Low IL-18 levels may predict long COVID risk in systemic autoimmune rheumatic diseases
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WASHINGTON — Among patients with systemic autoimmune rheumatic diseases, circulating interleukin-18 levels were lower in those with long COVID vs. those without, according to data presented at ACR Convergence 2024.
“We were interested to see if inflammatory cytokines were associated with long COVID among patients with rheumatic disease,” Jeffrey Sparks, MD, of Brigham and Women's Hospital and Harvard Medical School, told Healio. “This would help understand the pathogenesis and could lead to therapies and diagnostics.”
To examine potential inflammatory biomarkers for long COVID in patients with systemic autoimmune rheumatic diseases (SARDs), Sparks and colleagues analyzed data from RheumCARD. According to the researchers, RheumCARD is a prospective study of patients with SARDs and COVID-19 from a large health care system.
The analysis included 201 patients with a mean age of 56.3 years, who answered surveys and provided blood samples from March 2021 to July 2023. Recruitment occurred at least 28 days following acute COVID-19 onset. The cohort was 81% women. The most common systemic autoimmune rheumatic disease was inflammatory arthritis, with 60% of participants reporting this complication. Connective tissue disease occurred in 22% of participants. Results pertaining to patients using a cytokine-targeting DMARD were excluded.
According to the researchers, levels of IL-18 were lower — at 199 units — among those with long COVID, compared with 221 units in those without long COVID (P = .001). This trend persisted through the multivariate analysis ( = –55 units; SE, 17; P = .0011).
Additionally, IL-18 levels were “considerably lower” in patients with long COVID among all analyzed subgroups, including those with inflammatory arthritis (P = .021), those in remission or low disease activity (P = .02), those with moderate or high disease activity (P = .015), those who had pre-omicron variants of COVID-19 (P = .004), those who had omicron variants of COVID-19 (P = .06), and those who had long COVID defined as at least 90 days of persistent symptoms (P = .004), vs. comparators (P = .011), the researchers wrote.
Other cytokines associated with long COVID included colony stimulating factor 2, IL-2 and chemokine (C-C motif) ligand 6, according to Sparks.
“We found that lower levels of IL-18 were associated with increased risk of long COVID,” he said. “IL-18 induces cell-mediated immunity following infection, implicating a blunted immune response, rather than exuberant hyperinflammation, as a potential mechanism for long COVID among patients with rheumatic diseases. This may also tie into rheumatic patients exhibiting a longer duration of viral shedding due to immunosuppression.
“This provides rationale to investigate delayed viral clearance as a potential mechanism in rheumatic diseases and other immunosuppressing conditions,” Sparks added. “In addition to hyperinflammation, blunted immune response to initial infection may contribute to long COVID among immunosuppressed patients with rheumatic disease.”
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Sparks J. Abstract #2616. Presented at: ACR Convergence 2024; Nov. 14-19, 2024; Washington, D.C.
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