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1 Dept of Pharmacoepidemiology and Pharmacotherapy, Utrecht Institute for Pharmaceutical Sciences, 2 The PHARMO Institute, 3 Dept of Pulmonary Diseases, Heart Lung Centre Utrecht, Utrecht, The Netherlands
CORRESPONDENCE: R.M.C. Herings, Dept of Pharmacoepidemiology and Pharmacotherapy, Utrecht Institute for Pharmaceutical Sciences, PO Box 80082, 3508 TB, Utrecht, The Netherlands. Fax: 31 302345568. E-mail: Ron.Herings@Pharmo.nl
Keywords: chronic obstructive pulmonary disease, exacerbation, hospitalisation, mucolytics, N-acetylcysteine, pharmacoepidemiology
Received: July 15, 2002
Accepted January 6, 2003
The aim of this study was to evaluate the effect of oral N-acetylcysteine in the prevention of re-hospitalisation for chronic obstructive pulmonary disease (COPD) exacerbations.
Using the PHARmacoMOrbidity linkage (PHARMO) system the authors included all patients aged
A total of 1,219 patients, who were hospitalised for COPD between 19861998, were included in this study. After adjustment for disease severity, it was observed that the use of N-acetylcysteine was significantly associated with a reduced risk of readmission. The readmission risk was significantly lower in patients with high average daily doses of N-acetylcysteine.
In conclusion it was observed that N-acetylcysteine reduces the risk of re-hospitalisation for chronic obstructive pulmonary disease by
55 yrs who had been dispensed medication, labelled for respiratory indications (anatomical therapeutic chemical (ATC) classification system: R03), between 19861998 and who had also been hospitalised for COPD (International Classification of Diseases (ICD)-9: 491, 492, 496) in this time frame. These subjects were subsequently divided into two groups, those who had received N-acetylcysteine following discharge from their first admission between 19861998 and those who had not. All the patients were studied starting from their initial discharge, until their first readmission, death or end of data collection period. The maximum follow-up period was 1 yr.
30% and that this risk reduction is dose-dependent.
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