From Viral Recovery to Autoimmunity: A Case Report of Rheumatoid Arthritis Emergence After COVID‐19

TL;DR

A woman developed rheumatoid arthritis after recovering from COVID-19, showing how viral infections might trigger autoimmune conditions.

Contribution

This case uniquely documents the progression from postviral arthritis to rheumatoid arthritis with dynamic anti-CCP antibody changes.

Findings

Anti-CCP antibody levels correlated with clinical disease activity during steroid treatment.

Joint symptoms recurred and anti-CCP antibodies reappeared after discontinuing steroids.

The case suggests a link between COVID-19 and autoimmune dysregulation leading to rheumatoid arthritis.

Abstract

A woman in her 50s contracted Coronavirus disease 2019 (COVID‐19), initially presenting with mild symptoms, and managed conservatively. However, she developed a persistent low‐grade fever and insidious joint pain for 1 month, prompting further evaluation. Chest computed tomography revealed bilateral pulmonary infiltrates, leading to hospitalization for COVID‐19‐associated pneumonia. Despite a 2‐week course of ceftriaxone and azithromycin, her condition remained unchanged. Postadmission testing revealed elevated rheumatoid factor, anti‐cyclic citrullinated peptide (CCP) antibodies, and matrix metalloproteinase‐3, suggesting an inflammatory or autoimmune process. Given concerns for immune‐mediated inflammation, she was treated with high‐dose methylprednisolone. With pneumonia improvement, she was discharged on oral prednisolone (PSL) (20 mg/day) with a planned taper. Her joint symptoms resolved, and anti‐CCP antibody levels normalized during steroid therapy. However, upon PSL tapering and discontinuation, her joint pain recurred, and anti‐CCP antibodies became positive again. A rheumatology consultation confirmed rheumatoid arthritis (RA). This case provides rare longitudinal documentation of dynamic anti‐CCP antibody changes that paralleled clinical disease activity, illustrating the progression from postviral reactive arthritis to classifiable RA. It underscores COVID‐19’s potential to trigger autoimmune dysregulation and highlights the need for long‐term follow‐up with serial autoantibody monitoring in patients with persistent musculoskeletal symptoms after infection.

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