oxide levels in patients with asthma.

BACKGROUND: Airway hyperresponsiveness, induced sputum eosinophils, and exhaled nitric oxide (NO) levels have all been proposed as non-invasive markers for monitoring airway inflammation in patients with asthma. The aim of this study was to compare the changes in each of these markers following treatment with inhaled glucocorticosteroids in a single study. METHODS: In a randomised, double blind, placebo controlled, parallel study 25 patients with mild asthma (19-34 years, forced expiratory volume in one second (FEV1) >75% predicted, concentration of histamine provoking a fall in FEV1 of 20% or more (PC20) <4 mg/ml) inhaled fluticasone propionate (500 microg twice daily) for four weeks. PC20 to histamine, sputum eosinophil numbers, and exhaled NO levels were determined at weeks 0, 2, and 4, and two weeks after completing treatment. Sputum was induced by inhalation of hypertonic (4.5%) saline and eosinophil counts were expressed as percentage non-squamous cells. Exhaled NO levels (ppb) were measured by chemiluminescence. RESULTS: In the steroid treated group there was a significant increase in PC20, decrease in sputum eosinophils, and decrease in exhaled NO levels compared with baseline at weeks 2 and 4 of treatment. Subsequently, each of these variables showed significant worsening during the two week washout period compared with week 4. These changes were significantly different from those in the placebo group, except for the changes in sputum eosinophils and exhaled NO levels during the washout period. There were no significant correlations between the changes in the three markers in either group at any time. CONCLUSIONS: Treatment of asthmatic subjects with inhaled steroids for four weeks leads to improvements in airway hyperresponsiveness to histamine, eosinophil counts in induced sputum, and exhaled nitric oxide levels. The results suggest that these markers may provide different information when monitoring anti-inflammatory treatment in asthma.

Administration, Inhalation↗

Clinical control and histopathologic outcome of asthma when using airway hyperresponsiveness as an additional guide to long-term treatment. The AMPUL Study Group.

According to international guidelines, the level and adjustment of antiinflammatory treatment for asthma are based solely on symptoms and lung function. We investigated whether a treatment strategy aimed at reducing airway hyperresponsiveness (AHR strategy) in addition to the recommendations in the existing guidelines (reference strategy) led to: (1) more effective control of asthma; and (2) greater improvement of chronic airways inflammation. To accomplish this, we conducted a randomized, prospective, parallel trial involving 75 adults with mild to moderate asthma who visited a clinic every 3 mo for 2 yr. At each visit, FEV1 and AHR to methacholine were assessed, and subjects kept diaries of symptoms, beta2-agonist use, and peak expiratory flow (PEF). Medication with corticosteroids (four levels) was adjusted according to a stepwise approach (reference strategy), to which four severity classes of AHR were added (AHR strategy). At entry and after 2 yr, bronchial biopsies were obtained by fiberoptic bronchoscopy. Patients treated according to the AHR strategy had a 1.8-fold lower rate of mild exacerbations than did patients in the reference strategy group (0. 23 and 0.43 exacerbation/yr/patient, respectively). FEV1 also improved to a significantly greater extent in the AHR strategy group (p </= 0.05). In bronchial biopsies this was accompanied by a greater reduction in thickness of the subepithelial reticular layer in the AHR strategy group than in the reference strategy group (mean difference [95% confidence interval (CI): 1.7 micrometers (0.2 to 3.1) micrometers]). The changes in AHR in both strategy groups were correlated with eosinophil counts in the biopsies (r = -0.48, p = 0.003). We conclude that reducing AHR in conjunction with optimizing symptoms and lung function leads to more effective control of asthma while alleviating chronic airways inflammation. This implies a role for the monitoring of AHR or other surrogate markers of inflammation in the long-term management of asthma.

Administration, Inhalation↗

Lung function and sputum characteristics of patients with severe asthma during an induced exacerbation by double-blind steroid withdrawal.

