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

Constantinescu, Stefan Matei; Buysschaert, Benoît; Haufroid, Vincent; Broly, Franck; Jadoul, Michel; Morelle, Johann

doi:10.1186/s12882-017-0703-6

Cited by 8 publications

(12 citation statements)

References 10 publications

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“…3 Patients on dialysis and in those with a slow acetylator phenotype conferred by NAT2 polymorphisms are at increased risk of INH encephalopathy. 4 In our 1 st case the patient developed encephalopathy 7 days after initiation of INH. In Case 1c (Table-I) encephalopathy developed after 2 months of INH therapy.…”

Section: Discussionmentioning

confidence: 55%

Drug Induced Encephalopathy in Patients with Chronic Kidney Disease: A Case Series

et al. 2018

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Drug induced encephalopathy is an established side effect of many drugs when used in a higher dose. Though we do not encounter this side effect frequently in our day to day practice, yet with renal impairment this is not uncommon. Even with a reduced dose many of these can precipitate encephalopathy in this special group of patients. We are presenting here a series of seven such cases of drug induced encephalopathy in patients with renal impairment.Birdem Med J 2018; 8(2): 172-176

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Section: Discussionmentioning

confidence: 55%

Drug Induced Encephalopathy in Patients with Chronic Kidney Disease: A Case Series

et al. 2018

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“…Isoniazid-associated hepatotoxicity is the most frequent and its mechanisms are fairly well known, having been the subject of numerous studies [9]- [13]. Despite its hepatotoxicity, isoniazid is still widely used because it is inexpensive and has potent anti-mycobacterial activity [14].…”

Section: Toxicities Of Anti-tuberculosis Drugsmentioning

confidence: 99%

“…Renal failure is also a risk factor for isoniazid-induced hepatotoxicity [14]. In addition, other toxicities linked to the existence of a co-morbidity can also occur during the antituberculous treatment associating isoniazid.…”

Section: Polymorphisms Of Nat2 (N-acetyltransferase Type 2)mentioning

confidence: 99%

“…In addition, other toxicities linked to the existence of a co-morbidity can also occur during the antituberculous treatment associating isoniazid. Thus, a severe case of encephalopathy was reported in a 71-year-old patient of African origin after being put on anti-tuberculosis treatment [14].…”

Section: Polymorphisms Of Nat2 (N-acetyltransferase Type 2)mentioning

confidence: 99%

“…In hemodialysis patients and carriers of the slow isoniazid acetylator pheno-type, a reduction in the dosage of isoniazid associated with an increase in the doses supplemented with Vitamin B6 or Pyridoxine (>100 mg/day instead of 10 -25 mg/day) reduce the occurrence of hepatotoxicity, encephalopathy and neuropathy [14].…”

Section: Polymorphisms Of Nat2 (N-acetyltransferase Type 2)mentioning

confidence: 99%

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Genetic Polymorphisms and Toxicities of First-Line Antituberculosis Drugs: Systematic Review of the Literature

Sanni¹,

Sina²,

Baba-Moussa³

2022

JTR

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Introduction: Polymorphisms are the main genetic factors associated with toxicities of antituberculosis drugs. This literature review summarizes the polymorphisms of the genes that code for the enzymes of the metabolism of antituberculosis drugs and their transmembrane transporters. Some mechanisms of drug-associated toxicities and strategies for their management have also been described in this review. Methods: The bibliographic searches were exclusively carried out in PubMed, over a period of ten years (2010-2020). The search terms were the words "toxicity + antituberculosis drug + one or two word(s) among the following: polymorphism, genetics, mutation, SNP, HLA or haplotype". Publications in English or French, relating to the various toxicities associated with first-line anti-tuberculosis drugs (Rifampicin, Isoniazid, Ethambutol and Pyrazinamide) administered to patients with pulmonary tuberculosis, extrapulmonary tuberculosis or co-infected with TB/HIV were included in this review. Duplicates, in vitro, in silico or drug-induced toxicity studies other than antituberculosis drugs and genetic mutations of Mycobacteria strains were not included. Results: The studies selected and included were case reports, cohort studies, original research, systematic reviews and meta-analyses on human subjects of different ethnic origins. Hepatotoxicity is the most common toxicity associated with NAT2, CYP2E1, GSTM1 and GSTT1 polymorphisms in patients on antituberculosis drugs. Other forms of toxicity, less frequent, occurring in certain patients under concomitant treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), antiretrovirals (ARVs), antibiotics or antiepileptics have also been identified. Conclusion: The genetic polymorphisms associated with the toxicities of antituberculosis drugs concern both the main enzymes of the metabolic pathways (NAT2, CYP2E1, GST) and the transmembrane transporters (SLCO1B1 and ABCB1).

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Extracorporeal treatments for isoniazid poisoning: Systematic review and recommendations from the EXTRIP workgroup

et al. 2021

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Isoniazid toxicity from self‐poisoning or dosing errors remains common in regions of the world where tuberculosis is prevalent. Although the treatment of isoniazid poisoning is centered on supportive care and pyridoxine administration, extracorporeal treatments (ECTRs), such as hemodialysis, have been advocated to enhance elimination of isoniazid. No systematic reviews or evidence‐based recommendations currently exist on the benefit of ECTRs for isoniazid poisoning. The Extracorporeal Treatments in Poisoning (EXTRIP) workgroup systematically collected and rated the available evidence on the effect of and indications for ECTRs in cases of isoniazid poisoning. We conducted a systematic review of the literature, screened studies, extracted data on study characteristics, outcomes, and measurement characteristics, summarized findings, and formulated recommendations following published EXTRIP methods. Forty‐three studies (two animal studies, 34 patient reports or patient series, and seven pharmacokinetic studies) met inclusion criteria. Toxicokinetic or pharmacokinetic analysis was available for 60 patients, most treated with hemodialysis (n = 38). The workgroup assessed isoniazid as “Moderately Dialyzable” by hemodialysis for patients with normal kidney function (quality of evidence = C) and “Dialyzable” by hemodialysis for patients with impaired kidney function (quality of evidence = A). Clinical data for ECTR in isoniazid poisoning were available for 40 patients. Mortality of the cohort was 12.5%. Historical controls who received modern standard care including appropriately dosed pyridoxine generally had excellent outcomes. No benefit could be extrapolated from ECTR, although there was evidence of added costs and harms related to the double lumen catheter insertion, the extracorporeal procedure itself, and the extracorporeal removal of pyridoxine. The EXTRIP workgroup suggests against performing ECTR in addition to standard care (weak recommendation, very low quality of evidence) in patients with isoniazid poisoning. If standard dose pyridoxine cannot be administered, we suggest performing ECTR only in patients with seizures refractory to GABAA receptor agonists (weak recommendation, very low quality of evidence).

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

Cited by 8 publications

References 10 publications

Drug Induced Encephalopathy in Patients with Chronic Kidney Disease: A Case Series

Drug Induced Encephalopathy in Patients with Chronic Kidney Disease: A Case Series

Genetic Polymorphisms and Toxicities of First-Line Antituberculosis Drugs: Systematic Review of the Literature

Extracorporeal treatments for isoniazid poisoning: Systematic review and recommendations from the EXTRIP workgroup

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