More on Pulse Oximetry and Racial Disparities in Care
Research funded by the National Institute of Biomedical Imaging and Bioengineering and the National Institute of Diabetes and Digestive and Kidney Diseases added the evidence that pulse oximeter readings could be behind some of the racial disparities seen in health care.
The study found black patients may be given suboptimal levels of supplemental oxygen based on pulse oximeter readings that are falsely high.
The investigation was conducted among 3,069 ICU patients at one hospital in Boston, MA, 207 black, 112 Hispanic, and 83 Asian. The remaining patients in the trial were white. The researchers compared pulse oximetry readings to arterial blood gas results. They saw significantly higher pulse oximetry readings in black patients when compared to the arterial blood gas results.
Further analysis revealed that the non-white patients in the study received lower levels of supplemental oxygen and that race was a significant factor in how much supplemental oxygen a patient received. However, when the investigators looked at the discrepancy in blood oxygenation levels estimated by pulse oximetry or measured by a blood draw, they determined that while higher discrepancies between estimated and true blood-drawn oxygenation levels were associated with lower supplemental oxygen delivery, race was not a significant factor.
“We need to understand the drivers of health care disparities, and it turns out that one potential driver is the technology that clinicians rely on to triage patients and guide care,” said senior study author Leo Anthony Celi, MD, MS, MPH, who is affiliated with Massachusetts Institute of Technology, Beth Israel Deaconess Medical Center, and Harvard University.
“We need to be mindful that medical products developed using non-inclusive populations can contribute to the existing disparities that we are observing in the medical setting.”
The study was published by JAMA Internal Medicine. Read More
New Therapy for CF on the Horizon
A new technology called antisense oligonucleotides (ASOs) can help control protein levels in the cells and has already been used to develop an FDA-approved therapy for people with spinal muscular atrophy.
Could it also work for people with cystic fibrosis? Researchers from Cold Spring Harbor Laboratory are trying to find out. The team has discovered how to use ASOs to create an imperfect but still functional version of the CFTR protein that drives the disease and hopes to see their work translated into human use.
They explain that in people with CF, a genetic mutation causes cells to receive faulty instructions for making the CFTR protein. The cells eliminate those instructions, and the protein is not made.
The less-than-perfect CFTR protein created by the lab resulted from the fact that ASOs were able to trick the cells into following the faulty instructions and making the CFTR protein anyway. Though not ideal, the researchers found the imperfect CFTR protein was better than not having any CFTR protein at all because it was able to improve the function of lung cells.
They believe it could improve symptoms in people with CF as well.
The study appeared in Nature Communications. Read More
Nasal Spray Vaccine May Be Needed Too
According to researchers from the University of Virginia and elsewhere, mRNA vaccines alone will not be enough to halt the spread of COVID-19. Instead, they believe a nasal spray vaccine will have to be added to the mix.
The investigators found that the mRNA vaccines currently in use mainly ramp up the immune response to COVID-19 in the blood, which confers a strong protection against severe disease. However, the mucosal membranes experience moderate or little neutralizing antibody responses.
“The omicron variant almost completely escaped neutralization by mucosal antibodies in individuals who received mRNA vaccines and in previously infected individuals,” said study author Jie Sun. “Our data showed that mRNA vaccination also did not induce sufficient tissue-residing cellular immunity in the airways, another arm of our immune system to prevent the entry of the virus into our bodies.”
Only people who were unvaccinated and became seriously ill from COVID-19 mounted a vigorous defense against the virus in both their airways and bloodstreams.
The study went on to show that administering a nasal vaccine originating from an adenovirus, which also expresses the spike protein seen in the COVID-19 virus, caused robust neutralizing antibody responses in mice when combined with the mRNA vaccines. The response was effective against the original strain of COVID-19 and the omicron variant.
The authors stress much more study is needed on such a vaccine, though, because adenovirus-based nasal vaccines could have unwanted side effects, including an increased risk for Bell’s Palsy, a condition that causes muscle weakness in the face.
The study appeared in Science Immunology. Read More
How Asthma Influences COVID-19 Outcomes
How does asthma impact a person’s risk for severe outcomes from COVID-19? Unfortunately, the jury has been out on that question, but Michigan researchers helped to clear up the controversy in a study published by the American Journal of Managed Care.
The investigators looked at 140 asthma patients with COVID-19 in the first half of 2020 and 127 in the second half. Among the patients, 104 had mild asthma, 29 had moderate asthma, and 49 had severe asthma. About a third had eosinophilic asthma, and 58% had non-eosinophilic asthma.
In an unadjusted analysis, no differences in outcomes were seen between people with asthma and those without asthma. However, the adjusted analysis showed people with asthma were more likely than the general population to need mechanical ventilation and an ICU admission, and they had longer hospital stays and a higher risk for mortality.
Those with moderate asthma had higher odds of ICU admission, longer hospitalizations, and longer ICU stays when compared to those with mild asthma. Conversely, those with severe asthma had shorter hospital stays.
The results were adjusted to take factors like demographics, comorbidities, smoking status, and timing of illness into account. Read More
RSV May Be Only One Exposure Linked to Wheeze and Asthma in Children with Bronchiolitis
Researchers publishing in Pediatric Allergy and Immunology challenged the commonly held belief that RSV bronchiolitis in infancy increases the risk of preschool wheeze and childhood asthma more than other exposures that lead to bronchiolitis.
The investigators performed a systematic review and meta-analysis of previous studies comparing the association between preschool wheeze and childhood asthma and bronchiolitis in kids with and without bronchiolitis caused by RSV. While children who developed wheeze or asthma were more likely to have been hospitalized with RSV bronchiolitis than healthy children, they were no more likely to develop them than children who suffered a bout of non-RSV bronchiolitis, despite the fact that RSV bronchiolitis was more severe.
What’s more, results showed children with rhinovirus bronchiolitis were actually more likely to develop wheeze or childhood asthma than those with RSV bronchiolitis.
The investigators believe their findings call for more study on other exposures that might be involved in mediating the causal pathway from bronchiolitis to asthma. Read More
Long COVID Lung Fibrosis Similar to IPF
A study recently conducted out of the University of California, San Diego School of Medicine suggests the lung fibrosis seen in people with long COVID is similar to that seen in people with idiopathic pulmonary fibrosis (IPF).
The investigators used cutting-edge transdisciplinary approaches, such as artificial intelligence (AI)-assisted big data analysis, to assess more than 1,000 human lung transcriptomic datasets associated with various lung conditions. They specifically looked for gene expression patterns, inflammation signaling, and cellular changes. IPF most closely matched the condition seen in long COVID.
“Using an artificial intelligence approach, we found that lung fibrosis caused by COVID-19 resembles idiopathic pulmonary fibrosis,” said co-senior study author Pradipta Ghosh, MD. “At a fundamental level, both conditions display similar gene expression patterns in the lungs and blood, and dysfunctional processes within alveolar type II cells.”
The study was published by eBioMedicine. Read More
Email newsroom@aarc.org with questions or comments, we’d love to hear from you.
Debbie Bunch is an AARC contributor who writes feature articles, news stories, and other content for Newsroom, the AARC website, and associated emailed newsletters. In her spare time, she enjoys reading, traveling, photography, and spending time with her children and grandchildren. Connect with Debbie by email or on AARConnect or LinkedIn.
