Abstrakt

Acute inflammatory demyelinating polyneuropathy induced by SARs cov−2 viral infection

Arpankumar Patel*, Saumil Patel, Kaitlyn Spinella, Kenneth Heberling

Introduction: Guillain Barre Syndrome (GBS) in SARS- CoV-2 is estimated to be around 15 cases per 100,000 and most cases occur after active infection is resolved. We present a case where GBS occurred concurrently during an active infection, raising a broad clinical question about its immuno-mimicking or modulating properties and genetic susceptibility predisposing certain individuals. Case: A forty-one-year-old male presented with acute weakness in his bilateral lower extremities. The patient had ongoing flu-like symptoms. He was not vaccinated and tested positive for SARS-CoV-2. Past medical history was significant for acute inflammatory demyelinating polyneuropathy two years ago, with similar presentation as above shortly after influenza A. Neurological exam revealed bilateral lower leg weakness with reduced strength. Lumbar puncture showed elevated proteins. The patient was started on plasmapheresis and noted significant improvement after treatments for five days. Discussion: A review of literature demonstrated that SARS-CoV-2 is responsible for multiple autoimmune disorders. Hyperstimulation of the immune system occurs due to viral entry triggering cytokine storms, and production of multiple gamma globulins. This is one of the proposed mechanisms where low levels of antibody were already present in individuals and hypergammaglobulinemia precipitated autoimmunity. The similarity in primary sequence between humans and components of SARS-CoV-2 explains molecular mimicry as a second causative factor. Neutrophil Extracellular Traps activation produces extracellular fibers that traps and degrades organisms using elastase and proteases. This can cause the deimination of self-proteins, making them autoreactive. However, further research is warranted to study the underlying mechanism of autoimmunity