Reversal Of Terminal Congestive Heart Failure By EDTA Chelation Therapy Book Pdf
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Treatment of arsenic poisoning begins with the removal from the exposure source. Supportive measures and chelation therapy are the mainstays of management. Volume resuscitation is of paramount importance in the severely poisoned patient, and chelation with dimercaprol or succimer (2,3-dimercaptosuccinic acid, DMSA) should be considered in patients who have symptoms or increased body burden of arsenic. Hemodialysis may be considered for patients who have renal failure. However, using A375 cells, the role of arginine, a component of aqueous garlic extract, has been shown in remediation of sodium arsenite induced toxicity [48]. In addition, coadministration of folic acid and vitamin B12 has been shown to prevent cardiac tissues from arsenic induced oxidative damage in vivo. [49]
Removal of the patient from the source of the toxic exposure is the most important intervention. As elemental mercury typically has minimal toxicity when ingested, there is little role for GI decontamination. Although chelation therapy is considered the mainstay of treatment several controversies remain regarding its use. Chelators are charged molecules capable of binding the metal ion forming a neutral complex excreted by the kidney. Several agents are available such as succimer, dimercaprol, and D-penicillamine. Patients may require chelation for several months depending on the total body burden of mercury. In patients who have developed renal failure, hemodialysis may be required, with or without the inclusion of a chelation agent.
A lesser known side effect of chemotherapy drugs is cardiac toxicity. Cardiotoxicity is typically rare, yet may occur in more than 20% of patients treated with doxorubicin, daunorubicin or fluorouracil (Pai and Nahata 2000). Pai and Nahata (2000) describe the following cardiac events that may occur as a result of such chemotherapy drugs: mild blood pressure changes, thrombosis, electrocardiographic changes, arrhythmias, myocarditis, pericarditis, myocardial infarction, cardiomyopathy, cardiac failure (left ventricular failure) and congestive heart failure (Pai and Nahata 2000). ALA not only ameliorates these symptoms (Al-Majed et al.2002) but is also protective against the onset of cardiotoxicity (Balachandar et al. 2003).
Background: Digoxin is a common medication used in the treatment of congestive heart failure and arrhythmias. There are no reports of digoxin toxicity being treated with digoxin immune Fab fragment (DIF) in neonates.
Liang et al.49 demonstrated that the exposure to the low environmental level of lead (Pb) can accelerate the progressive renal failure in patients without diabetes, but who suffer from chronic kidney disease. The authors observed 202 patients with chronic renal failure during 24 months. Subsequently, 64 subjects with high levels of Pb in blood were divided, randomly, into two groups. During three months, the patients of the 'chelation' group received therapy with calcium disodium ethylenediaminetetraacetic acid (EDTA).Meanwhile, those in the 'control' group received placebo. Based on their results, they suggest that repeated chelation therapy can improve kidney function and delay the progression of renal failure. 153554b96e
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