Discussion
The precise etiology of autoimmune disorders is yet unclear, though there is growing evidence that there is a role for a multitude of elements, including genetic predisposition and environmental factors1. It is proposed that infections with bacterial or viral organisms trigger an exaggerated host immune response via molecular mimicry and activation of pre-primed auto-reactive T-cells and pro-inflammatory mediators1. This in turn may lead to tissue damage and multisystem organ dysfunction1.
COVID-19 has been shown to share similar pathogenic mechanisms driving an exaggerated immune response2. There is a growing evidence to suggest an association between prior COVID-19 infection and ensuing development of autoimmune disorders – primarily in the adult population – such as systemic Lupus Erythematosus, Guillain–Barré syndrome, Kawasaki disease, and Rheumatoid Arthritis2. In the pediatric population the most commonly reported autoimmune phenomena associated with COVID-19 infection is Multisystem Inflammatory Syndrome in Children (MIS-C)3.
Acute P-ANCA Vasculitis following COVID-19 infection is a rare but documented clinical presentation in the adult population4. Only one other pediatric case linking past COVID 19 infection with P-ANCA and MPO positive small vessel vasculitis was reported previously5. The other pediatric case also manifested with acute renal failure and DAH. These clinical manifestations are unlikely a direct result of acute COVID-19 infection, as both patients had multiple negative COVID-19 PCR tests while COVID-19 IgG was positive. These multisystem manifestations are likely to be a sequela of COVID-19 infection and its ability to trigger autoimmunity2.