Chronic obstructive pulmonary disease (COPD) is a progressive respiratory disorder characterized by persistent symptoms, airflow limitation, and chronic inflammatory response in the airways and lungs [1]. Globally, COPD is the third leading cause of death, accounting for approximately 3.2 million deaths annually (WHO, 2023). In India, the burden is disproportionately high, largely due to smoking, biomass fuel exposure, and occupational hazards [2,3,4]. Rajasthan, with its rural population and heavy reliance on biomass fuels, faces a particularly high prevalence of COPD. Beyond respiratory dysfunction, COPD has systemic manifestations, including oxidative stress, muscle wasting, metabolic disturbances, and cardiovascular comorbidities. Serum uric acid (SUA), the final metabolite of purine catabolism, is produced through xanthine oxidase activity, which is upregulated in hypoxia and oxidative stress [5,6]. Elevated SUA has been linked with ischemic heart disease, metabolic syndrome, and gout, but its role in COPD is less clearly established [7]. Previous studies suggest conflicting evidence. Bartziokas et al. (2017) reported that high SUA predicted mortality and frequent exacerbations in COPD patients. Koczulla et al. (2019) demonstrated SUA as a marker of systemic inflammation and hypoxemia. Conversely, Garcia-Pachon et al. (2011) found no consistent association between SUA and COPD severity. In India, Meena et al. (2020) observed significantly higher SUA in COPD patients in Rajasthan, while Sharma et al. (2018) suggested SUA may be confounded by renal status and smoking. These inconsistencies highlight the need for region-specific studies. Achrol, Jaipur, with its mixed urban–rural demographic, provides a unique setting to evaluate SUA in COPD patients, considering environmental exposures and smoking prevalence. Aim: To assess the association between SUA levels in individuals with and without COPD in Achrol, Jaipur. Objectives: 1. To compare SUA levels between COPD patients and non-COPD controls. 2. To analyze the correlation between SUA levels and disease severity (GOLD stage).

A cross-sectional, case–control study conducted in the Department of Pulmonary Medicine at a tertiary care hospital in Achrol, Jaipur, between January and June 2025. A total of 60 participants were included (30 COPD patients and 30 matched controls). COPD was diagnosed by spirometry (post-bronchodilator FEV1/FVC <0.7). Exclusion criteria were gout, chronic kidney disease, hepatic disease, malignancy, or drugs affecting uric acid metabolism. Data collected included demographics, smoking history, BMI, and spirometry findings. SUA was measured using enzymatic colorimetry. Ethical approval was obtained, and written informed consent was taken. Statistical analysis was performed using SPSS v25. Continuous variables were analyzed with t-test, categorical with chi-square test, p<0.05 was considered significant.

