Chronic obstructive pulmonary disease is not only a disorder of the airways but also a systemic inflammatory condition, even during its stable phase. Stable COPD refers to a period when patients are free from acute exacerbations and experience relatively constant respiratory symptoms.1 Despite clinical stability, low-grade chronic inflammation persists in these patients due to ongoing exposure to risk factors such as smoking, environmental pollutants, and occupational hazards. This persistent inflammatory milieu contributes to progressive airflow limitation, structural lung damage, extrapulmonary manifestations, and the development of multiple comorbidities including cardiovascular disease, metabolic syndrome, and skeletal muscle dysfunction2.In stable COPD, inflammatory biomarkers are generally lower than during acute exacerbations, but they remain elevated compared to healthy individuals. Conventional markers such as CRP, ESR, and circulating cytokines have been studied extensively to understand disease progression and long-term prognosis in stable COPD.3,4 However, these markers have shown inconsistent correlations with clinical outcomes when used in isolation. In this context, hematological indices like the neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR), derived from routine complete blood counts, have emerged as promising indicators of underlying systemic inflammation in stable COPD patients.5 These markers are inexpensive, rapidly available, and do not require specialized laboratory testing, making them practical tools in routine clinical practice.Studies have shown that patients with stable COPD have moderately elevated NLR and PLR values compared to healthy controls, reflecting a chronic inflammatory state dominated by neutrophilic activity6. Neutrophils play a central role in COPD pathogenesis by releasing proteases, reactive oxygen species, and inflammatory mediators that contribute to airway remodeling and alveolar destruction. Lymphocyte counts, on the other hand, tend to be relatively reduced, leading to a higher NLR. Although the degree of elevation is less pronounced than in AECOPD, higher baseline NLR values in stable COPD have been associated with increased disease severity, poorer lung function, and a higher risk of future exacerbations7.The role of NLR in stable COPD extends beyond inflammation, as it has also been linked to comorbid conditions frequently seen in these patients, such as cardiovascular disease and metabolic disorders. PLR, while less extensively studied, has similarly been associated with disease burden and systemic inflammation. Importantly, unlike acute exacerbations, inflammatory markers in stable COPD do not reliably predict short-term outcomes such as hospitalization or mortality, but they may help identify patients at higher risk for disease progression and future exacerbations8,9. Therefore, in stable COPD, NLR and PLR serve as indicators of chronic systemic inflammation rather than acute disease activity, and their longitudinal monitoring may aid in comprehensive disease assessment and long-term risk stratification. AIM To estimate the Inflammatory markers level in patients with COPD.

This observational analytical study was conducted in the Department of Medicine at Govt Medical College, Barmer from April 2025 to sept 2025, after obtaining approval from the institutional ethical committee. The study was carried out over a defined period extending from ethical clearance until the required sample size was achieved. Patients diagnosed with chronic obstructive pulmonary disease (COPD) according to the GOLD 2023 guidelines were included in the study. Adult patients aged more than 40 years, of both sexes, were enrolled after informed consent. Patients with coexisting respiratory conditions such as bronchiectasis, pulmonary tuberculosis, or bronchial asthma were excluded to avoid confounding of inflammatory markers. Individuals with a history of myocardial infarction or stroke within the preceding three months, collagen vascular diseases, or malignancies were also excluded. Clinical evaluation was performed in all patients, and blood samples were collected under aseptic precautions to estimate inflammatory markers, including neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio, derived from routine complete blood counts. These markers were analyzed to assess the inflammatory status of patients with COPD.

Table 1: age distribution of participants Age (years) Number of Patients (n) Percentage (%) ≤ 40 8 12% 41–50 11 17% 51–60 17 26% > 60 29 45% Among the study population, the highest proportion of patients were aged over 60 years, accounting for 45% (n = 29), followed by those in the 51–60 years age group at 26% (n = 17). Patients aged 41–50 years constituted 17% (n = 11), while the least representation was seen in those aged ≤40 years, comprising 12% (n = 8). Table 2:sex distribution of participants Sex Number of Patients (n) Percentage (%) Male 44 67% Female 21 33% Males constituted the majority of the study population, accounting for 67% (n = 44) of the patients. Females represented 33% (n = 21), indicating a clear male predominance in the study. Table 3: Smoking status of participants Smoking status Number of Patients (n) Percentage (%) Smoker 46 70% Non- smoker 19 30% The majority of patients were smokers, comprising 70% (n = 46) of the study population. Non-smokers accounted for the remaining 30% (n = 19). Table 4: Mean levels of inflammatory markers in COPD patients (N = 65) Inflammatory Marker Unit Mean ± SD Normal Reference Range C-reactive protein (CRP) mg/L 8.6 ± 3.2 < 5 Interleukin-6 (IL-6) pg/mL 18.4 ± 6.7 < 7 Tumor Necrosis Factor-α (TNF-α) pg/mL 22.1 ± 7.5 < 8 Fibrinogen mg/dL 465 ± 82 200–400 Total leukocyte count cells/mm³ 9,850 ± 2,150 4,000–11,000 ESR mm/hr 34 ± 12 < 20 The inflammatory markers showed elevated mean values, with CRP, IL-6, TNF-α, fibrinogen, and ESR all exceeding their normal reference ranges, indicating a heightened inflammatory state in the study population. Total leukocyte count remained within the normal range despite the presence of significant systemic inflammation. Table 5: Distribution of inflammatory marker levels according to severity of COPD (GOLD staging) Marker Mild (n=9) Moderate (n=24) Severe (n=20) Very Severe (n=12) p-value CRP (mg/L) 4.2 ± 1.1 7.1 ± 2.3 9.4 ± 3.1 12.8 ± 3.6 <0.001 IL-6 (pg/mL) 9.8 ± 2.4 15.6 ± 4.1 20.3 ± 5.2 26.1 ± 6.4 <0.001 TNF-α (pg/mL) 11.2 ± 3.0 18.9 ± 5.1 24.7 ± 6.8 31.5 ± 7.9 <0.001 Fibrinogen (mg/dL) 362 ± 54 428 ± 67 487 ± 72 538 ± 88 <0.001 All inflammatory markers, including CRP, IL-6, TNF-α, and fibrinogen, showed a progressive increase from mild to very severe disease categories. This rising trend was statistically significant for all markers (p < 0.001), indicating a strong association between disease severity and systemic inflammation.

