Plasma tumour necrosis factor alpha in cystic fibrosis.

Norman, Dean C.; Elborn, J. Stuart; Cordon, Sally M; Rayner, R J; Wiseman, M.S.; Hiller, E; Shale, Dennis J.

doi:10.1136/thx.46.2.91

Cited by 96 publications

(57 citation statements)

References 21 publications

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“…Pulmonary inflammation and consequent injury is linked to systemic inflammation in patients with COPD, 29 and increased circulating inflammatory markers have been detected in CF subjects. 30,31 Infection induces respiratory muscle weakness in animal models, 32 and respiratory muscle weakness is associated with upper-respiratory-tract infections in humans. 33 Induced chronic bronchopulmonary infection by P. aeruginosa significantly decreased diaphragm and limb strength in infected mice, 28 and tumor necrosis factor alpha depressed the diaphragmatic tetanic force in murine diaphragm and limb muscle preparations.…”

Section: Discussionmentioning

confidence: 99%

ChronicPseudomonas aeruginosaInfection and Respiratory Muscle Impairment in Cystic Fibrosis

et al. 2013

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BACKGROUND: Chronic infection with Pseudomonas aeruginosa in patients with cystic fibrosis (CF) is associated with increased morbidity. Chronic infection can cause limb and respiratory muscle compromise. Respiratory muscle function can be assessed via maximal inspiratory pressure (P Imax ), maximal expiratory pressure (P Emax ), and the pressure-time index of the respiratory muscles (PTI mus ). We studied the effect of chronic P. aeruginosa infection on respiratory muscle function in patients with CF. METHODS: This cross-sectional study assessed P Imax , P Emax , PTI mus , FEV 1 , FVC, maximum expiratory flow during the middle half of the FVC maneuver, body mass index, and upper arm muscle area in 122 subjects with CF, in 4 subgroups matched for age and sex at different stages of P. aeruginosa infection, according to the Leeds criteria. We compared respiratory muscle function in the subgroups according to P. aeruginosa infection state. RESULTS: Median P Imax was significantly lower in CF subjects with chronic P. aeruginosa infection (P Imax ‫؍‬ 62 cm H 2 O), compared to subjects who were never infected (P Imax ‫؍‬ 86 cm H 2 O, P ‫؍‬ .02), free of infection (P Imax ‫؍‬ 74 cm H 2 O, P ‫؍‬ .01), or intermittently infected (P Imax ‫؍‬ 72 cm H 2 O, P ‫؍‬ .02). Median PTI mus was significantly increased in CF subjects with chronic P. aeruginosa infection (PTI mus ‫؍‬ .142), compared to subjects who were free of infection (PTI mus ‫؍‬ .102, P ‫؍‬ .006). Median upper-arm muscle area was significantly lower in CF subjects with chronic P. aeruginosa infection (upper-arm muscle area ‫؍‬ 2,219 mm 2 ), compared to subjects who were never infected (2,754 mm 2 , P ‫؍‬ .03), free of infection (2,678 mm 2 , P ‫؍‬ .01), or intermittently infected (2,603 mm 2 , P ‫؍‬ .04). Multivariate logistic regression revealed P. aeruginosa state of infection as a significant determinant of PTI mus (P ‫؍‬ .03) independently of sex, upper-arm muscle area, and FEV 1 . CON-CLUSIONS: CF subjects with chronic P. aeruginosa infection exhibited impaired respiratory muscle function and decreased inspiratory muscle strength, and chronic P. aeruginosa infection independently impacts respiratory muscle function in subjects with CF.

