Have you had “Covid Toes”? A new study could explain why



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Researchers may have discovered the underlying cause of ‘Covid toes’, the inflammation and frostbite-like lesions reported by many patients with Covid-19.

The symptom, which was seen early in the COVID-19 pandemic, sees patients’ toes or fingers turning red or purple, often with painful bumps and sometimes pus. Dermatologists who typically saw four or five patients with these types of lesions – usually caused by inflammation of small blood vessels in cold weather – suddenly saw dozens of them in just a few weeks.

“This rash appears to be more common in young people,” writes the British Association of Dermatologists on its website. “It usually shows up later in the infection and can appear weeks after the onset of the viral infection. The fingers and toes are usually sore, but not itchy. When the rash recovers, the top layers of the skin are painful. skin may peel off where the purplish bumps were, with large scaly patches during the recovery period. “

Researchers investigating the new series of cases associated with COVID-19 believe the symptom may be the result of the immune system’s attempt to fight off the virus.

In their study, published in the British Journal of Dermatology, researchers from the University of Paris examined 50 patients at Saint-Louis Hospital, Paris, France, from April 9 to 16, 2020. All patients had been referred to dermatologists for frostbite. like lesions and had no history of similar problems. The study also looked at 13 other people who had similar lesions before Covid and were therefore unrelated to the disease.

As with all the problems of the television series lodge, the problem seems to be in the immune response.

“Infection with SARS-CoV-2 strongly triggers the expression of genes stimulated by type I interferon (IFN), which contribute to the antiviral protection of the host,” the team writes in their paper. “Type I IFN-mediated diseases, such as monogenic autoinflammatory interferonopathies or lupus erythematosus, are characterized by microangiopathy leading to clinical frostbite.”

Essentially, the patients with frostbite generated high levels of certain types of autoantibodies, which the team said targeted their own cells rather than the virus, causing inflammation. In addition to this, patients with the disease exhibited higher levels of type I interferon proteins, suggesting that these cytokines had a role in the inflammatory response.

The symptom, although commonly seen in previous waves of the pandemic, has become rarer as new variants such as Delta have become more prevalent and vaccination programs have been put in place. However, for patients with the symptom, this new study is good news.

“Confirmation of the cause will help develop new treatments to manage it more effectively,” podiatrist Dr Ivan Bristow told the BBC.



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