Indications: Lead Poisoning

The successful use of CaNa2EDTA in the treatment of lead poisoning is due, in part, to the capacity of lead to displace calcium from the chelate. Enhanced mobilization and excretion of lead indicate that the metal is accessible to EDTA. Bone provides the primary source of lead that is chelated by CaNa2EDTA. After such chelation, lead is redistributed from soft tissues to the skeleton.

Mercury poisoning, by contrast, does not respond to the drug despite the fact that mercury displaces calcium from CaNa2EDTA in vitro. Mercury is unavailable to the chelate, perhaps because it is too tightly bound by -SH groups or sequestered in body compartments that are not penetrated by CaNa2EDTA.

Although the lay press has reported that chelation therapy with CaNaf-DTA could minimize development of atherosclerotic plaques (which can accumulate calcium deposits), such use of CaNa2EDTA is without therapeutic rationale and not efficacious.


Less than 5% of CaNa2EDTA is absorbed from the GI tract. After intravenous administration, CaNa2EDTA disappears from the circulation with a t/2 of20-60 minutes. In blood, all of the drug is found in plasma. About 50% is excreted in urine in 1 hour and >95% in 24 hours. For this reason, adequate renal function is necessary for successful therapy. Renal clearance of the compound in dogs equals that of inulin, and glomerular filtration accounts entirely for urinary excretion. Altering either the pH or the rate of flow of urine has no effect on the rate of excretion. There is very little metabolic degradation of EDTA. The drug is distributed mainly in the extracellular fluids, but very little gains access to the spinal fluid (5% of the plasma concentration).

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