EDTA therapy

In patients on EDTA therapy, calcium cannot be determined by the Indirect colorimetric or fluorometrlc methods based on the chelation of a calcium - EDTA complex. However, In calcium determinations by atomic-absorption spectroscopy, the complexlng agent Is destroyed In the flame and the direct concentration of calcium can be determined. 

Blood from patients who were given an iodide-containing contrast agent or from patients under EDTA therapy is not suitable for this calcium method. 

Cases of anuria have been reported when EDTA was administered to treat lead poisoning. Such kidney injury is reversible and is probably not due to the chelate directly, but to the reabsorption of the metal in the tubules. Of 130 children that received dime-rcaprol and EDTA, 3% developed acute renal failure and 13% had biochemical evidence of nephrotoxicity. However, lead poisoning can cause kidney injury without EDTA therapy. In another study, 122 patients were given EDTA and none showed posttreatment increases in plasma creatinine. 

Hyperphosphatemia is usually secondary to the inability of the kidneys to excrete phosphate. In acute or chronic renal failure, a decrease in glomerular filtration rate (GFR) reduces the renal excretion of phosphate, resulting in hyperphosphatemia. Moderate increases of serum phosphate occur in individuals with low PTH (hypoparathyroidism), PTH resistance (pseudohypoparathyroidism), or acromegaly (increased growth hormone) caused by an increased renal phosphate threshold. Growdi hormone is responsible for the increased renal phosphate threshold and higher phosphate concentrations observed in children. EDTA therapy has also been associated with hyperphosphatemia. 

In the USA EDTA has been widely used for more than 30 years and some 100000 patients have been treated with over 2 million injections, often to remove the calcium-containing plaques which clog up the arteries in the prevalent disease atherosclerosis. More than 5000 references to EDTA therapy are to be found in the literature. 

Although the EDTA test has been shown to be safe even in the presence of renal failure [77], the cumulative nephrotoxicity of prolonged EDTA therapy in patients with markedly reduced glomerular filtration rates is unknown. Reports that CaNa2EDTA therapy has been followed by deterioration of renal function warrant careful follow-up of treated patients [78]. Despite these caveats, it may be appropriate to perform EDTA lead-mobilization tests in individuals with gout or hypertension and renal failure or interstitial nephritis of unknown etiology since a positive test may provide the best available indication of etiology. 

B. Lead encephalopathy (only in conjunction with calcium EDTA therapy [see p 440]). For acute pediatric lead encephalopathy, some clinicians initiate treatment with BAL, 3-4 mg/kg IM (75 mg/m ), followed in 4 hours by concomitant use of calcium EDTA and BAL, 3-4 mg/kg (75 mg/m ) every 4-6 hours for up to 3 days. 

H. Orai EDTA therapy is not recommended for prevention or treatment of iead poisoning, because it may increase the absorption of iead from the gastroin-testinai tract. 

CompIkralifHis. Therapy is usually discontinued after 5 days to avoid complications or toxicosis from calcium EDTA therapy. 

Administration of dimereaprol prior to initiation of calcium EDTA therapy may help alleviate acute neurologic signs, because it crosses the blood-biain barrier. In addition, lead excretion in both bile and urine is enhanced by dimereaprol. 

O Side effects are anorexia, lisdessness, aixl vomiling, which are minimized if smaller doses are given mote frequently, or if 5-7-flay test periods are dtemated with 5-7-day treatmerrt rumens. (The latter strategy is efl ve for caldum disodium EDTA therapy as well.)... 

Nutritional considerations Contains soy bean oil, egg lecithin, and glycerol. Provides 1.1 kcal/mL of emulsion may need to adjust nutritional regimen. One formulation contains EDTA. Prolonged therapy with the EDTA-containing product may decrease serum zinc levels. May need to monitor serum zinc levels and supplement. 

Chelation Therapy The History of EDTA. Leon Chaitow, N.D., D.O., http //www.healthy.net/library/books/chaitow/chelther/intro/history.htm... 

Chelation therapy (eg, EDTA) Coadministration of succimer with other chelation therapy is not recommended. 

Quantitative assay of biotinidase activity including evaluation for the presence of a Km defect requires 1 ml of plasma. Serum samples can be also used. Biotin therapy does not affect the assay [ 32 ]. The activity in plasma may decrease during storage (see Pitfalls and Limitations , below). We recommend the use of ethylene-diami-netetraacetic acid (EDTA)-plasma separated from whole blood and assayed within... 

EDTA has been shown to be of value in the therapy of lead intoxication. It can be administered either deep intramuscularly or by slow intravenous infusion. The dose of 75 mg/kg/day should be administered in 3-6 divided doses for up to 5 days this dosage... 

Ethylenediamine tetraacetic acid (EDTA) was introduced originally as a water-softener and as a textile dyeing assistant because of its ability to form very stable, water soluble complexes with many metal ions, including calcium and magnesium. The equilibria involved in chelation of metal ions by EDTA and related ligands have been exhaustively studied, notably by G. Schwarzenbach and his colleagues, and provide the basis for complexometric methods of chemical analysis. EDTA and its metal complexes have also become probably the most familiar examples of agents used in chelation therapy. 

Excess transition metals can be removed by chelation therapy using chelating agents such as deferoxamine, EDTA or D-penicillamine, and supplements can be used in cases of deficiency (e.g. iron(II) suphate or zinc(II) sulfate). 

Chelation therapy. Treatment of carbonic anhydrase with high concentrations of the metal chelator EDTA (ethylenediaminetetraacetic acid) results in the loss of enzyme activity. Propose an explanation. 

Adverse effects. Haemorrhage occurs but is less of a problem with low doses of heparin it remains a particular risk in patients treated after failed fibrinol5 c therapy for acute myocardial infarction. Platelet transfusion after cessation of abciximab is necessary for refractory or life threatening bleeding. After transfusion, the antibody redistributes to the transfused platelets, reduces the mean level of receptor blockade and improves platelet function. Thrombocytopenia may occur from 1 hour to days after commencing treatment in up to 1% of patients. This necessitates platelet counts at 2-4 hours and then daily if severe, therapy must be stopped and, if necessary, platelets transfused. EDTA-induced pseudothrombocytopenia has been reported and a low platelet count should prompt examination of a blood film for agglutination before therapy is stopped. 

In chronic intoxication, the therapeutic objective is removal of the patient from the site of exposure and elimination of the noxa from the body (e. g. detoxification measures, infusions of calcium-disodium EDTA in cases of lead poisoning, etc.). There is no justification whatsoever for therapeutic nihilism. With the aid of dietetic measures (if necessary) and adjuvant therapy (N-acetylcysteine, antioxidants, ursodeoxycholic acid, S-adenosyl-methionine, etc.), the clinical course and hence the prognosis can be favourably influenced. Insufficient regression or inadequate normalization of laboratory parameters and histological changes despite removal of the patient from the area of exposure must arouse suspicion of a further, still existing noxa (alcohol, medicaments, other chemicals). 

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