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Description

Background:

  • Methemoglobin (MetHb) is formed when the iron moiety of hemoglobin (Hgb) is oxidized from ferrous (Fe2+) to ferric (Fe3+) state à impaired O2 delivery to tissues
  • Acetaminophen Metabolism:

~90% is metabolized in liver via sulfation and glucuronidation

remainder is metabolized via CYP450 to a toxic oxidizing agent, N-acetyl-p-benzoquinone imine (NAPQI), which is detoxified via glutathione1

  • Acute Acetaminophen Overdose:

saturates sulfation and glucuronidation pathways

depletes glutathione stores

leads to excess NAPQI à oxidative stress à methemoglobinemia1

  • MetHb Reduction Pathway:

cytochrome b5 reductase removes 95% to 99% of endogenous MetHb

nicotinamide adenine dinucleotide phosphate (NADPH

Publication Date

2-24-2016

Keywords

Methemoglobinemia in Acetaminophen Overdose and Glucose-6-phosphate Dehydrogenase Deficiency

Disciplines

Pharmacy and Pharmaceutical Sciences

Comments

Poster presented at: Society of Critical Care Medicine at Orange County California.

Methemoglobinemia in Acetaminophen Overdose and Glucose-6-phosphate Dehydrogenase Deficiency

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