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At least 19 recordsLinked to original sources
PubMed2000

Toxicokinetics of ethylene glycol during fomepizole therapy: implications for management. For the Methylpyrazole for Toxic Alcohols Study Group.

STUDY OBJECTIVE: The elimination kinetics of ethylene glycol (EG) in human subjects treated with fomepizole (4-methylpyrazole) were analyzed to establish the efficacy of alcohol dehydrogenase (ADH) inhibition and to characterize elimination pathways. METHODS: Drug concentration data from patients enrolled in the EG arm of the Methylpyrazole for Toxic Alcohols trial, a prospective, multicenter, open-label trial of fomepizole, were analyzed and compared with published estimates. RESULTS: In 19 patients analyzed (EG concentrations of 3.5 to 211 mg/dL), elimination was first order during fomepizole monotherapy (half-life of 19.7+/-1.3 hours) and was not affected by the presence of ethanol. The elimination rate was significantly faster (half-life of <8.6+/-1.1 hours, P <.001) in the absence of fomepizole and ethanol. EG elimination by the kidneys was directly proportional to remaining renal function as estimated by creatinine clearance, with a fractional excretion of 25.5%+/-9.4%. Renal elimination and hemodialysis were the only significant routes of EG elimination as long as fomepizole concentrations were maintained well above 10 micromol/L (EG/fomepizole molar ratio, <100:1). All patients with normal serum creatinine concentrations at the initiation of fomepizole treatment had rapid rates of renal elimination (half-life of 16.8+/-0.8 hours). CONCLUSION: At doses used, fomepizole effectively inhibits ADH-mediated metabolism of EG. Serum creatinine concentration at presentation and creatinine clearance can be used to predict EG elimination during fomepizole therapy and can help determine which patients will require hemodialysis to expedite EG elimination. An absolute EG concentration above 50 mg/dL should no longer be used as an independent criterion for hemodialysis in patients treated with fomepizole.

Adolescent↗
PubMed2002

Role of fomepizole in the management of ethylene glycol toxicity.

OBJECTIVE: To systematically review English-language articles on fomepizole administration in patients with ethylene glycol poisoning. DATA SOURCES: MEDLINE, EMBASE, Current Contents, and PubMed. Search terms were fomepizole, 4-methylpyrazole, and ethylene glycol. The search was supplemented with a bibliographic review of all relevant articles. STUDY SELECTION: All published reports of fomepizole administration in patients with ethylene glycol poisoning were reviewed, irrespective of study design. We identified one clinical trial and subsequent pharmacokinetic study, one case series, and 13 case reports. RESULTS: Fomepizole has been investigated in 70 patients in open, unblinded studies. Most patients received an intravenous loading dose, with subsequent variable maintenance doses every 12 hours until plasma ethylene glycol levels became undetectable. Additional hemodialysis treatment generally was administered when patients had renal insufficiency or ethylene glycol levels above 50 mg/dl. Many patients had detectable ethanol levels either because of coadministration or as a result of adjunctive treatment at a referring center. Poorer patient outcomes, such as death and renal insufficiency, were associated with later clinical presentation time after ingestion. At therapeutic fomepizole levels (> 8.6 mg/ml), the half-life of ethylene glycol was prolonged to over 19 hours. Fomepizole appeared to be well tolerated by most patients. CONCLUSION: Fomepizole is an effective alcohol dehydrogenase inhibitor that decreases production of ethylene glycol metabolites. Reduced mortality and morbidity are undetermined because of the small number of patients evaluated to date. Data on comparative efficacy of fomepizole versus ethanol and data on administration of fomepizole in children are limited.

Alcohol Dehydrogenase↗
PubMed2000

Nystagmus secondary to fomepizole administration in a pediatric patient.

