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<p>Mycobacterial antigens interact with host tissues, triggering various autoimmune pathways that further complicate the treatment of tuberculosis. In a chronic state, the mycobacterial antigen-reactive T cells often react with self-antigens, potentially leading to systemic autoinflammatory disorders. Tumefactive demyelination (TDL) is an aggressive form of neuroinflammatory disorder, usually mimicking an abscess or a tumor, posing a diagnostic challenge in those without a pre-existing demyelinating disorder. Early diagnosis is crucial in such cases, as it can significantly impact the patient’s outcome. We report a 48-year-old gentleman with sputum smear–positive pulmonary tuberculosis on anti-tubercular therapy (ATT) for 2&#xa0;months and, on completion of the intensive phase, progressed to develop an acute onset of left-sided hemiparesis associated with severe frontal cognitive impairment, leading to a bedridden state, with imaging showing features of TDL with open ring enhancement. He had a good response to pulse methylprednisolone and maintenance steroids while continuing ATT. At follow-up, he was ambulant and had mild residual deficits. In addition, we present a systematic review of the literature on similar cases of tuberculosis-associated neurological autoimmunity.</p>

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Paradoxical Tuberculosis Reaction Presenting as Tumefactive Demyelination of the Central Nervous System—The Crossroad Between Infection and Immunity

  • 期刊论文

  • 发表日期：

    2025年5月23日

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  • Angel Miraclin T.,
  • Vanjare Harshad Arvind,
  • Lesley Ponraj,
  • Aditya Nair,
  • Selvakumar Selvaganesan,
  • Appaswamy Thirumal Prabhakar,
  • Ajith Sivadasan,
  • Vivek Mathew,
  • Sanjith Aaron

摘要

Mycobacterial antigens interact with host tissues, triggering various autoimmune pathways that further complicate the treatment of tuberculosis. In a chronic state, the mycobacterial antigen-reactive T cells often react with self-antigens, potentially leading to systemic autoinflammatory disorders. Tumefactive demyelination (TDL) is an aggressive form of neuroinflammatory disorder, usually mimicking an abscess or a tumor, posing a diagnostic challenge in those without a pre-existing demyelinating disorder. Early diagnosis is crucial in such cases, as it can significantly impact the patient’s outcome. We report a 48-year-old gentleman with sputum smear–positive pulmonary tuberculosis on anti-tubercular therapy (ATT) for 2 months and, on completion of the intensive phase, progressed to develop an acute onset of left-sided hemiparesis associated with severe frontal cognitive impairment, leading to a bedridden state, with imaging showing features of TDL with open ring enhancement. He had a good response to pulse methylprednisolone and maintenance steroids while continuing ATT. At follow-up, he was ambulant and had mild residual deficits. In addition, we present a systematic review of the literature on similar cases of tuberculosis-associated neurological autoimmunity.