In the present study, the mean age of COPD patients was 58.4 ± 9.2 years, which was comparable to the control group (56.7 ± 8.5 years), with no statistically significant difference (p = 0.42). Male predominance was evident in both groups, with 70% males in the COPD group and 67.7% in controls; however, this difference was not statistically significant (p = 0.842), showing that sex distribution was matched between groups. As 76.7% of COPD patients were smokers compared to only 33.3% of controls, and this difference was statistically significant (p < 0.01). Mean BMI was significantly lower in COPD patients (22.3 ± 2.4 kg/m²) compared to controls (24.6 ± 3.1 kg/m²), with p < 0.05, suggesting nutritional depletion and weight loss associated with chronic disease progression. Table 1: Demographic and Smoking Characteristics Variable COPD Group (n=30) Control Group (n=30) p-value Age (years) 58.4 ± 9.2 56.7 ± 8.5 0.42 Male sex (%) 21 (70%) 20 (67.7%) 0.842 Smokers (%) 76.7 33.3 <0.01 BMI (kg/m²) 22.3 ± 2.4 24.6 ± 3.1 <0.05 Serum uric acid (SUA) levels were found to be significantly higher in the COPD group compared to controls. The mean SUA level in COPD patients was 7.1 ± 1.3 mg/dL, whereas in the control group it was 5.4 ± 1.1 mg/dL. This difference was statistically highly significant (p < 0.001), suggest that elevated SUA is associated with COPD and may reflect systemic inflammation and oxidative stress commonly seen in chronic respiratory disorders. Table 2: Serum Uric Acid Levels Group Serum Uric Acid (mg/dL), Mean ± SD p-value COPD (n=30) 7.1 ± 1.3 <0.001 Controls (n=30) 5.4 ± 1.1 Patients in Stage I (mild COPD) had mean SUA levels of 6.1 ± 0.8 mg/dL, while Stage II patients showed levels of 6.7 ± 1.0 mg/dL. More advanced stages showed substantially higher values, with Stage III patients averaging 7.6 ± 1.2 mg/dL and Stage IV patients averaging 8.2 ± 1.4 mg/dL. The overall correlation between SUA and GOLD stage was statistically significant (p < 0.05), indicating a positive association between disease severity and uric acid level, highlights SUA as a potential surrogate marker for disease progression in COPD patients, with higher levels reflecting worsening pulmonary impairment and hypoxemia. Table 3: Correlation of SUA with GOLD Stage GOLD Stage Mean SUA (mg/dL) P value Stage I (Mild) 6.1 ± 0.8 <0.05 Stage II (Moderate) 6.7 ± 1.0 Stage III (Severe) 7.6 ± 1.2 Stage IV (Very Severe) 8.2 ± 1.4

In this study, serum uric acid (SUA) levels were significantly elevated in COPD patients compared with age- and sex-matched non-COPD controls. Additionally, SUA levels showed a positive correlation with disease severity as measured by GOLD staging, with progressively higher levels observed in patients with advanced COPD. Similar result reported by, Bartziokas et al. (2017), who reported that higher SUA levels predicted increased risk of exacerbations and mortality among COPD patients in Greece. As SUA reflected both systemic oxidative stress and tissue hypoxemia, mechanisms that may underpin disease progression. Similarly, Koczulla et al. (2019) reported that SUA was strongly associated with hypoxemia and systemic inflammation, suggesting its potential role as a marker for comorbidities in COPD, Meena et al. (2020) also reported significantly higher SUA levels in COPD patients from Rajasthan, with SUA correlating with spirometric severity, highlight the regional relevance of SUA as a biomarker. The present study also observed significantly lower BMI in COPD patients compared to controls, which aligns with systemic manifestations of chronic disease such as malnutrition, muscle wasting, and increased metabolic demand. This is supported by Sharma et al. (2018), who observed that malnourished COPD patients had higher SUA levels, possibly due to enhanced catabolism and hypoxia-driven metabolic pathways. Contrasting evidence, however, has been reported in some studies. Garcia-Pachon et al. (2011) found no consistent relationship between SUA and COPD severity in their Spanish cohort, suggesting that renal function, dietary habits, and medications might confound SUA levels. Similarly, Yao et al. (2016) reported that while SUA was elevated in some COPD patients, it did not consistently correlate with pulmonary function impairment, raising questions about its reliability as a universal biomarker. The biological plausibility of elevated SUA in COPD is supported by underlying mechanisms. Hypoxia upregulates xanthine oxidase activity, leading to increased breakdown of purines and production of uric acid, alongside generation of reactive oxygen species. This contributes to systemic oxidative stress, a hallmark of COPD progression. Elevated SUA may therefore not only reflect oxidative burden but also contribute to vascular dysfunction, potentially linking COPD with cardiovascular comorbidities. Limitations: Small sample size may limit generalizability. Dietary purine intake, renal clearance, and concomitant comorbidities were not controlled, all of which can influence SUA levels.

Serum uric acid levels were significantly higher in COPD patients compared to non-COPD controls in Achrol, Jaipur. SUA correlated positively with GOLD stage severity, suggesting its potential as a cost-effective biomarker. Further large-scale studies are required to establish prognostic value and explore interventions.

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