ArticleCureus2024
Myeloperoxidase Anti-Neutrophil Cytoplasmic Antibody (MPO-ANCA)-Associated Vasculitis With Rare Clinical Manifestations After SARS-CoV-2 Multisystem Inflammatory Syndrome in a 14-Year-Old Boy.
Article in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Vasculitis syndromes: the pathogenic roles of COVID-19 and related vaccinations.Virology journal · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA) microscopic polyangiitis is a rare but life-threatening small vessel vasculitis in childhood that affects multiple systems. Emerging clinical evidence suggests a possible association between SARS-CoV-2 infection or multisystem inflammatory syndrome in children (MIS-C) as well as the futuredevelopment of autoimmune diseases. A 14-year-old boy with a diagnosis of MIS-C two years prior to presentation was admitted to our hospital due to edema and left lower limb joint pain along with concomitant upper surface petechia. The patient had a positive higher SARS-CoV-2 IgG than MIS-C diagnosis titers and MPO-ANCA-positive antibody titers. Kidney biopsy favored a pauci-immune crescentic glomerulonephritis. Restrictive lung disease with concomitant diffusion abnormalities was also observed. Pancreatitis and gastrointestinal wall edema were additional clinical manifestations. SARS-CoV-2 breakthrough infection and MIS-C could contribute to the onset of autoimmune vasculitis through various immunological mechanisms. Further research is still needed to elucidate the role of SARS-CoV-2 in the pathophysiology of newly diagnosed autoimmune vasculitis.
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Registered trials
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