Higher serum levels of systemic inflammatory markers are linked to greater inspiratory muscle dysfunction in COPD

Abstract

Background Chronic obstructive pulmonary disease (COPD) is associated with an inflammatory response that becomes more pronounced in acute exacerbations. Considerable attention has recently focused on the value of several inflammatory mediators in predicting worsening of COPD‐related symptoms. Whereas respiratory muscle dysfunction is also widely present in this population, little is known about how systemic inflammation relates to inspiratory muscle dysfunction in COPD. Methods Fifty‐three males with mild‐to‐very severe airflow obstruction underwent blood sampling for 23 inflammatory markers, including acute‐phase proteins, cytokines and adipokines. Inspiratory muscle performance was assessed via the test of incremental respiratory endurance, providing measures of maximal (MIP) and sustained maximal (SMIP) inspiratory pressures. Results The mean ± SD MIP and SMIP were 75.32 ± 19.62 cmH2O and 406.15 ± 124.55 PTU. MIP negatively correlated with CRP, SAA and cystatin C (r‐values from −0.333 to −0.378, P < 0.02), while SMIP was inversely related to SAA and cystatin C (r = −0.534 and r = −0.396, P = 0.00). Significant differences in CRP, SAA, cystatin C and PARC were also found between subjects with and without inspiratory muscle weakness. No additional significant relationships were observed between either MIP or SMIP and other inflammatory markers in the study. Conclusions 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.

The association between cystatin C and COPD: a meta-analysis and systematic review

“…Consistent with previous studies, we found that the elevated levels of Cys C were significantly correlated with disease status and lung function. Hu et al [24] found that the elevated Cys C levels was an important and independent risk factor of increased mortality in a hospital setting during COPD exacerbation, Formiga et al [51] indicated that inspiratory muscle function was reduced with greater degrees of inflammation in COPD as expressed higher levels of Cys C. Combining with the results of previous studies and this meta-analysis, we thought that the elevated levels of serum Cys C might indicate the exacerbation and progression of COPD.…”

<p>Serum Amyloid A in Stable COPD Patients is Associated with the Frequent Exacerbator Phenotype</p>

“…14 Other studies showed increased circulating SAA concentration in COPD and other pulmonary diseases such as idiopathic pulmonary fibrosis (IPF). [22][23][24] Formiga et al reported that inspiratory muscle performance was considerably lower in COPD patients with greater SAA concentration. 23 In addition, SAA was greater in patients with IPF than in healthy controls.…”

“…[22][23][24] Formiga et al reported that inspiratory muscle performance was considerably lower in COPD patients with greater SAA concentration. 23 In addition, SAA was greater in patients with IPF than in healthy controls. 22 Furthermore, serum levels of SAA and CRP together with other inflammatory markers (eg, IL-6, IL-8, TNF-a, IP-10) were significantly greater in COPD patients experiencing an exacerbation than during remission and in healthy control subjects.…”

Serum Amyloid a in Stable COPD Patients is Associated With the Frequent Exacerbator Phenotype

“…Previous studies showed that SAA is dramatically increased during acute phase of a COPD exacerbation, and that SAA is a sensitive biomarker for exacerbation severity in COPD patients 14 . Other studies showed increased circulating SAA concentration in COPD and other pulmonary diseases such as idiopathic pulmonary brosis (IPF) [22][23][24] . Formiga et al reported that inspiratory muscle performance was considerably lower in COPD patients with greater SAA concentration 23 .…”

“…Other studies showed increased circulating SAA concentration in COPD and other pulmonary diseases such as idiopathic pulmonary brosis (IPF) [22][23][24] . Formiga et al reported that inspiratory muscle performance was considerably lower in COPD patients with greater SAA concentration 23 . In addition, SAA was greater in patients with IPF than in healthy controls 22 .…”