Dec. 3 (UPI) -- Researchers at the Stanford University School of Medicine came up with a new development that could greatly reduce incidents of surgical adhesion.
The findings, published in the journal Science Translational Medicine, report that combining the antibody responsible for adhesion formation with the one cancer cells use to penetrate the immune system in mice.
A slippery protein called mesothelium coats the outside of abdominal organs, allowing them to slide around each other smoothly when humans bend and twist.
When abnormal fibrous connections known as adhesions grow, they can bind organs to the abdominal wall following surgery, preventing the organs from sliding around as they should.
Symptoms of the condition can include bowel obstruction, chronic pain, female infertility and, sometimes, death.
In a test with lab mice, the Stanford team found that giving antibodies that connect to injured mesothelium greatly reduces the severity of adhesions. When the researchers combined that antibody with an anti-CD47 antibody, it worked even better.
The researchers say that the roving immune cells called macrophages eat up sick or dying cells and may help remove abnormal fibrous tissue and free up organs.
The National Institute of Health estimates that nearly 93 percent of abdominal surgeries result in adhesions and approximately 20 percent of surgical patients will return to the hospital to treat adhesion-related complications.
The findings are important because the researchers say the lab mice express similar genes and biological pathways to humans.
"Although we used a mouse model to study adhesion formation," said Irving Weissman, professor of pathology and of developmental biology at Stanford University, "we found similar characteristics in adhesions from patients, which makes us think this approach could be translated into the clinic."
The NIH places the annual cost of post-surgical adhesion treatment as high as $1 billion.
"This is a very common surgical complication, but it's not been well-studied," said Jonathan Tsai, a resident physician at Brigham and Women's Hospital and study co-author. "Until now, it wasn't even known what cell type was involved in originating the adhesions. Now we've come up with a way to isolate the injured tissue before they form the adhesions, and identify the molecular pathways involved."