BACKGROUND: Fomepizole is an alcohol dehydrogenase inhibitor used to treat ethylene glycol poisoning in adults, with only one report describing the use of fomepizole in the pediatric population. We report a case of nystagmus associated with fomepizole treatment of a 6-year-old female who ingested ethylene glycol 15 hours prior to admission. CASE REPORT: A previously healthy 6-year-old presented to the emergency department mottled, comatose, and with Kussmaul respirations. Initial arterial blood gases: pH 7.11, PO2 200, HCO3 2, base excess -29, and within 20 minutes her pH dropped to 7.03. The patient was responsive to pain only. Initially, crystalluria without fluorescence was observed in the emergency department; 2 hours after admission, the urine fluoresced under Wood's light. Laboratory data were significant for increased anion and osmolar gaps. She was fluid-resuscitated, NaHCO3, thiamine, and pyridoxine were administered, and she was admitted to the pediatric intensive care unit. Within 4 hours of admission, a loading dose of fomepizole (15 mg/kg) was infused due to the severity of the patient's clinical status. Hemodialysis was initiated but discontinued temporarily due to catheter thrombus formation. The initial (3-hour postadmission) ethylene glycol concentration was 13 mg/dL. She developed coarse vertical nystagmus within 2 hours of fomepizole infusion. The ethylene glycol concentration was 5 mg/dL 3 hours after hemodialysis which then was discontinued. No further fomepizole was administered and the child recovered uneventfully. CONCLUSION: There was no evidence of the more frequently cited adverse events, such as headache, nausea, and dizziness. Fomepizole has been incompletely evaluated in the pediatric population, and the nature and occurrence of adverse events have not been described adequately. The use of fomepizole appeared safe in this patient although she developed transient nystagmus.

Antidotes↗
PubMed2001

Fomepizole (orphan medical).

Orphan Medical has developed fomepizole as a potential treatment for both ethylene glycol and methanol poisoning. The drug was launched as Antizol in January 1998 for the treatment of ethylene glycol poisoning [273949] after US marketing approval was grantedin December 1997 [271563]. It has also received US approval for methanol poisoning [393217] and UK approval for ethylene glycol poisoning [329495]. In 1999, Orphan Medical's partner, Cambridge Laboratories, intended to pursue European approval under the mutual recognition procedure [329495]. However, by September 2000, Cambridge Laboratories had discontinued their involvement with fomepizole and IDIS World Medicines had licensed the rights to distribute the drug in the UK [412142]. In February 2000, the Canadian Therapeutic Products Programme (TPP) granted fomepizole Priority Review, provided that an NDA was submitted by March 14, 2000 [354665]. In August 2000, the TPP accepted this NDA and set a target date for approval in the fourth quarter of 2000 [379474]. The TPP granted fomepizole a Notice of Compliance permitting the sale of fomepizole in Canada in December 2000. The company's marketing partner in Canada, Paladin Labs had launched fomepizole by January 2001 [396953]. In June 2000, Tucker Anthony Cleary Gull stated that the Orphan Drug status which Orphan Medical had obtained for fomepizole would provide marketing exclusivity through December 2004. The analysts also stated that fomepizole had accounted for 40% of Orphan Medical's revenue in financial year 1999, although +/- 30% of sales were estimated to be due to stockpiling [409606].

Journal Article↗
PubMed2001

Treatment of acute methanol poisoning with fomepizole.

OBJECTIVE: To assess the efficacy and safety of fomepizole, a competitive alcohol dehydrogenase inhibitor, in methanol poisoning and to test the hypothesis that fomepizole obviates the need for hemodialysis in selected patients. DESIGN AND SETTING: Retrospective clinical study in three intensive care units in university-affiliated teaching hospitals. PATIENTS: All methanol-poisoned patients admitted to these ICUs and treated with fomepizole from 1987-1999 (n=14). MEASUREMENTS AND RESULTS: The median plasma methanol concentration was 50 mg/dl (range 4-146), anion gap 22.1 mmol/l (11.8-42.2), arterial pH 7.34 (7.11-7.51), and bicarbonate 17.5 mmol/l (3.0-25.0). Patients received oral or intravenous fomepizole until blood methanol was undetectable. The median cumulative dose was 1250 mg (500-6000); the median number of twice daily doses was 2 (1-16). Four patients underwent hemodialysis for visual impairment present on admission. Four patients with plasma methanol concentrations of 50 mg/dl or higher and treated without hemodialysis recovered fully. Patients without pretreatment visual disturbances recovered, with no sequelae in any case. There were no deaths. Fomepizole was safe and well tolerated, even in the case of prolonged treatment. Analysis of methanol toxicokinetics in five patients demonstrated that fomepizole was effective in blocking methanol's toxic metabolism. CONCLUSIONS: Fomepizole appears safe and effective in the treatment of methanol-poisoned patients. If our results are confirmed in prospective analyses, hemodialysis may prove unnecessary in patients presenting without visual impairment or severe acidosis.

