Role of neopterin among COPD patients

Chronic Obstructive Pulmonary Disease (COPD) is a major public health problem. It is the fourth leading cause of chronic morbidity and mortality worldwide. COPD is characterized by a specific pattern of inflammation involving many cells and mediators. Neopterin serves as a marker of systemic immune activation, which is of importance in the pathogenesis and progression of various diseases.Aim of the workThis study was conducted to elucidate the role of neopterin in the pathogenesis of COPD.Methods55 COPD patients and 20 healthy control subjects of similar age and sex were included in the study. Neopterin levels in the serum and sputum samples were measured in all subjects.ResultsThe mean values of neopterin in the serum (20.34 ± 4.70 nmol/l) and sputum (32.07 ± 8.14 nmol/l) samples of COPD patients were significantly higher than the mean values of neopterin in the serum and sputum samples of control subjects (6.27 ± 3.35 nmol/l and 4.13 ± 2.25 nmol/l respectively) (p < 0.001). Also, COPD patients with exacerbation had significantly higher (p < 0.001) serum and sputum neopterin levels (23.47 ± 2.56 nmol/l and 39.94 ± 5.47 nmol/l respectively) in comparison with stable COPD patients (18.69 ± 4.76 nmol/l and 27.91 ± 5.95 nmol/l respectively). There was statistically significant difference (p value < 0.05) between different COPD severity groups in the mean values of serum and sputum neopterin (nmol/l). There was statistically significant difference (p value < 0.05) in the mean values of serum and sputum neopterin between different COPD patients when they are classified according to the smoking state. Current smokers have higher mean values of serum (22.40 ± 3.04 nmol/l) and sputum (39.60 ± 7.56 nmol/l) neopterin than ex smokers (20.33 ± 4.67 nmol/l and 29.84 ± 6.33 nmol/l respectively) and nonsmokers (16.00 ± 5.3 nmol/l and 26.42 ± 6.60 nmol/l respectively).ConclusionsThis study found increased neopterin serum and sputum levels among COPD patients and suggests a role for neopterin in the pathogenesis of COPD. We recommend larger studies to support our results.