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Calcium Disodium Versenate

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Calcium Disodium Versenate

CLINICAL PHARMACOLOGY

The pharmacologic effects of edetate calcium disodium are due to the formation of chelates with divalent and trivalent metals. A stable chelate will form with any metal that has the ability to displace calcium from the molecule, a feature shared by lead, zinc, cadmium, manganese, iron and mercury. The amounts of manganese and iron mobilized are not significant. Copper1 is not mobilized and mercury is unavailable for chelation because it is too tightly bound to body ligands or it is stored in inaccessible body compartments. The excretion of calcium by the body is not increased following intravenous administration of edetate calcium disodium, but the excretion of zinc is considerably increased.1

Edetate calcium disodium is poorly absorbed from the gastrointestinal tract. In blood, all the drug is found in the plasma. Edetate calcium disodium does not appear to penetrate cells; it is distributed primarily in the extracellular fluid with only about 5% of the plasma concentration found in spinal fluid.

The half life of edetate calcium disodium is 20 to 60 minutes. It is excreted primarily by the kidney, with about 50% excreted in one hour and over 95% within 24 hours.2 Almost none of the compound is metabolized.

The primary source of lead chelated by Calcium Disodium Versenate (edetate calcium disodium injection) is from bone; subsequently, soft-tissue lead is redistributed to bone when chelation is stopped.3,4 There is also some reduction in kidney lead levels following chelation therapy.

It has been shown in animals that following a single dose of Calcium Disodium Versenate urinary lead output increases, blood lead concentration decreases, but brain lead is significantly increased due to internal redistribution of lead.5 (See WARNINGS.) These data are in agreement with the recent results of others in experimental animals showing that after a five day course of treatment there is no net reduction in brain lead.6

REFERENCES

1. Thomas DJ, Chisolm JJ. Lead, zinc and copper decorporation during calcium disodium ethylenediamine tetraacetate treatment of lead-poisoned children. J Pharmacol Exp Therapeu 1986; 239:829-835.

2. The Pharmacological Basis of Therapeutics, 7th edition, Goodman and Gilman, editors. MacMillan Publishing Company, New York, 1985, pp. 1619-1622.

3. Hammond PB, Aronson AL, Olson WC. The mechanism of mobilization of lead by ethylenediaminetetraacetate. J Pharmacol Exp Therapeu 1967; 157:196-206.

4. Van deVyver FL, D'Haese r WJ, et al. Bone lead in dialysis patients. Kidney Intl 1988;PC, Visse 33:601-607.

5. Cory-Slecta DA, Weiss B, Cox C. Mobilization and redistribution of lead over the course of calcium disodium ethylenediamine tetraacetate chelation therapy. J Pharmacol Exp Therapeu 1987; 243:804-813.

6. Chisolm JJ. Mobilization of lead by calcium disodium edetate. Am J Dis Child 1987; 141:1256-1257.

Last reviewed on RxList: 11/26/2008
This monograph has been modified to include the generic and brand name in many instances.

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