Harvard scientists have discovered how to treat pain due to endometriosis

The pain caused by endometriosis is largely explained by the interaction between pain receptors and macrophages, white blood cells that are experts at killing microorganisms, according to a study conducted on female mice and human samples published this Wednesday in the journal. Scientific translational medicine. Four drugs approved in the United States for the prevention and treatment of migraine relieve symptoms in rodents and are proposed as potential new treatments for endometriosis in women. Three of them are currently on sale in Spain.

“Blocking neuroimmune communication (between pain receptors and macrophages) may provide an innovative non-hormonal and non-opioid approach to the treatment of endometriosis,” the researchers note in the scientific paper. “Our data shows that treatment (with any of the four drugs) can shrink lesions and reduce pain,” he explains Vanguard Michael Rogers, an assistant professor at Harvard Medical School and a researcher at Boston Children’s Hospital who contributed to the paper.

Endometriosis causes lesions (red) that are promoted by excessive production of the peptide CGRP (green), which helps them grow.

Endometriosis causes lesions (red) that are promoted by excessive production of the peptide CGRP (green), which helps them grow.

Dr. Victor Fattori and Dr. Michael Rogers

The disease, which is estimated to affect at least 10% of women of reproductive age, has no effective treatment in many cases. The most common is to prescribe ibuprofen, analgesics or hormones, but a large number of patients do not respond to these, so sometimes the pain must be treated chronically with opioids.

The anti-migraine drugs tested in this new study, which have previously been studied for safety and have received approval from several regulatory agencies, open the possibility of a new therapeutic approach to endometriosis. “If the human trial is successful, it could significantly improve the lives of large numbers of women with this disease,” Rogers explains.

These tests on women are the next step in the research. However, warns a Harvard researcher, this is still a long way off. “We are not working on any clinical trials (…) and do not know that there are any,” he explains, “We have spoken to people who produce this type of drug and hope that our work will lead to clinical trials soon.” tests.”

Pain map

Researchers have characterized the process by which endometriosis worsens and causes pain

The key to the discovery is the movement of a peptide called CGRP. It is a type of molecule made up of several amino acids that certain pain receptors in our body release when they receive a harmful stimulus. The researchers found traces of these peptides in endometriosis lesions in both samples from women and female mice, leading them to hypothesize that this molecule may play a prominent role in the disease.

Experiments on female mice showed that those who suffer from endometriosis produce more CGRP than those who do not suffer from it. In addition, macrophages, white blood cells, which are experts in destroying microorganisms dangerous to our body, have receptors on their surface that can capture the peptide in question. If this happens, the nature of the macrophages changes and they take on characteristics that contribute to the growth in size and number of lesions caused by endometriosis. Accordingly, the pain intensifies.

That is, endometriosis favors the release of molecules that, when interacting with the immune system, increase the number and severity of lesions caused by the disease itself. So, to break this vicious cycle, it is necessary to break the connection between pain receptors and the immune system, and this is what several drugs approved for the treatment of migraines that have similar mechanisms of action already do.

The four drugs they tested yielded positive results: they all reduced the rodents’ pain, and one, the only one not approved in Spain, also reduced the size of the lesions. However, their number remained constant.


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CLAUDIA SEGURA

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