Rosuvastatin for chronic obstructive pulmonary disease (COPD) in people with HIV

Daily rosuvastatin stabilised clinical markers of chronic COPD progression and might reverse an important marker of pulmonary dysfunction commonly seen in HIV positive people, according to a pilot study reported by Alison Morris and colleagues from the University of Pittsburgh. [1]

COPD is found in approximately 15–20% of HIV positive individuals, and is usually related to smoking but it is not a complication that is improved by ART. [2] Impairments in diffusing capacity for carbon monoxide (DLCO) have also been reported in up to 64% of HIV positive people in some studies, and occurs both in smokers and non-smokers. [3]

Both conditions are associated with localised and systemic inflammation. Use of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) as opposed to inhaled corticosteroids is an attractive option for treatment of COPD because corticosteroids may have serious side effects in HIV positive people. Trials of statins for COPD in HIV positive people have so far produced conflicting results. Morris and colleagues conducted this prospective, randomised, double blind, placebo controlled, pilot-study of rosuvastatin (10 mg daily for 24 weeks) in HIV positive people with COPD, to determine feasibility for a larger multicentre study, and to assess impact on pulmonary function.

Inclusion criteria included a forced expiratory volume in 1 s/forced vital capacity (FEV1/FVC) below 0.70 and/or DLCO below 80%-predicted. Participants were not using lipid-lowering medication, were on or off ART and had a stable smoking status. The primary endpoint was difference between treatment and placebo in the 24-week change of post-bronchodilator FEV1%-predicted. Secondary endpoints included decline in other pulmonary function measures. The researchers used simulations to compare the observed values in each treatment group with the simulated null distribution.

Baseline spirometry for the 22 patients recruited, revealed median postbronchodilator FEV1 of 83%-predicted, and a median DLco value of 64%-predicted. For the placebo group, median FEV1%-predicted significantly declined by 4.5% (p = 0.027) at week 24 compared with baseline. In contrast, the median FEV1%-predicted remained stable in the rosuvastatin group at week 24 compared with baseline. The difference between groups was not significant. While there was no significant change in DLCO%-predicted between baseline and week 24 in the placebo group, DLCO%-predicted significantly increased by 6.7% between baseline and week 24 in the rosuvastatin group (p = 0.027). Again, this change was not significant between treatment groups.

The study demonstrated that rosuvastatin prevented any significant decline in FEV1%-predicted over 24 weeks in contrast to the placebo group, but was not powered to measure a difference between the groups. Rosuvastatin also led to improvements in DLCO, which was not seen in the placebo group. This is important because an impaired DLCO is the most common pulmonary function abnormality in HIV positive people and no therapies currently exist to treat it.

Nevertheless the authors concede that this study was limited by its small sample size and lacked statistical power. In addition, HIV positive people were recruited with pulmonary function deficits, who were current or former smokers. It is not clear what effect rosuvastatin may have had on COPD development in people with normal pulmonary function.