Edward M Erin

Imperial College London, Londinium, England, United Kingdom

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Publications (25)119.52 Total impact

  • T.T. Hansel · E. Erin · O.M. Kon · P.J. Barnes
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    ABSTRACT: There are considerable ongoing efforts from academic scientists and the pharmaceutical industry to develop new therapies for the treatment of allergy and asthma (Barnes 2004; Barnes & Hansel 2004; Bochner & Busse 2005; Buhl & Farmer 2005; Ballow 2006; Barnes 2006a) (see Fig. 83.1). Since the early 1970s asthma therapy has been dominated by use of inhaled synthetic β2-adrenoceptor agonists and corticosteroids, and the Global Initiative on Asthma (GINA) guidelines reflect the importance of using a combination long-acting β2 agonist (LABAs) and inhaled corticosteroid (ICS) in a single inhaler (National Institutes of Health 2005). Novartis and Theravance- GSK are involved in the development of once-daily "ultra" LABAs (Cazzola et al. 2005; Beeh et al. 2007). Novel recently licensed ICS include mometasone (Bousquet et al. 2000) and ciclesonide (Pearlman et al. 2005), while GSK 685 698 (Allermist) is a once-daily corticosteroid for allergic and nonallergic rhinitis submitted for marketing approval in July 2006. A humanized anti-IgE monoclonal antibody (Xolair, Novartis-Genentech) is the first biotechnology product to be licensed for the treatment of severe persistent allergic asthma that is not responding to high-dose inhaled ICS and LABAs (Holgate et al. 2005). There are a variety of novel IgEdirected approaches (Poole et al. 2005a), including anti-CD23 (low-affinity IgE receptor, FceRII) (Rosenwasser et al. 2003; Poole et al. 2005b). In the field of allergen immunotherapy, sublingual grass pollen immunotherapy has recently been licensed (Grazax, ALK-Abello) and peptide immunotherapy is also being assessed (Dahl et al. 2006; Durham et al. 2006). Thymic stromal lymphopoietin (TSLP) has attracted considerable attention as a target for allergy since it is produced by keratinocytes and may represent an important switch for dendritic cell control of allergic inflammation (Liu 2006). Specific biological therapy is under development to counteract individual cytokines, chemokines and adhesion molecules involved in allergy and asthma. Soluble interleukin (IL)-4 receptor (Nuvance, Immunex) was promising in preliminary studies involving abrupt withdrawal of inhaled steroids in patients with asthma (Borish et al. 1999; Borish et al. 2001) but larger-scale clinical studies in both mild and moderate asthma were discontinued in 2001 due to lack of efficacy. IL-13 has related but distinct properties and remains an attractive target for novel asthma therapy (Blanchard et al. 2005). IL-5 acts on the final stages of eosinophil maturation and release from the bone marrow, and humanized antibodies against IL-5 diminish eosinopoiesis and blood eosinophilia, but have no effect on responses to inhaled allergen (Gleich 2000). However, a bronchial biopsy study suggests that anti-IL-5 is not removing eosinophils from the airway wall, and that additional or alternative therapy will be required to ablate the eosinophil from the airways (Flood-Page et al. 2003a). It has been reported that anti-IL-5 was not effective in a clinical trial in severe asthma (Kips et al. 2003), but a study is ongoing on the effect of anti-IL-5 on asthma exacerbations in severe eosinophilic asthma. There is increasing evidence of a role for tumor necrosis factor (TNF)-a in severe asthma. A soluble TNF receptor construct (Nuvance, Immunex) has been found effective in a small study in severe asthma (Berry et al. 2006), while a monoclonal antibody (Remicade, Centocor) decreased exacerbations in less severe asthma (Erin et al. 2006). The chemokine CC receptor (CCR)3 is expressed on a range of cells including eosinophils and activated Th2 cells, and is an important target in asthma for a range of synthetic low-molecular-weight chemicals (Erin et al. 2002). VLA-4 antagonists have been considered for development in asthma, but there are concerns about Tysabri (natalizumab) being associated with progressive multifocal leukoencephalopathy (Berger & Koralnik 2005). Among specific receptor antagonists there are novel histamine H3 and H4 receptor antagonists (Leurs et al. 2005; Dunford et al. 2007) and prostaglandin (PG)D2 receptor antagonists (Yoshimura-Uchiyama et al. 2004). There has been extensive activity in developing inhibitors of cell signaling and transcription. Cilomilast (Ariflo, GSK) and roflumilast (Daxas, Nycomed) are oral tablets that inhibit phosphodiesterase type 4 (PDE4) (Lipworth 2005). Roflumilast has been shown to be effective in decreasing the early and late asthmatic reactions after inhaled allergen challenge (van Schalkwyk et al. 2005), and also in the treatment of asthma (Bateman et al. 2006; Bousquet