Researchers may have discovered the underlying cause of "COVID toes", the chilblain-like inflammation and lesions reported by many patients with COVID-19.
The symptom, which has been seen from early in the COVID-19 pandemic, sees patients' toes or fingers turn red or purple, often with painful bumps and occasionally pus. Dermatologists who would usually see four or five patients with these kinds of lesions – usually caused by inflammation in small blood vessels during cold conditions – suddenly saw dozens in just a few weeks.
"This rash seems to be more common in younger people," the British Association of Dermatologists write on their website. "It usually presents later in the infection and may 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 may peel where the purplish bumps were with large, scaly patches during the recovery period."
Researchers investigating the new slew of cases associated with COVID-19 believe that the symptom may be a result of the immune system attempting 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 9-16 2020. All of the patients had been referred to dermatologists with chilblain-like lesions and didn't have a history of similar problems. The study also looked at 13 others who had similar lesions pre-Covid, and so were unrelated to the illness.
As with every problem in the TV show House, the problem appears to be in the immune response.
"SARS-CoV-2 infection strongly triggers the expression of type I interferon (IFN)-stimulated genes, which assist in the host’s antiviral protection," the team write in their paper. "Diseases mediated by type I IFN, such as monogenic autoinflammatory interferonopathies or lupus erythematosus, are characterized by microangiopathy leading to clinical chilblains."
Essentially, patients with the chilblains had generated high levels of certain types of autoantibodies, which the team believe had targeted their own cells rather than the virus, causing the inflammation. As well as this, patients with the condition were found to have higher levels of type I interferon proteins, suggesting that these cytokines had a role in the inflammation response.
The symptom, while seen commonly during earlier waves of the pandemic, has become rarer as new variants such as Delta have become more prevalent, and vaccination programs have been delivered. However, for patients that do get the symptom, this new study is good news.
"The confirmation of the cause will help to develop new treatments to manage it more effectively," podiatrist Dr Ivan Bristow told the BBC.