Oral Corticosteroid Therapy in Cystic Fibrosis Patients Hospitalized for Pulmonary Exacerbation

Dovey, Mark; Aitken, Moira L.; Emerson, Julia; McNamara, Sharon; Waltz, David A.; Gibson, Ronald L.

doi:10.1378/chest.07-0843

Cited by 52 publications

(36 citation statements)

References 19 publications

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“…Concomitant systemic corticosteroids did not substantially impact the majority of plasma protein measurements, consistent with previous findings that adding oral prednisone to standard CF exacerbation treatment resulted in no significant change in clinical outcomes and no additional reductions in sputum markers of inflammation (15). In our study, though, systemic corticosteroids did lead to greater reductions in hsCRP and IL-8, an effect that has been observed in other acute proinflammatory states treated with corticosteroids (16)(17)(18).…”

Section: O2 Saturationsupporting

confidence: 90%

Effect of Treatment of Cystic Fibrosis Pulmonary Exacerbations on Systemic Inflammation

et al. 2015

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Rationale: In cystic fibrosis (CF), pulmonary exacerbations present an opportunity to define the effect of antibiotic therapy on systemic measures of inflammation.Objectives: Investigate whether plasma inflammatory proteins demonstrate and predict a clinical response to antibiotic therapy and determine which proteins are associated with measures of clinical improvement.Methods: In this multicenter study, a panel of 15 plasma proteins was measured at the onset and end of treatment for pulmonary exacerbation and at a clinically stable visit in patients with CF who were 10 years of age or older.Measurements and Main Results: Significant reductions in 10 plasma proteins were observed in 103 patients who had paired blood collections during antibiotic treatment for pulmonary exacerbations. Plasma C-reactive protein, serum amyloid A, calprotectin, and neutrophil elastase antiprotease complexes correlated most strongly with clinical measures at exacerbation onset. Reductions in C-reactive protein, serum amyloid A, IL-1ra, and haptoglobin were most associated with improvements in lung function with antibiotic therapy. Having higher IL-6, IL-8, and a 1 -antitrypsin (a1AT) levels at exacerbation onset were associated with an increased risk of being a nonresponder (i.e., failing to recover to baseline FEV 1 ). Baseline IL-8, neutrophil elastase antiprotease complexes, and a1AT along with changes in several plasma proteins with antibiotic treatment, in combination with FEV 1 at exacerbation onset, were predictive of being a treatment responder. Conclusions:Circulating inflammatory proteins demonstrate and predict a response to treatment of CF pulmonary exacerbations. A systemic biomarker panel could speed up drug discovery, leading to a quicker, more efficient drug development process for the CF community.

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Section: O2 Saturationsupporting

confidence: 90%

Effect of Treatment of Cystic Fibrosis Pulmonary Exacerbations on Systemic Inflammation

et al. 2015

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“…They have been studied mostly as chronic suppressive medications in CF, however, long-term use has been limited by concerns of side effects [27]. A randomized controlled trial examining the short-term use of oral prednisone in all CF patients presenting with pulmonary exacerbations demonstrated a modest improvement in lung function [28]. Focusing this anti-inflammatory treatment on CF patients with exacerbations who are not responding to antibiotic treatment may maximize its potential benefit while minimizing harmful side effects.…”

Section: Discussionmentioning

confidence: 99%

Factors associated with response to treatment of pulmonary exacerbations in cystic fibrosis patients

Waters

Stanojevic

Sonneveld

et al. 2015

Journal of Cystic Fibrosis

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“…For example, intravenous corticosteroids during acute exacerbations of respiratory inflammation (45,104), chest physiotherapy (28,60,93), and chronic administration of azithromycin (9,131) have been shown improve the symptoms in both patient populations. An important exception is that dornase alpha, which clinically improves lung function and acute respiratory exacerbation frequency in CF patients (34), was found to be harmful in COPD patients (105).…”

Section: Treatments For Copdmentioning

confidence: 99%

Cigarette smoke and CFTR: implications in the pathogenesis of COPD

Rab

Rowe

Raju

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

141

127

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Chronic obstructive pulmonary disease (COPD) is a progressive respiratory disorder consisting of chronic bronchitis and/or emphysema. COPD patients suffer from chronic infections and display exaggerated inflammatory responses and a progressive decline in respiratory function. The respiratory symptoms of COPD are similar to those seen in cystic fibrosis (CF), although the molecular basis of the two disorders differs. CF is a genetic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene encoding a chloride and bicarbonate channel (CFTR), leading to CFTR dysfunction. The majority of COPD cases result from chronic oxidative insults such as cigarette smoke. Interestingly, environmental stresses including cigarette smoke, hypoxia, and chronic inflammation have also been implicated in reduced CFTR function, and this suggests a common mechanism that may contribute to both the CF and COPD. Therefore, improving CFTR function may offer an excellent opportunity for the development of a common treatment for CF and COPD. In this article, we review what is known about the CF respiratory phenotype and discuss how diminished CFTR expression-associated ion transport defects may contribute to some of the pathological changes seen in COPD.

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Oral Corticosteroid Therapy in Cystic Fibrosis Patients Hospitalized for Pulmonary Exacerbation

Cited by 52 publications

References 19 publications

Effect of Treatment of Cystic Fibrosis Pulmonary Exacerbations on Systemic Inflammation

Effect of Treatment of Cystic Fibrosis Pulmonary Exacerbations on Systemic Inflammation

Factors associated with response to treatment of pulmonary exacerbations in cystic fibrosis patients

Cigarette smoke and CFTR: implications in the pathogenesis of COPD

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