et al. 2006). A range of kinase inhibitors have been developed primarily for the treatment of malignancies and some of these have potential for treatment of allergy and asthma (Adcock et al. 2006; Barnes 2006b). Targets include receptor tyrosine kinase inhibitors (c-kit, EGFR and VEGFR), Syk kinase inhibitors, phosphoinositide 3-kinase (PI3K) inhibitors, p38 MAP kinase inhibitors, and IKK2 (NF-κB) inhibitors. Among approaches directed against transcription factors and nuclear receptors, we consider glucocorticoid receptors and peroxisome proliferator-activated receptor (PPAR) agonists and therapy directed against JNK and AP-1. Of especial promise for the future is the advent of nucleic acid therapy (antisensense oligodeoxynucleotides) and interference RNA that targets specific mRNA (Popescu 2005; Sel et al. 2006; Ulanova et al. 2006) and can be delivered topically. Based on better understanding of the genetics and molecular pathophysiology that underlies allergy and asthma, novel rational biotechnology therapies are currently being tested in clinical trials. Proof-of-concept studies with highly specific protein therapeutics in novel clinical models are currently ongoing, and these studies should answer fundamental questions about the mechanisms of airway diseases, and enable the rational development of a range of novel synthetic chemical antiinflammatory therapies.
    No preview · Article · Feb 2009
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    ABSTRACT: Ciclesonide is a novel inhaled corticosteroid for the treatment of asthma, and it is important to measure the onset of effect of this therapy on airway hyperresponsiveness (AHR), exhaled nitric oxide (NO), and levels of eosinophils in induced sputum. In a randomized, double-blind, crossover study, 21 patients with mild asthma inhaled ciclesonide 320 microg (ex-actuator) qd, ciclesonide 640 microg (ex-actuator) bid, and placebo for 7 days. Exhaled NO and AHR to adenosine monophosphate (AMP), measured as the provocative concentration of AMP producing a 20% reduction in FEV1 (PC20FEV1), were assessed after inhalation on days 1, 3 and 7. Eosinophil levels in induced sputum were also measured. Ciclesonide 320 microg qd and 640 microg bid produced significantly greater improvements in PC20FEV1 compared with placebo on day 1 (within 2.5 h), and on days 3 and 7 (all p < 0.0001). On day 3, both ciclesonide doses significantly reduced exhaled NO levels by - 17.7 parts per billion (p < 0.0001) and - 15.4 parts per billion (p < 0.003) vs placebo, respectively. Significant reductions were maintained during the study with both ciclesonide doses (p < 0.01). A nonsignificant trend towards a decrease in eosinophil cell numbers was observed after 7 days of ciclesonide treatment, especially in patients receiving the higher dose. A single dose of ciclesonide decreased AHR to AMP and exhaled NO within 3 h, while FEV, improved at 3 days and 7 days.
    No preview · Article · May 2008 · Chest
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    ABSTRACT: Dithiothreitol (DTT) is commonly used to liquefy induced sputum samples before assessment of cytology, but causes reduction of disulfide bonds and denaturation of proteins. To process sputum supernatants containing DTT to enable quantification of cytokines and chemokines. A standard solution of 22 pooled chemokines and cytokines was incubated with DTT at the concentrations used during sputum liquefaction and then dialyzed under 20 different denaturant and redox conditions. After incubation of the standard solution with DTT there was loss of detectable protein mediators on immunoassay, but optimized dialysis permitted recovery of chemokines to 96 +/- 4% and cytokines to 91 +/- 6%. Optimized dialysis of DTT supernatants from subjects with asthma covering a range of severities (n = 35) was performed in the presence of a cocktail of protease inhibitors and demonstrated significantly elevated levels of the chemokine CXCL10 (IFN-gamma-inducible protein-10), CXCL8 (IL-8), and CCL3 (macrophage inflammatory protein-1alpha); with lower but significantly elevated levels of CCL2 (monocyte chemotactic protein-1), CCL11 (eotaxin), and CCL5 (regulated on activation, normal T-cell expressed and secreted) in severe asthma. In sputum from subjects with severe asthma there were also significantly elevated levels of IL-4, IL-5, IL-13, tumor necrosis factor-alpha, IL-6, granulocyte-macrophage colony-stimulating factor, and IL-12(p40). The technique of optimized dialysis and protease inhibition of sputum DTT supernatants aids the detection of chemokines and cytokines. The detection of elevated levels of particular sputum chemokines and cytokines in individual patients may provide a rationale for specific therapies.
    Full-text · Article · Feb 2008 · American Journal of Respiratory and Critical Care Medicine
  • E.M. Erin · M.K. Onn · P.J. Barnes · T.T. Hansel

