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Concise review: methemoglobinemia

A Mansouri1, A A Lurie

  • 1Department of Medicine, Overton Brooks VAMC, Shreveport, Louisiana 71101-4295.

American Journal of Hematology
|January 1, 1993
PubMed
Summary
This summary is machine-generated.

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Methemoglobinemia occurs when hemoglobin oxidizes and cannot carry oxygen. Red blood cell enzymes normally prevent this, but deficiencies or toxins can cause methemoglobinemia, which may require treatment in specific cases.

Area of Science:

  • Biochemistry
  • Hematology
  • Physiology

Background:

  • Hemoglobin's ferrous iron can oxidize to methemoglobin, impairing oxygen transport.
  • Methemoglobin (ferrihemoglobin) must be reduced to functional hemoglobin (ferrohemoglobin).
  • Red cell NADH-cytochrome b5 reductase is crucial for physiological methemoglobin reduction.

Purpose of the Study:

  • To explain the mechanism of methemoglobin formation and its physiological regulation.
  • To identify causes and consequences of methemoglobinemia.
  • To outline treatment strategies for different methemoglobinemia scenarios.

Main Methods:

  • Review of biochemical pathways of hemoglobin oxidation and reduction.
  • Analysis of factors leading to increased methemoglobin formation.

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  • Discussion of clinical implications and therapeutic interventions.

    • Main Results:

    • Oxidant exposure, abnormal hemoglobin variants (hemoglobin M), or enzyme deficiencies (cytochrome b5 reductase) can cause methemoglobinemia.
    • Most methemoglobinemia cases are asymptomatic and require no treatment.
    • Rapid treatment is indicated for severe oxidant exposure or in infants; cosmetic improvement is a goal in hereditary conditions.

    Conclusions:

    • Efficient endogenous reduction mechanisms usually prevent clinically significant methemoglobin levels.
    • Methemoglobinemia can arise from exogenous or endogenous factors disrupting this balance.
    • Treatment decisions depend on the cause, severity, and clinical context of methemoglobinemia.