Chelation Therapy Associated with Antioxidant Supplementation Can Decrease Oxidative Stress and Inflammation in Multiple Sclerosis: Preliminary Results.

An imbalance of oxy-inflammation status has been involved in axonal damage and demyelination in multiple sclerosis (MS). The aim of this study was to investigate the efficacy of an antioxidant treatment (calcium disodium ethylenediaminetetracetic acid-EDTA) chelation therapy associated with a micronutrient complex in MS patients. A total of 20 MS patients and 20 healthy subjects, enrolled as a control group (CTR), were recruited.

Neuron Protection by EDTA May Explain the Successful Outcomes of Toxic Metal Chelation Therapy in Neurodegenerative Diseases.

Many mechanisms have been related to the etiopathogenesis of neurodegenerative diseases (NDs) such as multiple sclerosis, amyotrophic lateral sclerosis, Parkinson's disease, and Alzheimer's disease. In this context, the detrimental role of environmental agents has also been highlighted. Studies focused on the role of toxic metals in the pathogenesis of ND demonstrate the efficacy of treatment with the chelating agent calcium disodium ethylenediaminetetraacetic acid (EDTA) in eliminating toxic metal burden in all ND patients, improving their symptoms.

EDTA Chelation Therapy in the Treatment of Neurodegenerative Diseases: An Update.

We have previously described the role played by toxic-metal burdens in the etiology of neurodegenerative diseases (ND). We herein report an updated evaluation of toxic-metal burdens in human subjects affected or not affected by ND or other chronic diseases. Each subject underwent a chelation test with the chelating agent calcium disodium ethylenediaminetetraacetic acid (CaNAEDTA or EDTA) to identify the presence of 20 toxic metals in urine samples using inductively coupled plasma mass spectrometry.

EDTA Chelation Therapy for the Treatment of Neurotoxicity.

Neurotoxicity can be caused by numerous direct agents, of which toxic metals, organophosphorus pesticides, air pollution, radiation and electromagnetic fields, neurotoxins, chemotherapeutic and anesthetic drugs, and pathogens are the most important. Other indirect causes of neurotoxicity are cytokine and/or reactive oxygen species production and adoptive immunotherapy. The development of neurodegenerative diseases has been associated with neurotoxicity.

Rationale for the Successful Management of EDTA Chelation Therapy in Human Burden by Toxic Metals.

Exposure to environmental and occupational toxicants is responsible for adverse effects on human health. Chelation therapy is the only procedure able to remove toxic metals from human organs and tissue, aiming to treat damage related to acute and/or chronic intoxication. The present review focuses on the most recent evidence of the successful use of the chelating agent ethylenediaminetetraacetic acid (EDTA).

Defibrotide in the treatment of hepatic veno-occlusive disease.

Hepatic veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome (SOS), represents the most frequent complication in patients in early phase following hematopoietic stem-cell transplantation (HSCT). In its severe form, VOD/SOS can be associated with multiorgan failure and with a mortality rate >80% by day +100. Defibrotide (DF) (a mixture of 90% single-stranded phosphodiester oligonucleotides and 10% double-stranded phosphodiester oligonucleotides derived from controlled depolarization of porcine intestinal mucosal DNA) has been proposed for the treatment of SOS due to its ability to restore thrombo-fibrinolytic balance and protect endothelial cells.

Efficacy of chelation therapy to remove aluminium intoxication.

There is a distinct correlation between aluminium (Al) intoxication and neurodegenerative diseases (ND). We demonstrated how patients affected by ND showing Al intoxication benefit from short-term treatment with calcium disodium ethylene diamine tetraacetic acid (EDTA) (chelation therapy). Such therapy further improved through daily treatment with the antioxidant Cellfood.

Aluminium involvement in neurotoxicity.

The aetiology of neurodegenerative diseases (ND) seems to involve susceptibility genes and environmental factors. Toxic metals are considered major environmental pollutants. Following our study of a case of multiple sclerosis (MS) improvement due to removal of aluminium (Al) and other toxic metals, we have examined the possible relationship between Al intoxication and ND.

Improvement of oxidative and metabolic parameters by cellfood administration in patients affected by neurodegenerative diseases on chelation treatment.

