Abstract
A relationship is emerging between SARS-CoV-2 infections and ANCA-associated vasculitis (AAV) because: (i) the pulmonary involvement of COVID-19 may mimic that observed in patients with AAV; (ii) the two diseases may occur together; (iii) COVID-19 may trigger AAV. However, few cases of AAV have been identified so far in COVID-19 patients. To define the frequency of ANCA autoimmunity in patients with SARS-CoV-2 infection, we analyzed the serum ANCAs and the serum PR3 and MPO antigens by immunoassays in 124 adult patients with a diagnosis of SARS-CoV-2 infection (16 were asymptomatic and 108 were hospitalized) and 48 control subjects. The serum ANCAs were significantly higher in the hospitalized patients compared with either the controls or the asymptomatic patients and increased with the progression of the COVID-19 severity. After one week of hospitalization, the values were significantly lower. In contrast, no differences emerged among the controls, asymptomatic and hospitalized patients for the PR3 and MPO serum levels. None of the patients had clinical signs of AAV with the exception of a severe pulmonary involvement. Further studies are necessary to define whether the increase in the serum ANCAs might mask subclinical vasculitis in a percentage of patients with SARS-CoV-2 infection or it is an epiphenomenon of SARS-CoV-2 infection with no clinical manifestations.
Highlights
IntroductionVascular complications have been reported in patients with a SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection
Vascular complications have been reported in patients with a SARS-CoV-2 infection
The production of ANCAs in patients with SARS-CoV-2 infection seems to be triggered by the enhanced release of the PR3 and MPO antigens by neutrophils; in the patients with SARSCoV-2 infection of the first wave, the serum levels of PR3 and MPO were parallel to the trend of the serum ANCAs
Summary
Vascular complications have been reported in patients with a SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection. Necroscopies of COVID-19 patients revealed that endothelial cell inflammation with the accumulation of lymphocytes, 4.0/). Circulating neutrophils, which are increased in COVID-19 patients [5], contribute to the endothelial damage by releasing tumor necrosis factor-alpha, interleukin (IL)-1 and IL-8. Acute kidney disease was described in up to one third of severe patients with COVID19 [6] and may appear within a more complex picture of ANCA (anti-neutrophil cytoplasmic antibody)-associated vasculitis either after or during COVID-19 [7]. ANCA-associated vasculitis (AAV) comprises granulomatosis with polyangiitis (GPA), microscopic polyangiitis and eosinophilic GPA [8]. AAV may be triggered by the release of proteinase 3 (PR3)
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