© 2004 BMJ Publishing Group Ltd & British Thoracic Society
EDITORIAL
Salt transport in CF
Unravelling salt transport in cystic fibrosis
1 Department of Respiratory Medicine, Belfast City Hospital, Belfast, Northern Ireland, UK
2 Institute of Child Health, University of Liverpool, Royal Liverpool Children’s Hospital, UK
Correspondence to:
Correspondence to:
Dr P G Noone
Department of Respiratory Medicine, Belfast City Hospital, Lisburn Road, Belfast BT9 7AB, Northern Ireland, UK; peadar.noone@bch.n-i.nhs.uk
Sodium hyperabsorption may be a key therapeutic target in CF
Keywords: nasal potential difference; cystic fibrosis; ion transport; genotype/phenotype
| The first 150 words of the full text of this article appear below. |
Cystic fibrosis (CF) lung disease is characterised by thick viscid airway secretions, the development of progressive airways obstruction and bronchiectasis, and colonisation with specific bacteria, notably Pseudomonas aeruginosa.1 Although the precise pathogenic pathways in CF are still debated (see below), airway epithelial ion transport has been known to be defective in CF for two decades. This can be assessed in the airway in vivo by measuring potential difference (PD)—that is, the voltage generated across an electrically tight epithelium by the active transport of charged sodium and chloride ions.2 In patients with CF the magnitude of sodium absorption across airway epithelia and the response to the sodium channel blocker amiloride are substantially increased compared with normal subjects, coupled with an inability to secrete chloride ions.3 In the 1990s the putative gene (the cystic fibrosis transmembrane conductance regulator (CFTR) gene) was cloned4 and the affected
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