Improving QoL in Patients With Bronchiectasis and Pseudomonas aeruginosa

Pseudomonas aeruginosa
Pseudomonas aeruginosa
High-doses of atorvastatin reduced inflammation and improved health-related quality of life in patients with bronchiectasis.

High-dose atorvastatin reduced systemic inflammation and improved health-related quality of life (QoL) in patients with bronchiectasis and Pseudomonas aeruginosa, although it did not significantly improve cough, the primary end point. Atorvastatin (80 mg) significantly improved QoL as measured by the St George’s Respiratory Questionnaire (SGRQ) and other secondary end points, according to data published in Chest.

Pallavi Bedi, MD, from the University of Edinburgh’s MRC Centre for Inflammation Research in Scotland, and colleagues sought to determine whether atorvastatin would reduce cough severity and ameliorate inflammation in patients with severe bronchiectasis and chronic P aeruginosa infection ( Identifier: NCT01299194).

In the 7.5-month double-blind, crossover, randomized, controlled study, 16 patients (median age: 62.3±2.4) received 80 mg atorvastatin once daily, and 16 patients (median age 67.8±2.5) received placebo for 3 months. At 3 months, the groups were assessed with the Leicester Cough Questionnaire, followed by a 6-week washout period, after which they switched groups and were assessed again after 3 months.

Patients were included in the study if they had computed tomography (CT)-confirmed bronchiectasis, a chronic cough, 2 or more exacerbations in the previous year, and chronic infection with P aeruginosa. Patients were excluded if they were current smokers; had emphysema on CT scan; had cystic fibrosis, active allergic bronchopulmonary aspergillosis, tuberculosis, uncontrolled asthma, malignant disease, active inflammatory diseases; or were pregnant or breastfeeding.

Of the 27 patients who completed the study, atorvastatin did not significantly improve cough, the primary end point (mean difference: 1.92, 95% CI, −0.57 to 4.41, P =.12).

Statistically significant results, however, occurred in 5 secondary end points: SGRQ (mean difference: −5.62 points; 95% CI, −10.13 to −1.13; P =.016), serum interleukin 8 (mean difference: −27.96 pg/mL; 95% CI, −54.95 to −0.96; P =.04), tumor necrosis factor (TNF; mean difference: −14.24 pg/mL; 95% CI, −25.63 to −2.85; P =.01), intercellular adhesion molecule (ICAM1; mean difference: −126.67 ng/mL; 95% CI, −249.61 to −3.72; P =.04), and total cholesterol (mean difference: −1.642 mmol/L; 95% CI, −2.168 to −1.117;P <.0001).

There were no serious adverse events related to atorvastatin. Of the 5 patients who dropped out of the study, 3 were in the active drug group, and 1 withdrew due to a transient ischemic attack. While the patients were on the study drug, there was no significant difference in the creatinine kinase or alanine aminotransferase levels.

“This study confirms the efficacy of atorvastatin as an anti-inflammatory agent in this clinical population and justifies larger multicentre studies,” the researchers noted.

Study Limitations

  • The study was not powered for the secondary end points
  • The active and placebo drugs were not matched in appearance, but the researchers were not aware of the study drug administered to the patients because pharmacists dispensed it directly to the patients
  • A 3-month study may be inadequate to observe atorvastatin’s anti-inflammatory effects


Donald J. Davidson, PhD, received a Medical Research Council Senior Non-clinical Fellowship (G1002046).

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Bedi P, Chalmers JD, Graham C, et al. A randomised control trial of atorvastatin in bronchiectasis patients infected with Pseudomonas aeruginosa—a proof of concept study [published online May 26, 2017]. Chest. doi:10.1016/j.chest.2017.05.017

This article originally appeared on Pulmonology Advisor