MISOGYNISTIC MEDICINE
Fewer women receive lung transplants despite policy changes
UCLA Health study finds gender disparities persist under new national organ allocation system
New research from UCLA Health reveals that women continue to face barriers in accessing lung transplants compared to men, despite recent national policy changes aimed at making organ distribution more equitable.
“Female lung transplant candidates have historically faced unique challenges in organ allocation due to a combination of biological and social factors,” said Dr. Abbas Ardehali, director of the UCLA Heart, Lung, and Heart-Lung Transplant Programs at UCLA Health and senior author of the study, published in The Annals of Thoracic Surgery.
Women often have a smaller body size, which limits the number of donor lungs that are physically compatible. They are also more likely to develop antibodies from prior pregnancies, blood transfusions, or autoimmune conditions, making it harder for their bodies to accept many potential donor organs. Together, these factors significantly narrow the pool of compatible donors, Ardehali said.
Efforts to reduce these disparities have been ongoing. The Lung Allocation Score (LAS) system, introduced in 2005, prioritized transplants based on medical urgency but did not fully account for biological differences that affect women. To improve fairness, the Organ Procurement and Transplantation Network (OPTN) implemented the Composite Allocation Score (CAS) system in March 2023. The new system added variables such as height, blood type, and immune sensitivity to better match donors and recipients.
However, researchers found that even with this improved system, inequities remain. Before CAS was implemented, women were 32% less likely than men to receive a lung transplant. After CAS went into effect, women were 16% less likely to undergo transplantation.
“There was a modest improvement in narrowing the gap, but we still have a lot of work to do,” Ardehali said. “Further refinements to the scoring system are needed to ensure a fair and effective organ allocation system for all patients, regardless of gender.”
Journal
The Annals of Thoracic Surgery
Method of Research
Data/statistical analysis
Subject of Research
People
Article Publication Date
18-Oct-2025
‘Chronic lung-transplant rejection has been a black box.’ New study gives answers, drug targets.
More than 50% of lung-transplant recipients experience a rejection of their new lung within five years
image:
Photo from inside Dr. Ankit Bharat's laboratory at Northwestern University Feinberg School of Medicine in Chicago, IL.
view moreCredit: Northwestern Medicine
- Study found which abnormal cells talk to each other in harmful ways and perpetuate lung damage
- Scientists are already exploring therapeutic strategies based on this study’s discoveries
- Treatments also could help patients with other lung-scarring diseases (COPD, COVID-19, etc.)
CHICAGO --- More than 50% of lung-transplant recipients experience a rejection of their new lung within five years of receiving it, yet the reason why this is such a prevalent complication has remained a medical mystery.
Now, a new Northwestern Medicine study has found that, following transplant and in chronic disease states, abnormal cells emerge and “conversations” between them drives the development of lung damage and transplant rejection.
These findings not only help answer why rejection occurs, but they also have spurred immediate exploration of new drugs to treat transplant rejection and other lung-scarring diseases.
“Chronic lung-transplant rejection has been a ‘black box.’ We knew it happened but did not exactly know why,” said corresponding author Dr. Ankit Bharat, professor of thoracic surgery at Northwestern University Feinberg School of Medicine and executive director of the Northwestern Medicine Canning Thoracic Institute. “Our study provides the first comprehensive cellular and molecular roadmap of the disease.”
The study will be published Oct. 22 in JCI Insight.
Leading cause of death after the first year of transplantation
Surgeons perform approximately 3,000 to 3,500 lung transplants each year in the U.S., and more than 69,000 have been performed worldwide to date. Chronic lung allograft dysfunction (CLAD), which encompasses several manifestations of chronic lung rejection, remains the leading cause of death after the first year of transplantation. There currently are no effective treatments for CLAD once it develops, leaving patients with only one option: re-transplantation.
In the new study, after evaluating almost 1.6 million cells, scientists distinguished between abnormal cells from the donor lung versus cells from the recipient’s own immune system. They discovered the donor-derived structural cells and recipient’s immune cells talk to each other in harmful ways that perpetuate lung damage. The findings could lead to new drug targets and provide insights that could help patients with various lung-scarring diseases, not just transplant recipients.
More findings
The scientists discovered a rogue cell type (KRT17 and KRT5 cells) that drives lung scarring across multiple diseases, including idiopathic pulmonary fibrosis, interstitial lung disease, COPD, COVID-19 lung damage and transplant rejection. By integrating data from this array of scarring lung diseases, the scientists created the first comprehensive reference map showing which molecular features are shared across conditions and which are unique to each disease.
“By comparing chronic rejection to other scarring lung diseases, we identified both shared and unique features,” said Bharat, who also is a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University. “This means treatments developed for one condition might help others. The benefits extend far beyond transplant patients.”
The scientists also identified previously unrecognized cell populations in rejected lungs. These include “exhausted” T cells (which participate in immune response) that remain activated but dysfunctional, and “super-activated” macrophages (immune cells that act like the body’s “clean-up crew”) that promote inflammation and scarring.
Lastly, the scientists developed new computational methods to analyze data from multiple studies together, overcoming technical barriers that previously prevented this kind of comprehensive analysis, Bharat said.
New drug targets identified
The scientists pinpointed specific genes and signaling pathways (like PDGF, GDF15 and TWEAK) that drive scarring, which allows them to identify potential targets for new drugs, Bharat said. Some existing medications, such as nintedanib (sold under the brand names Ofev and Vargatef), and pirfenidone (commonly sold under the brand name Esbriet), which are approved for other lung diseases, might be repurposed for transplant rejection, he said.
“The findings have immediate translational potential,” Bharat said. “We’re already exploring therapeutic strategies based on these discoveries.”
Broad impact on pulmonary fibrosis
While addressing CLAD was the main focus of the paper, this research has major implications for understanding and treating all forms of pulmonary fibrosis, Bharat said.
“The molecular pathways and cell types we identified are relevant to conditions affecting hundreds of thousands of patients with various lung-scarring diseases, not just transplant recipients,” Bharat said. “This work essentially provides a ‘Rosetta Stone’ for understanding lung scarring regardless of the initial trigger.”
Other Northwestern study authors include Dr. Yuanqing Yan, Taisuke Kaihou, Emilia Lecuona, Xin Wu, Masahiko Shigemura,Haiying Sun, Chitaru Kurihara, Ruli Gao, Felix L Nunez and G. R. Scott Budinger.
Journal
JCI Insight
No comments:
Post a Comment