Inflammatory Biomarkers Linked to More Severe Disease in COPD With Bronchiectasis

Inflammatory Biomarkers Linked to More Severe Disease in COPD With Bronchiectasis
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People with chronic obstructive pulmonary disease (COPD) have higher levels of inflammatory biomarkers if they also have bronchiectasis, or damage to the lung’s airways, according to a new study. Such patients experience more severe disease and a greater number of exacerbations. 

The study, “Serum Biomarkers in Patients with Stable and Exacerbated COPD‐Bronchiectasis Overlap Syndrome,” was published in The Clinical Respiratory Journal.  

Bronchiectasis is characterized by the progressive dilation, inflammation, and scarring of the airways (bronchi) leading to the lungs. In turn, COPD is an inflammatory lung disease that causes wheezing, shortness of breath, and cough with mucus. Up to 40% of people with COPD also have bronchiectasis, which previously has been described as an overlap syndrome.

Compared with COPD patients who do not have bronchiectasis, those with this condition typically experience greater lung function deterioration, and a higher number of exacerbations and infections. 

Biomarkers — objective measures that capture what is happening in a cell or organism at a given moment — are a useful way to identify a disease process in the body and monitor disease progression. However, inflammatory biomarkers to detect exacerbations in patients with COPD and bronchiectasis have yet to be studied. 

To fill this gap, researchers at the Suleyman Demirel University, in Turkey, recruited 87 COPD patients — 85 of them men — with a mean age of 68 (all older than 40). All were either current smokers or ex-smokers, and 87% were symptomatic.  

Using CT scans, bronchiectasis was confirmed in 38 patients (43.7%). A comparison of those with and without bronchiectasis showed similar age, smoking history, and comorbidities, or more than one disease or condition present in a person at the same time.

However, during the initial assessment, the COPD patients with bronchiectasis were found to have lower body mass index, worse lung function, and a higher GOLD classification, representing greater airflow restriction. These individuals also had experienced more symptoms and more frequent exacerbations in the previous year, although these differences were not statistically significant. 

The participants were followed for a mean of 9.6 months, which included a winter season. The total number of exacerbations and of severe exacerbations was significantly higher in COPD patients with bronchiectasis than in those without. 

Symptoms such as shortness of breath, increased amount of sputum, increased respiratory rate, fast heart rate (tachycardia), fever, wheezing, and cough during exacerbations were significantly increased in COPD plus bronchiectasis. 

In blood samples, significantly higher levels of the inflammatory marker C-reactive protein (CRP) — a protein made by the liver — were found in COPD patients with exacerbations as well as those with bronchiectasis compared with people with COPD but without exacerbations or bronchiectasis.

In addition, the amount of fibrinogen, also a protein produced by the liver, was significantly higher in the same two groups. Notably, fibrinogen is involved in blood clotting and an indicator of inflammation.

CRP and fibrinogen levels also correlated with CT scan-based scores for bronchiectasis, in which patients with high levels of these inflammatory biomarkers had more advanced disease.

In turn, levels of suPAR — a protein associated with immune system activation and inflammatory diseases — tended to be higher in participants with bronchiectasis, but the difference was not statistically significant. 

Likewise, plasminogen activator inhibitor-1 (PAI-1) levels — a protein important in blood clotting and secreted in response to inflammatory reactions — were higher, but not significantly, in those with COPD and bronchiectasis.

In conclusion, “bronchiectasis coexistence is common in COPD patients and causes frequent exacerbations of the disease,” the scientists wrote.

“In addition to fibrinogen and CRP, suPAR and PAI-1 may play important roles in increased systemic inflammation associated with COPD bronchiectasis,” they added. “Large scale long-term prospective studies are needed about the roles of suPAR, PAI-1 in the inflammation of COPD patients with or without bronchiectasis.” 

Steve holds a PhD in Biochemistry from the Faculty of Medicine at the University of Toronto, Canada. He worked as a medical scientist for 18 years, within both industry and academia, where his research focused on the discovery of new medicines to treat inflammatory disorders and infectious diseases. Steve recently stepped away from the lab and into science communications, where he’s helping make medical science information more accessible for everyone.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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Steve holds a PhD in Biochemistry from the Faculty of Medicine at the University of Toronto, Canada. He worked as a medical scientist for 18 years, within both industry and academia, where his research focused on the discovery of new medicines to treat inflammatory disorders and infectious diseases. Steve recently stepped away from the lab and into science communications, where he’s helping make medical science information more accessible for everyone.
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