Isoniazid
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Isoniazid Hepatotoxicity and motor-sensory axonal neuropathy: 3 case reports
A case series described 3 men aged 18–32 years, who developed hepatotoxicity or motor-sensory axonal neuropathy, while receiving isoniazid for tuberculosis [routes and dosages not stated]. Case 1: The 23-year-old man presented with symptoms of fever and dry cough for 2 weeks. Based on findings of tuberculosis, he started receiving unspecified anti-tubercular therapy regimen, containing isoniazid. After 3 months, he presented with weakness and sensory disturbance of both lower extremities. Further investigations suggested generalised (lower limb>upper limb), fairly, symmetric, severe sensory-motor, mixed axonal demyelinating type of peripheral neuropathy. He was noted to have a heterozygous mutation of NAT2*6 gene, indicative of reduced enzyme activity. He then started receiving isoniazid 225mg (dose was redcued) along with rifampicin, ethambutol and pyridoxine. Over the following 6–8 months, his neurological signs and symptoms improved gradually. Case 2: The 32-year-old man presented with prolonged symptoms of mild fever and cough for 3 weeks. He had been receiving concomitant insulin therapy. He was diagnosed with tubercular pleural effusion. Subsequently, he started receiving unspecified anti-tubercular therapy regimen, containing isoniazid tablet. After 1 month, he developed generalised weakness of bilateral lower limbs. Clinical examination and nerve conduction studies suggested bilateral lower limb axonal sensory-motor neuropathy. He was noted to have NAT2 gene mutation, possessing compound heterozygous gene mutation for both NAT2*5 (CT) and NAT2*6 (GA) genes, indicative of reduced enzyme activity. Isoniazid was discontinued, and he stared receiving pyridoxine. Over the following 2 months, the symptoms of lower limb weakness reduced. Case 3: The 18-year-old man, who was recently diagnosed to be HIV, started receiving unspecified anti-retroviral therapy. After 3 months, he presented with fever for more than 20 days, not responding to any treatment [specific drugs not stated]. He developed tuberculosis. Subsequently, he started receiving anti-tubercular therapy regimen containing isoniazid. Eventually, his fever subsided. Two months following the initiation of anti-tubercular therapy, he presented with persistent fatigue, abdominal pain, icterus and loss of appetite. His serum glutamic pyruvic transaminase (SGPT) and serum glutamic oxaloacetic transaminase (SGOT) values were found to be more than 2 times the normal values. He was noted to have a homozygous mutation with NAT2*6 gene, indicative of reduced enzyme activity. Isoniazid was withdrawn. Within 3 weeks, liver function improved. Shetty P, et al. A case series of three patients presenting with isoniazid induced toxicity and N-acetyl transferase 2 gene mutation: A management conundrum for programmatic therapy of tuberculosis in India. Indian Journal of Tuberculosis 67: 407-410, No. 3, Jul 2020. Available from: URL: http://doi.org/10.1016/ j.ijtb.2020.01.005
0114-9954/20/1825
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