Alpha-1 antitrypsin deficiency, a rare genetic cause of COPD, has some unique features compared to the more common forms of COPD in which individuals have normal alpha-1 antitrypsin levels.

In this study, we studied medical records (with names and other personal identifying information removed) to determine if there are features that may predict whether an individual with COPD had alpha-1 antitrypsin deficiency. We developed a computer model that focused on known patients with alpha-1 antitrypsin deficiency. The computer model appeared to have high levels of “predictive sensitivity.” In other words, it correctly identified which individuals with COPD also had alpha-1 antitrypsin deficiency.

This computer model now needs to be tested in real-world populations of patients with COPD to determine if the prediction model is accurate for finding those affected by alpha-1 antitrypsin deficiency.

Individuals with alpha-1 antitrypsin deficiency often acquire progressive emphysema. We have discovered that a unique protease (an enzyme in the body that breaks down proteins) named chymotrypsin-like elastase 1 (Cela1) is secreted by cells in the lungs and is important in emphysema progression. This enzyme is normally neutralized or canceled by alpha-1 antitrypsin but that is less possible in individuals with alpha-1 antitrypsin deficiency.

We have developed an antibody that neutralizes or inactivates the Cela1 protease. Specifically, we have developed a monoclonal antibody which is a protein made in the lab that can target and attack a specific foreign body or antigen in the body, like our own immune system does. The antibody we created is called KF4 and has previously been shown to protect mice from emphysema progression. In this latest study, we wondered whether it would do the same in alpha-1 antitrypsin deficient mice and whether it would be better than replacing the mice’s missing alpha-1 antitrypsin. We found that in mice with emphysema caused by being alpha-1 antitrypsin deficient, both alpha-1 antitrypsin and our developed antibody, KF4, were protective, but when given together, the results were not better or greater.

Our study shows that KF4 is as effective as alpha-1 antitrypsin in preventing emphysema in a mouse model.

Smoking is known to cause muscle loss, which can lead to poor health outcomes. While exercise and nutrition can help improve muscle health, it is not clear how common medications may impact muscle loss over time in smokers.

Our study looked at 4,191 current and former smokers who participated in the COPDGene study to see how the use of certain medications affected their chest muscles over a five-year period. We measured changes in muscle size and quality using computed tomography (CT) scans. We found that people taking statins, which are drugs used to lower cholesterol, had less muscle loss compared to those not taking them. On the other hand, people using aspirin, commonly taken for heart health, experienced more muscle loss. This suggests that statins may help protect muscles, while aspirin might be linked to greater muscle decline.

Our findings are important because they suggest that medications already being taken for other health reasons may affect muscle health in smokers. More research is needed to confirm these results and to explore how these findings can be used to improve health outcomes for smokers in the future.

Many people with COPD experience symptoms of depression and anxiety, but may not meet diagnostic criteria (the signs, symptoms, or tests used to determine if an individual has a particular disease or disorder) for these conditions. While numerous studies have examined the impact of these symptoms on COPD results or outcomes, there is limited understanding of how a diagnosis of a major depressive or anxiety disorder may affect outcomes reported by patients.

In this national study, we identified people with COPD meeting diagnostic criteria for depression or anxiety disorders using a proven mental health interview and evaluated how their depression or anxiety was affecting their COPD. We found that depression and anxiety disorders were linked to increased breathlessness, COPD symptoms, difficulty completing daily activities, poor sleep, and lower health-related quality of life. Despite these effects, fewer than half of those with depression or anxiety disorders were receiving medication or mental health counseling.

Depression and anxiety disorders are common among people with COPD and worsen quality of life, but are underrecognized and undertreated. There are currently limited guidelines on the best “real-world” ways to screen for, treat, and monitor depression and anxiety disorders in people with COPD. This study highlights the need to prioritize mental health as an important part of complete COPD care.

Patients hospitalized for an acute exacerbation of chronic obstructive pulmonary disease (COPD) have a high risk of being readmitted to the hospital less than 30 days after being discharged.

At our institution, we implemented a “Transitions of Care Pharmacist” service to help improve how well patients do during their hospital stay and to reduce the number of Medicare patients with COPD being readmitted to the hospital. Our team stayed in contact with patients from the time they were admitted to the hospital until 30 days after they left the hospital. When a patient was preparing to leave the hospital, we focused on prescribing affordable inhalers with the medications most recommended by experts.

Inhalers are an important part of managing and treating COPD, but high costs make them unaffordable for many patients, even with insurance. Having a pharmacist help select and prescribe an inhaler for patients as they leave the hospital allows for the detailed selection of an inhaler the patient can afford, which means the patient is more likely to continue to receive the medicines they need to treat their COPD.

Our study suggests that having a pharmacist prescribe an inhaler when a patient is preparing to leave a hospital may lead to fewer patients having to be readmitted to the hospital and may increase the number of patients receiving inhalers and medicines most recommended by experts and guidelines for treating COPD. This approach may help other institutions reduce readmissions.

