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Erschienen in:
27.01.2022 | Original Article
The role of anti-ribosomal P autoantibodies in the prediction of neuropsychiatric damage in systemic lupus erythematosus based on CSTAR cohort (XIV)
Erschienen in: Clinical Rheumatology | Ausgabe 5/2022
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Objectives
To identify the predictive value of anti-ribosomal P protein (anti-RibP) antibodies on the accrual of neuropsychiatric damage in systemic lupus erythematosus (SLE) patients in a large cohort in the Chinese SLE Treatment and Research group (CSTAR) database.
Methods
This single-center prospective study was conducted based on data from the CSTAR registry. At baseline, we collected demographic characteristics, autoantibody profiles, clinical manifestations, disease activity status, and organ damage. Follow-up data were collected by reviewing clinical records and telephone interviews. Anti-RibP antibodies were identified by immunoblot containing all three native RibP (P0, P1, P2) antigenic proteins.
Results
Of 2395 SLE patients with complete follow-up data, 659 (27.5%) were anti-RibP antibody positive. At baseline, positive anti-RibP antibodies were associated with a higher proportion of neurological involvement (𝑃 < 0.05). During follow-up, patients with positive anti-RibP antibodies were more likely to accumulate neuropsychiatric damage (adjusted HR = 3.8, 95% CI 2.7–57), p < 0.001). What is more, the cumulative probability of new-onset neurological involvement increased gradually in anti-RibP antibody–positive patients.
Conclusion
Anti-RibP antibodies can provide information about not only organ involvement at baseline, but also neuropsychiatric damage accrual and new-onset neurological involvement during follow-up. We suggested that anti-RibP antibody detection should be done in the newly diagnosed SLE patients to predict organ involvement and even the accumulation of neuropsychiatric damage.
Key Points
• Positive anti-RibP antibodies were associated with baseline neurological involvement.
• Baseline positive anti-RibP antibodies can predict the neuropsychiatric damage accrual and new-onset neurological involvement.
