Fact checked byShenaz Bagha

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May 02, 2024
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Dementia risk lower in patients with rheumatoid arthritis treated with biologic DMARDs

Fact checked byShenaz Bagha
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Key takeaways:

  • Conventional synthetic DMARDs did not show a similar protective effect.
  • TNF inhibitors should undergo controlled clinical trials assessing their “neuroprotective potentials.”

Dementia risk decreases among patients with rheumatoid arthritis treated with biologic disease-modifying antirheumatic drugs, according to a systematic review and meta-analysis published in RMD Open.

“Chronic systemic inflammation is believed to be involved in the development of dementia,” Wenhui Xie, PhD, of the department of rheumatology and clinical immunology at Peking University First Hospital, in Beijing, and colleagues wrote.

An infographic showing 76% relative risk for dementia among patients with RA treated with biological DMARDs vs. conventional synthetic DMARDs.
Data derived from Xie W, et al. RMD Open. 2024;doi:10.1136/rmdopen-2023-004016.

“Existing epidemiological evidence also suggests an increased risk of incident dementia associated with RA,” they added. “Under such conditions, modulating systemic inflammation is hypothesized to attenuate the development of dementia, and antirheumatic drugs are, therefore, considered as a potential strategy for dementia intervention in patients with RA.”

To assess the impact of DMARD treatment in RA on the risk for dementia, Xie and colleagues conducted a systematic review and meta-analysis of 14 studies. These studies — all either case-controlled, prospective or retrospective in nature — included data from 940,442 patients with RA and were collected from PubMed, EMBASE and the Cochrane Library. The overall findings of the studies were summarized using pooled risk ratios with confidence intervals of 95%.

According to the researchers, the analysis demonstrated a “significant reduction” in dementia risk among patients receiving biological DMARDs (RR = 0.76; 95% CI, 0.72-0.8) vs. those taking conventional synthetic DMARDs. A separate analysis on TNF inhibitors vs. conventional synthetic DMARDs also showed relative risk of 0.76 (95% CI, 0.71-0.82), as did analysis of non-TNF targeted DMARDs (RR = 0.76; 95% CI, 0.7-0.83) vs. conventional synthetic DMARDs.

Additionally, significant differences were observed among varying kinds of TNF inhibitors, with etanercept (Enbrel, Amgen) demonstrating the lowest relative risk (RR = 0.58; 95% CI, 0.53-0.65) and infliximab (Remicade, Janssen) having the highest (RR = 0.8; 95% CI, 0.72-0.88). Conversely, there was no significant impact on dementia incidence among those receiving conventional synthetic DMARDs overall (RR = 0.84; 95% CI, 0.59-1.2), except for an increased risk with sulfasalazine (RR = 1.27; 95% CI, 1.06-1.5).

“The present study provides comprehensive evidence on the beneficial effects of [biologic DMARDs], however, not [conventional synthetic DMARDs], on dementia development in patients with RA,” Xie and colleagues wrote. “These findings have clinical implications in choosing DMARDs for patients with RA at high risk for dementia and may also provide important insights into the prevention and treatment of dementia. Controlled clinical trials on TNF inhibitors are necessary to test their neuroprotective potentials.”