Objective: This prospective pilot study aimed at evaluating the effects of therapy with antioxidant compounds (Cellfood, and other antioxidants) on patients affected by neurodegenerative diseases (ND), who displayed toxic metal burden and were subjected to chelation treatment with the chelating agent calcium disodium ethylenediaminetetraacetic acid (CaNa2EDTA or EDTA).

Methods: Two groups of subjects were studied: (a) 39 patients affected by ND and (b) 11 subjects unaffected by ND (controls). The following blood parameters were analyzed before and after three months' treatment with chelation+Cellfood or chelation+other antioxidants: oxidative status (reactive oxygen species, ROS; total antioxidant capacity, TAC; oxidized LDL, oxLDL; glutathione), homocysteine, vitamin B12, and folate.

A case of multiple sclerosis improvement following removal of heavy metal intoxication: lessons learnt from Matteo's case.

Multiple sclerosis (MS) is a chronic progressive disease of the central nervous system (CNS) provoking disability and neurological symptoms. The exact causes of SM are unknown, even if it is characterized by focal inflammatory lesions in CNS accompanied by autoimmune reaction against myelin. Indeed, many drugs able to modulate the immune response of patients have been used to treat MS.

Ozonated autohemotherapy: protection of kidneys from ischemia in rats subjected to unilateral nephrectomy.

Background: Ozonated autohemotherapy (OA) has been previously successfully used in the treatment of patients affected by peripheral occlusive arterial disease. OA consists of an intrafemoral reinfusion of autologous blood previously exposed to a mixture of oxygen/ozone (O2/O3). This study analyzes the effects of OA in protecting rat kidney from ischemia and ischemia/reperfusion damage.

Mn bioavailability by polarized Caco-2 cells: comparison between Mn gluconate and Mn oxyprolinate.

Background: Micronutrient inadequate intake is responsible of pathological deficiencies and there is a need of assessing the effectiveness of metal supplementation, frequently proposed to rebalance poor diets. Manganese (Mn) is present in many enzymatic intracellular systems crucial for the regulation of cell metabolism, and is contained in commercially available metal supplements.

Methods: We compared the effects of two different commercial Mn forms, gluconate (MnGluc) and oxyprolinate (MnOxP).

Metal chelation therapy in rheumathoid arthritis: a case report. Successful management of rheumathoid arthritis by metal chelation therapy.

Toxic metals are involved in the pathogenesis of some neurodegenerative and vascular diseases and are known to impair the immune system functions. We report here the case of a patient affected by heavy metal intoxication, who had developed an autoimmune disease. There was evidence of aluminium, cadmium and lead intoxication in a 63-year old Italian woman affected by rheumatoid arthritis (RA).

Purinoceptors in inflammation: potential as anti-inflammatory therapeutic targets.

Purinergic receptors or purinoceptors are expressed in many mammalian cells and are activated by extracellular purines (adenine, purine nucleotides and nucleosides). Both adenosine (P1) and nucleotide/nucleoside (P2, grouped in P2X and P2Y subtypes) receptors exert important role in the inflammatory processes. The significative up-regulation of many purinoceptors located on the immune cells (neutrophils, eosinophils, monocytes, macrophages, mast cells and lymphocytes) in the course of inflammatory diseases supports the interpretation of their functions.

The usefulness of chelation therapy for the remission of symptoms caused by previous treatment with mercury-containing pharmaceuticals: a case report.

Introduction: A great deal of data regarding the toxicology of mercury has been recently reported. Although the most common human exposures to mercury are currently mercury vapour from amalgam tooth fillings, methylmercury from seafood and ethylmercury as a preservative in vaccines, in the past mercury compounds have been used in the treatment of syphilis.

Case Presentation: Mercury intoxication was found in a 67 year-old Italian man affected by neurological symptoms of apparently unknown origin.

Rationale of the combined use of inspiratory and expiratory devices in improving maximal inspiratory pressure and maximal expiratory pressure of patients with chronic obstructive pulmonary disease.

Objective: To examine the rationale of the combined use of a new expiratory device in association with a previously assessed inspiratory device in improving 3 indicators of the respiratory muscle strength, for example, maximal inspiratory pressure (MIP), maximal expiratory pressure (MEP), and dyspnea grade.

Design: Randomized trial.

Setting: Home-based pulmonary rehabilitation.

Unexpected perinatal loss versus Sids-a common neuropathologic entity.

