The inflammatory and autoimmune spheres can be influenced by various factors (i.e. virus) and they can change over time [17]. In our recent work, we observed how SARS-CoV-2 infection is also linked to these status [9]. In the study we analysed 40 patients from both an inflammatory and immunological point of view, highlighting modifications of the most common markers of inflammation. Furthermore, as regards the autoimmune profile, a significant prevalence of autoantibodies to ANA, X-ANCA, ASCA IgA was observed (Fig. 1). Taking in account that the autoimmune response alterations could be transitory or persist longer and lead to chronic autoimmune disease, we decide to perform a follow-up study. Thirteen patients of the previous study were analysed at 3- and 6-months post hospitalization for the same autoantibodies considered at t0.
The 13 patients considered had an age between 19 and 77 years old (average = 55.69 years). None of the 13 patients was affected, in the last five years, by the following diseases: coronary disease, cerebrovascular disease, hepatitis B infection, cancer, immunodeficiency, ischemic heart disease, ictus, dementia, chronic liver disease, HIV infection. The mean hospitalization time was 22.54 days. At the time of discharge, 3 patients (P1, P6, P9) were diagnosed with COVID-19 interstitial pneumonia, 7 patients (P2, P4, P7, P8, P11, P12, P13) were dismissed having severe respiratory failure derived from COVID-19 bilateral interstitial pneumonia. Two of these 7 (P11, P13) presented severe respiratory failure type 1, whereas another (P12) had also thrombocytopenia most probably as consequence of heparin administration. One patient (P5) had immune thrombocytopenic purpura and another one (P10) was defined to have only interstitial anomalies. For one patient we did not have the diagnosis at the discharge (Fig. 3).
Concerning the autoimmune sphere, 9/13 patients had ANA antibodies at t0 (Fig. 2 table a). A patient (P3), negative at t0, was tested again after 16 days after admission and she resulted positive for ANA, with a cytoplasmatic and granular pattern (1:320). The same patient at t3 showed a combination of granular, cytoplasmic and centriolar pattern, however the granular pattern disappeared at t6. In addition, immunoblot analysis performed at all three time points confirmed the presence of M2-β and Ku autoantibodies. In total, 6 patients (P3, P4, P5, P6, P8 and P13) maintained the positivity during the follow-up, both at t3 and t6. P4 showed a granular pattern at t0 (1:160) and homogeneous pattern (1:80) was also added to t3 and t6 (1:80). P5 showed a centriolar pattern (1:160) which was maintained at follow-up. Furthermore, she was positive at the CTD screen. P6 showed a mid-body and mitotic spindle pattern which was maintained at follow-up. P8 had homogeneous ANA pattern (1:320). P13 showed at t0 a cytoplasmic pattern (1:160) which was maintained at t3 (1:80) and t6 (1:160), furthermore at t6 he also showed a nucleolar pattern (1:160).
Three patients (P7, P9, 10), showing at t0 a cytoplasmic pattern, became negative at t3 and t6. A patient (P12) was positive only at t0 and t3, although the pattern changed slightly from cytoplasmic-granular, at t3 it was detected only the cytoplasmic one. Two patients (P1, P2) were negative at t0 and remained negative also during the follow-up. One patient (P11) developed ANA at t3 showing a homogeneous pattern and unfortunately it was not possible to test the patient at t6.
Regarding the other autoantibodies (Fig. 2 table b), 1 patient (P1) positive for ENA at t0, he was positive also during the follow-up. Two patients (P9 and P10) had also X-ANCA at t0 and one of them (P10) was also positive for ASCA IgG autoantibodies at all the three time points, whereas ASCA IgA were borderline at t0 and then positive at t3 and t6. A patient (P11) was positive for ASCA IgA and IgG only at t0, whereas another patient (P12) developed these autoantibodies during the follow-up.
None of the 13 patients showed the presence of the following autoantibodies: anti-β2glicoprotein, anti-cardiolipin, anti PR3, anti MPO (data not shown).