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Pyridoxine in Clinical Toxicology: a Review Philippe Lheureux, Andrea Penaloza and Mireille Gris

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Pyridoxine in Clinical Toxicology: a Review Philippe Lheureux, Andrea Penaloza and Mireille Gris 78 Review Pyridoxine in clinical toxicology: a review Philippe Lheureux, Andrea Penaloza and Mireille Gris Pyridoxine (vitamin B6) is a co-factor in many enzymatic controversial. This paper reviews the various indications pathways involved in amino acid metabolism: the main of pyridoxine in clinical toxicology and the supporting biologically active form is pyridoxal 5-phosphate. literature. The potential adverse effects of excessive Pyridoxine has been used as an antidote in acute pyridoxine dosage will also be summarized. intoxications, including isoniazid overdose, Gyromitra European Journal of Emergency Medicine 12:78–85 mushroom or false morrel (monomethylhydrazine) c 2005 Lippincott Williams & Wilkins. poisoning and hydrazine exposure. It is also recommended as a co-factor to improve the conversion of glyoxylic acid European Journal of Emergency Medicine 2005, 12:78–85 into glycine in ethylene glycol poisoning. Other indications Keywords: Antidotes, crimidin, drug-induced neuropathy, ethylene glycol, are recommended by some sources (for example crimidine hydrazine, isoniazid, metadoxine, pyridoxine poisoning, zipeprol and theophylline-induced seizures, adjunct to d-penicillamine chelation), without significant Department of Emergency Medicine, Erasme University Hospital, Brussels, Belgium. supporting data. The value of pyridoxine or its congener Correspondence to Philippe Lheureux, Department of Emergency Medicine, metadoxine as an agent for hastening ethanol metabolism Erasme University Hospital, 808 route de Lennik, 1070 Brussels, Belgium. or improving vigilance in acute alcohol intoxication is E-mail: [email protected] Introduction ing. More controversial issues include alcohol intoxication Pyridoxine or vitamin B6 is a highly water-soluble and zipeprol or theophylline-induced seizures. vitamin. Its main biologically active form is a phosphate ester of its aldehyde form, pyridoxal 5-phosphate (P5P). The purpose of this paper is to review the literature It plays a major role in many biological pathways, allowing supporting these indications as well. the proper functioning of over 60 enzymes, especially involved in amino acid metabolism including decarbox- Isoniazid overdose ylation, desamination, transamination and transsulphura- Isoniazid has been used as a first-line agent for the tion. Examples are the metabolism of tryptophan to prophylaxis and treatment of tuberculosis since 1952. It niacin, methionine to cysteine and glutamic acid to undergoes nearly complete gastrointestinal absorption, is gamma-aminobutyric acid (GABA). The normal adult poorly protein bound ( < 10%), and has a short elimina- needs (1–2 mg/day) are usually fully provided by nutri- tion half-life (0.7 h or 2–4 h in rapid or slow acetylators, tional sources, especially meats and vegetables, but respectively); 75–95% of the ingested dose is eliminated requirements are increased during pregnancy. In addition, as metabolites in urine within 24 h [1]. some individuals are likely to suffer pyridoxine deficiency, including malnourished patients, those with HIV infec- Acute life-threatening toxicity may develop rapidly tion, alcoholism, or diabetes, or those taking drugs or (30–45 min after ingestion), but is usually short lived exposed to substances that promote pyridoxine depletion (less than 24 h). Although acute ingestions of 20 mg/kg (isoniazide, cycloserine, hydralazine, phenelzine, penicil- (approximately 1.5 g in adults) usually result in only mild lamine, theophylline, carbon disulphidey). toxicity, ingestions greater than 30 mg/kg may produce generalized tonic–clonic seizures [2]. Higher doses Pyridoxine hydrochloride is available as an antidote, in ( > 80 mg/kg, 10–15 g in adults) are responsible for the form of ampoules (commonly 100 mg/2 ml and 200 or recurrent seizures, lactic acidosis and coma, the classical 250 mg/5 ml) or vials (1 g/10 ml) for parenteral use, triad of INH poisoning that may result in death if not usually intravenously. It is sensitive to light and alkali; properly managed [3,4]. The prognosis is, however, good it must be stored in the dark and should never be mixed when the adequate treatment is instituted early [1,2,5,6]. with sodium bicarbonate. INH intoxications from long-term over-ingestions (1200 mg a day for 6 weeks) resulting in encephalopathy Commonly recommended indications include isoniazid and coma have also been reported [7]. (or isonicotinic acid hydrazide; INH) overdose, Gyromitra mushroom (false morel) poisoning (monomethylhydra- Central nervous system (CNS) hyperexcitability mainly zine or monomethylhydrazine syndrome), hydrazine