Objective: To evaluate the involvement of alterations of the central autonomic nervous system, particularly of the brainstem and cerebellum, in a wide set of victims of sudden and unexplained perinatal and infant death.

Material And Methods: The study population consisted of 63 stillbirths, 28 neonatal deaths and 140 suspected SIDS. The victims were subjected to in-depth anatomopathological examination following appropriate guidelines.

Cracked mercury dental amalgam as a possible cause of fever of unknown origin: a case report.

Introduction: Sudden fever of unknown origin is quite a common emergency and may lead to hospitalization. A rise in body temperature can be caused by infectious diseases and by other types of medical condition. This case report is of a woman who had fever at night for several days and other clinical signs which were likely related to cracked dental mercury amalgam.

The vasostatin-I fragment of chromogranin A inhibits VEGF-induced endothelial cell proliferation and migration.

Unlabelled: A growing body of evidence suggests that chromogranin A (CgA), a secretory protein released by many neuroendocrine cells and frequently used as a diagnostic and prognostic serum marker for a range of neuroendocrine tumors, is a precursor of several bioactive fragments. This work was undertaken to assess whether the N-terminal fragment CgA(1-76) (called vasostatin I) can inhibit the proangiogenic activity of vascular endothelial growth factor (VEGF), a factor involved in tumor growth. The effect of recombinant human vasostatin I (VS-1) on VEGF-induced human umbilical endothelial cells (HUVEC) signaling, proliferation, migration, and organization has been investigated.

Protective effect of EDTA preadministration on renal ischemia.

Background: Chelation therapy with sodium edetate (EDTA) improved renal function and slowed the progression of renal insufficiency in patients subjected to lead intoxication. This study was performed to identify the underlying mechanism of the ability of EDTA treatment to protect kidneys from damage.

Methods: The effects of EDTA administration were studied in a rat model of acute renal failure induced by 60 minutes ischemia followed or not by 60 minutes reperfusion.

Inhibition of chemokine expression in rat inflamed paws by systemic use of the antihyperalgesic oxidized ATP.

Background: We previously showed that local use of periodate oxidized ATP (oATP, a selective inhibitor of P2X7 receptors for ATP) in rat paw treated with Freund's adjuvant induced a significant reduction of hyperalgesia Herein we investigate the role of oATP, in the rat paws inflamed by carrageenan, which mimics acute inflammation in humans.

Results: Local, oral or intravenous administration of a single dose of oATP significantly reduced thermal hyperalgesia in hind paws of rats for 24 hours, and such effect was greater than that induced by diclofenac or indomethacin. Following oATP treatment, the expression of the pro-inflammatory chemokines interferon-gamma-inducible protein-10 (IP-10), mon ocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) within the inflamed tissues markedly decreased on vessels and infiltrated cells.

Distribution of 99mTc-labeled lymphocytes in control and inflamed rats.

We studied the in vivo fate of CD8(+) lymphocytes, of naive (CD8(+)CD45RC(bright)) or memory (CD8(+)CD45RC(dim)) phenotype, injected in syngeneic rats, after their sorting and labeling with [(99m)Tc] HM-PAO. By using the scintigrafic method we showed that memory CD8(+) lymphocytes were able to recirculate into liver and lungs. The same method was also successfully used to in vivo study the homing of total blood lymphocytes obtained from inflamed rats.

In vivo vascular leakage assay.

This chapter describes the methods for measuring the increase in vascular permeability induced by tumor necrosis factor alpha (TNFalpha, or other mediators, in vivo in animal models. Mouse liver or kidney are perfused through the portal vein or the renal artery, respectively, by intravascular injection of a blue dye (trypan blue or Evans blue) combined with albumin. When endothelial permeability is increased, the dye extravasates and reaches the subendothelial spaces.

Chromogranin A protects vessels against tumor necrosis factor alpha-induced vascular leakage.

Elevated levels of circulating chromogranin A (CgA), a protein stored in the secretory granules of many neuroendocrine cells and neurons, have been detected in the blood of patients with neuroendocrine tumors or heart failure. The pathophysiological role of increased secretion of CgA is unknown. Using mice bearing subcutaneous tumors genetically engineered to secrete CgA in circulation, we have found that increased blood levels of this protein prevent vascular leakage induced by tumor necrosis factor-alpha (TNF) in the liver venous system.