Psychosis in systemic lupus erythematosus (SLE): 40-year experience of a specialist centre

Author:

Abrol Esha1,Coutinho Ester2,Chou Michael3,Hart Melanie3,Vincent Angela45,Howard Robert1,Zandi Michael S5,Isenberg David6ORCID

Affiliation:

1. Division of Psychiatry, University College London

2. Department of Basic and Clinical Neuroscience, Institute of Psychiatry Psychology and Neuroscience, King’s College London

3. Neuroimmunology Laboratory, National Hospital for Neurology and Neurosurgery, London

4. Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford

5. Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology

6. Centre for Rheumatology, Division of Medicine, University College London (UCL), London, UK

Abstract

Abstract Objectives The long-term outcome of psychosis in association with systemic lupus erythematosus (SLE) has been insufficiently characterised. We used a specialist centre cohort of patients with SLE and psychosis to investigate their clinical outcome and phenotypic and laboratory characteristics. Methods Retrospective cohort study of 709 SLE patients seen at a specialist centre between January 1978 and November 2018. Clinical, biochemical and immunological characteristics (Bonferroni corrected), and serum neuronal surface antibody profile using novel cell-based assays, were compared between patients with and without psychosis. Results Eighteen (18/709, 2.5%) patients developed lupus psychosis over a mean ± SD of 17.5 ± 11.0 years follow-up. Psychosis fully remitted in 66.7% (12/18) with a combination of antipsychotic (in 38.9%) and immunosuppressive therapy (methylprednisolone 72.2%, cyclophosphamide 55.6%, rituximab 16.7%, plasma exchange 27.8%, prednisolone 50%). Patients who developed lupus psychosis may be more likely to have anti-RNP antibodies (50.0% vs 26.5%) and less likely to have anti-cardiolipin antibodies (5.6% vs 30.0%), but this was not significant in our small sample. Neuronal surface autoantibody tests found GABABR autoantibodies in 3/10 (30.0%) lupus psychosis patients compared with only 3/27 (11.1%) in age- and sex-matched SLE controls using fixed cell-based assays (P =0.114). However, GABABR antibodies were not replicated using a live cell-based assay. NMDAR-antibodies were not detected with fixed or live cell assays in any samples. Conclusion Lupus psychosis is rare but treatable. In this rare sample of eighteen patients from a 40-year cohort, no significant biomarker was found, but some preliminary associations warrant further exploration in a larger multicentre analysis.

Funder

NIHR

Publisher

Oxford University Press (OUP)

Subject

Pharmacology (medical),Rheumatology

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