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Buerger's disease

Buerger's disease (also known as thromboangiitis obliterans) is an acute inflammation and thrombosis (clotting) of arteries and veins of the hands and feet. It is strongly associated with use of tobacco products, primarily from smoking, but also from smokeless tobacco. more...

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There is an acute inflammation and thrombosis of arteries and veins of the hands and feet. The main symptom is pain in the affected areas. Ulcerations and gangrene in the extremities are common complications, often resulting in the need for amputation of the involved extremity.


A concrete diagnosis of thromboangiitis obliterans is often difficult as it relies heavily on exclusion of the conditions. The commonly followed diagnostic criteria are below although the criteria tend to differ slightly from author to author. Olin (2000) proposes the following criteria:

  1. Age younger than 45 years
  2. Current (Or recent) history of tobacco use
  3. Presence of distal extremity ischemia (indicated by claudication, pain at rest, ischemic ulcers or gangrene) documented by noninvasive vascular testing such as etc
  4. Exclusion of autoimmune diseases, hypercoagulable states and diabetes mellitus by laboratory tests.
  5. Exclusion of a proximal source of emboli by echocardiography and arteriography
  6. Consistent arteriographic findings in the clinically involved and noninvolved limbs.


There are characteristic pathologic findings of acute inflammation and thrombosis (clotting) of arteries and veins of the hands and feet (the lower limbs being more common). The mechanisms underlying Buerger's disease are still largely unknown. It is suspected that immunological reactions play a role.


Immediate and absolute cessation of tobacco use is necessary to prevent any further progression of the disease. Even a few cigarettes a day or nicotine replacements can keep the disease active. Vascular surgery can sometimes be helpful in treating limbs with poor perfusion secondary to this disease.


Buerger's disease is rarely fatal, but amputation is common in patients who continue to use tobacco. It often leads to vascular insufficiency.


The disease occurs exclusively in tobacco users, so not using tobacco prevents you from getting the disease. Diet has no influence.


Prevalence of the disease has decreases with the decreased prevalence of smoking. It is more common among men. It is more common in Israel, Japan and India than in the United States and Europe. The disease is most common among natives of Bangladesh, who smoke special cigarettes made of raw tobacco (bidi).


Buerger's disease was first reported by physician Leo Buerger in 1908.


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Preventing amputations for peripheral vascular disease - Letters to the Editor
From Townsend Letter for Doctors and Patients, 12/1/03 by Wayne Martin


There are far too many amputations among our older people. I have heard a figure of 60,000 such diabetic amputations each year in the USA. There could be very few such amputations.

I am age 92 and in 1929 at age 17 I was hit by an auto on a motorcycle and lost my left leg below the knee. I see older people who suffered diabetic amputations who never learn to use an artificial leg. There are many ways to prevent diabetic amputations or amputations from vascular disease in general.

First, let us tell about Isidore Snapper, MD of Brooklyn, New York. He had spent ten years in a hospital in North China. He had returned to the USA when the Japanese occupied North China. He had taken note that the very poor Chinese living in the North of China had as many diabetic patients as in the USA, however the diabetic patients among the poor Chinese had none of the vascular problems that diabetics have here. They did not suffer amputations and they did not go blind.

He expressed these observations in a book published in 1941, Chinese Lessons to Western Medicine, New York, Interscience 1941. The diet of these poor Chinese was vegetarian and millet and soya food was the main items in diet. I spent from 1939 to 1944 working in Brooklyn and I met Dr. Snapper once for lunch in 1942.

It was in 1970 that I had an exchange with Professor of Hematology R.G. MacFarlane of Oxford University. He had two reports, one in The Lancet 1946 ii p 888 and the other in the journal Physiology 1947 vol 105 p 104, on the great benefit of soya protease inhibitor. He said all whole grains and beans had protease inhibitors like the one in soya beans, that these protease inhibitors acted like warfarin in the inhibition of the red or fibrin portion of a blood clot. Unlike warfarin, they would not cause internal bleeding.

