Clinical Review – Resolution of Arterial Ulcer with EDTA Chelation Therapy

Efrain Olszewer, MD

A 72-year-old female patient, with arterial hypertension, consulted for an arterial ulcer in the right ankle (See photo 1, dated 3 March 2021). She had been treated conventionally for the last three months with no apparent results. 

Arterial ulcers are skin lesions caused by problems with blood circulation. They appear in the lower limbs (usually near the shin), are painful and difficult to treat. The origin of this type of ulcer is linked to complications in the circulation.

After clinical laboratory evaluation, the patient decided, after exchanging information with the bedside physician, to use chelation treatment with EDTA (ethylene diamine tetra acetic acid) since all conventionally established treatments had ended without the expected success. 

The treatment is carried out with a weekly application of chelating agents,1 which include Sf (0.9% saline solution) 250 ml,  disodium EDTA 10 ml/15%,  vitamin C 1 gram,  B complex 2 ml,  and magnesium sulfate 10 ml/10%). 

After six months and 24 applications, the patient shows complete healing (See photo 5 dated 10 August 2021), as shown in the photographs.  Kidney function was not altered after 24 infusions based on BUN and creatinine levels.

Arterial ulcers are painful and difficult to treat. The origin of this type of ulcer is linked to complications in the circulation. A lot of attention is needed because, despite having very similar causes compared to venous ulcers, the treatment is different. That is, the diagnosis directly influences the healing process of the lesion and, if done wrongly, can have serious consequences. 

This type of skin lesion begins with the obstruction of the arteries by fatty plaques. 

This obstruction leads to a lack of blood rich in oxygen and nutrients to irrigate the tissues, resulting in cell death and, consequently, in lesions.

Due to the fragility of the skin in the region, any small bump or trauma can cause wounds.  Therefore, the appearance of lesions in more exposed regions and with bony prominence, such as malleolus, sides of the feet, shins or fingers, is very common. Some external factors also favor the appearance of arterial ulcers, such as smoking, uncontrolled diabetes, hypertension, and high cholesterol. 

Arterial ulcers can be identified from the following symptoms: 

  • Severe pain in the lesion (in some cases, the patient starts to limp);
  • Even when resting the limbs still hurt; the pain can get worse at night;2,3 
  • When elevating the affected limb, the pain increases even more; 
  • Pain relief only when the leg is left to rest downwards; 
  • Circular-shaped lesion; 
  • The skin around the lesion loses its hair, has a cold temperature, and becomes whitish; 
  • The blood pulse in the region decreases; 
  • Nails become thicker.

The father of modern biochemistry was the French-Swiss chemist Alfred Werner. In 1893 he developed the theory of coordination compounds, today referred to as chelates. 

For this turning point in the reclassification of inorganic compounds, he was awarded the Nobel Prize in 1913. He went on to define the mechanisms for the process by which metals bind to organic molecules, which is the basis for the chemistry of chelation. 

Chelation therapy began to be used in cardiovascular pathologies by Soffer et al., and Norman Clarke in the 1960s. Historically, as calcium EDTA or versenate lost its patent in the 1960s and 70s, EDTA became an orphan drug, and its scientific discussion began to lose its due importance.4,5

Several works done by Carter, Olszewer, and collaborators in the 1980s and 90s show the efficacy of EDTA in peripheral vascular pathology.6,7 

As of 2020, published works by the group of Lamas and collaborators, called the TACT study, show the effectiveness of chelation therapy in cardiovascular pathologies, showing a 40% reduction in the second coronary event in patients with ischemic cardiomyopathy secondary to diabetes in double-blind studies, currently in the TACT 2 work phase.8,9 

The EDTA premier use was in the form of calcium,10 but as the hypothesis of endothelial relaxation was used as an explanation of EDTA chelation pharmacological use, the use of EDTA calcium switched to sodium EDTA to decrease free calcium levels. Sodium EDTA is associated with magnesium, which has greater potential for association with plasma calcium, maintaining magnesium levels in the reduction of pre- and post-load so that patients do not present with symptoms of hypocalcemia or laboratory alterations. 

EDTA has an affinity for many minerals, most importantly zinc, and for several heavy metals, in particular lead; calcium is on an intermediate scale.11,12 

EDTA’s main mechanisms of action in vascular pathology12-16 were postulated as being the following:

  1. Decreases platelet aggregation;
  2. Decreases post-load, by endothelial relaxation mechanisms in the sodium, magnesium, phosphorus pump; 
  3. Increases the virtual diameter of vessels by 10% by Poiseuille’s law; 
  4. Chelates heavy metals such as lead and iron, decreasing excessive production of free radicals in regions of clinical and subclinical ischemia; 
  5. Modulates metalloenzymes. 

