Acute isoniazid intoxication: an uncommon cause of convulsion, coma and acidosis

Uzman, Sinan; Yanaral, Tümay Uludağ; Toptaş, Mehmet; Koç, Alparslan; Taş, Aytül; Bican, Gülşen

doi:10.5578/tt.1897

Cited by 11 publications

(12 citation statements)

References 11 publications

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“…Lactic acidosis can result from both lack and accumulation of certain substances. The former type is typically seen in thiamine and pyridoxine deficiency [19, 20]. The latter type can occur in severe ethanol and methanol intoxication, and in subjects treated with antiretroviral drugs, linezolid, or propofol.…”

Section: Lactic Acidosis Excluding Metforminmentioning

confidence: 99%

Etiology and Management of Acute Metabolic Acidosis: An Update

Matyukhin

Patschan

Ritter

et al. 2020

Kidney Blood Press Res

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Background: The etiology of acute metabolic acidosis (aMA) is heterogeneous, and the consequences are potentially life-threatening. The aim of this article was to summarize the causes and management of aMA from a clinician's perspective. Summary: We performed a systematic search on PubMed, applying the following search terms: "acute metabolic acidosis," "lactic acidosis," "metformin" AND "acidosis," "unbalanced solutions" AND "acidosis," "bicarbonate" AND "acidosis" AND "outcome," "acute metabolic acidosis" AND "management," and "acute metabolic acidosis" AND "renal replacement therapy (RRT)/dialysis." The literature search did not consider diabetic ketoacidosis at all. Lactic acidosis evolves from various conditions, either with or without systemic hypoxia. The incidence of metformin-associated aMA is actually quite low. Unbalanced electrolyte preparations can induce hyperchloremic aMA. The latter potentially worsens kidney-related outcome parameters. Nevertheless, prospective and controlled data are missing at the moment. Recently, bicarbonate has been shown to improve clinically relevant endpoints in the critically ill, even if higher pH values (> 7.3) are targeted. New therapeutics for aMA control are under development, since bicarbonate treatment can induce serious side effects. Key Messages: aMA is a frequent and potentially life-threatening complication of various conditions. Lactic acidosis might occur even in the absence of systemic hypoxia. The incidence of metformin-associated aMA is comparably low. Unbalanced electrolyte solutions induce hyperchloremic aMA, which most likely worsens the renal prognosis of critically ill patients. Bicarbonate, although potentially deleterious due to increased carbon dioxide production with subsequent intracellular acidosis, improves kidneyrelated endpoints in the critically ill.

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Section: Lactic Acidosis Excluding Metforminmentioning

confidence: 99%

Etiology and Management of Acute Metabolic Acidosis: An Update

Matyukhin

Patschan

Ritter

et al. 2020

Kidney Blood Press Res

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“…The major sign of SE in patients with isoniazid poisoning is repeated convulsions, which often leads to the formation of toxic substances that damage the brain cells. Although isoniazidinduced seizure is known to respond poorly to currently available anticonvulsant drugs, intravenous diazepam is still used to control the seizure episodes in the absence of pyridoxine [4,5,6,7]. On this basis, diazepam and pyridoxine, serving as reference drugs, were compared with the current study test substance.…”

Section: Introductionmentioning

confidence: 99%

“…On this basis, diazepam and pyridoxine, serving as reference drugs, were compared with the current study test substance. However, pyridoxine is reported as the only effective antidote for isoniazid toxicity and should be given in doses equivalent to the amounts of the ingested isoniazid in order to be effective [5,6,7].…”

Section: Introductionmentioning

confidence: 99%

Antioxidant and Anticonvulsant Effect of Dennettia Tripetala on Rat Model of Isoniazid-induced Seizure

Finbarrs-Bello

Ozor

Ojuolape

et al. 2019

EJMP

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Aims:This study aimed at investigating the antioxidative, anticonvulsive and histological effects of ethanolic fruit extract of Dennettia tripetala on the pre-frontal lobe of the brain in isoniazid-induced (300 mg/kg, i.p) seizure in adult wistar rat. Introduction: Neuronal hyper-excitability and excessive production of free radicals have been implicated in the pathogenesis of a considerable range of neurological disorders, including epilepsy. The high rate of oxidative metabolism, coupled with the low antioxidant defenses and the richness in polyunsaturated fatty acids, makes the brain highly vulnerable to free radical damage. Study Design: This is an original research conducted in Finbarrs-Bello et al.; EJMP, 30(2): 1-10, 2019; Article no.EJMP.52261 2 Methodology: A total number of twenty four wistar rats were used for this experiment, the animals were grouped into six groups with four animals per group, Group I served as the negative control, Group II served as the positive control, Group III received the standard drug as well as the Isoniazid, while group IV, V and VI were treated with ethanolic extract of Dennettia tripetala at different dosages; 250 mg/kg, 500 mg/kg and 750 mg/kg, intraperitoneally (i.p) respectively and its effects compared with a standard drug (Pyridoxine) treated group. Results: The extract significantly prolonged the onset of seizure at high dose administration (750 mg/kg) but completely prevented seizure occurrence at low and medium dose administration (250 mg/kg and 500 mg/kg, i.p) when induced with isoniazid (300 mg/kg, i.p.). Conclusion: The results obtained from this work suggest that ethanolic extract of Dennettia tripetala has anticonvulsant activity, and this supports the use of the formulation traditionally in the treatment of convulsions, thus should be considered for clinical trials. Original Research Article

