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.