Neuro-Behçet’s Disease Onset in the Context of Tuberculous Meningoencephalitis: A Case Report

Author:

Antonescu Florian12,Butnariu Ioana12ORCID,Antonescu-Ghelmez Dana12,Tuta Sorin12,Voinescu Bianca Adriana3,Manea Mihnea Costin14,Bucur Amanda Ioana2,Chelmambet Altay Sercan2,Moraru Adriana2

Affiliation:

1. Department of Clinical Neurosciences, “Carol Davila” University of Medicine and Pharmacy, 020023 Bucharest, Romania

2. Department of Neurology, National Institute of Neurology and Neurovascular Diseases, 041915 Bucharest, Romania

3. “Victor Babes” Clinical Hospital for Infectious and Tropical Diseases, 030303 Bucharest, Romania

4. “Prof. Dr. Alexandru Obregia” Clinical Psychiatry Hospital, 041915 Bucharest, Romania

Abstract

Behçet’s disease (BD) is a systemic vasculitis that frequently presents with a relapsing–remitting pattern. CNS involvement (Neuro-Behçet) is rare, affecting approximately 10% of patients. Its etiological mechanisms are not yet fully understood. The most commonly accepted hypothesis is that of a systemic inflammatory reaction triggered by an infectious agent or by an autoantigen, such as heat shock protein, in genetically predisposed individuals. Mycobacterium tuberculosis is known to be closely interconnected with BD, both affecting cell-mediated immunity to a certain extent and probably sharing a common genetic background. We present the case of a 34-year-old Caucasian woman who had been diagnosed with tuberculous meningitis 15 months prior, with significant neurological deficits and lesional burden on MRI with repeated relapses whenever treatment withdrawal was attempted. These relapses were initially considered as reactivation of tuberculous meningoencephalitis, and symptoms improved after a combination of antituberculous treatment and corticosteroid therapy. After the second relapse, the diagnosis was reconsidered, as new information emerged about oral and genital aphthous lesions, making us suspect a BD diagnosis. HLA B51 testing was positive, antituberculous treatment was stopped, and the patient was started on high doses of oral Cortisone and Azathioprine. Consequently, the evolution was favorable, with no further relapses and slow improvements in neurological deficits. To our knowledge, this is the first report of Neuro-Behçet’s disease onset precipitated by tuberculous meningitis. We include a review of the available literature on this subject. Our case reinforces the fact that Mycobacterium tuberculosis infection can precipitate BD in genetically predisposed patients, and we recommend HLA B51 screening in patients with prolonged or relapsing meningoencephalitis, even if an infectious agent is apparently involved.

Publisher

MDPI AG

Subject

General Medicine

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