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“…Isoniazid, an anti-tuberculosis drug, induces SE by depleting brain level of Gamma-Aminobutyric Acid (GABA), a major inhibitory transmitter substance in the mammalian brain, through inhibition of pyridoxal-5-phosphate-dependent Glutamic Acid Decarboxylase (GAD) (Corda, Costa, & Guidtti, 1982; Uzman et al, 2013). Pyridoxal-5-phosphate is the active form of pyridoxine, a cofactor for GAD, and an enzyme required for GABA synthesis (Bassin et al, 2002; Brophy et al, 2012; Meierkord et al, 2010; Corda et al, 1982; Uzman et al, 2013). The decrease in GABA levels results in recurrent seizures that characterized SE (Corda et al, 1982; Uzman et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

“…Pyridoxal-5-phosphate is the active form of pyridoxine, a cofactor for GAD, and an enzyme required for GABA synthesis (Bassin et al, 2002; Brophy et al, 2012; Meierkord et al, 2010; Corda et al, 1982; Uzman et al, 2013). The decrease in GABA levels results in recurrent seizures that characterized SE (Corda et al, 1982; Uzman et al, 2013). Although isoniazid-induced seizure is known to respond poorly to currently available anticonvulsant drugs, intravenous diazepam is still used to control the seizure episodes in the absence of pyridoxine (Corda et al, 1982; Uzman et al, 2013; Tajender & Saluja, 2006; Romero & Kuczler, 1998).…”

Section: Introductionmentioning

confidence: 99%

Effects of Jobelyn® on Isoniazid-Induced Seizures, Biomarkers of Oxidative Stress and Glutamate Decarboxylase Activity in Mice

Asehinde

Ajayi

Bakre

et al. 2018

Basic Clin. Neurosci. J.

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Introduction:Isoniazid-induced seizure, often described as Status Epilepticus (SE), is an emergency condition characterized by repeated convulsive episodes that responds poorly to the currently available anticonvulsant drugs. The current study aimed at ascertaining the effect of Jobelyn® (JB), an African dietary supplement, on seizures, altered oxidative stress, and glutamate decarboxylase activity induced by isoniazid in mice.Methods:A total of 6 mice received JB (10–50 mg/kg, PO), pyridoxine (300 mg/kg), diazepam (5 mg/kg), or distilled water (10 mL/kg) 30 minutes prior to the induction of SE with injection of isoniazid (300 mg/kg, IP). Thereafter, the mice were observed for the onset of convulsions for a period of two hours. Moreover, the effect of JB on Glutamate Decarboxylase (GAD) activity and biomarkers of oxidative stress (glutathione and malondialdehyde) was also evaluated in the brain homogenates of another set of isoniazid-treated mice.Results:JB (50 mg/kg, PO) prolonged the latency to convulsions, but could not prevent the occurrence of seizure episodes caused by isoniazid. Moreover, JB neither showed any protection against death nor delayed the latency to death caused by isoniazid. However, this dose of JB positively modulated the concentrations of malondialdehyde and glutathione in the brains of mice treated with isoniazid. The activity of GAD, the enzyme responsible for GABA synthesis, increased by JB, which suggested enhanced GABAergic neurotransmission.Conclusion:The current study findings suggest that JB prolongs the latency to convulsions, enhances GABAergic neurotransmission, and demonstrates anti-oxidative effect in isoniazid-treated mice.

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Acute isoniazid intoxication: an uncommon cause of convulsion, coma and acidosis

Abstract: ÖZET Akut izoniazid intoksikasyonu: konvülziyon, koma ve asidozun nadir bir nedeni

Cited by 11 publications

References 11 publications

Etiology and Management of Acute Metabolic Acidosis: An Update

Etiology and Management of Acute Metabolic Acidosis: An Update

Antioxidant and Anticonvulsant Effect of Dennettia Tripetala on Rat Model of Isoniazid-induced Seizure

Effects of Jobelyn® on Isoniazid-Induced Seizures, Biomarkers of Oxidative Stress and Glutamate Decarboxylase Activity in Mice

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