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Acquired defects in CFTR-dependent β-adrenergic sweat secretion in chronic obstructive pulmonary disease.

Abstract：

RATIONALE:Smoking-induced chronic obstructive pulmonary disease (COPD) is associated with acquired systemic cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction. Recently, sweat evaporimetry has been shown to efficiently measure β-adrenergic sweat rate and specifically quantify CFTR function in the secretory coil of the sweat gland. OBJECTIVES:To evaluate the presence and severity of systemic CFTR dysfunction in smoking-related lung disease using sweat evaporimetry to determine CFTR-dependent sweat rate. METHODS:We recruited a cohort of patients consisting of healthy never smokers (N = 18), healthy smokers (12), COPD smokers (25), and COPD former smokers (12) and measured β-adrenergic sweat secretion rate with evaporative water loss, sweat chloride, and clinical data (spirometry and symptom questionnaires). MEASUREMENTS AND MAIN RESULTS:β-adrenergic sweat rate was reduced in COPD smokers (41.9 ± 3.4, P < 0.05, ± SEM) and COPD former smokers (39.0 ± 5.4, P < 0.05) compared to healthy controls (53.6 ± 3.4). Similarly, sweat chloride was significantly greater in COPD smokers (32.8 ± 3.3, P < 0.01) and COPD former smokers (37.8 ± 6.0, P < 0.01) vs. healthy controls (19.1 ± 2.5). Univariate analysis revealed a significant association between β-adrenergic sweat rate and female gender (β = 0.26), age (-0.28), FEV1% (0.35), dyspnea (-0.3), and history of smoking (-0.27; each P < 0.05). Stepwise multivariate regression included gender (0.39) and COPD (-0.43) in the final model (R()2 = 0.266, P < 0.0001). CONCLUSIONS:β-adrenergic sweat rate was significantly reduced in COPD patients, regardless of smoking status, reflecting acquired CFTR dysfunction and abnormal gland secretion in the skin that can persist despite smoking cessation. β-adrenergic sweat rate and sweat chloride are associated with COPD severity and clinical symptoms, supporting the hypothesis that CFTR decrements have a causative role in COPD pathogenesis.

journal_name

Respir Res

journal_title

Respiratory research

authors

Courville CA,Tidwell S,Liu B,Accurso FJ,Dransfield MT,Rowe SM

doi

10.1186/1465-9921-15-25

subject

Has Abstract

pub_date

2014-02-25 00:00:00

pages

eissn

1465-9921

issn

1465-993X

pii

1465-9921-15-25

journal_volume

pub_type

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Acquired defects in CFTR-dependent β-adrenergic sweat secretion in chronic obstructive pulmonary disease.