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(067) Altered Mental Status Due to Golimumab: A Case of Tnf-alpha Inhibitor Induced Lupus-like Syndrome


Authors:

Jason P. Caplan, MD, FACLP, FAPA – Professor of Psychiatry, Creighton University School of Medicine - Phoenix

Evan Cordrey, BA – MS4, Creighton University School of Medicine: Phoenix Regional Campus

Dawn Benford, MSN, PMHNP-BC – Psychiatric Nurse Practitioner, St. Joseph's Hospital and Medical Center


Co-Authors:

Presenting Author: Jason Caplan, MD, FACLP, Creighton University School of Medicine - Phoenix
Co-Author: Evan Cordrey, BA, Creighton University School of Medicine: Phoenix Regional Campus
Co-Author: Dawn Benford, MSN, PMHNP-BC, St. Joseph's Hospital and Medical Center

Abstract:

Introduction:

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease for which first-line treatment is disease-modifying antirheumatic drugs (DMARDs). If these medications are unsuccessful, tumor necrosis factor alpha (TNF-alpha) inhibitors, sometimes known as anti-TNF-alpha medications, typically serve as second-line treatment. Since TNF-alpha plays a role in the native immune system, these medications can trigger the production of autoantibodies and a subsequent autoimmune response mimicking the symptoms of systemic lupus erythematosus (SLE) and, in rare circumstances, lead to major life-threatening organ damage including inflammation of the brain (cerebritis). This phenomena has previously been documented as TNF-alpha inhibitor induced lupus-like syndrome (TAILS).




Case Presentation:


We report a case of a 69 year-old woman with a chronic history of RA who was switched from methotrexate monotherapy to the anti-TNF-alpha medication golimumab. Within 6 months of starting this medication she developed gradual polyneuropathy, limb paresthesias, pancytopenia, and eventual cerebritis requiring an intensive care unit (ICU) admission. Upon psychiatric consultation, patient demonstrated psychomotor retardation, confusion, and global aphasia. Patient was oriented only to self for most of her ICU admission. Despite stopping golimumab, the patient had seroconversion of antinuclear antibodies (ANA), anti-double-stranded DNA, and anti-Sjögren’s-syndrome-related antigen A (Anti-SSA). Extensive neurological, neoplastic, vascular and infectious work-up were not revealing of any other cause of her autoimmunity, leading to the conclusion this was a drug-induced form of lupus cerebritis. Further weight was added to this hypothesis when the patient rapidly recovered after 48 hours of high dose methylprednisolone.




Discussion:


To our knowledge, this is the first reported case of golimumab-induced autoimmune cerebritis. Previous reports of automimmunity with this agent have only presented with cutaneous forms of this lupus-like syndrome. Autoimmune cerebritis has previously been reported with other anti-TNF-alpha agent such as adalimumab and have included a variety of neuropsychiatric symptoms including seizures and clonus.




Conclusion:

This case highlights that TAILS can present with a variety of CNS symptoms without the cutaneous involvement typically associated with a lupus-like syndrome. and should be considered in the differential diagnosis of neuropsychiatric symptoms in a patient using anti-TNF-alpha medications including golimumab.


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