Adolescent↗
PubMed1999

Fomepizole for the treatment of ethylene glycol poisoning. Methylpyrazole for Toxic Alcohols Study Group.

BACKGROUND: Ethylene glycol poisoning causes metabolic acidosis and renal failure and may cause death. The standard treatment is inhibition of alcohol dehydrogenase with ethanol, given in intoxicating doses, and adjunctive hemodialysis. We studied the efficacy of fomepizole, a new inhibitor of alcohol dehydrogenase, in the treatment of ethylene glycol poisoning. METHODS: We administered intravenous fomepizole to 19 patients with ethylene glycol poisoning (plasma ethylene glycol concentration, > or =20 mg per deciliter [3.2 mmol per liter]). Patients who met specific criteria also underwent hemodialysis. Treatment was continued until plasma ethylene glycol concentrations were less than 20 mg per deciliter. Acid-base status, renal function, the kinetics of fomepizole, and ethylene glycol metabolism were assessed at predetermined intervals. RESULTS: Fifteen of the patients initially had acidosis (mean serum bicarbonate concentration, 12.9 mmol per liter). Acid-base status tended to normalize within hours after the initiation of treatment with fomepizole. One patient with extreme acidosis died. In nine patients, renal function decreased during therapy; at enrollment, all nine had high serum creatinine concentrations and markedly elevated plasma glycolate concentrations (> or =97.7 mg per deciliter [12.9 mmol per liter]). None of the 10 patients with normal serum creatinine concentrations at enrollment had renal injury during treatment; all 10 had plasma glycolate concentrations at or below 76.8 mg per deciliter (10.1 mmol per liter). Renal injury was independent of the initial plasma ethylene glycol concentration. The plasma concentration of glycolate and the urinary excretion of oxalate, the major metabolites of ethylene glycol, uniformly fell after the initiation of fomepizole therapy. Few adverse effects were attributable to fomepizole. CONCLUSIONS: In patients with ethylene glycol poisoning, fomepizole administered early in the course of intoxication prevents renal injury by inhibiting the formation of toxic metabolites.

Adult↗
PubMed2001

Fomepizole for the treatment of methanol poisoning.

BACKGROUND: Methanol poisoning may result in metabolic acidosis, blindness, and death. The inhibition of alcohol dehydrogenase is fundamental to the treatment of methanol poisoning. We performed a multicenter study to evaluate fomepizole, an inhibitor of alcohol dehydrogenase, in the treatment of patients with methanol poisoning. METHODS: We administered intravenous fomepizole to 11 consecutive patients who presented with methanol poisoning at a participating center. Serial clinical and laboratory studies, including measurements of plasma formic acid and fomepizole, were performed. The outcomes measured were the preservation of visual acuity, the resolution of metabolic acidosis, the inhibition of formic acid production, the achievment of therapeutic plasma concentrations of fomepizole with the dosing regimen, residual illness or disability, and death. RESULTS: Plasma formic acid concentrations were detectable in eight patients, and these concentrations were closely correlated with the initial arterial pH values (r=0.92, P<0.001). In response to fomepizole, plasma formic acid concentrations fell and metabolic abnormalities resolved in all patients. Nine patients survived. Seven patients initially had visual abnormalities, but at the end of the trial no surviving patient had any detectable visual deficits related to methanol poisoning. Fomepizole had few adverse effects. The two patients who died had anoxic brain injury that was present at the time of enrollment. During treatment, methanol had an elimination half-life of 54 hours. CONCLUSIONS: Fomepizole appears to be safe and effective in the treatment of methanol poisoning.

Acidosis↗
PubMed2005

Methanol and formate kinetics during treatment with fomepizole.

