Low-dose aspirin was associated with a decreased risk for lung cancer and lung cancer-related mortality in patients with chronic obstructive pulmonary disease (COPD), according to a study published in PLOS Medicine.

For the retrospective cohort analysis, Hong Kong researchers compared patients with COPD who received vs did not receive treatment with aspirin. Investigators sourced data from the Clinical Data Analysis Reporting System in Hong Kong and conducted inverse probability of treatment weighting to balance baseline covariates between aspirin vs nonaspirin groups. Patients had a mean age of 75.7 years, and 80.3% were men.

In total, 4.2% of the cohort was diagnosed with lung cancer during a median 2.6 years (IQR, 1.4-4.8) of follow-up. Receiving treatment with aspirin vs no aspirin was associated with a 25% decreased risk for lung cancer (subdistribution hazard ratio [SHR], 0.75; 95% CI, 0.65-0.87; P<.001), meaning every 125 patients treated for 5 years with aspirin was associated with 1 fewer case of lung cancer. Receiving treatment with aspirin vs no aspirin was also associated with a 26% reduction in lung cancer-related mortality (SHR, 0.74; 95% CI, 0.64-0.86; P<.001), an increased risk for hemoptysis (SHR, 1.96; 95% CI, 1.73-2.23; P<.001), but it was not associated with increased risk for upper gastrointestinal bleeding (SHR, 1.19; 95% CI, 0.94-1.53; P=.16).


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The study authors suggest that aspirin could be preventive treatment for lung cancer in COPD patients, although adverse effects need to be further elucidated.

COPD predicts lung cancer, per the literature. The chemoprotective benefits of aspirin are evident even after short follow-up, according to results of the current study, which contrasts with previous research that have indicated that such benefit is significant only after 5 years or greater.

Proposed mechanisms of cancer prevention could be due to the anti-inflammatory and the antiplatelet properties of aspirin. Aspirin at low doses preferentially targets COX-1 activity, and COX-1 activity is the primary driver of prostanoids, such as thromboxane A and prostaglandin E2. These prostanoids are inhibited by low-dose aspirin, with this inhibition possibly playing a role in crosstalk between platelets and cells in the tumor microenvironment. The inhibition of platelets could stymie tumor progression and mitigate the risk of epithelial-to-mesenchymal transition, which facilitates respiratory malignant transformation.

Limitations of the current study include its observational design, which precludes any determination of causality. Furthermore, it’s possible that patients who take aspirin could pursue additional treatments.

“While the current retrospective study should not to be considered sufficient evidence for the inclusion of aspirin in the management strategy for COPD, the protective association between aspirin and lung carcinoma merits elucidation by future randomized studies to thoroughly study its benefits and associated adverse effects, to allow for rigorous cost-effective analyses, and to improve patient autonomy in clinical decision-making,” the study authors wrote.

Reference

Yu S-Y, Ip MS-M, Li X, et al. Low-dose aspirin and incidence of lung carcinoma in patients with chronic obstructive pulmonary disease in Hong Kong: A cohort study. PLOS Medicine. Published online on January 13, 2022. doi:10.1371/journal.pmed.1003880