A large cohort study from the UK Biobank suggested that patients with impaired pulmonary function may face an elevated risk of developing gout.
In the study, published in BMC Medicine, investigators analyzed data from 420,002 participants and observed that those who had preserved ratio impaired spirometry (PRISm) and chronic obstructive pulmonary disease (COPD) had nearly double the prevalence of gout compared with those who had normal lung function.
The study reported a gout prevalence of 6.31% in participants with PRISm and 6.26% in those with COPD compared with 3.45% in participants with normal pulmonary function. After adjusting for various factors, PRISm was associated with a 24% higher risk (odds ratio [OR] = 1.24, 95% confidence interval [CI] = 1.17–1.31), and COPD with a 14% higher risk (OR = 1.14, 95% CI = 1.07–1.22) of gout. A longitudinal analysis further showed that impaired pulmonary function was linked to a 32% increased risk of incident gout (hazard ratio = 1.32, 95% CI = 1.24–1.40).
To test the robustness of the findings, sensitivity analysis using the E-value (1.97) indicated that the observed associations were unlikely to be fully explained by unmeasured confounding. Mendelian randomization analysis suggested potential causal relationships, with genetic data showing that decreased lung function (e.g., FVC: OR = 0.80, 95% CI = 0.66–0.96) may influence gout risk.
The study explored mediating pathways, identifying urate levels as the most significant factor, accounting for 49.1% of the mediation effect. Additional contributors included C-reactive protein (6.62%), monocyte counts (1.33%), and neutrophil counts (4.85%), suggesting systemic inflammation and immune dysregulation as key mechanisms.
"Our study revealed a significant association between impaired pulmonary function and an increased risk of developing gout," the study authors indicated. "The association might be partially mediated by biomarkers including urate levels, inflammatory markers, and immune cell counts," they added.
A nonlinear relationship between pulmonary function indicators and gout risk was also observed. Participants with a forced vital capacity (FVC) below 88% or forced expiratory volume in 1 second (FEV1) below 79% demonstrated a pronounced increase in gout risk, as depicted in an inverse S-shaped curve.
The study used propensity score matching to balance demographics, lifestyle, and comorbidities between the participants with normal and impaired lung function. Three models, adjusted for varying levels of confounders, consistently showed a higher risk of gout in those with impaired pulmonary function.
The findings highlighted the potential role of pulmonary function tests in identifying patients at increased risk of gout. The investigators recommended greater collaboration between pulmonologists and rheumatologists to improve patient outcomes and management strategies.
The reliance on a predominantly Caucasian UK Biobank cohort limits the generalizability of the findings to more diverse populations. Additionally, the cross-sectional nature of spirometry data and potential underreporting of gout cases could introduce bias. Future studies should include more diverse populations and longitudinal assessments to validate these results.
The authors declared no competing interests.