    No preview · Article · Feb 2007
  • Edward M. Erin · Onn Min Kon · Peter J. Barnes · Trevor T. Hansel

    No preview · Article · Jan 2007 · American Journal of Respiratory and Critical Care Medicine

  • No preview · Article · Jan 2007
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    Full-text · Article · Jan 2007
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    ABSTRACT: Neutralization of tumor necrosis factor-alpha (TNF-alpha) is an effective antiinflammatory therapy for several chronic inflammatory diseases. We undertook a double-blind, placebo-controlled, parallel-group design study in 38 patients with moderate asthma treated with inhaled corticosteroids but symptomatic during a run-in phase. Infliximab (5 mg/kg) or placebo was administered by intravenous infusion at Weeks 0, 2, and 6. We assessed clinical response by monitoring lung function, symptoms, and inhaled beta(2)-agonist usage using hand-held electronic devices. The primary endpoint, change in morning PEF at Days 50-56 compared with the last 7 d of the run-in, was not significantly different on treatment. However, infliximab was associated with a decrease in mean diurnal variation of PEF at Week 8 (p = 0.02; 95% confidence interval [CI], -8.1 to -0.72). Furthermore, there was a decrease in the number of patients with exacerbations of asthma (p = 0.01; 95% CI, 4.4 to 52.7) and an increased probability of freedom from exacerbation with time (p = 0.03) in patients on infliximab (n = 14) compared with placebo (n = 18). In addition, infliximab decreased levels of TNF-alpha (p = 0.01) and other cytokines in sputum supernatants. There were no serious adverse events related to the study agent. Treatment with infliximab was well tolerated and caused a decrease in the number of patients with exacerbations in symptomatic moderate asthma. The promising preliminary findings underscore the need to evaluate therapy directed against TNF-alpha in larger trials enrolling patients with more severe asthma.
    Full-text · Article · Nov 2006 · American Journal of Respiratory and Critical Care Medicine
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    Angela Zacharasiewicz · Edward M Erin · Andrew Bush
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    ABSTRACT: Management of pediatric asthma is currently based on symptoms (often a second-hand report from parents) and lung function. Inhaled steroids are the mainstay of asthma management targeted at controlling airway inflammation. They should be used in the lowest possible doses. A number of noninvasive methods to assess inflammation have been developed in an effort to optimize anti-inflammatory treatment. The first longitudinal studies have been published demonstrating an improvement in asthma control in children by adding noninvasive monitoring of inflammation into the clinical management. New methods include exhaled nitric oxide measurements, induced sputum and markers in exhaled breath condensate. Further studies will show the practicability of including these measurement methods into everyday clinical practice. Their addition to the conventional assessment of asthma control appears promising. Using these methods to evaluate the current inflammatory state seems obligatory in research into new asthma therapeutics and management strategies. Managing asthma in children in specialist practice relying only on symptoms and lung function is no longer state of the art.
    Full-text · Article · Jul 2006 · Current Opinion in Allergy and Clinical Immunology
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    ABSTRACT: beta-Tryptase is a multifunctional mast cell serine protease released during mast cell degranulation and tryptase/trypsin inhibitors are a novel potential therapeutic approach for allergic inflammatory diseases. This study was performed to assess the effects of RWJ-58643 on nasal symptoms, eosinophil influx, and cytokine and chemokine release following nasal allergen challenge (NAC). Male patients with grass pollen allergic rhinitis (n=16) out of season received single doses of RWJ-58643 (100, 300, 600 microg) or matched placebo given 30 min before NAC in a double-blind, randomized crossover design. A single dose of 200 microg budesonide was studied in an open-label extension phase. NAC was performed with Timothy grass pollen (ALK) via a nasal device, and nasal lavage was performed at times 0 (pre-drug, pre-allergen), 0.5 (30 min post-drug, pre-NAC) 1.5, 2.5, 4.5, 6.5, 8.5, and 24 h after drug administration. Nasal lavage mediators were analysed using a sensitive multiplexed bead immunoassay system. Low-dose RWJ-58643 (100 microg) and budesonide (200 microg) significantly reduced symptoms, eosinophils and levels of IL-5 following NAC. However, higher doses of RWJ-58643 (300 and 600 microg) caused a late eosinophilia and preceding increases in IL-5 compared with placebo. This study suggests that combined beta-tryptase and trypsin inhibition has therapeutic potential in allergic inflammation, however, this property is dose responsive and higher doses are ineffective and may cause eosinophilia.
