Correlation analysis indicated that serum CX3CL1 in COPD smokers was negatively correlated with FEV<sub>1</sub>/FVC (justified r = -0.319, P < 0.001), FEV<sub>1</sub>/Pre (justified r = -0.476, P < 0.001), FEV<sub>3</sub>/FVC (justified r = -0.354, P < 0.001), MMEF25-75/Pre (justified r = -0.428, P < 0.001), but positively correlated with CRP (justified r = 0.331, P < 0.001) and MMP-12 (justified r = 0.352, P < 0.001).
Levels were higher in COPD patients [1.55 (0.45)g/L] and individuals with respiratory symptoms [1.57 (0.47)g/L] than in controls [1.43 (0.47)g/L], p<0.001, a finding which persisted after correction for age and CRP.
Linear regression models, adjusting for age, FEV1 % predicted, and coronary artery disease, assessed the relationships between PA and CRP and IL-6 in those with OVS versus those with COPD alone.
We investigated whether elevated baseline serum C-reactive protein (CRP) levels in healthy individuals are associated with the risk of incident COPD by smoking status.
Point-of-care testing of C-reactive protein (CRP) may be a way to reduce unnecessary use of antibiotics without harming patients who have acute exacerbations of chronic obstructive pulmonary disease (COPD).
On day-30, no difference in symptom score, quality of life or serious adverse events was detected.Use of CRP as a biomarker to guide antibiotic treatment in severe acute exacerbations of COPD leads to a significant reduction in antibiotic treatment.
Besides, SDC-1 but not SDC-4, was negatively correlated with C-reactive protein (CRP) in COPD patients and downregulated in frequent exacerbators (FEs) of COPD.
In contrast, coexisting chronic obstructive pulmonary disease and higher C-reactive protein levels were independent risk factors for 1-year mortality in the HF without CKD group.
Serum Romo1 was correlated inversely with FEV1% predicted in COPD patients (푟 = - 0.347, 푃 = 0.016), while it was correlated positively with CRP and ROS levels, respectively.
MIP and SMIP are markedly reduced with greater degrees of inflammation in COPD as expressed by higher levels of CRP, SAA and cystatin C. Future research is needed to further examine the above findings and determine the impact of systemic inflammation along with its underlying mechanisms on inspiratory muscle function in COPD.
Correlations between serum amyloid A, C-reactive protein and clinical indices of patients with acutely exacerbated chronic obstructive pulmonary disease.
CysC levels showed negative correlation with forced expiratory volume in 1 second (FEV<sub>1</sub>) and a positive correlation with C-reactive protein (CRP) levels in patients with stable COPD.
We established a sequential COPD-AE-RW rat model by cigarette-smoke and bacterial exposures in the first 8 weeks, and was challenged with Klebsiella pneumonia to mimic an AE on Day 1 of week 9, and found that body temperature, white blood cell, neutrophils, serum amyloid A (SAA) and C-reactive protein (CRP) increased in AECOPD rats 24 h after challenge, and declined in 3-6 d, while lung function declined in 48 h, and recovered in 7-16 d. When sacrificed, pulmonary forced expiratory volume (FEV)100 and FEV300 decreased, while elevated bronchoalveolar lavage fluid (BALF) neutrophils and marked airway inflammation, remodeling and emphysema were observed.
CRP levels were significantly higher in TS COPD patients than in BS COPD group (p < 0.05), whereas fibrinogen was raised in COPD patients with a history of smoking (TS and TS + BS) when compared to control subjects (p < 0.01).
There were no significant differences in the number of subjects with high levels of inflammatory biomarkers (>90th percentile of never-smokers without COPD), including white blood cell count, total bilirubin, interleukin (IL)-6, IL-8, and C-reactive protein, or radiologic measurements (including emphysema index and mean wall area percentage) between never-smokers with COPD and those without COPD.
Serum CyPA positively correlated with serum interleukin-6, matrix metalloproteinase-9 and high-sensitivity C-reactive protein in both the exacerbation and convalescence phases of COPD.
There were differences in gender, smoking, time of cough, education, forced expiratory volume in the first second (FEV1) and serum CRP levels between COPD patients with or without depression.
Plasma Nrf2 and CRP levels significantly increased in a stepwise manner with an increase in inflammatory status (control vs. COPD-stable vs. COPD-exacerbation) (p = 0.002, p < 0.001).
There was a significant negative correlation between c-term FGF23 and total lung capacity (r = - 0.4; p = 0.01), and between c-term FGF23 and CRP in COPD patients (r = 0.48; p = 0.002). iFGF23 and c-term FGF23 were positively correlated with phosphate and PTH in the control group.
The aim of this study was to determine whether a panel of blood biomarkers [C-reactive protein (CRP), neutrophils, eosinophils, albumin and vitamin D] could predict mortality in COPD.
High CRP levels were associated with younger age, higher body mass index (BMI), chronic obstructive pulmonary disease (COPD), lower peak oxygen consumption and higher endothelin-1 and aldosterone levels.