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<p>Isoniazid, a widely used anti-tuberculous drug, is known to cause peripheral neuropathy as a side effect. To mitigate this risk, pyridoxine is commonly administered as a preventive measure, particularly in individuals at higher risk, such as those with HIV infection, chronic alcohol use, or chronic kidney disease (CKD). We report the case of a 39-year-old female with chronic kidney disease and tuberculous lymphadenitis who developed peripheral neuropathy while receiving anti-tuberculous therapy (ATT) along with prophylactic pyridoxine. Suspecting isoniazid-induced neuropathy, her pyridoxine dose was increased to a therapeutic level (100&#xa0;mg). However, her symptoms continued to worsen despite the higher dose. Further evaluation revealed pyridoxine toxicity as the underlying cause of her neuropathy. Her condition gradually improved after discontinuation of pyridoxine. This case highlights the need for individualized dosing and careful monitoring of pyridoxine therapy, particularly in patients with renal impairment. In individuals with CKD, altered drug metabolism can result in accumulation and toxicity, even at standard prophylactic or therapeutic doses. Early identification and appropriate management are crucial to prevent long-term neurological complications.</p>

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When the Cure Hurts: Pyridoxine Induced Neuropathy in A Patient Treated for Tuberculosis—A Case Report

  • 期刊论文

  • 发表日期：

    2025年6月17日

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  • Neeraj Sharma,
  • Robin Chaudhary,
  • Vivek Sharda,
  • Vignesh Jayprakash

摘要

Isoniazid, a widely used anti-tuberculous drug, is known to cause peripheral neuropathy as a side effect. To mitigate this risk, pyridoxine is commonly administered as a preventive measure, particularly in individuals at higher risk, such as those with HIV infection, chronic alcohol use, or chronic kidney disease (CKD). We report the case of a 39-year-old female with chronic kidney disease and tuberculous lymphadenitis who developed peripheral neuropathy while receiving anti-tuberculous therapy (ATT) along with prophylactic pyridoxine. Suspecting isoniazid-induced neuropathy, her pyridoxine dose was increased to a therapeutic level (100 mg). However, her symptoms continued to worsen despite the higher dose. Further evaluation revealed pyridoxine toxicity as the underlying cause of her neuropathy. Her condition gradually improved after discontinuation of pyridoxine. This case highlights the need for individualized dosing and careful monitoring of pyridoxine therapy, particularly in patients with renal impairment. In individuals with CKD, altered drug metabolism can result in accumulation and toxicity, even at standard prophylactic or therapeutic doses. Early identification and appropriate management are crucial to prevent long-term neurological complications.