Chronic obstructive pulmonary disease (COPD) has been introduced as a major public health problem. It has been suggested that disruption in function or some adipokines and serum proteins' signaling could play crucial roles in lung diseases. This study's purpose was to investigate the association between serum levels of S100A1, ZAG, and adiponectin with FEV1 in COPD patients.
In this cross-sectional study, 90 clinically stable outpatient males with age ranging from 40 to 70 years with COPD diagnosis – FEV1/FVC < 70% – were divided into two groups: mild–moderate COPD patients; FEV1 ≥ 50 (n=52) VS severe and very severe COPD patients; FEV1 < 50 (n=38). The serum levels of ZAG, S100A1, and adiponectin were measured by the use of enzyme-linked immunosorbent assay.
In the present study, lower FEV1 was significantly associated with increased risk of cachexia (OR = 5.76, 95% CI: 2.28–14.54). The serum level of ZAG was significantly higher in the mild–moderate COPD patients in comparison with the severe–very severe COPD patients (p<0.035). However, the resting metabolic rate (RMR) level was significantly higher in FEV1<50 group compared to FEV1≥50 group (p<0.024). Also, strong positive associations between serum S100A1–ZAG, serum adiponectin–ZAG, and serum adiponectin–S100A1 (β>0.800, p<0.001) were shown.
In the present study, we found that low FEV1 was associated with increased risk of cachexia in COPD patients. Additionally, lower serum level of ZAG and higher RMR were observed in patients with severe–very severe COPD as compared to mild–moderate COPD. Therefore, it could be claimed that there is a mechanistic chain of causality between FEV1, serum ZAG, RMR, and cachexia.