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Before COVID-19, few had heard of the antimalarial drug hydroxychloroquine. The pandemic soon put paid to that. Early on, the drug garnered much publicity as a possible means of preventing or treating the virus – an idea much encouraged by the then-occupant of the White House. However, multiple studies showed that hydroxychloroquine offers no identifiable benefit as a post-exposure prophylaxis or a treatment for COVID-19.
Hydroxychloroquine for CRPS
However, while its hoped-for efficacy for the virus proved unfounded, a study published by Stanford University suggests that hydroxychloroquine “may target the autoinflammatory component of CRPS.”
It’s thought an injury to the sympathetic nervous system – which is responsible for our so-called ‘fight or flight response’ – can trigger CRPS. But that’s a massive over-simplification because many mechanisms, including autoimmune and autoinflammatory components, are at work.
Autoinflammation
Following an injury or infection, our immune system triggers inflammation. Its purpose is to isolate ‘foreign’ substances and attract white blood cells to dispose of dead or damaged cells and anything harmful to the body. Autoinflammation is a term used to describe a situation where our inflammatory response continues long after the injury has healed or even when there’s no identifiable injury.
Autoimmune conditions
Doctors have long used hydroxychloroquine’s ability to suppress an overactive immune response to treat autoimmune conditions such as lupus and rheumatoid arthritis. And this made researchers wonder whether it might also be effective against otherwise therapy-resistant CRPS. So, they prescribed hydroxychloroquine to seven volunteers with long-established CRPS, five of whom then reported reduced pain.
Before treatment, the seven scored their pain at an average of 6.8 out of 10. Following treatment, this decreased to an average of 3.8 out of 10.
Although the reduction in pain was the primary benefit, some of the group also reported an improvement in other symptoms. One experienced decreased redness and swelling in her affected foot, with these symptoms returning to their previous level on cessation of hydroxychloroquine. When recommenced, the symptoms again improved.
On repeating the experiment in mice, they achieved comparable results. Researchers believe the mechanism at work involves inflammatory cells in the brain and spinal cord called ‘microglia’. The inflammatory response is the result of the microglia releasing specific proteins. Earlier research demonstrated that hydroxychloroquine reduced the activation of microglia, lessening inflammation.
Taken together, the researchers believe these results and observations make a strong case for further feasibility studies for using hydroxychloroquine as a treatment in patients with therapy-resistant CRPS.