Antibodies to Ribosomal P in Lupus Psychosis Resolving after Rituximab plus Cyclophosphamide – A Case Report
|Nicola C. G. Stein1,2, Karsten Conrad3 and Martin Aringer1*|
|1Department of Medicine III, University Medical Center Carl Gustav Carus, TU Dresden, Dresden, Germany|
|2Division of Rheumatology, Medizinische Klinik und Poliklinik IV, University of Munich, Munich, Germany|
|3Institute of Immunology, Faculty of Medicine Carl Gustav Carus, TU Dresden, Dresden, Germany|
|Corresponding Author :||Martin Aringer, MD
Division of Rheumatology
Department of Medicine III
University Medical Center Carl Gustav Carus at the TU Dresden
Fetscherstrasse 74, 01309 Dresden, Germany
E-mail: [email protected]
|Received October 01, 2013; Accepted October 23, 2013; Published October 30, 2013|
|Citation: Stein NCG, Conrad K, Aringer M (2013) Antibodies to Ribosomal P in Lupus Psychosis Resolving after Rituximab plus Cyclophosphamide – A Case Report. J Clin Cell Immunol 4:168. doi:10.4172/2155-9899.1000168|
|Copyright: © 2013 Stein NCG, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
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Background: Central nervous disease manifestations in systemic lupus erythematosus (SLE) are variable, but may be severe. A subset of these manifestations in the central nervous system (CNS) is caused by antibodies. One antibody in particular, against ribosomal P, is supposed to play a significant role in neuropsychiatric SLE, especially lupus psychosis. Our case supports this idea.
Case: We present a case of a young female who developed severe lupus psychosis after discontinuation of her immunosuppressive treatment for systemic lupus erythematosus without prior central nervous or psychiatric manifestations. Cerebral imaging and liquor analysis was unremarkable, serum analysis showed high titers of both, anti-dsDNA and anti-ribosomal P antibodies. When disease could not be controlled with high dose methylprednisolone, a combination of cyclophosphamide and rituximab was administered. Approximately two weeks after the immunosuppressive combination therapy, mood stabilization and clinical recovery were apparent. After two months the patient was recovered completely. Serology showed a striking decrease in anti-ribosomal P antibodies at this time.
Conclusion: The disease course of this young patient with severe lupus psychosis suggests that the effect of pulse methylprednisolone was on the blood-brain barrier, with only with a dose of 1 g q.d. being effective. Therewith, it supports the idea of lupus psychosis being caused by auto-antibodies entering the CNS. The very high titres of antiribosomal P antibodies in full-blown psychosis, and the pronounced fall of these antibodies thereafter, concomitant with reaching clinical remission, support the concept of anti-ribosomal P antibodies causing lupus psychosis.