The age-wise distribution of the study population is shown in the table. Patients aged more than 60 years constituted the largest group, accounting for 45% of the total cases. This was followed by the 51–60 years age group, which comprised 26% of the patients. Individuals aged 41–50 years represented 17% of the study population. The youngest group, aged 40 years or less, accounted for 12% of cases. The study population was predominantly middle-aged and elderly.Eagan, T. M. L., et al10 The study included 272 females and 368 males.Among the COPD the average age was 63.6±6.9. The sex-wise distribution of the study population is presented in the table. Males constituted the majority of the patients, accounting for 67% of the total study population. Female patients comprised 33% of the cases. This indicates a clear male predominance in the study group. The male-to-female ratio was approximately 2:1. Such a distribution suggests that the condition under study was more commonly observed in males. The smoking status of the study population is summarized in the table. A majority of the patients were smokers, accounting for 70% of the total cases. Non-smokers constituted 30% of the study population. This shows a marked predominance of smokers among the participants. The high proportion of smokers suggests a possible association with the condition under study. Smoking emerged as a common habit in the study group. Jindal SK et al11 Chronic obstructive pulmonary disease was diagnosed in 4.1% of 35295 subjects, with a male to female ratio of 1.56:1 and a smoker to nonsmoker ratio of 2.65:1. Prevalence among bidi and cigarette smokers was 8.2% and 5.9%, respectively. The inflammatory marker profile of the study population is presented in the table. The mean C-reactive protein level was 8.6 ± 3.2 mg/L, which was elevated above the normal reference value of less than 5 mg/L. Interleukin-6 levels were also increased, with a mean value of 18.4 ± 6.7 pg/mL compared to the normal limit of less than 7 pg/mL. Tumor necrosis factor-α showed a raised mean level of 22.1 ± 7.5 pg/mL, exceeding the normal reference range. The mean fibrinogen level was 465 ± 82 mg/dL, which was higher than the normal range of 200–400 mg/dL. Although the mean total leukocyte count of 9,850 ± 2,150 cells/mm³ was within normal limits, the ESR was elevated at 34 ± 12 mm/hr, indicating an ongoing inflammatory state.In study by Meshram et al12 of various inflammatory markers, it was found out that all the biomarkers( CRP, TNF-α, and IL-6 )were significantly raised in the study group The comparison of inflammatory markers across disease severity categories is shown in the table. Mean CRP levels showed a progressive rise from mild to very severe disease, increasing from 4.2 ± 1.1 mg/L to 12.8 ± 3.6 mg/L. Similarly, IL-6 levels increased steadily with severity, ranging from 9.8 ± 2.4 pg/mL in mild cases to 26.1 ± 6.4 pg/mL in very severe cases. TNF-α levels also demonstrated a marked escalation across the severity spectrum, with the highest values observed in very severe disease. Fibrinogen levels increased consistently from mild to very severe categories, indicating heightened coagulation and inflammatory activity. The differences in all markers across severity groups were statistically significant. (p < 0.001).López-Campos JL et al13 The distribution of COPD stages was as follows: GOLD I, 14 patients (15.9%); GOLD II, 41 patients (46.6%); GOLD III, 19 patients (21.6%); and GOLD IV, 14 patients (15.9%). Simonovska L et al14 The statistical analysis conducted using the Student’s t-test showed significant statistical differences in the mean values of CRP in patients with different levels of bronchial obstruction. The highest mean value of CRP was registered in patients with very severe bronchial obstruction

The present study demonstrates that COPD predominantly affects middle-aged and elderly individuals, with a clear male predominance and a high prevalence among smokers, highlighting age, male sex, and smoking as major risk factors. The inflammatory marker profile revealed significantly elevated levels of CRP, IL-6, TNF-α, fibrinogen, and ESR, confirming the presence of systemic inflammation in COPD patients. Importantly, all key inflammatory markers showed a progressive and statistically significant increase with worsening disease severity, indicating a strong correlation between inflammatory burden and COPD severity. These findings are consistent with previous studies and reinforce the role of systemic inflammation in the pathogenesis and progression of COPD. Inflammatory markers may serve as useful indicators of disease severity and could aid in risk stratification and monitoring of patients with COPD.

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