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Twelve months ago, few of us had heard of the antimalarial drug, hydroxychloroquine. COVID-19 put paid to that. In the early months of the pandemic, the drug was suggested as a possible means of prevention or treatment for the virus, an idea actively encouraged by the now-former occupant of the White House. But multiple studies have subsequently demonstrated that hydroxychloroquine offers no identifiable benefit as either a post-exposure prophylaxis or as a treatment for COVID-19.
CRPS
However, while its efficacy for COVID-19 has been dispelled, a study published recently by Stanford University suggests that hydroxychloroquine “may target the autoinflammatory component of CRPS.”
Complex Regional Pain Syndrome (CRPS) is a chronic pain condition which develops following trauma and is typically characterised by intense, burning and persistent pain, increased skin sensitivity, changes in skin colour and temperature and abnormal nail and hair growth. The areas affected are most often the arms, hands, legs and feet, but it can affect many other areas of the body. While the trigger for CRPS is thought to be an injury to the sympathetic nervous system, there are many mechanisms at work in the condition, including autoimmune and autoinflammatory components.
Autoinflammation
When we suffer an injury or develop an infection, our immune system triggers inflammation to help isolate any foreign substances and attract white blood cells to dispose of dead or damaged cells and anything harmful to the body. Autoinflammation refers to a situation where the inflammatory response continues long after the original injury has healed, or even when no identifiable injury has occurred.
Hydroxychloroquine for CRPS
Because of its ability to suppress an overactive immune response, hydroxychloroquine is commonly used to treat autoimmune conditions such as rheumatoid arthritis and lupus. This caused the researchers at Stanford University to wonder whether it might also prove effective for people with therapy-resistant CRPS.
Seven volunteers, each suffering CRPS and for whom past treatment had been ineffective, were started on hydroxychloroquine. Five of the seven reported reduced pain. Before treatment with hydroxychloroquine, the seven reported their pain as an average of 6.8 out of 10, but once treatment began, this decreased to an average of 3.8 out of 10.
While a reduction in pain was the major benefit reported, for some, there was also an improvement in their physical symptoms. One volunteer experienced decreased swelling and redness of her affected foot; these symptoms returning to their previous severity when she ceased taking hydroxychloroquine. When recommenced, the symptoms improved again.
Subsequently, the experiment was repeated in mice, with comparable results. Further investigation suggests that the mechanism at work involves inflammatory cells located in the spinal cord and brain called microglia. These cells cause an inflammatory response by releasing specific proteins. Earlier research had already demonstrated that hydroxychloroquine can reduce the activation of microglia and, therefore, has the potential to lessen inflammation.
Taken together with the clinical observations, the researchers believe these results support further feasibility studies into the use of hydroxychloroquine as a treatment option for patients with therapy-resistant CRPS.