Antonio R. Anzueto, MD: Biomarkers in COPD

Antonio R. Anzueto, MD

The role of biomarkers in chronic obstructive pulmonary disease (COPD) are still riddled with unknowns, but Antonio R. Anzueto, MD, of UT Health San Antonio, is working to further define their function and role in the disease. While walking between sessions at the 2018 CHEST Annual Meeting in San Antonio, TX, Anzueto spoke with MD Magazine^® on the latest research regarding biomarkers in COPD, outlining possible avenues of investigation and addressing regional causes of the disease.

MD Mag: What was the inspiration for conducting this study?

Anzueto: The reason I wanted to look into biomarkers [in COPD] was to see if there was some type of biological indicator of diagnosis, severe progression—and most importantly—an ability to identify the patients who are at risk to having exacerbations or running into problems.

The objective was how a blood test, like troponin, can tell me, ‘Hey, something bad is happening, I need to be proactive and change the way I treat my patient.”

What are the observed hallmarks in the data you looked at with biomarkers?

The issues are, we are looking to biomarkers for other markers of inflammation, but the data doesn’t help us. We’re looking to see if they can help us to guide therapies, so can we use these as a way to treat patients—for example, the use of inhaled cortical steroids [ICS]. Can I use eosinophils?

Clearly, in patients who have higher eosinophils and more exacerbations, they highly benefit from the use of ICS. The biomarker here is a clinical biomarker with the history of exacerbations, and you also have the indicator for pharmacotherapy—the use of ICS.

What would you say are the main role of biomarkers in COPD? Is any 1 more than important than another?

We don’t know. We have not yet identified which is going to be the most important biomarker. The only 1 we have more data on is broad eosinophils as a guidance for therapies, but we don’t have any other to guide on severity.

What is fibrinogen’s role in COPD?

Fibrinogen has been studied. Patients with elevated fibrinogen have an increased risk for mortality, but the risk is really low. Fibrinogen is something we don’t measure on a regular basis, and when we measure it in the patient, we don’t know what it means. I cannot tell my patient, ‘If your fibrinogen is 12, you’re at increased risk for mortality.”

We don’t know what the meaning is in the individual patient. We know the meaning as a population source.

What is the significance of clinical phenotypes to biological endotypes on COPD?

For the clinical phenotypes, we have to combine the clinical refractory states, the patient’s lung function, and the quality of life, and we need to correlate that with biologicals and anatomical abnormalities, a computed tomography (CAT) scan of the chest, low FEV1. We need to try and put all this together and correlate it with blood.

If it increases fibrinogen, for example, it’s going to be a marker for mortality in individuals with “x” and “y” characteristics, and that’s what we need to identify.

What are the next steps with this data?

We need to put it all together. We need to not only look at individual blood tests and individual results form different blood tests, but we also need to integrate the results of the blood tests with the clinical features and pharmacological indicators in patients to better characterize the patient.

What are the current trends in therapy for COPD, and what is leading for clinical consideration?

The treatment for COPD is bronchodilators. Clinical studies show combinations of active bronchodilators show significant improvement in lung function and quality of life, and reductions in exacerbations.

Groups of patients will require ICS, especially the ones who have high eosinophils and have frequent exacerbations, but in the future, we need to try and individualize therapy. We need to base it [therapy] on patients’ clinical characteristics—who has a more rapid progression of the disease, what therapy we should give, who are the individuals who exacerbate more, what are the therapies we should give to try to tailor appropriate therapies to patients’ conditions?

Are there any regionally related issues with COPD?

We know smoking is one of the major contributing causes of COPD, but here in South Texas, we see a lot of women who, when they were young, were exposed to biomass, or wood smoke in ovens in their house.

These women are now in their fifties and their sixties, and now they are experiencing shortness of breath—symptoms that mimic COPD. We know they are causes of COPD even though they were experienced 30 years ago.

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