Triple inhaler therapy includes 2 long-acting bronchodilator drugs and an inhaled corticosteroid and is recommended for treating chronic obstructive pulmonary disease (COPD). Specifically, it is recommended for patients who have flare-ups or exacerbations and have high levels of eosinophils (a kind of white blood cell) in their blood. Triple inhaler therapy can be given using a single inhaler or with multiple inhalers.

We conducted the current study to determine if switching from multiple inhaler triple therapy to single inhaler triple therapy would bring about any clinical benefits among Chinese COPD patients.

Our study showed that among Chinese COPD patients, switching from multiple inhaler triple therapy to single inhaler triple therapy may allow them to have fewer errors or mistakes when using their inhalers—mistakes that stop the medicine from getting into the lungs completely. We also found that switching from multiple inhalers to a single inhaler may improve how well the patients did at taking their medicines regularly and as directed by their doctor.

Our study explored the association between chronic obstructive pulmonary disease (COPD) and the risk of death among patients with arthritis (joint inflammation). Using rigorous statistical methods, we analyzed data from over 11,000 individuals across the United States who self-reported having arthritis.

During an average follow-up period of 8.8 years, we found that individuals with both arthritis and COPD had a significantly increased risk of death from any cause (including heart disease) compared to those with only arthritis. Specifically, arthritis patients with COPD had a 41% increased risk of death from any cause and a 29% increased risk of death from heart disease. Furthermore, our research revealed that arthritis patients with COPD had a strikingly higher risk of death related to lung infections, with a 446% increase, compared to a 24% increased risk of death from nonlung infection-related causes.

These findings highlight the importance of effective management and control of COPD in arthritis patients to reduce their risk of death.

Chronic obstructive pulmonary disease (COPD) is often complicated by additional diseases that individuals may have along with their COPD. These comorbidities can cause individuals to have worse symptoms and a higher risk of death. Anemia, which can be caused by iron deficiency—low levels of iron—is one such condition known to cause an individual’s COPD to become worse. Iron deficiency, which can exist without anemia, has not yet been well-studied in COPD and may be a treatable condition.

This study used information about adults with COPD treated at an academic center to investigate how common iron deficiency is in individuals with COPD, both with and without anemia, and to better understand how low iron might impact an individual’s risk or chance of being hospitalized. Fifty-two percent of the patients studied were iron deficient, of whom 27% did not have anemia. We also showed that particularly among females, lower iron even without anemia, was associated with a higher risk of being hospitalized for any cause. Among males, a similar pattern was observed, but not to the extent observed among females.

In conclusion, iron deficiency is an important comorbidity that is unique and different from anemia in COPD patients and affects males and females differently. These results support the need for future studies considering increasing iron levels to improve COPD results.

Chronic obstructive pulmonary disease (COPD) leads to the narrowing of the airways, which causes difficulty in moving air in and out of the lungs. This negatively impacts lung capacity (the amount of air the lungs can breathe in) and overall quality of life. Cigarette smoking and environmental pollution are the most frequent causes of COPD, and lifestyle changes such as quitting smoking are crucial to prevent further lung damage. Medications including bronchodilators, which help to open the airways, and inhaled corticosteroids, which reduce inflammation, are the preferred medical treatment for COPD. However, they may not be effective enough, can be difficult to take, and may cause side effects.

Phosphodiesterase 3 (PDE3) and PDE4 are enzymes involved in the function of the airway smooth muscle in the lungs—which has a role in the narrowing of the airways that can be part of why individuals with COPD experience breathlessness. PDE3 and PDE4 also contribute to inflammation in the lungs’ airways. Medications that stop either PDE3 or PDE4 from being produced are beneficial in patients with COPD. When both PDE3 and PDE4 are both stopped or inhibited, inflammation in the lungs is reduced and the airways are opened or expanded. In this review, we explain the process of COPD progression, describe current treatments for COPD, and discuss how dual PDE3 and PDE4 inhibition can be a beneficial addition to currently available COPD treatments.

Pulmonary rehabilitation is an effective treatment for people with chronic obstructive pulmonary disease (COPD) and other lung conditions. However, many people face significant barriers to attending an in-person, center-based program.

We surveyed Australian pulmonary rehabilitation services to understand what types of rehabilitation programs were available to patients—in-person, “center-based” programs or remote, online “telerehabilitation” programs. We asked participants to indicate how their current program may have changed compared with before and during the COVID-19 pandemic.

Almost all programs (97%) were currently providing center-based pulmonary rehabilitation which was similar to pre-pandemic availability. Nearly half of the programs (43%) also offered pulmonary rehabilitation via telerehabilitation. The availability of telerehabilitation services was lower than during the pandemic but remained higher than pre-pandemic. Whether delivered at the center, or by telerehabilitation, most programs provided the components considered essential for pulmonary rehabilitation, although specific staff training in telerehabilitation delivery could be improved.

Understanding and supporting the wider availability of alternative models of pulmonary rehabilitation delivery may help more people to access the program.