Unlabelled: We report a case of hypotension and bradycardia associated with intravenous fomepizole infusion.
Case Report: A 59-year-old man presented to hospital 10 hours after ethylene glycol ingestion with ataxia, slurred speech, metabolic acidosis, heart rate 70/min, blood pressure 160/100 mmHg. Treatment with hemodialysis and fomepizole began 7.5 hours after admission. Severe bradycardia (29/min) and hypotension (69 mmHg systolic) occurred immediately following a 30 minute intravenous infusion of the first (19 mg/kg) fomepizole dose, but rapidly corrected with 1 mg atropine. Transient bradycardia (48/min) and hypotension (89/57 mmHg) recurred immediately after the second (10 mg/kg) fomepizole dose, also given during dialysis.
Discussion: Hemodialysis may cause a drop in blood pressure and heart rate; however, the close temporal relationship with fomepizole infusions, dose-related symptom intensity and recurrence with rechallenge suggest a causal relationship with fomepizole. Hemodialysis, acidosis and high initial fomepizole dose may have enhanced patient susceptibility, as a post-dialysis fomepizole dose was well tolerated.
Conclusion: Fomepizole may precipitate bradycardia and/or hypotension during hemodialysis. Monitor vital signs closely during and immediately after infusion.
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http://dx.doi.org/10.1080/15563650701725128 | DOI Listing |
Clin Toxicol (Phila)
August 2024
Utah Poison Control Center, College of Pharmacy, University of Utah, Salt Lake City, UT, USA.
Background: Ethylene glycol poisoning causes metabolic acidosis, organ injury, and death. Ethylene glycol testing is unavailable in many areas. Our laboratory uses an automated glycerol dehydrogenase enzymatic assay to screen for ethylene glycol.
View Article and Find Full Text PDFPhytopathology
March 2024
College of Life Sciences, Qingdao University, Qingdao 266071, P.R. China.
, the pine wood nematode (PWN), is the causal agent of pine wilt disease (PWD), which causes enormous economic loss annually. According to our previous research, fomepizole, as a selective inhibitor of PWN alcohol dehydrogenase (ADH), has the potential to be a preferable lead compound for developing novel nematicides. However, the underlying molecular mechanism is still unclear.
View Article and Find Full Text PDFClin Nephrol Case Stud
March 2024
Indiana University School of Medicine, Indianapolis, IN, USA.
Acetaminophen ingestion is routinely managed with the antidote, N-acetylcysteine (NAC). Massive acetaminophen poisoning has been treated successfully with adjunctive therapies such as fomepizole and hemodialysis. Fomepizole functions by inhibiting cytochrome p560, which prevents tylenol from forming its toxic metabolite, NAPQI.
View Article and Find Full Text PDFBiochem Pharmacol
October 2024
Department of Pharmacology, Toxicology & Therapeutics, University of Kansas Medical Center, Kansas City, KS, USA. Electronic address:
Liver injury and acute liver failure caused by an acetaminophen (APAP) overdose is a significant clinical problem in western countries. With the introduction of the mouse model of APAP hepatotoxicity in the 1970 s, fundamental mechanisms of cell death were discovered. This included the recognition that part of the APAP dose is metabolized by cytochrome P450 generating a reactive metabolite that is detoxified by glutathione.
View Article and Find Full Text PDFToxicol Sci
March 2024
Department of Pharmacology, Toxicology & Therapeutics, University of Kansas Medical Center, Kansas City, Kansas 66160, USA.
Acute kidney injury (AKI) is a common complication in acetaminophen (APAP) overdose patients and can negatively impact prognosis. Unfortunately, N-acetylcysteine, which is the standard of care for the treatment of APAP hepatotoxicity does not prevent APAP-induced AKI. We have previously demonstrated the renal metabolism of APAP and identified fomepizole (4-methylpyrazole, 4MP) as a therapeutic option to prevent APAP-induced nephrotoxicity.
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