COVID-19 RNA Vaccine Produces Fingertip Necrosis

And still the Democrats are mandating this poison.

Related: Vaccinated Suffering Strange, Terrifying New Illness

https://twitter.com/pathnoerror/status/1581443174387499008?s=20&t=vo23E5nrIvXCYZjO8UlpOA

Pfizer–biontech COVID-19 RNA vaccination induces phosphatidylserine autoantibodies, cryoglobulinemia, and digital necrosis in a patient with pre-existing autoimmunity☆

Published in Science Direct

We describe a 64-year-old Caucasian female with a history of Raynaud’s disease, hand arthritis, photosensitivity, Sjogren’s syndrome and leukocytoclastic vasculitis who presented with progressively worsening fingertip necrosis that began three days after receiving a first dose of Pfizer–BioNTech COVID-19 RNA vaccine. Our workup revealed cryoglobulinemia, hypocomplementemia, elevated antinuclear antibodies (ANA) and IgM antiphospholipid autoantibodies (aPL) directed against phosphatidylserine (aPL-PS), suggesting a diagnosis of systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). The patient failed to develop anti-spike IgG antibodies up to two months following vaccination. Disease progression was halted by plasmapheresis, anticoagulation, and immune suppression. We conclude that the vaccine RNA moiety may induce SLE manifesting in APS, cryoglobulinemia, hypocomplementemia, and digital necrosis.

Digital necrosis
Introduction

Systemic vasculitides are heterogeneous disorders that share the common feature of vascular inflammation. They vary depending on which organs are involved, which size of blood vessels is affected and how severe the inflammation is. In the end, there is diminished blood flow, alterations in the vascular system, and eventual occlusion with variable ischemia, necrosis, and damage to tissues. Cryoglobulinemic vasculitis is a small vessel vasculitis that is characterized by the presence in the serum of one or more immunoglobulins that precipitate below core body temperatures and re-dissolve upon rewarming [1].

Vasculitides have been linked to infectious agents, connective tissue diseases, malignancies, drugs, and toxins among other still unknown factors. Various forms of vasculitides have also been observed and reported as adverse events following immunization after different vaccines [2]. The Pfizer–BioNTech COVID-19 vaccine is a lipid nanoparticle-formulated, nucleoside-modified mRNA vaccine encoding the pre-fusion spike glycoprotein of SARS-CoV-2, the virus that causes COVID-19 [3]. To our knowledge, there has not been any described case of worsening of vasculitis following administration of the vaccine.
Case presentation

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A 64-year old Caucasian female presented to our emergency department with painful fingertip discoloration on 3/20/2021. Her past medical history included Raynaud’s disease, hand arthritis, and Sjogren’s syndrome diagnosed in August 2020. Two months prior to admission, in January of 2021, she presented to with purpuric rash over her lower extremities, which was diagnosed as biopsy-proven leukocytoclastic vasculitis and treated with a prednisone taper by her dermatologist for 2 weeks.

On 03/03/21 she received a 1st COVID-19 vaccine. On 03/11/21 she saw her dermatologist for the bluish discoloration of her fingertips, when her right third distal phalanx started to turn black for the first time, which was accompanied by overall worsening upper extremity Raynaud’s disease. She was again started on prednisone, 10 mg daily, which did not help with the fingertip lesions. Eventually, the patient presented to the Upstate Emergency Department (ED) on 03/20/21 with stabbing pain and decreased sensation in all her fingertips. She was hemodynamically stable. Nasopharyngeal SARS-CoV-2 RNA RT-PCR test was negative. On physical exam, there was a bluish discoloration of all fingertips, the right third distal phalanx was showing signs of necrosis, and purpuric rash was seen on her legs (Fig. 1). Rheumatological work-up revealed photosensitivity, malar rash, bilateral symmetrical leg purpura, positive ANA, low complement levels with undetectable C4, elevated IgM antiphospholipid antibody directed to phosphatidylserine (aPL-PS), cryocrit of 14% (Table 1), suggesting systemic lupus erythematosus (SLE) with antiphospholipid syndrome (APS) and cryoglobulinemia. Hepatitis B surface antigen, hepatitis B core antibody, hepatitis C antibody and HIV were all nonreactive.

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