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Background: It is amply reported that patients with chronic obstructive pulmonary disease (COPD) have increased risk of cardiovascular disease (CVD). Recent evidence suggests that COPD patients have elevated concentrations of plasma homocysteine (Hcy), a transsulfuration pathway analyte that is commonly regarded as a CVD risk factor. Design: We comprehensively investigated the plasma concentrations of transsulfuration pathway analytes, and their relationship with markers of oxidative stress and inflammation, to identify which low molecular thiols might play a pathophysiological role both in CVD and in COPD. Hcy, cysteine (Cys), glutathione (GSH), cysteinylglycine (CysGly), glutamylcysteine (GluCys), taurine (Tau), oxidative stress markers (TBARS and protein‐SH, PSH) and the inflammation marker kynurenine/tryptophan (Kyn/Trp) ratio were measured in 54 COPD patients and 54 control subjects. Results: We found increased concentrations of total Hcy (P <.01) and total CysGly (P <.05) in COPD patients when compared to controls. Total Hcy and CysGly were also significantly associated with abnormal lung function parameters and COPD severity. In COPD patients, total Hcy was significantly associated with the Kyn/Trp ratio (P =.0017) whereas total CysGly was significantly associated with both PSH (P =.0298) and the Kyn/Trp ratio (P = <.0001). Conclusion: Both total Hcy and CysGly concentrations were significantly associated with the presence and severity of COPD and with markers of oxidative stress (total CysGly) and inflammation (total Hcy and CysGly). This suggests that specific low molecular mass thiols might play a role in the inflammatory and oxidative stress pathways involved in both CVD and COPD. [ABSTRACT FROM AUTHOR]

Abstract: Introduction: The main white blood cell populations, neutrophils and lymphocytes, are involved in the pathophysiology of chronic obstructive pulmonary disease (COPD). We conducted a systematic review and meta‐analysis of studies investigating the relationship between the neutrophil to lymphocyte ratio (NLR, a marker of subclinical inflammation), presence of COPD, and its exacerbations. Methods: A comprehensive literature search was conducted in Pubmed, Web of Science and Scopus databases; two investigators independently reviewed suitable studies. Results: Nine studies, from 247 initially identified, were included in the meta‐analysis. Seven studies, in 775 COPD patients with stable disease and 496 healthy controls, showed a significant increase in NLR values in stable COPD (standardised mean difference, SMD, 0.773, 95% CI 0.410‐1.136; P < 0.001). Furthermore, in six studies in 527 COPD patients with acute exacerbation and 620 COPD patients with stable disease, NLR values were significantly higher in patients with exacerbations (random effects SMD 0.850, 95% CI 0.549‐1.151; P < 0.001). Conclusions: Our meta‐analysis showed that NLR values are significantly higher in stable COPD patients when compared to healthy individuals, although the magnitude of the difference is reduced after trim and fill adjustment, and in patients with COPD exacerbations when compared to patients with stable disease. Further studies, in larger cohorts, are needed to confirm whether the NLR is a useful tool in discriminating between COPD patients with stable disease, those with acute exacerbations, and subjects without the disease. [ABSTRACT FROM AUTHOR]