OBJECTIVE: Methanol is metabolized by alcohol dehydrogenase to formaldehyde, and further to formic acid, which is responsible for the toxicity in methanol poisoning. Fomepizole (4-methylpyrazole) is a potent competitive inhibitor of alcohol dehydrogenase and is used as an antidote to treat methanol poisonings. We report serum methanol kinetics in eight patients treated with bicarbonate and fomepizole only. METHODS: Prospective case series study of eight patients with methanol poisoning, who were selected to fomepizole and bicarbonate treatment only, because of moderate metabolic acidosis. Three of the patients were later dialyzed, because of high serum methanol concentrations and very slow methanol elimination. RESULTS: Upon admission the median pH was 7.27 (range 7.12-7.50), median base deficit was 15 mmol/L (5-22 mmol/L) and median serum methanol was 20.4 mmol/L (65 mg/dL) (range 8.4-140.6 mmol/L). The kinetics of methanol during fomepizole treatment in six patients was best described by a first-order elimination one-compartment model. The mean correlation coefficient (R2) describing the first-order elimination model in all eight patients was 0.95 (range 0.90-0.99). The mean plasma half-life (t(1/2)) of methanol during fomepizole treatment was 52 h (range 22-87); the higher the serum methanol, the longer the T(1/2). Mean half-life of serum formate was 2.6 h, when methanol metabolism was assumed blocked by fomepizole and no folinic acid was given. This rapid formate elimination in nonacidotic patients may be explained by high renal excretion of formate. CONCLUSION: Based on our data, methanol-poisoned patients with moderate metabolic acidosis and methanol levels up to 19 mmol/L (60 mg/L) may safely be treated with bicarbonate and fomepizole only, without dialysis.

Acidosis↗
PubMed2001

Reversal of severe methanol-induced visual impairment: no evidence of retinal toxicity due to fomepizole.

CASE REPORT: We report a case of methanol poisoning exhibiting complete recovery from severe visual impairment following treatment with ethanol, fomepizole, and hemodialysis. An adult male presented with central blindness after ingesting methanol. Initial visual acuity was <20/800 (finger counting at 1-2 feet) with retinal edema on fundoscopy, arterial pH 7.19, methanol 97 mg/dL (30 mmol/L), formate 14.3 mmol/L, and ethanol undetectable. The patient was treated with ethanol, then fomepizole intravenously (15, 10, then 5 mg/kg), and hemodialysis. Methanol metabolism was effectively blocked by fomepizole even after ethanol had been eliminated, and the patient recovered 20/20 vision by day 14 with normal fundoscopy. This case report confirms highly efficient inhibition of alcohol dehydrogenase by fomepizole, as well as demonstrate the safety of fomepizole in a patient already exhibiting end-organ retinal toxicity. The potential for fomepizole to inhibit retinol dehydrogenase, an isoenzyme of alcohol dehydrogenase essential to vision, did not appear to be clinically significant in this symptomatic methanol-poisoned patient.

Adult↗
PubMed2000

Fomepizole treatment of ethylene glycol poisoning in an infant.

The enzyme alcohol dehydrogenase metabolizes ingested ethylene glycol (EG) to the toxic compounds glycolic and oxalic acids. Renal failure, acidosis, hypocalcemia, and death may follow. Traditional treatment of EG poisoning may require ethanol, a competitive substrate of alcohol dehydrogenase, and hemodialysis, that removes both EG and its toxic metabolites. A new alcohol dehydrogenase inhibitor, fomepizole (4-methylpyrazole), was approved in 1997 for patients at least 12 years old with suspected or confirmed EG poisoning. Fomepizole has not been studied adequately in the pediatric population. We present a case of an 8-month-old male infant who drank up to 120 mL of EG and developed acidosis and oxalate crystalluria. He was treated with fomepizole and hemodialysis. Even after the completion of hemodialysis, fomepizole appeared to effectively block the production of EG toxic metabolites and to allow the resolution of acidosis; the patient recovered within 48 hours. This is the first report of fomepizole treatment of EG poisoning in an infant.4-methylpyrazole, fomepizole, poisoning, ethylene glycol, hemodialysis, infant, child, pediatrics.

Antidotes↗
PubMed2000

Inhibition of canine and feline alcohol dehydrogenase activity by fomepizole.

OBJECTIVE: To determine and compare substrate specificity and kinetic rate constants of feline and canine alcohol dehydrogenase (ADH) with ethanol (EtOH) and ethylene glycol (EG) as substrates in vitro, with and without fomepizole. SAMPLE POPULATION: Livers from 3 dogs and 3 cats. PROCEDURE: Canine and feline ADH activity, in cytosolic fractions of homogenized liver, was determined by use of various concentrations of nicotinamide adenine dinucleotide (NAD), EtOH, or EG as substrates. Initial reaction velocities were calculated, and kinetic inhibition rate constants (Ki) for fomepizole were determined. RESULTS: Substrate specificity of canine and feline ADH for EtOH or EG was not significantly different. A 2-fold difference was detected in the maximal velocity of canine, compared with feline, ADH, using either substrate. Fomepizole Ki in feline hepatic homogenates was significantly greater than Ki in canine hepatic homogenates when either EtOH or EG was used as substrate (10- and 30-fold, respectively). A 6-fold increase in the concentration of fomepizole was required to achieve ADH inhibition, with feline homogenates equivalent to those of canine homogenates. CONCLUSIONS AND CLINICAL RELEVANCE: Feline ADH has lower enzymatic capacity for turnover or is less concentrated in liver than canine ADH with regard to EtOH and EG catalysis. Canine ADH was more effectively inhibited by fomepizole than feline ADH. Results suggest that higher dosages of fomepizole may be more effective to treat cats with EG intoxication than dosages reported to treat dogs.

