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. 2023 Feb;10(1):e000835.
doi: 10.1136/lupus-2022-000835.

Clinical associations of cognitive dysfunction in systemic lupus erythematosus

Sudha Raghunath  1   2 , Yifat Glikmann-Johnston  3 , Vera Golder  4   2 , Rangi Kandane-Rathnayake  4 , Eric F Morand  4   2 , Julie C Stout  3 , Alberta Hoi  4   2
Affiliations

Clinical associations of cognitive dysfunction in systemic lupus erythematosus

Sudha Raghunath et al. Lupus Sci Med. 2023 Feb.

Abstract

Objective: Cognitive dysfunction in SLE is common, but clinical risk factors are poorly understood. This study aims to explore the associations of cognitive dysfunction in SLE with disease activity, organ damage, biomarkers and medications.

Methods: We performed cross-sectional cognitive assessment using a conventional neuropsychological test battery, with normative values derived from demographically matched healthy subjects. Endpoints included two binary definitions of cognitive dysfunction and seven individual cognitive domain scores. Clinical parameters included disease activity (SLEDAI-2K) and organ damage (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index). We performed regression analyses to determine associations between clinical parameters and cognitive endpoints.

Results: 89 patients with SLE were studied, with median age of 45 and disease duration of 15 years. Organ damage was significantly associated with severe cognitive dysfunction (OR 1.49, CI 1.01-2.22) and worse cognitive test performance in three of the seven individual cognitive domains. In contrast, no significant associations were found between SLEDAI-2K at the time of cognitive assessment and any cognitive endpoints on multivariate analysis. Higher time-adjusted mean SLEDAI-2K was associated with better verbal memory scores but had no significant associations with other cognitive endpoints. The presence of anti-dsDNA antibodies and high IFN gene signature were negatively associated with severe cognitive dysfunction; there were no significant associations with the other autoantibodies studied or any medications. Substance use was significantly associated with lower psychomotor speed. Only 8% of patients who had cognitive dysfunction on testing had been recognised by clinicians on their SDI score.

Conclusions: In SLE, cognitive dysfunction was positively associated with organ damage, but not associated with disease activity, and serological activity and high IFN signature were negatively associated. Cognitive dysfunction was poorly captured by clinicians. These findings have implications for preventative strategies addressing cognitive dysfunction in SLE.

Keywords: autoimmune diseases; lupus erythematosus, systemic; systemic lupus erythematosus.

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Conflict of interest statement

Competing interests: SR reports a research grant from Lupus Victoria and postgraduate scholarships from the National Health and Medical Research Council (NHMRC), Arthritis Australia and the Australian Rheumatology Association. YG-J, VG, RK-R and JCS have nothing to disclose. EFM reports grants from Abbvie, Amgen, AstraZeneca, Biogen, BristolMyersSquibb, Eli Lilly, EMD Serano, Genentech, GlaxoSmithKline, Janssen and UCB, as well as consulting fees from AstraZeneca, Biogen, BristolMyersSquibb, Eli Lily, EMD Serano, Novartis, Servier and Zenas, all of which were outside the submitted work. EFM also reports payment or honoraria for educational events from AstraZeneca, Gilead and ONO, meeting support from AstraZeneca, patents with Monash University and AstraZeneca and director role for Rare Voices Australia. AH reports grants from AstraZeneca and Merck Serono outside the submitted work, Sponsorship of the Australian Lupus Registry and Biobank which is chaired by AH is received from Janssen, BMS, AstraZeneca and UCB. AH also reports meeting support from Janssen and consulting fees from Abbvie, Janssen and GSK. AH is honorary treasurer and board member for the Australian Rheumatology Association.

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