Abstract
It is presumed that bronchial hyperreactivity (BHR) can occur with any inhaled agent and may be a reason for discontinuation of inhalation therapy in cystic fibrosis (CF) patients. On the other hand, inhalation of antibiotics is being increasingly used to eradicate or treat infections. This review focuses on identifying the mechanisms of BHR for a better understanding of its impact on inhalation treatment. BHR in CF is suggested to be secondary to underlying airway disease (associated to poor pulmonary function, chronic inflammation and aerosol distribution) or to be a separate condition occurring more in CF. Furthermore, certain characteristics of the aerosol solution itself, such as the active molecule, chemical additives and particle size, can cause BHR. Recombinant human DNase (rhDNase), hypertonic saline (HS) and the antibiotics tobramycin, colistin and aztreonam lysine for inhalation (AZLI) are frequently used inhalation drugs in the treatment of CF. Prevalence of BHR related to both short and long-term inhalation of these drugs as reported in the literature was investigated. Acute BHR is documented in up to two thirds of CF patients. Despite the widespread use of rhDNase, HS, tobramycin, colistin and AZLI, only one long-term trial looked for, but did not demonstrate, BHR at the end of the trial period.
Highlights
Cystic fibrosis (CF) is the most common life-shortening autosomal recessive multi-organ disease; it is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene [1,2]
bronchial hyperreactivity (BHR) in CF is suggested to be secondary to underlying airway disease or to be a separate condition occurring more in CF
Half of the CF patients experience bronchial hyperreactivity on a metacholine challenge test, but not all of these patients respond with BHR to histamine as seen in asthma
Summary
Cystic fibrosis (CF) is the most common life-shortening autosomal recessive multi-organ disease; it is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene [1,2]. The most important site of disease and the predominant cause of both morbidity and mortality in CF is the respiratory tract [3,4] CFTR deficiency results in a modified epithelial ion transport and alters airway epithelial cell function by changing epithelial surfaces, leading to increased bacterial adherence and exaggerated airway cell inflammatory responses. These modifications lead to changes in both quality and quantity of mucus secretions and eventually lead to impairment of mucociliary clearance and loss of pulmonary function [5]. The second aspect is the suppression of bacterial colonization and infection with intravenous and/or inhaled antibiotics, [6] such as tobramycin, colistin and aztreonam lysine for inhalation (AZLI)
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