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- Title
COVID‐19 pandemic‐associated chilblains: more links for SARS‐CoV‐2 and less evidence for high interferon type I systemic response.
- Authors
Bessis, Didier; Trouillet‐Assant, Sophie; Secco, Léo‐Paul; Bardin, Nathalie; Blanc, Brigitte; Blatière, Véronique; Chable‐Bessia, Christine; Delfour, Christophe; Girard, Céline; Richard, Jean‐Christophe; Gros, Nathalie; Le Moing, Vincent; Molinari, Nicolas; Pallure, Valérie; Pisoni, Amandine; Raison‐Peyron, Nadia; Reynaud, Elisa; Schwob, Émilie; Pescarmona, Rémi; Samaran, Quentin
- Abstract
From left to right: patients with COVID 19-associated chilblains (n = 19); nonhospitalized patients with nonsevere COVID-19 without CAC (n = 8); and critically ill patients with COVID-19 in the intensive care unit (n = 72). We confirmed that IFN-I signalling was increased in whole blood of patients with CAC but the kinetics of ISG over time were like those of SARS-CoV-2 infection without CAC. Since the onset of the SARS-CoV-2 pandemic, the direct causative role of the virus in COVID-19-associated chilblains (CAC) has remained under question due to the low rate of positivity to SARS-CoV-2 nasopharyngeal polymerase chain reaction (PCR) and blood serology.[1] Likewise, the suspected pivotal pathogenic role of upregulation of interferon type I (IFN-I) is mainly indirectly supported by assessment of I in situ i immune response.[2] From April 2020 to January 2022, we prospectively assessed children and adults with new-onset CAC seen in the dermatology, infectious diseases, and adult and paediatric emergency departments, as well as the intensive care unit of the University Hospital of Montpellier.
- Subjects
TYPE I interferons; SARS-CoV-2; COVID-19
- Publication
British Journal of Dermatology, 2022, Vol 187, Issue 6, p1032
- ISSN
0007-0963
- Publication type
Article
- DOI
10.1111/bjd.21820