NEW YORK (Reuters Health) - Most patients with cystic fibrosis (CF) and normal lung function have neutrophilic airway inflammation that worsens over time, according to a new study, and recombinant human deoxyribonuclease (rhDNase) may favorably alter the inflammatory process.
“This is the first study demonstrating that rhDNase is not only an effective mucolytic drug but also affects the progression of airway inflammation in CF,” investigators note in the second issue for March 2004 of the American Journal of Respiratory and Critical Care Medicine.
The enzyme has previously been shown to improve lung function and reduce pulmonary exacerbations in CF patients, but its long-term effect on airway inflammation is largely unknown, Dr. Felix Ratjen, from the University of Essen in Germany and colleagues note in their report.
They determined the effects of rhDNase on airway inflammation over a 3-year period using bronchoalveolar lavage (BAL) in a group of CF patients with mild lung disease but normal lung function. Among a total of 105 patients, 46 were randomly assigned to rhDNase (2.5 mg/day) and 39 to no treatment.
The percentage of neutrophils in BAL fluid at baseline was similar in these two groups. The remaining 20 patients had a low percentage of neutrophils in BAL fluid at baseline and served as a control group.
According to the investigators, neutrophils in BAL increased significantly over the 3-year study in both untreated and control subjects, but remained unchanged in those treated with rhDNase.
Concentrations of proinflammatory interleukin-8 as well as elastase activity also increased in untreated and control subjects but remained stable in patients on rhDNase.
These results combined with prior studies, the team concludes, “would favor an early use of this drug in patients with CF having mild lung disease.” Further follow-up of this cohort will tell whether the positive effects of rhDNase on airway inflammation will affect the decline in lung function over time, they add.
Source: Am J Respir Crit Care Med 2004;169:719-725. [ Google search on this article ]
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