Chronic obstructive pulmonary disease (COPD) is the third most common cause of death by disease in the United States and one of the costliest diseases to treat, with no cure at present. More than 300 million people worldwide suffer from COPD. Current and former smokers, especially the older segments of the population, are most likely to suffer from it. In addition, it’s a common source of billing and reimbursement issues, with a high rate of readmission.
Given these grim facts, it is naturally the focus of a great deal of research and, fortunately, recent advancements have been made in understanding this very common disease. Notably, a recent study at Kanazawa Medical University (see Yamamura, Nishiki, et al., 2022) found a genetic component to the disease. Non-genetic conditions, notably tobacco use and to a lesser degree, environmental pollutants, are the primary causes of COPD, however, there may be a genetic aspect to the severity of the illness. A tumor suppressor called p53 normally appears in lung tissue in the presence of oxidative stress, inhibiting the reproduction tumor cells and triggering their destruction. In some COPD cases, a polymorphism occurs in p53 codon 72, and in patients carrying that genotype, a greater percentage of low-attenuation areas was found, along with greater airflow limitation and muscle atrophy. While the exact correlation, if any, between p53 polymorphism and COPD severity remains under investigation, this may be a significant step in understanding the root causes of the most severe cases.
Another advancement in understanding may point toward the eventual development of better medical COPD treatments. Researchers at the University of Technology, Sydney, have pinned down a biological component that may become a drug target. An enzyme secreted by mast cells in the immune system, mast cell chymase-1, was found by researchers to worsen the development of COPD. Levels of chymase-1 in COPD patients were found to be double that of the amount found in people without the disease. After determining an analogous enzyme in the immune system of mice, researchers showed that inhibiting the enzyme offered protection against inflammation, emphysema, and other aspects of the illness.
Other advances in COPD treatment are coming from the tech sector. Remote monitoring, telehealth, and health-related apps all skyrocketed in use during the pandemic, and it’s likely we will see an uptick in software solutions to monitor a wide range of health concerns. A company called Wellinks recently partnered with a clinic group in Connecticut to try to curb COPD readmissions through monitoring devices and an app. According to the company’s press release, they seek to combine “virtual pulmonary rehabilitation, personalized health coaching and monitoring through connected devices and a patient-friendly app to create a truly integrated approach to COPD management.” They hope that with communication and monitoring, readmissions—which are costly to all involved—can be decreased significantly.
While the data needs to be updated about the accuracy of remote CT readings—studies in the last decade showed a pretty hefty margin of error—the technology continues to advance. A study published in the American Journal of Roentgenology showed the ability of an artificial intelligence tool to detect an interstitial pulmonary embolus (iPE). The study shows that out of 40 iPEs detected in the team’s study sample, seven of them were detected only by the clinical reports, while AI detected four missed by clinicians. The study doesn’t speak on the idea of AI taking over altogether, and that is likely a long way off if it will ever happen. But it’s not unreasonable to see that AI could successfully serve as a secondary reader.