He reported on the freedom from death from myocardial infarction among the black population of Uganda as told by Robert O'Neal et al. in the January 1960 issue of the American Journal of Cardiology. This population lived on a vegetarian diet of whole grains, millet, corn and barley.

MacFarlane thought that the soya and grain protease inhibitors were preventing the coronary blood clots that cause most heart attacks. MacFarlane was greatly disappointed that he could not interest a single drug firm in selling soya or grain protease inhibitor. He was greatly interested in Snapper's report about the lack of amputations and blindness among the poor North Chinese diabetics. He said if it was looked into, the same would be true among the black population of Uganda.

So we have Snapper telling of the poor North Chinese diabetics being free from amputations and blindness and we have MacFarlane suggesting that this happy circumstance was due to the warfarin-like effect of a vegetarian whole-grain and beans diet.

Diabetic patients here in the USA may want to live on such a vegetarian diet. First one should eat only whole grain bread. Polished white rice is nearly devoid of the beneficial protease inhibitor but brown rice can be had with a protease inhibitor as can all kinds of beans, dry or frozen. Canned beans are devoid of protease inhibitor due to the heat used in the canning process. One can buy millet in a food co-op.

Dr. M.S. Mazel owned the Edgewater Hospital in Chicago. I visited his hospital in 1977. In the lobby was the life-size photo of a smiling man walking out of his hospital. Alongside of it was a before and after photo of the patient's foot and lower leg.

Mazel was an early user of the proteolytic enzyme urokinase in treating patients having a heart attack. In the photo of this patient's foot and leg there was a great toe with an ulcer and some black and blue coloration on it and another ulcer on his leg with black and blue coloration. The patient was a diabetic and he was suffering great pain from the two ulcers. The foot was cold and well below body temperature. The patient had been to three major hospitals and they had all urged amputation at once. At Edgewater Hospital the patient was treated with an intravenous infusion of urokinase. I do not know if the patient had one infusion or more than one, but the urokinase had lysed the blood clots in his leg and foot. His foot had returned to body temperature and the two ulcers had quickly healed. A second photo of the patient's foot and leg showed the ulcers healed. Amputation had been avoided.

There are now more of the clot-busting proteolytic enzyme drugs but I have not heard of any of them being used to treat diabetic patients with foot ulcers to prevent amputations by a doctor other than Dr. Mazel. I should think that many diabetic amputations could be avoided by the infusion of a proteolytic enzyme drug.

I was a dear friend of Evan Shute, MD, Med. ScD of London, Canada from 1946 until the time of his death. He spent from 1946 onward fostering the treatment of coronary heart disease with what he called Big E, vitamin E at 400 iu to 800 iu daily.

He had formed the Shute Foundation and had a publication called The Summary. In The Summary for December 1973 he had dramatic photos of the feet of two diabetic patients with portions of their feet being black. The feet were cold. One had all of the heel black. This patient was a cigarette smoker who continued to smoke. On 800 iu of vitamin E as d alpha tocopherol, healing began to take place at the demarcation of the black area. The foot returned to body temrpature after about two weeks. After eight months the entire black heel self-amputated. So the patient lost his heel, but the leg was saved.

With the second patient, the entire front three inches of the foot was black. With this patient it took 15 months for the entire black front area of the foot to self-amputate and fall off, on treatment with vitamin E. So this patient lost one-third of the foot but was saved from amputation.

Dr. Shute said that it was not often that he would see a patient with so much black area of the foot. Such patients usually suffered amputation long before they had so much of their foot turn black. Dr. Shute would show one photo after another of patients with small ulcers on toes that healed on treatment with vitamin E--in which case no part of the foot was lost and amputation was prevented. He said that once the foot had returned to body temperature, it was a sign that amputation would not be needed.

Vitamin E at 800 iu a day may be considered safe so it is suggested that diabetic patients might take 800 iu of vitamin E a day in hope that it will prevent getting a cold foot and perhaps ulcers that would lead to amputation.

In 1975, I visited Kurt Oster, MD at Fairfield University. He was a cardiologist and had his own way to prevent amputations among older diabetic patients.