revolves around the effect of INH on pyridoxine meta- exposure, crimidine poisoning or ethylene glycol poison- bolism Three additive mechanisms are involved. The first 0969-9546 c 2005 Lippincott Williams & Wilkins Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Pyridoxine in clinical toxicology Lheureux et al. 79 Fig. 1 Fig. 2 (a) Dehydrazination Isoniazid hydrazones Ethylene glycol 2 Inhibition Isoniazid (INH) alcohol deshydrogenase Acetylation Glycoaldehyde and hydrolysis Pyridoxine aldehyde deshydrogenase Hydrazines Pyridoxine and phosphokinase Hydrazides Glycolic acid Pyridoxal lactate deshdrogenase and inactivates 5-phosphate glycolic acid oxidase Pyridoxine Thiamine Complexation Glyoxylic acid with Pyridoxine Isonicotinyl 1 P5P hydrazide Glycine Oxalic acid Formic acid α-hydroxy-β-ketoadipic ac. Urinary elimination Metabolism of ethylene-glycol: effect of pyridoxine. The main pathways of ethylene glycol metabolism. Supplementation with pyridoxine and (b) Glutamine Glutamic acid thiamine may be of theoretical benefit by shunting the conversion of glyoxylate to the less toxic metabolites glycine and alpha-hydroxy-beta- NH3 ketoadipic acid, respectively, rather than to oxalate and formate. GAD Pyridoxal 5- phosphate Inhibition by INH hydrazones 3 seizures in animal models, whereas combinations of these anticonvulsants and pyridoxine are effective (synergistic CO2 effect) [8]. Pyridoxine reduces the severity of seizures and prevents the mortality caused by a lethal dose of INH in dogs [8]. Such an efficacy was, however, not observed in rats [9]. Gamma aminobutyric acid (GABA) Clinical experience reported in humans with INH overdose is likely to be biased because it mainly consists Mechanism of isonicotinic acid hydrazide-induced central nervous of isolated case reports or short uncontrolled series system hyperexcitability (a and b). See text for details. CO2, carbon dioxide; GAD, glutamic acid decarboxylase; INH, isonicotinic acid showing favourable results, including rapid seizure hydrazide; P5P, pyridoxal 5-phosphate. control and no fatalities [10–12]. The ratio of grams of pyridoxine administered to grams of INH ingested is highly variable, ranging from 0.14 to 1.3. However, most patients received approximately a gram-for-gram amount is a pyridoxine depletion (Figure 1a; step 1): it is mainly of pyridoxine, as this ratio is commonly recommended on caused by the combination of P5P (not excreted in urine) an empirical or theoretical basis. Variable results in the with INH to form isonicotinilhydrazide, a compound control of seizures sometimes occurred in children when easily excreted in urine [2,7]. The second mechanism relatively smaller doses of pyridoxine were used. If consists of a decrease of pyridoxine activation in P5P by pyridoxine fails to control the seizures, the addition of the inhibition of pyridoxal phosphokinase (PPK) by diazepam seems to be more effective than other anti- hydrazone derivatives (Figure 1a; step 2). Finally, the convulsants such as phenytoin or barbiturates [13]. P5P depletion decreases the GABA synthesis from Thiopenthal was also used in a patient who failed to glutamic acid because P5P is an essential co-factor of respond to 12 g pyridoxine [14]. glutamic acid decarboxylase (GAD) (Figure 1b; step 3). Isoniazid hydrazones also inactivate P5P directly. The In a retrospective series by Wason et al. [15], the clinical lack of GABA and the accumulation of glutamic acid are course of five patients who received a gram-to-gram dose the presumed aetiology for CNS excitation and seizures. of pyridoxine was compared with the evolution of 41 patients in the literature who received lower doses or no The usual anticonvulsants such as phenobarbital, pheny- pyridoxine at all. In that study, pyridoxine appeared not toin or diazepam do not prevent or correct INH-induced only to be effective in treating INH-induced seizures, Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 80 European Journal of Emergency Medicine 2005, Vol 12 No 2 but also the changes in mental status, suggesting that including intubation and respiratory support, as needed. pyridoxine deficiency also plays a role in the impairment Haemodialysis is highly efficient in removing INH of consciousness. However, the dose required to allow because of its small distribution volume and its low awakening may be higher than that required to control protein binding. However, the short half-life of INH seizures [15–17]. Brent et al. [16] have reported three often makes active elimination unnecessary. Although the cases of obtundation secondary to INH overdose: in use of haemodialysis may be considered in patients who two cases, status seizures were stopped by intravenous fail to respond to supportive and antidotal therapy, pyridoxine, but the patients remained comatose for and those with very high
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