    Full-text · Article · May 2006 · Clinical & Experimental Allergy
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    ABSTRACT: Cytokines and chemokines produced by allergen-reactive T-helper type 2 (Th2) cells may be pivotal to the pathophysiology of allergic disorders. This study was performed to assess the effect of 7 days of topical corticosteroid on nasal allergen challenge (NAC) in terms of eosinophils, cytokines and chemokines obtained by nasal lavage and filter paper methods. Patients with grass pollen seasonal-allergic rhinitis (n = 13) out of season received nasal challenge following matched placebo (twice daily into each nostril for 7 days) and fluticasone propionate (100 microg twice daily into each nostril for 7 days). Chemokine and cytokine levels were analysed using a sensitive automated bead immunoassay system at intervals up to 8 h after NAC. Levels of cytokines and chemokines from filter paper were generally higher than from nasal lavage. Fluticasone propionate caused a reduction in symptoms, total leukocyte counts and eosinophils, and abrogation of IL-4, IL-5, IL-6 and IL-13 responses in the filter paper taken in the late phase (P < 0.05 for IL-4 and IL-13, P < 0.01 for IL-5 and IL-6). Levels of chemokines (eotaxin, RANTES, MCP-1, MIP-1alpha, IL-8 and IP-10) were also reduced in the late phase (P < 0.01 at 8 h). However, levels of IL-2, IL-3, IL-7, IL-12 (p40 and p70), -15, TNF-alpha, IFN-gamma and GM-CSF were not affected. Fluticasone propionate has selective inhibitory effects on Th2 cytokine synthesis following nasal challenge, while also decreasing release of chemokines, but not affecting levels of Th1 cytokines.
    No preview · Article · Dec 2005 · Clinical & Experimental Allergy
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    ABSTRACT: Nasal lavage is a noninvasive method of obtaining inflammatory exudates following nasal allergen challenge (NAC), and permits cells and released mediators to be evaluated. Objective: To determine the effects of a single dose of topical steroid on eosinophils and levels of chemokines and cytokines in nasal lavage fluid following NAC in patients with allergic rhinitis. Patients with grass pollen seasonal allergic rhinitis (n = 32) out of the allergy season received either nasal budesonide (100 microg per nostril) or matched placebo before allergen challenge in a double blind two-way crossover design. A semi-automated mixed bead array system was employed to measure multiple chemokines and cytokines in small volumes (50 microl) of nasal lavage supernatants. Following NAC there was a rapid onset of nasal symptoms together with nasal eosinophilia, and the appearance of IL-5 and IL-13 in lavages between 4 and 8 h. Elevated levels of eotaxin, RANTES, IL-8 and MCP-1 were also detected following allergen challenge. A single dose of nasal budesonide caused a decrease in symptoms (P < 0.05) and nasal eosinophils (P < 0.05) with selective abrogation of IL-5 and IL-13 responses (P < 0.05), but a lack of effect on levels of eotaxin, RANTES, IL-8 and MCP-1. This study suggests that a single dose of nasal steroid has the capacity to selectively abolish IL-5 and IL-13 responses following NAC. This model should be convenient for testing novel anti-inflammatory and immunoregulatory agents intended for the treatment of allergic rhinitis.
    Full-text · Article · Dec 2005 · Allergy
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    ABSTRACT: Inhaled anticholinergic drugs are effective bronchodilators in the treatment of COPD, and tiotropium bromide has recently been introduced as a once-daily bronchodilator for use as a maintenance treatment. Racemic glycopyrrolate is an anticholinergic drug that has been used orally to control gastric acidity, parenterally as an antisialogogue and to reverse neuromuscular blockade, and has been studied by inhalation for asthma and COPD. We investigated the duration of protection against the constrictor effects of inhaled methacholine of a single dose of inhaled nebulized racemic glycopyrrolate (0.5, 1.0, and 2.0 mg) compared with ipratropium bromide (0.5 mg) and placebo in 10 atopic asthmatic volunteers in a double-blind, five-way, crossover study. Protection against methacholine-induced bronchospasm after administering glycopyrrolate was maintained to 30 h, the last time point measured. Both bronchodilatation and bronchoprotection were significantly longer with glycopyrrolate than after ipratropium bromide, and bronchoprotection was significant at all time points from 2 to 30 h compared to placebo. Dryness of the mouth and nose was described in 18% of patients after the highest dose of glycopyrrolate. The prolonged bronchodilator response and the protection against methacholine-induced bronchospasm demonstrated in asthma suggests that inhaled racemic glycopyrrolate would be superior to ipratropium bromide for treatment of stable COPD.
    No preview · Article · Nov 2005 · Chest