Some patients with severe asthma are difficult to control and suffer from frequent exacerbations, whereas others remain stable with anti-inflammatory therapy. To investigate mechanisms of exacerbations, we compared 13 patients 20 to 51 yr of age (11 female, two male) with difficult-to-control asthma (two or more exacerbations during the previous year) and 15 patients 20 to 47 yr of age (13 female, two male) with severe but stable asthma (no exacerbations) after matching for sex, age, atopy, lung function, airway responsiveness, and medication. Exacerbations were induced by double-blind, controlled tapering of inhaled corticosteroids (fluticasone propionate) at weekly intervals. FEV1, airway responsiveness for methacholine (PC20MCh) and hypertonic saline (HYP slope), eosinophils and soluble markers (ECP, albumin, IL-6, IL-8) in induced sputum were assessed at baseline and during exacerbation (peak flow < 60% of personal best), or after 5 wk if no exacerbation occurred. Steroid tapering caused a decrease (mean +/- SEM) in FEV1 (12.1 +/- 3.1% pred; p = 0.045), PC20MCh (2.1 +/- 0.4 doubling dose; p = 0.004) and HYP slope (1.7 +/- 0.3 doubling dose; p = 0.001), and an increase in sputum eosinophils (10 +/- 3%; p = 0.008) and soluble markers for the two groups combined, without significant differences between the groups. Patients with difficult-to-control asthma had more exacerbations than did the stable asthmatics during both steroid tapering (7 versus 2; p = 0.022) and corticosteroid treatment (6 versus 0; p = 0.003). Exacerbations during steroid treatment in the patients with difficult-to-control asthma were associated with a decrease in FEV1 and PC20MCh, but not in HYP slope or increase in sputum eosinophils. We conclude that tapering of inhaled corticosteroids induces a rapid, reversible flare-up of eosinophilic airway inflammation. Patients with difficult-to-control asthma may develop exacerbations despite treatment with inhaled corticosteroids, which appear to have an eosinophil-independent mechanism. This implies that assessment of the nature of exacerbations may contribute to improved treatment for these patients.

Administration, Inhalation↗

Anti-leukotriene therapy in asthma.

There is ample evidence that leukotrienes are important inflammatory mediators of asthma. Anti-leukotriene therapy is a novel, specific anti-asthma strategy providing both reliever and controller effects. Currently, two types of anti-leukotriene drugs are being registered in several countries: leukotriene receptor antagonists and leukotriene biosynthesis inhibitors. Both types of drugs have shown comparable bronchodilator effects, and provided protection against bronchoprovocation tests with cold dry air, exercise, allergen and aspirin. Moreover, beneficial effects have been shown in the treatment of day-to-day asthma resulting in improvement of clinical symptoms, lung function parameters, and a reduction in beta 2-agonist- and corticosteroid-use. Furthermore, some studies showed a decrease in the airway eosinophil counts after longterm administration of anti-leukotriene drugs, suggestive of anti-inflammatory effects. Because of these properties in combination with generally mild adverse effects, anti-leukotrienes seem promising in the treatment of patients with various types and severities of asthma, including children. However, their definitive place in the management of asthma will eventually depend on their effectiveness to modulate the chronic airway inflammation, which induces the structural changes within the airways, determining the severity of clinical symptoms of asthma.

Asthma↗

CD11b and L-selectin expression on eosinophils and neutrophils in blood and induced sputum of patients with asthma compared with normal subjects.

BACKGROUND: Patients with asthma show altered surface expression of the adhesion molecules CD11b and L-selectin on airway granulocytes compared with blood granulocytes. OBJECTIVE: To investigate whether this modulation is related to disease activity or due to transendothelial migration, we compared the CD11b and L-selectin expression on blood and induced sputum eosinophils and neutrophils between patients with asthma and normal subjects. METHODS: Eleven normal subjects (21-43 years), nine patients (21-34 years) with mild atopic asthma and 10 patients (20-47 years) with moderate to severe atopic asthma on regular treatment with inhaled steroids underwent sputum induction by inhalation of nebulized hypertonic saline (4.5%). CD11b and L-selectin expression on granulocytes from blood and DTT-homogenized sputum were analysed by flow cytometry. Eosinophils could be discriminated from neutrophils by using depolarized light scatter. Disease activity was assessed by baseline FEV1 and airway responsiveness to histamine (PC20). RESULTS: Sputum eosinophils showed higher expression of CD11b (P<0.001) and lower expression of L-selectin (P<0.001) compared with peripheral blood eosinophils. CD11b and L-selectin expression on eosinophils from blood or sputum did not differ between the three groups. Similar results were obtained for neutrophils. The PC20 in the patients with moderate-to-severe asthma was related to CD11b expression on blood (R=-0.92, P=0.001) and sputum eosinophils (R=0.75, P=0.02). CONCLUSIONS: Flow cytometry of induced sputum granulocytes from asthmatic as well as normal subjects is feasible. We conclude that the modulated expression of CD11b and L-selectin on airway granulocytes is not specific for asthmatic airway inflammation, but is probably the result of tissue migration per sé. This implies that CD11b and L-selectin expression on granulocytes in induced sputum cannot be used as marker of disease activity.

Adult↗