Disodium Edetate 3 g plus Sodium Ascorbate 5 g (Biological Therapies)

What it is used for

1. Disodium Edetate is particularly effective in treating lead accumulation and lead poisoning. This is especially so where there is a concomitant hypercalcaemic problem (refer “Indications (2)”). However it must be noted that Disodium Edetate is equally effective with Calcium Disodium Edetate in removing heavy metals, even in the absence of hypercalcaemia. For patients with elevated serum calcium or hypermobility of their body pools of calcium where there may be transiently or prolonged raised serum calcium (see “Indications (2)”), the EDTA of choice for removing heavy metals may be Disodium Edetate. There are no recognised safe limits for lead intoxication. Lead poisoning may occur by ingestion or inhalation of lead dust or fumes. Poisoning is manifested by a metallic taste, anorexia, irritability, apathy, abdominal colic, vomiting, diarrhoea, constipation, headache, leg cramps, black stools, oliguria, stupor, convulsions, palsies and coma. Chronic lead poisoning causes variable involvement of the Central Nervous System, the blood forming organs and the gastrointestinal tract. Diagnostic laboratory tests include blood lead, hair analysis, urine coproporphyrin, urine delta-aminolevulinic acid, x-ray of abdomen and x-ray of long bones. Comparing the results of a 12-hour urine collection, pre-EDTA therapy, with the results of a 12-hour urine collection, during/post initial EDTA chelation, should confirm the early excretory surge of lead. As long as significant quantities of lead remain in the bone, any intercurrent illness which causes demineralisation can cause mobilisation of toxic quantities of lead into soft tissues and exacerbate plumbism. 2. Disodium Edetate may be used to temporarily reduce serum Calcium in patients with hypercalcaemia. Transient or prolonged hypercalcaemia may exceed the solubility product of calcium and result in tissue damage. Increased plasma calcium may give rise to renal lithiasis or acute pancreatitis. Calcium may also precipitate in the eyes (band keratopathy) and in soft tissues around the joints. There are many primary and secondary causes of transient and prolonged hypercalcaemia, which include the following: i) The injection of Calcium Disodium EDTA may itself give rise to a transient hypercalcaemia. ii) IMMOBILISATION, which may be associated with all sorts of conditions. For example, in Paget’s Disease it is sometimes warranted to supplement with calcium unless there is chronic immobilisation (greater than 3 days immobilisation in bed may precipitate a hypercalcaemia), in which case patients should be placed on a calcium restricted diet. iii) Increased ingestion and uptake of calcium, as in dairy foods or calcium supplements such as calcium citrate. iv) Increased ingestion and uptake of vitamin D. v) Hypervitaminosis A. vi) Osteoarthritis, Rheumatoid Arthritis, Hyperthyroidism, Hyperparathyroidism, Malignancies, Multiple Myeloma, prolonged use of Heparin, Immunosuppressant Drugs, Acromegaly. 3. Disodium Edetate may be valuable in the management of severe digitalis arrhythmias, when a rapid response is required. 4. Disodium Edetate is useful in helping to eliminate some radioactive metals, including Calcium, Strontium, Radium, Cobalt and the very toxic Plutonium.