  • No preview · Article · Sep 2005 · Clinical & Experimental Allergy
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    ABSTRACT: The use of noninvasive methods of monitoring airway inflammation, such as exhaled nitric oxide (eNO) and induced sputum, has been shown to improve asthma monitoring and optimize treatment in adult patients with asthma. There is a lack of comparable data in children. Forty children with stable asthma eligible for inhaled steroid reduction were reviewed every 8 weeks, and their inhaled steroid dose halved if clinically indicated. eNO, sputum induction combined with bronchial hyperreactivity testing, and exhaled breath condensate collection were performed at each visit to predict success or failure of reduction of inhaled steroids. Thirty of 40 (75%) children tolerated at least one dose reduction, 12 of 40 (30%) were successfully weaned off, and in total, 15 of 40 (38%) children experienced loss of asthma control. Treatment reduction was successful in all children who had no eosinophils in induced sputum before the attempted reduction. Using multiple logistic regression, increased eNO (odds ratio, 6.3; confidence interval, 3.75-10.58) and percentage of sputum eosinophils (odds ratio, 1.38; confidence interval, 1.06-1.81) were significant predictors of failed reduction. These findings suggest that monitoring airway inflammation may be useful in optimizing treatment in children with asthma.
    Full-text · Article · Jun 2005 · American Journal of Respiratory and Critical Care Medicine
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    ABSTRACT: Despite having been recognized for a long time as a cheap and effective therapy for the treatment of asthma and chronic obstructive pulmonary disease (COPD), theophylline is relegated to third-line therapy in the treatment of airway diseases due to the drug's frequent side effects and relatively low efficacy. However, regardless of the current situation, there are reasons for thinking that the use of theophylline, in addition to inhaled steroids, may come back into fashion for the treatment of chronic asthma, as it may have an anti-inflammatory and immunomodulatory effect when given in low doses. At these low doses, the drug is easier to use, side effects are uncommon and the problems of drug interaction are less of an issue, thus making the clinical use of theophylline less complicated. In COPD, low-dose theophylline is the first drug to demonstrate clear anti-inflammatory effects, and thus it may even have a role in preventing progression of the disease. Furthermore, the reversal of the steroid resistance induced by oxidative stress suggests that theophylline may increase responsiveness to corticosteroids.
    No preview · Article · Feb 2004 · Drugs of today (Barcelona, Spain: 1998)
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    ABSTRACT: The incidence of both asthma and chronic obstructive pulmonary disease (COPD) is increasing throughout the world, and acts as a major incentive for the development of new and improved drug therapy. For the large range of bronchodilator and anti-inflammatory agents in current clinical development, reliable decision-making is imperative in phase II, before entering large-scale phase III clinical studies. With anti-inflammatory therapies for asthma, many studies have been performed utilising the inhaled allergen challenge as a proof of concept study, effects on airway hyper-reactivity (AHR) can be assessed, and it is also possible to directly study limited numbers of symptomatic asthma patients. Additional clinical trial designs in asthma include studies to assess bronchodilation, bronchoprotection against a variety of inhaled constrictor agents, exercise tolerance, add-on and titration studies with inhaled and oral corticosteroids, and prevention and treatment of exacerbations. In contrast, it is a major issue for the development of new anti-inflammatory drugs for COPD that large-scale phase II studies are generally required in this disease in order to detect clinical efficacy. In COPD, clinical trial designs range from studies on lung function, symptoms and exercise performance, inflammatory biomarkers, natural history of chronic stable disease, prevention and treatment of exacerbations, and effects on cachexia and muscle function. Compared with asthma, inclusion criteria, monitoring parameters, comparator therapies and trial design are less well established for COPD. The large variety of potential clinical endpoints includes lung function, symptoms, walking tests, hyperinflation, health-related quality of life (HR-QOL), airway reactivity, and frequency and severity of exacerbations. In addition, surrogate biomarkers may be assessed in blood, exhaled breath, induced sputum, bronchial mucosal biopsy and bronchoalveolar lavage (BAL), and advanced radiographic imaging employed. Of particular utility is ex vivo whole blood stimulation to enable pharmacokinetic/pharmacodynamic modelling in establishing an optimal dosage regimen relatively early in human clinical studies. There have been considerable recent advances in the development of non-invasive biomarkers and novel clinical trial designs, as well as clarification of regulatory requirements, that will facilitate the development of new therapies for patients with asthma and COPD.
    No preview · Chapter · Jan 2004
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    ABSTRACT: There is a pressing need to develop new treatments for chronic obstructive pulmonary disease (COPD), as no currently available drug has been shown to reduce the relentless progression of this disease. Furthermore, recognition of the global importance and rising prevalence of COPD and the absence of effective therapies has now led to a concerted effort to develop new drugs for this disease [1, 2]. However, there have been disappointingly few therapeutic advances in the drug therapy of COPD, in contrast to the enormous advances made in asthma management that reflect a much better understanding of the underlying disease [3, 4].
    No preview · Article · Jan 2004

