Inflammatory myopathy occurring shortly after severe acute respiratory syndrome coronavirus 2 vaccination: two case reports

• Published in: Journal of medical case reports 2022-01, Vol.16 (1), p.57-57, Article 57
• Main Authors: Vutipongsatorn, Kritchai, Isaacs, Anthony, Farah, Ziad
• Format: Article
• Language: English
• Subjects: Aged; Antibodies; Biopsy; Blood tests; BNT162 Vaccine; Case Report; Case reports; Coronavirus disease 2019; Coronaviruses; Corticosteroids; COVID-19; COVID-19 vaccines; Creatine; Creatine kinase; Creatinine; Drug dosages; Edema; Epidemics; Family medical history; Female; Hemoglobin; Humans; Idiopathic inflammatory myopathies; Immunoglobulins; Inflammation; Inflammatory diseases; Magnetic resonance imaging; Messenger ribonucleic acid vaccine; Methylprednisolone; Middle Aged; mRNA vaccines; Musculoskeletal diseases; Myositis - drug therapy; Neutrophils; Patients; Phosphatase; Potassium; Prednisolone; RNA; RNA polymerase; SARS-CoV-2; Severe acute respiratory syndrome; Severe acute respiratory syndrome coronavirus 2; Steroids; T cell receptors; Vaccination
• ISSN: 1752-1947; 1752-1947
• DOI: 10.1186/s13256-022-03266-1

Vaccination remains the cornerstone approach to exiting the current global coronavirus disease 2019 pandemic caused by severe acute respiratory syndrome coronavirus 2. The novel messenger ribonucleic acid vaccines offer a high level of protection and are widely used throughout the world. With more people receiving the vaccines, better understanding of their relative safety can be reached. In this report, we describe two patients who developed inflammatory myopathy within 48 hours of receiving the Pfizer BNT162b2 vaccine. Patient A, a 55-year-old South East Asian woman, presented with a 6-week history of pruritic facial and torso rash and a 1-week history of worsening proximal myopathy. Her rash first developed 2 days after receiving the first dose of BNT162b2 vaccine. Patient B, a 72-year-old Caucasian woman, presented with a 2-week history of proximal myopathy a day after receiving the second dose of BNT162b2 vaccine. Both patients had elevated creatine kinase on admission. Patient A tested positive for anti-Mi-2a antibody and anti-Ro-52 antibody, while Patient B was positive for anti-fibrillarin antibody. Magnetic resonance imaging subsequently confirmed generalized acute muscle inflammation and subcutaneous inflammation consistent with inflammatory myositis. Both patients did not have a previous history or family history of autoimmune disease. Patients A and B were diagnosed with dermatomyositis and inflammatory myositis, respectively. They were initially treated with pulsed intravenous methylprednisolone followed by oral prednisolone. However, as their conditions were resistant to corticosteroids, both eventually received and responded well to intravenous immunoglobulin therapy. There are previously reported cases of severe acute respiratory syndrome coronavirus 2-induced and other vaccine-related inflammatory myopathies. However, the precise mechanisms are not elucidated. Without more evidence and convincing pathophysiology, it is not possible to conclude that our patients developed inflammatory myopathy because of the vaccine. However, the timing of the disease onset and the lack of previous history raise an important question of this novel messenger ribonucleic acid therapy.