Based on these premises and on the lack of therapeutic response for more than three months of conventional treatments without therapeutic results, treatment with chelating agents for arterial ulcer is indicated with a periodicity of once a week until the closure of the ulcer. Closure happens on average in six months, totaling 24 intravenous applications, as was the case with the present patient, as shown by the dates in the photos. 

The patient, who had constant pain for months, found progressive relief from the sixth application, becoming asymptomatic after the 10th intravenous infusion. 

Experience has shown that arterial and venous ulcers respond very well to the treatment of associated chelating agents in the absence of response to conventional treatment, and should be thought of in these extraordinary situations


Conclusion

EDTA chelation therapy in the present case seems to be a safe and effective therapy for arterial limb ulcers that did not have a positive response to traditional therapies.


References

  1. Rozema TC. Special issue: protocols for chelation therapy.  J Adv Med. 1997;10;5-100.
  2. Cleveland Clinic. Lower Extremity (Leg and Foot) Ulcers.         Cleveland Clinic. http://my.clevelandclinic.org/heart/disorders/vascular/legfootulcer.aspx. Updated November 2010. Accessed August 22, 2019.
  3. Gabriel A. Vascular Ulcers. Medscape 3. http://emedicine.medscape.com/article/1298345–overview. Updated July 11, 2012. Accessed August 22, 2019.
  4. Clarke NE, Sr. Atherosclerosis, occlusive vascular disease and EDTA. Am J Cardiol. 1960;6:233236.
  5. Soffer A, Toribara T, Sayman A. Myocardial responses to chelation. Br Heart J. 1961 Nov;23:690.
  6. Olszewer E, Carter JC. EDTA chelation therapy in chronic degenerative disease. Med Hypotheses. 1988;27:41–49. 5. 
  7. Olszewer E, Carter JP. EDTA chelation therapy: a retrospective study of 2,870 patients. J Adv Med. 1989;2:197–211
  8. Lamas GA, Goertz C, Boineau R, et al. Effect of disodium EDTA chelation regimen on cardiovascular events in patients with previous myocardial infarction: The TACT Randomized Trial. JAMA. 2013;309(12):1241-1250. doi:10.1001/jama.2013.2107.
  9. Lamas GA, Boineau R, Goertz C, et al. Oral High-Dose Multivitamins and Minerals or Post Myocardial Infarction Patients in TACT. Annals of Internal Medicine. 2013;159(12):797-805.
  10. Calcium disodium edetate and disodium edetate. Federal Register, Volume 35, No. 8, Tuesday, January 13, 1970, 585-587
  11. Aronson AL and Hammond PB: Effect of two chelating agents on the distribution and excretion of lead. J Pharmacol Exp Ther 146:241-251, 1964.
  12. Blaurock-Busch E.  Toxic metals and antidotes: the chelation therapy handbook.  Germany, MTM Publishing, 2010.
  13. Aronov DM: First experience with the treatment of atherosclerosis patients with calcinosis of the arteries with trilon-B (disodium salt of EDTA). (Russ, Moscow) Klin Med 41:19, 1963.
  14. Scientific Rationale for EDTA Chelation Therapy Mechanism of Action Elmer M. Cranton, M.D. James P. Frackelton, M.D.  This chapter is adapted from A Textbook on EDTA Chelation Therapy, Second Edition, 2001 edited by Elmer M. Cranton, M.D., Hampton Roads Publishing Company, Charlottesville, Virginia.
  15. Wartman, A., Lampe, T.L., McCann, D.S., and Boyle, A.J. Plaque reversal with Mgedta in experimental atherosclerosis: Elastin and collagen metabolism. J Atherosclerosis Res, 1967, 7: 331-341
  16. Aronson AL, Hammond PB and Strafuss AC: Studies with calcium ethylenediaminetetraacetate in calves; toxicity and use in bovine lead poisoning. Toxicol Appl Pharmacol 12:337-349, 1968

 Published March 25, 2023.


About the Author

Efrain Olszewer, MD, who specializes in internal medicine and cardiology, is clinical director of the International Center of Prevention Medicine (CMP) in Brazil. He is the president of the Brazilian Orthomolecular Society and editorial director of the Journal of Orthomolecular Practice. He has written 93 books on health and medicine.