Chelation therapy

The origins of chelation therapy can be traced back to the treatment of First World War soldiers who had suffered from gas attacks that used the arsenic-based toxin, Lewisite. A dithiol, British anti-Lewisite (BAL), was developed to remove the toxic metal. 

During the Second World War there was a need to treat workers who had been exposed to lead in the paint, particularly white lead or lead(II) carbonate, used on military vehicles and ships. This was achieved with the well known chelating agent ethylenediamine tetraacetic acid (EDTA). Since then other chelating agents have been identified or synthesized for the purpose of binding specific metals. 

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Elaborate precautions must be taken to prevent the entrance of Pu iato the worker s body by ingestion, inhalation, or entry through the skin, because all common Pu isotopes except for Pu ate a-emitters. Pu is a P-emitter, but it decays to Am, which emits both (X- and y-rays. Acute intake of Pu, from ingestion or a wound, thus mandates prompt and aggressive medical intervention to remove as much Pu as possible before it deposits in the body. Subcutaneous deposition of plutonium from a puncture wound has been effectively controlled by prompt surgical excision followed by prolonged intravenous chelation therapy with diethylenetriaminepentaacetate (Ca " —DTPA) (171). 

No reports were located regarding death in humans that could be associated with acute-, intermediate,- or chronic-duration dermal exposure to americium. An explosion and accidental exposure of a 64-year-old man to 1-5 Ci (37-185 GBq) of241 Am was followed by immediate treatment to reduce contamination to approximately 6 mCi (222 MBq) and to 1 mCi (37 MBq) after the first day (Thompson 1983 Toohey and Kathren 1995). Survival was likely the result of intense and long-term chelation therapy, such as with diethylenetriaminepentaacetic acid (DTPA). The patient lived until natural death 11 years after the accident (see Section 3.2.3.2 for more detailed information regarding this accidental exposure and subsequent treatment and follow-up). 

Breitenstein BD. 1983. 1976 Hanford americium exposure incident Medical management and chelation therapy. Health Phys 45(4) 855-866. 

A study of 55 adolescents who had been treated for lead intoxication in early childhood (11-17 years earlier) revealed no evidence of chronic nephropathy, as evidenced by endogenous creatinine clearance, BUN, serum uric acid, and routine urinalysis (Chisolm et al. 1976). PbB levels during the acute poisoning episode ranged from 100 to 650 pg/dL all patients received immediate chelation therapy. At the time of the study, their PbB levels had decreased to less than 40 pg/dL. 

Understand developmental benefits of National Institute of chelation therapy and other measures Environmental Health to reduce lead in the range of Sciences... 

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

Roels HA, Balis-Jacques MN, Buchet J-P, et al. 1979. The influence of sex and of chelation therapy on erythrocyte protoporphyrin and urinary delta-aminolevulinic acid in lead-exposed workers. J Occup Med 21 527-539. 

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

Chelators of transition metals, mainly iron and copper, are usually considered as antioxidants because of their ability to inhibit free radical-mediated damaging processes. Actually, the so-called chelating therapy has been in the use probably even earlier than antioxidant therapy because it is an obvious pathway to treat the development of pathologies depending on metal overload (such as calcium overload in atherosclerosis or iron overload in thalassemia) with compounds capable of removing metals from an organism. Understanding of chelators as antioxidants came later when much attention was drawn to the possibility of in vivo hydroxyl radical formation via the Fenton reaction ... 

At present, numerous free radical studies related to many pathologies have been carried out. The amount of these studies is really enormous and many of them are too far from the scope of this book. The main topics of this chapter will be confined to the mechanism of free radical formation and oxidative processes under pathophysiological conditions. We will consider the possible role of free radicals in cardiovascular disorders, cancer, anemias, inflammation, diabetes mellitus, rheumatoid arthritis, and some other diseases. Furthermore, the possibilities of antioxidant and chelating therapies will be discussed. 

The most successful up-to-date treatment of thalassemic patients is chelating therapy, which is based on patient s lifetime application of iron chelators. Removal of excess iron is supposed to be effective route for suppressing free radical-mediated damage. There is a great number of studies showing successful treatment of thalassemic patients with intravenous chelator desferal (desferrioxamine) and oral chelator deferiprone (LI). Biochemical studies show the efficacy of both chelators in removal of excess iron. For example, the incubation of thalassemic erythrocytes with 0.5 mmol 1 1 LI during 6h resulted in 96% removal of membrane-free iron [392], It was demonstrated that LI is able to remove pathologic deposits of... 

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