The notion that it is related to M. lepromatosis may be true according to some authors. However, others showed that the correlation is not that strong, looking at leprosy clinical types in different countries 6 ; M. lepromatosis may resemble M. leprae in causing different manifestations depending on the host immunity. 2 From the group around Rea and Modlin, Maria Achoa reported at the World Congress Dermatology in Milano that of their Mexican patients with lepra bonita, the majority was indeed infected with M. lepromatosis, while some had a single M. leprae infection or a mixed infection. Whether M. lepromatosis affects the internal organs more than M. leprae is yet to be proven. The difference in the type of infection may in part account for clinical and geographical variabilities associated with leprosy infection; however, according to our opinion, the survival of the bacilli in the environment and the socioeconomic factors are relatively more important. For the practising dermatologist, the bacilli causing leprosy are of academic interest only. The treatment is the same, and it is the resistance to therapy that counts. As far as the role of physical medicine is concerned, she is right, but to direct this requires publishing of another article.

Summary Background The outbreak of chilblain‐like lesions (CLL) during the COVID‐19 pandemic has been reported extensively, potentially related to SARS‐CoV‐2 infection, yet its underlying pathophysiology is unclear. Objectives To study skin and blood endothelial and immune system activation in CLL in comparison with healthy controls and seasonal chilblains (SC), defined as cold‐induced sporadic chilblains occurring during 2015 and 2019 with exclusion of chilblain lupus. Methods This observational study was conducted during 9–16 April 2020 at Saint‐Louis Hospital, Paris, France. All patients referred with CLL seen during this period of the COVID‐19 pandemic were included in this study. We excluded patients with a history of chilblains or chilblain lupus. Fifty patients were included. Results Histological patterns were similar and transcriptomic signatures overlapped in both the CLL and SC groups, with type I interferon polarization and a cytotoxic–natural killer gene signature. CLL were characterized by higher IgA tissue deposition and more significant transcriptomic activation of complement and angiogenesis factors compared with SC. We observed in CLL a systemic immune response associated with IgA antineutrophil cytoplasmic antibodies in 73% of patients, and elevated type I interferon blood signature in comparison with healthy controls. Finally, using blood biomarkers related to endothelial dysfunction and activation, and to angiogenesis or endothelial progenitor cell mobilization, we confirmed endothelial dysfunction in CLL. Conclusions Our findings support an activation loop in the skin in CLL associated with endothelial alteration and immune infiltration of cytotoxic and type I IFN‐polarized cells leading to clinical manifestations.

No abstract