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Correspondence on ‘Onset of rheumatoid arthritis after COVID-19: coincidence or connected?’

We read with great interest the letter by Derksen et al on ‘Onset of rheumatoid arthritis (RA) after COVID-19: coincidence or connected?’ in which they have conducted serology studies on 61 patients, 5 weeks after COVID-19 infection and found no increase in the incidence of anticitrullinated cyclic peptide (antiCCP) antibodies. Also, they found that the clinical and autoantibody characteristics of three patients from another cohort with seroconversion were similar to the regular patients with RA. Based on this, they have proposed that RA after COVID-19 may be a coincidence rather than connected. Triggering of autoimmunity by severe COVID-19 infection has been proposed and shown by demonstration of various autoantibodies, mainly antinuclear antibodies, antineutrophil cytoplasmic antibodies and antiphospholipid antibodies (APLA), in the sera of such patients. 4 Autoimmune diseases like lupus, Kawasaki disease, systemic vasculitis, APLA syndrome and reactive arthritis have been reported post COVID-19. Multiple arthritic manifestations of COVID-19 infection have been reported including a few cases of reactive arthritis 6 and a few of seropositive RA. 7 8 However, information on arthritisrelated antibodies like rheumatoid factor (RF) and antiCCP antibody are sparse. In this correspondence, we describe a case of a 56yearold woman who developed seropositive RA after COVID-19 infection. She is a known hypertensive since 3 years, well controlled on 5 mg of amlodipine. She was admitted at the hospital with fever, cough and dyspnoea in July, 2020. She had no prior history of smoking or joint pains. She was hypoxic and required oxygen support. Her reverse transcriptionpolymerase chain reaction (RTPCR) for SARSCoV-2 was positive and she was treated with ceftriaxone, azithromycin and discharged after a week. Two weeks after discharge, she started developing bilateral wrist joint pain and swelling followed by involvement of bilateral knees associated with morning stiffness lasting for about an hour. She was evaluated and had raised C reactive protein and erythrocyte sedimentation rate. Her RF and antiCCP antibodies were negative in August 2020. She was treated with short courses of steroids with intermittent relief and hydroxychloroquine for possible postCOVID reactive arthritis. However, her symptoms persisted and she presented to us in March 2021 with pain in bilateral wrist and knee joints. This time, laboratory evaluation revealed RF titres of 131 IU/ mL (normal range <10 IU/mL) and antiCCP titres of 35 U/ mL (normal <20 U/mL). Power Doppler ultrasound showed increased vascularity, synovial proliferation with erosions in bilateral wrist joints. She received intraarticular injections in both wrists with prompt relief in pain and was started on Methotrexate 15 mg/week for RA. To the best of our knowledge, this is the sixth case of seropositive RA after a COVID-19 infection (table 1). All these patients have previously documented negative serology. This case is unique because the patient had a negative serology at the onset of arthritis, which turned positive on subsequent testing for persistent symptoms. It probably suggests an ongoing autoimmune process even after the acute infection, which triggered the autoimmunity, has subsided. Derksen et al studied autoantibody characteristics of five Dutch patients who suffered from moderate to severe COVID-19 infection and presented with polyarthritis. They found antiCCP antibodies in three of them. Two other cases of seropositive RA after COVID-19 infection also had significant pulmonary involvement, 8 as did our case. The serum of one out of 29 severely ill COVID-19 patients revealed antiCCP antibodies but information on joint pain was lacking. Local airway inflammation and neutrophil extracellular trap (NET) formation has been hypothesised to drive antiCCP production in the lungs of first degree relatives of patients with RA. NET derived proteases can cause the release of peptidylarginine deiminases (PADs) which citrullinate self proteins and are known to be pathogenic in RA. Presence of NETs have been demonstrated in COVID-19 infected postmortem lung tissue and in sera of COVID-19 patients. 11 NETs and PADs have been proposed as potential therapeutic targets for COVID19. Further, viruses have been hypothesised to drive aberrant innate and acquired immune response with increased production of cytokines leading to autoinflammatory and autoimmune diseases, mainly via molecular mimicry and hyperstimulation of Correspondence