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Journal of General Internal Medicine ; 37:S405, 2022.
Article in English | EMBASE | ID: covidwho-1995668

ABSTRACT

CASE: JW is a previously healthy 27-year-old woman who presented with several months of progressive weakness, neuropathy, and tachycardia that began shortly after her second dose of the Pfizer COVID-19 vaccine. Initially, she noticed fatigue followed by occipital neuralgia and paresthesia. Weeks later, she was febrile with extremity tremors and neuralgia. She went to the ED where she was lymphopenic, group A strep positive (GAS+), and had unremarkable imaging;she was given antibiotics and gabapentin. Her fever resolved, but her pain/tremor continued. Occipital nerve blocks provided temporary relief;acyclovir and duloxetine had no effect. On two subsequent ED visits, she was again GAS+ and was given additional antibiotics. Later, she developed non-pruritic rash, dermatographia, and blepharitis;skin biopsy showed non-vasculitic progressive pigmented purpura. An extensive rheumatologic, post-infectious, and paraneoplastic workup was unrevealing. Notably, she had high anti-COVID-19 spike antibody on qualitative assay. During workup, her symptoms rapidly worsened, leading to admission. On exam, she had intact sensation, profound gait imbalance, and HR to 150s with standing. LP was negative;EMG ruled out large fiber polyneuropathy (LFPN). She was diagnosed with autoimmune small fiber polyneuropathy (SFPN) and POTS. She improved rapidly with IVIG and steroids. Given her negative workup, the COVID-19 vaccine was identified as the likely trigger. IMPACT/DISCUSSION: Despite being common, SFPN is undiagnosed in many patients, likely due to its non-specific symptoms and low awareness among physicians. Furthermore, SFPN and LFPN often coexist, complicating the diagnosis of SFPN which typically requires confirmatory skin biopsy. Postvaccine SFPN has been described, including a milder case following the Pfizer COVID-19 vaccine. Symptoms typically progress chronically, follow a Guillain-Barré-like presentation, and may include dysautonomia. SFPN is thought to be mediated via humoral autoimmunity and autoreactive B-cells. Treatment is immunoglobulins and steroids. That JW's case progressed through the healthcare system for several months prior to diagnosis demonstrates two key points: 1) despite the ubiquity of SFPN, scant diagnostic tools and the subjective and chronic nature of symptoms may result in underdiagnosis;2) given the public discourse around vaccination and the rarity of adverse effects, there may be a tendency to dismiss complaints related to vaccines. Despite JW's early suggestion that the COVID19 vaccine caused her symptoms, post-vaccine syndromes were not considered until late in the course. CONCLUSION: SFPN should be considered in any patient with neuropathy. Clearer diagnostic criteria for SFPN are needed and may improve patient outcomes and enable more clinical trials. COVID-19 vaccination can trigger polyneuropathy. Vaccine-related adverse outcomes should remain on the differential when symptoms begin shortly after vaccination, despite the rarity of such outcomes.

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