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Edetate Disodium (EDTA) Injection

Edetate disodium is a chelating agent with affinity for divalent and trivalent metals. When applied as a treatment for hypercalcemia, ETDA can decrease blood calcium levels too rapidly, which may lead to cardiac arrhythmias and respiratory arrest; because of this risk, the drug is rarely used. Edetate disodium was once used to treat arrhythmias associated with digitalis toxicity, but preferred alternative agents have taken its place. Edetate disodium should not be confused with its calcium salt (calcium EDTA), which is used to treat lead toxicity. Decades ago, edetate disodium was used for atherosclerotic vascular disease despite a lack of clinical data to support its efficacy. Only one large study has been conducted to evaluate this use and the study showed no significant improvement relative to placebo. Nevertheless, interest persists in using EDTA to treat atherosclerosis. A recent clinical trial suggests no evidence to support the benefit of chelation therapy in patients with ischemic heart disease including stable angina. EDTA has been approved by the FDA, but because of potentially lethal adverse effects, edetate disodium should not be used for the treatment of arteriosclerosis due to advancing age.

Mechanism of Action

Edetate disodium binds calcium ions, forming a stable, soluble complex that is eventually excreted by the kidneys. Following IV administration of edetate disodium, serum calcium levels decrease rapidly, since 1 gm of edetate disodium can combine with 120 mg of calcium. The decrease in calcium antagonizes the effects of digitalis glycosides on the ventricles of the heart, thereby helping to control digitalis-induced ventricular arrhythmias. Edetate disodium is also known to exhibit negative cardiac inotropic activity; the sudden decrease in serum calcium caused by EDTA can lead to hypocalcemic tetany, seizures, cardiac arrhythmias, and respiratory arrest. These effects are usually related to high doses or rapid infusion rates, which means a slower IV infusion allows time for the body to mobilize calcium in bone to replenish the serum calcium pool, reducing the risk of negative effects. EDTA does not affect the concentration of calcium ions in the cerebrospinal fluid.

Edetate disodium also enhances the excretion of other trace metals including magnesium and zinc, and although the drug does not have this effect on potassium, administration can increase renal excretion and decrease serum concentration of this mineral, which can produce hypokalemia. It was once believed that EDTA could be used to manage atherosclerosis, but this has been disproven. Edetate disodium is still advocated as a treatment for this condition through mechanisms that have not been verified.

Pharmacokinetics
General Administration Information
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Pregnancy/ Breastfeeding
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