© 2005 American Thoracic Society
Fluticasone Reduces CRP in COPDTo the Editor:I have read the observational study by Sin and colleagues (1) and an accompanying editorial by Calverley (2) published in the AJRCCM. It remains unclear whether the C-reactive protein (CRP) in these patients was elevated as a consequence of their COPD or whether it was due to concomitant atherosclerosis or coronary artery disease. Second, there is still uncertainty whether elevated concentrations of CRP are causally related to the increased risk for cardiovascular complications or are merely a consequence of this elevated risk. In addition, the questions of whether elevated CRP levels reflect the degree of the underlying atherosclerosis or plaque vulnerability or might be related to other environmental or infectious stimuli, or whether CRP can directly influence platelet aggregation or coagulation, are unanswered. In contrast to Dr. Sin's speculation, there is little evidence that a reduction in CRP will lead to an improvement in outcome of COPD. In my view, the most important aspect missed by Drs. Sin and Calverley is the point that one could argue the converse. Corticosteroids could alter markers of systemic inflammation without any therapeutic benefit. A reduction in CRP by fluticasone or prednisolone is not necessarily "likely to have clinical relevance" and may not "improve health and/or cardiovascular outcomes in patients with COPD" as Dr. Sin suggests. In fact, the opposite might be the case: Monakier and colleagues (3) have recently suggeted that rofecoxib, a COX-2 inhibitor, lowers CRP (mean reduction by > 50%, namely, 0.84 mg/dL at 1 month and 1.3 mg/dL at 3 months; baseline 1.33 ± 3.99 mg/dL) and interleukin-6 levels significantly. The authors speculate that this "may translate into reduction of acute coronary events" (3). Despite these presumably beneficial actions of rofecoxib, this drug has recently been withdrawn from the market because its long-term use (> 1 year) might be associated with an increase in cardiovascular and cerebrovascular morbidity (4). What seems to appear obvious or "logical" in medicine may not be so. Observational studies such as the one by Dr. Sin and colleagues should be analyzed carefully, and allegations about possible "salutary effects" of corticosteroids "on cardiovascular morbidity and mortality in COPD" (1) should not be based on such studies. I am afraid that Dr. Sin's study does not add clinically relevant information to the question of whether corticosteroids reduce mortality in COPD. Long-term interventional studies are clearly needed.
University of Rostock Rostock, Germany FOOTNOTES
Conflict of Interest Statement: J.C.V. received REFERENCES
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
4,000 from GlaxoSmithKline (GSK) for speaking at conferences sponsored by this company and