The manipulation of potassium efflux during fluoride intoxication: Implications for therapy

Michael E. McIvor, Charles C. Cummings, Morton M. Mower, Romulo F. Baltazar, Robert E. Wenk, Jack A. Lustgarten, Joseph Salomon

Research output: Contribution to journalArticlepeer-review

Abstract

Based on findings in fluoride-toxic patients, it was suspected that hyperkalemia played a clinically impotant role in the etiology of sudden death from fluoride poisoning. Using fluoridated human erythrocytes as an in vitro model, it was confirmed that fluoride produced a marked potassium efflux from intact cells. Further, neither glucose and insulin in pharmacologic doses, nor various buffers could halt the efflux by shifting the potassium intracellularly. If these results can be estrapolated to the clinical situation, removal of potassium and fluoride via exchange resins or dialysis remains the only reasonable approach to this life threatening problem. Aside from sudden hyperkalemia and hypocalcemia, no serologic marker for fluoride toxicity has been identified. A high degree of clinical suspicion is therefore essential to the diagnosis.

Original languageEnglish (US)
Pages (from-to)233-239
Number of pages7
JournalToxicology
Volume37
Issue number3-4
DOIs
StatePublished - Dec 1985

Keywords

  • Acute fluoride intoxication
  • Calcium dependent potassium channels
  • Erythrocytes
  • Hyperkalemia
  • Potassium
  • Sodium fluoride
  • Sudden death

ASJC Scopus subject areas

  • Toxicology

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