  • No preview · Article · Jan 2004
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    ABSTRACT: A study was undertaken to assess the correlation between cough frequency in asthmatic children with lung function and two non-invasive markers of airway inflammation. Thirty two children of median age 12.0 years (interquartile range (IQR) 9.5-13.4) with stable asthma were recruited. They underwent spirometric testing, exhaled nitric oxide (eNO) measurement, sputum induction for differential cell count, and ambulatory cough monitoring over 17 hours and 40 minutes. Coughing episodes were counted both as individual spikes and as clusters. Complete cough frequency data were available in 29 children (90%) and their median forced expiratory volume in 1 second (FEV1) and eNO were 88.5% (IQR 79.5-98) and 23.9 ppb (IQR 11.4-41.5), respectively. The median number of cough episodes was 14 (IQR 7.0-24.0) which was significantly higher than that of normal children (6.7 (IQR 4.1-10.5), p<0.001). Sputum induction was successful in 61% of the subjects; the median induced sputum eosinophil count was 0.05% (IQR 0-9.0). Cough frequency was found to have a significant positive correlation with eNO (Spearman's r =0.781, p<0.001) but not with FEV1 or sputum eosinophil count (r =-0.270, p=0.157; r =0.173, p=0.508, respectively). Children with stable asthma have increased cough frequency compared with normal controls and cough frequency was greater during the day than at night. Cough may be a more sensitive marker of airway inflammation than simple spirometry.
    Full-text · Article · Dec 2003 · Thorax

Publication Stats

941 Citations
119.52 Total Impact Points


  • 2002-2008
    • Imperial College London
      • Section of Leukocyte Biology
      Londinium, England, United Kingdom
  • 2006-2007
    • Royal Brompton and Harefield NHS Foundation Trust
      • Department of Paediatrics
      Harefield, England, United Kingdom