Serum eosinophil cationic protein (ECP) in chronic asthma. Relationship to spirometry, flow-volume curves, PC20, and exacerbations

Wever, A.M.J.; Wever-Hess, J.; Hensgens, H.E.S.J.; Hermans, J.

doi:10.1016/s0954-6111(05)80010-1

Cited by 66 publications

(51 citation statements)

References 20 publications

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“…Since many of the patients showed high MPO levels during the follow-up period an ongoing neutrophil activation seemed to take place. Depending on the triggering agent at exacerbation differences in the levels of ECP have been described [10]. Lower ECP values were found at infection induced exacerbations and higher values at inflammatory exacerbations caused by different allergenic agents…”

Section: Discussionmentioning

confidence: 99%

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Serum eosinophil cationic protein (ECP) as a mediator of inflammation in acute asthma, during resolution and during the monitoring of stable asthmatic patients treated with inhaled steroids according to a dose reduction schedule

Kunkel

Rydén

1999

Inflammation Research

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Section: Discussionmentioning

confidence: 99%

“…It was further established that patients with the highest ECP levels in acute asthma showed the largest improvement in lung function after increased steroid treatment [7]. Elevated ECP levels in patients with inflammatory exacerbations also suggest that increased ECP could denote patients at risk of exacerbations [10].…”

Section: Introductionmentioning

confidence: 99%

Serum eosinophil cationic protein (ECP) as a mediator of inflammation in acute asthma, during resolution and during the monitoring of stable asthmatic patients treated with inhaled steroids according to a dose reduction schedule

Kunkel

Rydén

1999

Inflammation Research

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“…In bronchial lavage fluid samples from patients with chronic bronchitis, increased levels of ECP and MPO were found [Riise et al, 1995]. Serum ECP has been suggested to be a sensitive marker of inflammatory airflow obstruction in chronic asthma [Wever et al, 1994]. Higher concentrations of sputum ECP in symptomatic asthmatic patients have been reported [Konno et al, 1996] as well as a correlation between sputum ECP and airflow obstruction [Virchow et al, 1992].…”

Section: Commentsmentioning

confidence: 96%

Airways inflammation and glucan exposure among household waste collectors

1998

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“…ECP is released from activated eosinophils, is a marker of eosinophil activity and is elevated in serum from asthmatics, providing an indicator of inflammatory airflow obstruction [26]. In this study, serum levels of ECP were elevated in 10 subjects (25%).…”

Section: Discussionmentioning

confidence: 53%

Investigations on the renin-angiotensin system in acute severe asthma

Ramsay¹,

Dagg²,

McKay³

et al. 1997

Eur Respir J

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The renin-angiotensin system is activated in acute severe asthma, although not in all asthmatics [1,2]. The mechanism of this activation is unclear, but recent evidence has shown elevation of renin and angiotensin II in response to nebulized and intravenous salbutamol [3,4]. A wide variation in plasma β 2 -agonist levels has been found in acute asthmatics in previous studies [5], and could, therefore, account for the variation in renin and angiotensin II levels.However, the degree of activation of the renin-angiotensin system following administration of β 2 -agonists is less than that seen in acute asthma, suggesting an additional mechanism. The generation of angiotensin II via an "alternative" pathway, through the action of inflammatory proteases [6] either circulating or locally within the airways, could occur in addition to the "classical" activation of the renin-angiotensin system. Endogenous catecholamines released during an acute attack of asthma [7] could stimulate adrenoceptors on juxtaglomerular cells in the kidney [8] resulting in renin release, and may act synergistically with systemically absorbed albuterol.Serum angiotensin-converting enzyme (ACE) levels vary between individuals and correlate with a genetic polymorphism of the ACE gene [9]. Homozygotes for the deletion polymorphism have a higher ACE activity [10], and, therefore, the capacity to produce greater levels of angiotensin II in response to activation of the renin-angiotensin system. Thus, serum ACE activity could contribute to the variation seen in angiotensin II levels in acute asth-ma.We hypothesize that activation of the renin-angiotensin system in acute severe asthma is partly due to high levels of circulating β 2 -agonists in some asthmatics, and that other factors, as suggested above, may also contribute, possibly with a synergistic effect. Thus, we have examined the associations between renin, angiotensin II and multiple factors during acute attacks of asthma, with particular emphasis on the mechanisms outlined above. Materials and methods PatientsForty adult asthmatic patients (26 females and 14 males; mean (SD) age 45 (17) yrs) were recruited into the study. All presented nonconsecutively at the accident and emergency department, with acute exacerbations of asthma unresponsive to their regular medication and requiring hospital admission for treatment. Admission parameters were measured with peak expiratory flow rate (PEFR) 35 (18) % predicted, oxygen saturation 94 (4) %, cardiac frequency 108 (16) beats·min -1 , systolic blood pressure 139.5Investigations on the renin-angiotensin system in acute severe asthma. S.G. Ramsay, K.D. Dagg, I.C. McKay, B.J. Lipworth, C. McSharry, N.C. Thomson. ERS Journals Ltd 1997. ABSTRACT: The renin-angiotensin system is activated in acute severe asthma. The precise mechanism of activation is at present unknown, but may involve, β 2 -agonists, catecholamines or proteases released in airway inflammation.This study aims to identify potential factors involved in the activation of the reninangiotensin ...

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Serum eosinophil cationic protein (ECP) in chronic asthma. Relationship to spirometry, flow-volume curves, PC20, and exacerbations

Cited by 66 publications

References 20 publications

Serum eosinophil cationic protein (ECP) as a mediator of inflammation in acute asthma, during resolution and during the monitoring of stable asthmatic patients treated with inhaled steroids according to a dose reduction schedule

Serum eosinophil cationic protein (ECP) as a mediator of inflammation in acute asthma, during resolution and during the monitoring of stable asthmatic patients treated with inhaled steroids according to a dose reduction schedule

Airways inflammation and glucan exposure among household waste collectors

Investigations on the renin-angiotensin system in acute severe asthma

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