Alcohol Dehydrogenase↗
PubMed2002

Treatment of a 1,4-butanediol poisoning with fomepizole.

BACKGROUND: Toxicity of 1,4-butanediol, an industrial solvent and a substance of abuse, is still misunderstood and not well documented. To date, only supportive treatments are used in this poisoning. CASE REPORT: The case of a 43-year-old man who ingested 30 mL of a homemade 1,4-butanediol solution and who developed general seizures and coma has been reported here. An intravenous loading dose of fomepizole 10 mg/kg was started on admission and followed by two other doses of 10 mg/kg every 12 hour. He awoke shortly after fomepizole administration. Initial plasma 1,4-butanediol and gamma-hydroxybutyric acid concentrations, measured by gas chromatography-mass spectrometry, were 24 and 222 mg/L, respectively. Subsequent 1,4-butanediol and gamma-hydroxybutyric acid determination suggest that there was some further formate of gamma-hydroxbutyric acid after fomepizole was administered. CONCLUSION: Fomepizole administration appeared safe in this 1,4-butanediol-intoxicated patient. It is unknown whether fomepizole influenced his clinical course, but the rapid awakening observed suggests that it may have been usefuL Further experience is needed, however, to define the efficacy of this antidotal therapy in 1,4-butanediol intoxication.

Adult↗
PubMed2002

Fomepizole as an antidote for ethylene glycol poisoning.

OBJECTIVE: To assess the use of fomepizole in the treatment of ethylene glycol poisoning in the absence of hemodialysis. DATA SOURCES: A MEDLINE search (1966-May 2001) of English-language literature pertaining to the use of fomepizole in ethylene glycol poisoning was performed. Key search terms included fomepizole, ethylene glycol poisoning, and hemodialysis. References cited in those articles were also evaluated. DATA SYNTHESIS: Results from a number of case reports and a prospective trial suggest that fomepizole is a safe and effective antidote in the treatment of ethylene glycol poisoning. CONCLUSIONS: Case reports and 1 prospective trial have shown that, in the absence of both renal dysfunction and significant metabolic acidosis, the use of fomepizole should obviate the need for hemodialysis. However, the decision to add hemodialysis in the treatment of ethylene glycol poisoning based on plasma ethylene glycol concentrations is still debatable. A randomized, controlled trial is needed to determine the exact criteria for adding hemodialysis.

Acid-Base Imbalance↗
PubMed2002

[Severe ethylene glycol poisoning treated wtih fomepizole (4-methylpyrazole)].

BACKGROUND: Poisoning with ethylene glycol causes severe metabolic acidosis and renal failure, and is potentially lethal if not treated rapidly. Until recently the standard therapy for this poisoning has been bicarbonate to counteract the metabolic acidosis, inhibition of alcohol dehydrogenase (ADH) with ethanol to prevent the production of toxic metabolites and haemodialysis to remove ethylene glycol and its toxic metabolites. The new potent inhibitor of ADH, 4-methylpyrazole (fomepizole), has recently been approved for the treatment of methanol and ethylene glycol poisonings. MATERIAL AND METHODS: Three patients severely poisoned by ethylene glycol and treated with fomepizole are presented. RESULTS: Of our three patients treated with fomepizole two were managed without haemodialysis. One patient had an exceptionally high serum ethylene glycol concentration (90 mmol/l; 585 mg/dl) and was successfully treated with fomepizole without the need for haemodialysis despite pronounced metabolic acidosis. INTERPRETATION: Ethylene glycol poisonings may be treated effectively with fomepizole without haemodialysis.

Adult↗
PubMed2004

Fomepizole as a therapeutic strategy in paediatric methanol poisoning. A case report and review of the literature.

