A patient was admitted to a district general hospital within an hour of ingesting a fatal dose of sodium fluoride. The results of laboratory investigations, together with some in vitro findings, support the hypothesis that the hypocalcaemia of fluoride poisoning is the result of fluorapatite formation and not calcium fluoride precipitation, and that its persistence reflects the severity of the calcium deficit and not an inhibition of normal homeostatic mechanisms. It is suggested that the role of renal clearance of fluoride may be more important than had been realised hitherto.
References
1.
WaldbottGL. Acute fluoride intoxication. Acta Med Scand1963; Supplement 400 (174).
NeumanWFNeumanMW. Emerging concepts of the structure and metabolic functions of bone. Am J Med1957; 22: 123–131.
6.
JoostlarsenMFejerskouOJosephsenKHammarströmL. The action of acute doses of fluoride on serum calcium level in relation to dental hard tissue formation in rats. Calcif Tissue Res1977; 22: 454–457.
7.
WadkinsCLLubenRA. Effects of fluoride on in vitro calcification of tendon matrix. Calcif Tissue Res1978; 26: 51–59.
8.
MesserHHArmstrongWDSingerL. Fluoride, parathyroid hormone and calcitonin: Inter-relationships in bone calcium metabolism. Calcif Tissue Res1973; 13: 217–225.
9.
ZarembskiPMHodgkinsonA. Plasma oxalic acid and calcium levels in oxalate poisoning. J Clin Pathol1967; 20: 283–285.
10.
SchmidtESchmidtF W. Brief Guide to Practical Enzyme Diagnosis17. Mannheim, W Germany: Boehringer Mannheim GmbH. 1976.
11.
BermanLTavesDMitraSNewmarkK. Inorganic fluoride poisoning: Treatment by hemodialysis. N Engl J Med1973; 289: 922.