COPD stands for Chronic Obstructive Pulmonary Disease and is a chronic inflammatory lung disease characterized by restricted airflow that mainly affects middle-aged or elderly adults who smoke. Chronic obstructive pulmonary disease is a progressive disease that results in symptoms such as shortness of breath, coughing, and mucus production. Restricted airflow is caused by a mixture of obstructive bronchitis and fibrosis in the small airways and the destruction of the lung parenchyma, leading to emphysema.

How many people have COPD?
COPD is an underdiagnosed disease with a prevalence of 251 million cases worldwide. With 3.2 million deaths in 2015, chronic obstructive pulmonary disease caused 5% of all deaths worldwide, making it the third leading cause of death. Tobacco smoke is the main cause of COPD, but other important risk factors include indoor and outdoor air pollution and workplace dust or fumes.

How is COPD treated?
There is no cure for COPD, but bronchodilators are the most common type of treatment to improve lung function and relieve symptoms temporarily. The treatment regimen is based on symptoms, lung function and risk of exacerbations.

How is COPD diagnosed?
Current diagnosis is based on spirometry with a forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) value below 0.7 after bronchodilation. This confirms persistent airflow limitation and, together with symptoms, leads to a diagnosis.

The medical need for biomarkers in COPD is to enable precision medicine. First, a diagnostic biomarker that identifies different subtypes would be of great value because of the great heterogeneity of chronic obstructive pulmonary disease.

Second, a prognostic biomarker that identifies patients at risk of rapid progression would stratify patient selection for clinical trials and guide treatment strategy.

Third, a predictive biomarker to select patients likely to respond to a therapeutic drug in clinical trials could reduce the duration of trials and the number of participants needed to determine therapeutic efficacy.

Visit our lung biomarker portfolio and choose a panel that fits your clinical research or drug development targets!

In COPD, prolonged exposure to cigarette smoke or other irritants leads to chronic inflammation. A normal repair response results in a balance between extracellular matrix (ECM) proteins that are broken down and rebuilt to maintain tissue structure and function.

However, in chronic inflammation, the balance between degradation and rebuilding is disrupted, resulting in altered tissue remodeling in COPD. Tissue-derived Protein Fingerprint biomarkers can be measured in serological samples and used to accurately quantify changes in tissue turnover in the individual patient's lungs.

In COPD, only plasma fibrinogen has qualified as a biomarker for enrichment studies because elevated levels are associated with a higher risk of acute exacerbations and death. Plasma fibrinogen levels reflect systemic wound healing that occurs continuously throughout the body, so their capacity is limited. In addition, there are no biomarkers for subtyping or predicting response to treatment.

Therefore, there is still a need in medicine and drug development for biomarkers that can characterize and quantify structural tissue changes and predict disease progression and response to treatment. Tissue-derived Protein Fingerprint biomarkers, as well as neo-epitope biomarkers of wound healing, are important for evaluating pathological changes in the lungs of patients with COPD. Our biomarkers can be used individually or in combination to detect abnormal lung tissue remodeling, wound healing, and inflammation.

Serologically measured protein fingerprint biomarkers are generally elevated in COPD patients compared with healthy individuals. Smoking status in healthy individuals alters lung tissue turnover, which may also be reflected in Protein Fingerprint biomarkers.

Our laboratory services offer customized solutions for your COPD biomarker needs.

Lung tissue remodeling, quantified by type VI collagen formation (PRO-C6) and MMP-mediated degradation (C6M) and elastin degradation mediated by neutrophil elastase (EL-NE) or proteinase-3 (ELP-3), and wound healing, quantified by X- FIB, are increased in COPD compared with smoking and even more so compared with healthy controls who never smoke.

References: Bihlet A et al 2017 Respir Res; Rønnow SR et al 2019 SciRep; Manon-Jensen T and Langholm LL et al 2019 Respir Med

Protein Fingerprint biomarkers measured in serum are associated with subtypes of COPD, such as chronic bronchitis or emphysema.

Lung tissue degradation quantified by MMP degraded type VI collagen (C6M) is associated with the COPD subtype characterized by chronic bronchitis.

Reference: Bihlet A et al 2017 Respir Res

Protein Fingerprint biomarkers measured in serum are associated with acute exacerbations of COPD (AECOPD). AECOPD are periods of worsening respiratory symptoms that drive disease progression. Therefore, the Protein Fingerprint biomarkers are associated with disease activity in patients with COPD.

Lung tissue degradation quantified by MMP degraded type I, III, IV and VI collagen (C1M, C3M, C4M, C6M), and neutrophil elastase degraded elastin (EL-NE) are all increased during hospitalized acute exacerbations of COPD as compared to baseline and 4 weeks follow-up.

References: Sand JM et al 2015 Respir Res; Stolz D et al 2017 Chest; Schumann DM et al 2018 Chest

Protein Fingerprint biomarkers measured in serum may predict disease progression as determined by decline in lung function (FEV1).

Associations are shown per increase of 1 SD in each biomarker. Protein Fingerprint biomarkers (C1M and C6M) are associated with rate of change in FEV1 to a higher degree than the standard serological biomarkers.

Reference: Leeming DJ et al 2017 BMC Pulm Med

Protein Fingerprint biomarkers measured in serum are associated with mortality in COPD and may be useful in predicting outcome and aid therapeutic decision making.

COPD patients with high baseline serum levels of Protein Fingerprint biomarkers (Q4) have increased risk of all-cause mortality.

Reference: Sand JM et al 2016 Respir Res

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