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The Mechanism of Fluoride-Induced Hypocalcaemia

Laboratory of Toxicology, P.O. Box 1, 3720 BA Bilthoven, Department of Clinical Chemistry, University ospital Utrecht, Utrecht

J. Wemer

Laboratory of Medicines and Medical Devices, P.O. Box 3720 BA Bilthoven

J. Meulenbelt

National Poison Control Centre, P.O. Box 1, 3720 BA Bilthoven, Department of Intensive Care and Clinical Toxicology, University Hospital Utrecht, Utrecht

H.A.M.G. Vaessen

Laboratory of Residue Analysis of the National Institute of Public Health and Environmental Protection, P.O. Box 1, NL-3720 BA Bilthoven

D.J. de Wildt

Laboratory of Medicines and Medical Devices, P.O. Box 3720 BA Bilthoven, Department of Medical Pharmacology, Rudolf Magnus Institute, Utrecht University, Utrecht, The Netherlands

1 Fluoride intoxication leads to sudden cardiac death which has been assumed to result from the accompanying severe hypocalcaemia. The aim of this study has been to investigate the suggestion that fluorapatite formation rather than CaF₂ precipitation is responsible for this low calcium.

2 Measurements of free Ca²⁺ and F^- ion concentrations in HEPES buffered solutions containing F-, Ca²⁺, and phosphate ions at different concentrations in the absence and presence of hydroxyapatite showed that the presence of hydroxyapatite enhanced the decrease of Ca²⁺ and F- concentration.

3 The ratio of Ca²⁺:F^- clearance was 5:1 which is consistent with formation of fluorapatite. These results support the hypothesis that hydroxyapatite acts as a nucleation catalyst for fluorapatite formation and this process is responsible for the hypocalcaemia induced by fluoride intoxication.

4 The proposed mechanism explains also the metabolic acidosis which is frequently seen in cases of fluoride intoxication.

Human & Experimental Toxicology, Vol. 13, No. 3, 149-155 (1994)
DOI: 10.1177/096032719401300302


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