Sarcoidosis meets COVID-19: do they share common pathogenetic mechanisms?

<bold>Background:</bold> In recent years, the spread of SARS-CoV-2 infection has been associated with several immune disorders. Angiotensin-converting enzyme(ACE), which is expressed also by lymphocytes, seems to promote SARS-CoV-2 infection. Unsurprisingly, a possible correlation between COVID-19 and sarcoidosis onset/exacerbation has been debated. <bold>Aim:</bold> To phenotypically characterize patients diagnosed with sarcoidosis after a close SARS-CoV-2 infection. <bold>Methods:</bold> Patients with a histological diagnosis of sarcoidosis between Jan. 2021 and June 2023 were enrolled. Patients were divided into two groups: those with a previously documented SARS-CoV-2 infection(SARCOVID) and those with a diagnosis of sarcoidosis alone(S). An expert thoracic radiologist evaluated the CT scan at sarcoidosis diagnosis defining an atypical pattern when any of those are present:diffuse or focal ground glass opacity, confluent nodules, mass-like opacities, asymmetrical or calcified lymphadenopathy, honeycombing, emphysema, inter-and intra-lobular septa thickening, mosaic attenuation, pleural effusion. <bold>Results:</bold> 13/26(50%) patients presented a diagnosis of sarcoidosis after SARS-CoV-2 infection [median:8 months(3-26)]. SARCOVID presented more frequently an atypical CT pattern compared to S, although this difference was not statistically significant (31 vs.15%,p=0.64), higher levels of ACE[56(35-128) vs.35U/L(8-145),p=0.05] and blood lymphocytes [31(16-38) vs. 20%(4-29),p=0.02]. <bold>Conclusion:</bold> During the SARS-Cov-2 pandemic, half of the patients diagnosed with sarcoidosis presented a recent SARS-CoV2 infection. Larger studies are needed to unravel whether human coronaviruses(HCoV), including SARS‐CoV‐2, can induce granulomatous inflammation and sarcoidosis.