During the 20th Century, it was as if the food and water industries were trying to think up more ways to cause deaths from heart attacks. In an article of mine in The Townsend Letter for Doctors & Patients for August/September 2003, I told how water softeners came on the market in a big way after 1950 and caused a great many deaths from heart attacks by removing highly beneficial magnesium from drinking water. In the same article I told of how the new oil seed industry was formed after 1925 and how heart attack deaths increased in direct proportion to the sale of their product--the new polyunsaturated vegetable oils and margarine.

In 1936 the entire dairy industry began to sell homogenized milk. Oster holds that the homogenizing of milk has caused a vast increase in heart attack deaths and has caused many amputations of diabetic patients' legs.

Here is Oster's explanation for the harm due to the homogenizing of milk. Nature put xanthine oxidase, an oxidizing enzyme, in milk in big particles. As such, they will not pass through the intestinal tract and they will not get into the blood. Once milk is homogenized, the xanthine oxidase particles are made very small and all of them get into the blood circulation. This according to Oster, is most harmful to the vascular tree, causing heart attacks and foot and leg ulcers in diabetic patients.

Professor Stephen Seely of the University of Sheffield found this of interest and did a study of liquid milk and cheese consumption vs heart attacks. His report was in Medical Hypotheses 1981 vol 7 p 907-10. At the time of his study, milk worldwide was homogenized.

Finland had the highest death rate from heart attacks of any nation in the world. Protein from liquid milk in Finland was 30.4 grams a day. In Germany liquid milk protein was 14.1 grams a day. In Japan liquid milk protein was only 2.5 grams a day. Finland had twice the death rate from heart attacks as had Germany and the death rate from heart attacks in Finland was ten times the death rate from heart attacks in Japan. Then Seely did a study of milk protein in cheese consumption in several nations. He could find no increase in heart attacks due to eating cheese. In the making of cheese the milk is never homogenized.

Now back to Oster. He showed me three photos of diabetic patients with leg and foot ulcers. In all three cases other doctors had advised amputation at once. He showed before and after photos with the ulcers healed and amputations prevented. He said that folic acid is an antagonist to xanthine oxidase and will tend to nullify the harm of it. His treatment was to get the patient to avoid homogenized milk and to take 80 mg of folic acid a day and ten grams of vitamin C a day. That is about 100 times as much folic acid as in average vitamin pills.

I told him of the results that Dr. Evan Shute was having with vitamin E in the treatment of diabetic foot and leg ulcers. He thought it well to add 800 iu of vitamin E to his treatment. He, like Shute, felt that if a cold foot came to body temperature it was a very good sign that an amputation could be avoided.

In the February/March 2003 issue of The Townsend Letter, I had a letter on Coley's Toxins. In it I told of a doctor at the Veterans Administration Hospital in Newington, Connecticut. Dr. Harry Gray, who in the period of 1932 to 1934 treated 26 patients with Buerger's disease. All had ulcers--some with gangrene in the foot. All, by orthodox treatment, would have suffered amputation. All had cold feet and lack of a pulse in the foot and lower leg. All were treated with injections of Coley's toxins into the gluteus maximus muscle with a febrile reaction of 102[degrees]F. With all these patients, the foot returned to body temperature, the pulse was restored to the foot and the ulcers were healed. One patient was traced ten years later, working on his feet in an aircraft factory.

The duration of treatment was not stated but it is presumed that treatment and a full recovery happened in days rather than in weeks. Dr. Gray felt that the same treatment could be used to treat diabetic patients with foot ulcers. All of Dr. Gray's patients were spared amputation.

My friend Glen Wilcoxson, MD of Spanish Fort, Alabama is treating patients with Coley's Toxins. I hope that a diabetic patient with a cold foot and ulcers may come to him for treatment with Coley's Toxins to see if amputation may be prevented.

Wayne Martin, BS, ChE

25 Orchard Court

Fairhope, Alabama 36532 USA

251-928-3975 / Fax 251-928-0150

COPYRIGHT 2003 The Townsend Letter Group
COPYRIGHT 2004 Gale Group

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