UNLABELLED: Methanol poisoning is not frequently observed in children; however, without treatment, serious intoxication can be complicated by visual impairment, coma, metabolic acidosis, respiratory and circulatory insufficiency and death. Treatment in a paediatric intensive care is therefore compulsory. Methanol is metabolised in the liver by alcohol dehydrogenase to the toxic metabolites formaldehyde and formic acid. Classically, ethanol is given as a competitive inhibitor in order to avoid the formation of these compounds. We report on the use of fomepizole (4-methylpyrazole),a new and potent inhibitor of alcohol dehydrogenase, in a 3-year-old boy after the intake of a toxic amount of methanol. The course was uneventful and the use of fomepizole was not accompanied by any side-effects. An overview is given of all cases of paediatric poisoning in which fomepizole was used. CONCLUSION: Fomepizole seems to be a safe and valid alternative to ethanol in cases of paediatric methanol poisoning.

Antidotes↗
PubMed2001

Treatment of methanol and isopropanol poisoning with intravenous fomepizole.

CASE REPORT: We report a case of mixed methanol and isopropanol poisoning in a patient who refused dialysis but agreed to treatment with intravenous fomepizole. The patient was asymptomatic on arrival, with initial blood methanol and isopropanol concentrations of 146 mg/dL and 39 mg/dL, respectively. Blood ethanol was undetectable. The patient was treated with fomepizole twice daily intravenously until blood methanol was undetectable. No side effects of therapy, other than transient eosinophilia, were observed. The evolution was uneventful and no metabolites of either alcohol were detected at any time during the hospitalization. The decay of plasma methanol and isopropanol under fomepizole treatment were well described by first-order kinetics. The plasma elimination half-lives of methanol and isopropanol were 47.6 hours and 27.7 hours, respectively. Fomepizole appears to have been effective in blocking the toxic metabolism of both methanol and isopropanol and was associated with a favorable outcome.

2-Propanol↗
PubMedDate not supplied

Compliance with poison center fomepizole recommendations is suboptimal in cases of toxic alcohol poisoning.

We sought to examine hospital compliance with poison center antidotal alcohol dehydrogenase inhibition recommendations in cases of ethylene glycol (EG) and methanol (ME) ingestion. A 2-year analysis of all potential EG and ME ingestion cases reported to a regional poison center was conducted. Excluded from analysis were exposures without an ingestion, without a confirmatory EG or ME serum assay, or without complete medical charting. During the study period, 579 EG or ME exposures were reported to the poison center: 133 cases met study eligibility as an ingestion. Of the 133 cases, 102 (77%) had complete data and were included in the analysis. Immediate alcohol dehydrogenase inhibition was recommended by the poison center in 79 of the 102 cases. Fomepizole was recommended in 61/79 (77%); ethanol was recommended as an alternative therapeutic choice in 32/61 (52%) of these cases if fomepizole was not immediately available. Ethanol alone was recommended in 18/79 (23%). Fomepizole was eventually administered in 39/61 (64%) cases where recommended. The mean time to antidote administration was 3 times longer in cases where a choice in antidote was given [57 min (95% confidence interval, 43-70) vs. 146 min (95% confidence interval, 93-200)]. Despite its ease of administration, fomepizole is used less frequently than recommended by poison center staff. Delays to antidote administration occurred more commonly in cases where the poison center gave a choice in antidotal therapy.

Adolescent↗
PubMed2004

Fomepizole alone for severe infant ethylene glycol poisoning.

OBJECTIVE: To report a case of a massive ingestion of ethylene glycol in an infant successfully treated by fomepizole without hemodialysis. DESIGN: Descriptive case report. SETTING: Pediatric intensive care unit. PATIENT: A 5-mo-old boy who ingested 200 mL of an antifreeze solution. INTERVENTIONS: Antidotal therapy with a total of seven doses of fomepizole administered intravenously with an interval of 12 hrs (15 mg/kg as loading dose, then 10 mg/kg). Hemodialysis was not performed. MEASUREMENTS AND MAIN RESULTS: Iterative determination of ethylene glycol concentration was obtained in blood and urine. Kinetics were calculated for ethylene glycol and fomepizole elimination. The infant made a complete recovery with no change in renal function. CONCLUSIONS: Although not yet approved for this indication in the child, fomepizole seemed safe and effective in a case of severe ethylene glycol poisoning, without the need for hemodialysis.

Accidents, Home↗