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Underlying claims, studies suggest that inflammation prevents chronic pain

Underlying claims, studies suggest that inflammation prevents chronic pain


FOr 20 years ago, Ruda Diachenko investigated the underlying biology of the pain that detectives chase after clues. What role does this gene play? How about that protein?

But she always wondered what would be found if she could see how all the genes in the cell behave as pain progresses in the body. It’s like Sherlock Holmes exchanging his magnifying glass for a video of the crime being committed.

But when such techniques finally became cheaply available in 2018, the footage shocked her, thanks to advances in RNA sequencing.


“This was very, very unexpected,” said Diachenko, a professor of medicine at McGill University.

The resultReported on Wednesday in Scientific Translation Medicine, She and other pain researchers have denied much of their belief in how the first stroke of acute pain develops into a chronic and debilitating condition. Many studies suggest that chronic inflammation is a major driver of chronic pain, so many pain professionals control inflammation from early signs of injury and immunology before it goes out of control. Focused on extinguishing a fire.


However, Diachenko’s results suggest that early inflammation is needed for the body to recover. In the true case, decades-old protocols for treating pain with IV steroids in the hospital, or aspirin and ibuprofen at home, are actually counterproductive and risk for patients developing chronic pain. It means that you are increasing.

In other words, “standard medical care for this type of pain probably exacerbates the problem, but it’s not good,” said Jeffrey, a neuroscientist at McGill University and another senior author of the paper. Mogil said. “What I’m saying here is pretty radical.”

Like many radical claims, it has the potential to divide outside researchers. Despite mostly positive reviews, Mogil wrote that one reviewer “will not overturn decades of medical practice” until the group presents more compelling evidence. The paper stated that it was rejected by the New England Journal of Medicine. Patients who receive anti-inflammatory drugs are more likely to develop chronic pain than those who receive placebo.

And even if the findings are maintained, they may only do so for a subset of patients. Michael Kent, a professor of anesthesiology at Duke University, said Diachenko’s work focuses on patients with back pain.

Many of his patients have postoperative pain. Their inflammatory system is so unmanageable that he said he needed a class of medicines, including the nonsteroidal anti-inflammatory drugs steroids aspirin and ibuprofen.

“People are so inflamed and not moving that they are in pain,” he said. “And because they don’t move, they put themselves at greater risk of blood clots and pneumonia.”

But for a handful of researchers who have long pushed the field of pain to recognize the more agile role of inflammation in the body, the results are a big step forward.

And they suggest that a surprisingly simple fix can make (small) dents in more and more people — Currently 1 in 5 Americans — People with chronic pain: Switch from aspirin to tylenol, which relieves pain without affecting inflammation.

“That is, this is a paradigm-changing paper,” said Thomas Buchheit, director of Duke’s Regenerative Pain Treatment Program, who was not involved in the study. “We have been treating everything that has been injured by steroid injections and anti-inflammatory drugs for years.”

To be precise, patients who see pain relieve after the first injury and those who see it last for more than 3 months (clinical definition of chronic pain) have long remained a mystery. Most researchers assumed that patients with chronic pain had some form of active dysfunction, Mogil said.

When Diachenko began her research, she expected her molecular imaging to capture the genes that cause the dysfunction of the action. In theory, you could develop some kind of medicine to shut down or tune them.

She, along with an Italian collaborator, collected blood from 98 Italian back pain patients and followed them for 3 months. With the help of McGill University computational biologist Mark Parisien, they used a technique called RNAseq. With this technique, researchers sequence the immune cells of both patients and all the RNA in the patient’s cells that have been pain-relieved by the last visit. Who didn’t.

RNAseq reveals which genes in the cell are active. This is the best proxy for what is happening inside the cell at a particular moment. Diachenko expected the cells of patients with chronic pain to be vibrant with activity. This is a sign of an ongoing illness process.

Instead, the cells of the chronic patient were silent. “Completely dead,” said Diachenko.

Meanwhile, the patient’s immune cells were noisy when the pain was resolved. More than half of those genomes altered expression. “They are in the process of this massive immunological process,” she said.

That was the first surprise: instead of something happening error Something was happening in patients who developed chronic pain right In patients who did not. But what?

Further analysis showed that activated genes are involved in inflammation in patients who did not develop chronic pain. The cells first upregulated the inflammation and then quickly downregulated it.

It suggested that inflammation was protective. But when Diachenko called Mogil, who specializes in mouse research, he told her about the consequences that it was impossible. Everyone knows that giving mice an anti-inflammatory drug for chronic pain reduces pain.

However, they found that no one had been tracking the mouse for a very long time. Mogil went on to study and injured mice, giving one group an over-the-counter anti-inflammatory drug, one group the commonly used IV steroid dexamethasone, and another group saline.

Mice treated with over-the-counter anti-inflammatory drugs or dexamethasone initially had less pain symptoms than saline mice. However, within a few weeks, most saline mice saw the pain completely subside. In contrast, mice treated with anti-inflammatory drugs are still fluttering when you touch their feet.

“It took 150 days instead of two weeks to resolve their pain,” Daitchenko said.

To confirm that anti-inflammatory drugs can actually have this debilitating effect, researchers then went to UK Biobank, a large database of diverse patient data, to report acute pain. I examined the patients who had inflammation.

Indeed, they found that people taking anti-inflammatory drugs were about 75% more likely to develop chronic pain as a control. Other types of analgesics, including Tylenol, they examined showed no similar correlation.

Some experts have said it shouldn’t be shocking, but it’s not yet clear exactly why inflammation may have this protective effect. Long-term inflammation is known to be debilitating, but doctors may intentionally induce inflammation in areas of concentration to promote tissue repair.

And researchers have long known that exercise can have a regenerative effect, even if it is highly inflammatory.

“Basically, inflammation is a double-edged sword,” said Ru-Rong Ji, a professor of neurobiology at Duke who wasn’t involved in the job.

Pain expert Kent imagined that postoperative pain always needed anti-inflammatory drugs, but this study found that the inflammatory Goldie doctors should reach for such drugs. It suggests that there may be a lock zone. He envisioned performing a titration study to find new optimal levels of anti-inflammatory drug use.

Mogil and Diatchenko are also currently working on the start of randomized clinical trials requested by NEJM reviewers. Randomized trials are notorious for being expensive, but he said this should be fairly straightforward.

“I don’t expect people to change soon,” Mogil said. “But yeah, I think the writing is on the wall.”




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