McIvor M E, Cummings C C, Mower M M, Baltazar R F, Wenk R E, Lustgarten J A, Salomon J
Toxicology. 1985 Dec;37(3-4):233-9. doi: 10.1016/0300-483x(85)90086-1.
Based on findings in 2 fluoride-toxic patients, it was suspected that hyperkalemia played a clinically important 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 extrapolated 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.
基于对2例氟中毒患者的研究结果，怀疑高钾血症在氟中毒所致猝死的病因中起重要临床作用。以氟化人红细胞作为体外模型，证实氟可使完整细胞出现明显的钾外流。此外，药理剂量的葡萄糖和胰岛素以及各种缓冲液均不能通过促使钾进入细胞内而阻止钾外流。如果这些结果可外推至临床情况，那么通过离子交换树脂或透析去除钾和氟仍是解决这一危及生命问题的唯一合理方法。除了突发的高钾血症和低钙血症外，尚未发现氟中毒的血清学标志物。因此，高度的临床怀疑对诊断至关重要。
