Poisoning chelation therapy

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. 

The interaction of ligands derived from salicylic acid and its derivatives has been extensively investigated (83, 147, 149, 160, 170, 176, 183-205). A similar situation obtains with regard to l-hydroxy-2-naphthoic acid (185, 194, 196, 198, 206-215). Salicylic acid derivatives may be useful in chelation therapy for beryllium poisoning (2). 

Treatment of acute arsenic poisoning includes removal from the exposure source, supportive measures for loss of fluids, and chelation therapy (Ibrahim et al., 2006). Chelators that can be used include dimercaprol or 2,3-dimercaptosuccinic acid. In cases of renal failure, hemodialysis should be considered. 

The toxicological action of tetraethyllead is different from that of inorganic lead. As one manifestation of this difference, chelation therapy is ineffective for the treatment of tetraethyllead poisoning. The toxic action of tetraethyllead appears to involve its metabolic conversion to the triethyl form. 

Toxic heavy metals, such as cadmium, lead, and mercury, are sulfur seekers that bind strongly with thiol groups, which is one of the ways in which they interact adversely with biomolecules, including some enzymes. Advantage has been taken of this tendency to use thiols in chelation therapy in heavy metal poisoning. Among the thiols tested for this purpose are meso-2,3-dimer-captosuccinic acid, diethyldimercapto succinate, a-mercapto-P-(2-furyl), and a-mercapto-P-(2-thienyl) acrylic acid.3 The structural formulas for the first two are... 

I think I had MCS tendencies all along and that perhaps mercury poisoning and/or chelation therapy pushed me over the edge into full-blown MCS. At any rate, after I finished my chelation therapy I developed a heightened sense... 

The high affinity for oxidized iron makes the siderophores ideal candidates for chelation therapy where the body is becoming overwhelmed by iron(III) either through acute poisoning or conditions like haemochromatosis that can occur when patients receive frequent blood transfusions. While enterobactin would seem to be the primary choice it has two major drawbacks its synthesis is complicated and, although both isomers bind iron(III) to the same extent, only the L-isomer has activity in vivo. Consequently desferrioxamine B is the agent of choice. 

A Note about Chelation Therapies. Chelation therapies are used to prevent or treat metal-induced toxicities. They are often used in acute poisoning scenarios, but can also be used to assess exposure. One of the major challenges in the management of chelation therapies is the tendency for chelating agents to interact with essential metals, particularly calcium and zinc. Chelation therapies should only be administered by a physician due to the potential to disrupt essential metal functions. The Food and Drug Administration does not regulate dietary supplements, and several do it yourself chelation therapies are available. These are not advisable. 

Lead nephropathy is important because it is one of the few renal diseases that is preventable. Moreover, lead-induced acute renal dysfunction can sometimes be reversed by chelation therapy [19, 28, 63]. The salutary effect of chelation therapy appears to be on the acute reduction in GFR and the acute elevation of blood pressure associated with elevated blood lead concentration rather than on the long-term effects of cumulative exposure associated with endothelial dysfunction, hypertension, and interstitial nephritis. There is no evidence that such therapy reverses established interstitial nephritis. The partial remission achieved among moonshiners and lead workers appears to represent reversal of the physiologic effects of acute poisoning superimposed on chronic lead nephropathy. No improvement in renal function has been observed once advanced interstitial nephritis is present and the steady-state serum creatinine concentration exceeds about 3 mg/ dL [64]. 

In summary, chelation therapy is justified in cases of symptomatic lead poisoning or when the blood lead exceeds about 80 pg/dL. When no symptom end-point... 

Chelating agents for mercury, such as cysteine and penicillamine, have been used as intervention measures to reduce the concentration of inorganic mercury. However, chelation therapy has yielded variable success in cases of alkyl mercury poisoning. Studies of MMM suggest that chelators may reduce brain and blood mercury levels if started within a few days after exposure. Surgical gallbladder drains and oral administration of a nonabsorbable thiol resin have been applied in order to interrupt biliary excretion and reabsorption of mercury by the intestine. 

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