Abstract

BackgroundConcomitant diagnosis of neuromyelitis optica spectrum disease and pulmonary tuberculosis has rarely been reported.Case reportWe report a case involving a young Tunisian male patient who developed dry cough followed, 2 months later, by weakness in the lower limbs. The findings of central nervous system imaging and anti-aquaporin-4 antibody positivity were compatible with the diagnosis of neuromyelitis optica spectrum disease. Constellation of the clinical and the typical radiological pulmonary findings in our patient, coming from an endemic region, allowed the diagnosis of pulmonary tuberculosis, although sputum smear examination for acid-fast bacilli and cultures was negative. The patient received anti-tuberculous polytherapy associated with immunomodulation, consisting of methylprednisolone and intravenous immunoglobulins. Pulmonary infection symptoms initially improved but with no motor recovery. The patient suddenly died at home 4 months after the onset of the first symptoms. Current data regarding the clinical presentation of this underreported concomitant or associated condition, the possible pathophysiological mechanisms, and the therapeutic options were reviewed.ConclusionsThis case underscores the necessity to understand the exact mechanism of these coincident entities and to clarify the best immunomodulatory choice since immunosuppression targeting neuromyelitis optica spectrum disease can lead to dissemination of pulmonary tuberculosis.

Highlights

  • Neuromyelitis optica spectrum disease (NMOSD) is an autoimmune inflammatory disease affecting the central nervous system

  • This case underscores the necessity to understand the exact mechanism of these coincident entities and to clarify the best immunomodulatory choice since immunosuppression targeting neuromyelitis optica spectrum disease can lead to dissemination of pulmonary tuberculosis

  • As our region is endemic for Mycobacterium tuberculosis (MT) and the radiological findings were typical with a positive tuberculin skin test, diagnosis of smear-negative pulmonary tuberculosis (PT) coincident with NMOSD was retained

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Summary

Conclusions

MT infection should be considered by the practitioner as a possible additional condition to the neurological signs of NMOSD. MT infection can be concomitant or associated with NMOSD. This is important, especially in high-burden settings. Our work as well as earlier reports reinforce the hypothesis that MT infection is a possible infectious environmental factor involved in the development of NMOSD, even in the absence of CNS invasion by MT. A better understanding of the mechanism by which MT exerts its pathological effect, contributing to astrocyte damage, can be helpful for the clarification of the therapeutic approach of this complex association

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