Isoniazid-Induced Encephalopathy

Adams, Philip C.; White, Charles A.

doi:10.1016/s0140-6736(65)91833-7

Cited by 21 publications

(3 citation statements)

References 6 publications

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“…As there were no signs of the many other causes of optic neuropathy [11,19], we believe that the progressive optic atrophy in the reported patient was due to the neurotoxic effects of Ethambutol and/or INH. The occurrence of an encephalopathy induced by INH has been reported [1,5,6]. The occurrence of an encephalopathy induced by INH has been reported [1,5,6].…”

Section: Discussionmentioning

confidence: 99%

Neurotoxicity of antituberculous drugs in a patient without active tuberculosis

Leppert

Waespe

1988

Ital J Neuro Sci

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A 56-year old patient presented 3 months after initiation of an antituberculous regimen with Isoniacid (INH, 5 mg/kg daily), Ethambutol (20 mg/kg daily) and Rifampicin (675 mg daily) a mild sensory polyneuropathy and a bilateral retrobulbar neuritis which progressed to a severe optic atrophy. Multiple hyperintense foci were detected with NMR-imaging in the cerebral white matter suggestive of demyelination. INH and Ethambutol are known for their neurotoxic effects but suggestion was made that neurologic signs may not be due to drug neurotoxicity but could be induced by immunological processes initiated by the tubercle bacillus. In the reported patient the suspected tuberculosis of the urogenital tract was never proved histologically. Most likely his neurological symptoms were therefore cause by the administration of INH and Ethambutol. Patients with a low serum zinc level and a slow acetylation of INH are reported to be at special risk; both factors were present in our patient.

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Section: Discussionmentioning

confidence: 99%

Neurotoxicity of antituberculous drugs in a patient without active tuberculosis

Leppert

Waespe

1988

Ital J Neuro Sci

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“…However, isoniazid may lead to serious adverse events, including hepatotoxicity, peripheral neuropathy and encephalopathy, especially in populations at risk [ 2 ]. The following case illustrates the impact of end-stage renal disease and NAT2 polymorphisms on the risk of isoniazid toxicity, and discusses how these life-threatening complications may be prevented and managed.…”

Section: Introductionmentioning

confidence: 99%

Chronic dialysis, NAT2 polymorphisms, and the risk of isoniazid-induced encephalopathy – case report and literature review

et al. 2017

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Background: Isoniazid is the most widely used anti-tuberculosis agent, yet it may lead to life-threatening complications. Case presentation: Here we report the case of a chronic hemodialysis patient who developed severe encephalopathy after the start of isoniazid. Blood levels of isoniazid were elevated, and acetyl-isoniazid over isoniazid ratio was decreased 3 h after intake of the medication, suggesting that a slow acetylator phenotype may have contributed to drug toxicity, in addition to pyridoxal phosphate removal by dialysis. This hypothesis was confirmed by sequencing of NAT2, the gene responsible for isoniazid elimination, and identification of NAT2 polymorphisms compatible with a slow acetylator phenotype. Isoniazid withdrawal along with supplementation using high doses of pyridoxine successfully reversed the drug toxicity. Isoniazid toxicity occurs in populations at risk, including patients with chronic kidney failure or NAT2 polymorphisms, who have a disturbed metabolism of pyridoxine or isoniazid, respectively, and those on renal replacement therapies, in whom pyridoxal phosphate -the active metabolite of pyridoxine -is inadvertently removed by dialysis. Conclusions: Physicians should be aware of the increased risk of isoniazid toxicity in patients on dialysis and in those with a slow acetylator phenotype conferred by NAT2 polymorphisms. Adaptation of prescription -either with higher doses of pyridoxine or decreased doses of isoniazid, respectively -has been suggested to reduce the risk of potentially life-threatening toxicity of isoniazid.

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“…Hepatotoxicity is a common complication of Isonicotinic Acid Hydrazide (INH) or Isoniazid (an anti-tuberculosis drug), a condition that may lead to hepatic failure and subsequently hepatic encephalopathy requiring liver transplantation [2]. The existing body of literature reveals that drug-induced encephalopathies are important pharmacological side effects which occur seldom in clinical practice [3] and Isoniazid-induced encephalopathy is one of them [4]. INH hepatotoxicity presents a difficult management challenge and is associated with a high risk of mortality.…”

Section: Introductionmentioning

confidence: 99%

Isoniazid Preventive Therapy Associated Hepatotoxicity among Children Living with HIV: Descriptive Case Series at Mildmay Uganda HIV/AIDS Clinic, Uganda

Nsobya¹,

Nsobya²,

Nakaweesi³

et al. 2015

IJCM

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Provision of Isoniazid Preventive Therapy (IPT) as part of the comprehensive TB/HIV prevention intervention for people living with HIV & AIDS was recommended by WHO in 2011. Literature shows that Isoniazid (INH) associated hepatotoxicity is a common drug adverse event among people taking INH, and that it's associated with a high risk of mortality. These case series document INH associated hepatotoxicity in HIV-infected children receiving IPT in a resource constrained setting. They also further describe the challenges and lessons learnt while providing routine IPT among HIV-infected children in a resource-limited setting where laboratory tests for liver function monitoring are not performed routinely. The case series describe observed cases which presented to the Mildmay Uganda HIV/AIDS clinic between December 2013 and March 2014. The findings demonstrate that: 1) there was a 1.5% INH related hepatotoxicity incidence among children of four to ten years old; 2) 20% death rate-one out of the five children died and; 3) hepatotoxicity events on average occurred at 10.8 weeks after INH initiation while at the same time, all the cases had liver enzymes elevated above 10 times the upper normal limit values and reported late for medical intervention. The insidious onset of symptoms and signs of INH related hepatotoxicity coupled with lack of adequate resources needed to manage the condition were the major challenges to provision of routine IPT among children living with HIV in resource-limited settings in sub-Sahara Africa. Clinical vigilance, continuous education of clients and caretakers about the * Corresponding author. L. Nsobya et al. 385 side effects or adverse events of INH and routine laboratory examination of liver function tests during follow-up of IPT in HIV-infected children are recommended to enhance early detection and prompt management of IPT associated hepatotoxicity.

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Isoniazid-Induced Encephalopathy

Cited by 21 publications

References 6 publications

Neurotoxicity of antituberculous drugs in a patient without active tuberculosis

Neurotoxicity of antituberculous drugs in a patient without active tuberculosis

Chronic dialysis, NAT2 polymorphisms, and the risk of isoniazid-induced encephalopathy – case report and literature review

Isoniazid Preventive Therapy Associated Hepatotoxicity among Children Living with HIV: Descriptive Case Series at Mildmay Uganda HIV/AIDS Clinic, Uganda

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