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Section: Discussionmentioning

confidence: 99%

ChronicPseudomonas aeruginosaInfection and Respiratory Muscle Impairment in Cystic Fibrosis

et al. 2013

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“…Several investigators have observed that pHLE complexes are increased in the blood of patients with CF [19,[29][30][31]. Increases in pHLE complexes have been reported in various studies of oxidant stress, antioxidant supplementation and other aspects of CF lung disease [31][32][33][34]; however, other investigators have found that HLE complexes in the blood of CF patients do not re ect respiratory exacerbations and do not correlate with lung function [27].…”

Section: Discussionmentioning

confidence: 99%

Plasma biomarkers and cystic fibrosis lung disease

Cantin

Bilodeau²,

Larivée³

et al. 2012

CIM

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Plasma biomarkers and cystic brosis lung disease AbstractPurpose: e purpose of this study was to determine whether plasma biomarkers re ect changes in lung function and respiratory exacerbations associated with CF lung disease.Methods: Plasma human leukocyte elastase/alpha1 antitrypsin complex (pHLE complex) values were measured in 28 adult CF patients and 47 healthy volunteers and correlated with forced expiratory volume (FEV1) and forced vital capacity (FVC). pHLE complexes were studied during respiratory exacerbations and a er antibiotic therapy. Plasma cytokines and sialic acid were also measured.Results: pHLE complexes were increased in CF patients (p < 0.01), were inversely correlated with FEV1 (r = 0.71) and FVC (r = 0.67) and returned to normal levels a er intravenous antibiotics (p < 0.001). Plasma cytokines did not correlate with lung function. Total sialic acid increased during CF respiratory exacerbations and decreased a er antibiotic therapy.Conclusion: Plasma sialic acid and pHLE complexes re ect clinically meaningful changes in CF lung disease. In contrast, plasma cytokine levels did not correlate with lung function.

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“…However, a systemic marker may not be sensitive enough to detect a meaningful change in lung disease, given that the inflammatory response to infection in the CF lung is largely confined to the lung. Assessments in blood have included antibodies to Pseudomonas aeruginosa (81)(82)(83) or products of inflammation (84), neutrophil elastase ␣ 1 -antiprotease complexes (63,85), C-reactive protein (CRP) (85,86), and various cytokines from serum or plasma (27,(87)(88)(89)(90)(91)(92)(93)(94)(95)(96)(97), and blood cells themselves (32,33,(98)(99)(100)(101)(102)(103). C-reactive protein is gaining increased recognition as a marker of inflammation for other diseases, but in CF, it is widely variable due to transient increases during pulmonary exacerbations (104,105).…”

Section: Assessing Inflammation In the Cf Lungmentioning

confidence: 99%

Sputum Biomarkers of Inflammation in Cystic Fibrosis Lung Disease

Sagel

Chmiel²,

Konstan³

2007

Proceedings of the American Thoracic Society

158

162

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Pulmonary biomarkers are being used more frequently to monitor disease activity and evaluate response to treatment in individuals with cystic fibrosis (CF). This article summarizes the current state of knowledge of biomarkers of inflammation relevant to CF lung disease, and the tools to measure inflammation, with specific emphasis on sputum. Sputum is a rich, noninvasive source of biomarkers of inflammation and infection. Sputum induction, through the inhalation of hypertonic saline, has expanded the possibilities for monitoring airway inflammation and infection, especially in individuals who do not routinely expectorate sputum. We critically examine the existing data supporting the validity of sputum biomarkers in CF, with an eye toward their application as surrogate endpoints or outcome measures in CF clinical trials. Further validation studies are needed regarding the variability of inflammatory biomarker measurements, and to evaluate how these biomarkers relate to disease severity, and to longitudinal changes in lung function and other clinical endpoints. We highlight the need to incorporate sputum collection, by induction if necessary, and measurement of sputum biomarkers into routine CF clinical care. In the future, pulmonary biomarkers will likely be useful in predicting disease progression, indicating the onset and resolution of a pulmonary exacerbation, and assessing response to current therapies or candidate therapeutics.

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Plasma tumour necrosis factor alpha in cystic fibrosis.

Cited by 96 publications

References 21 publications

ChronicPseudomonas aeruginosaInfection and Respiratory Muscle Impairment in Cystic Fibrosis

ChronicPseudomonas aeruginosaInfection and Respiratory Muscle Impairment in Cystic Fibrosis

Plasma biomarkers and cystic fibrosis lung disease

Sputum Biomarkers of Inflammation in Cystic Fibrosis Lung Disease

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