|Blood Group Link||Colitis shows a slightly higher incidence of group O over other ABO groups.|
As the name suggests ulcerative colitis involves only the colon and rectum although some "backwash" may be occur in the last part of the small intestine. In contract to ChrohnĘs disease, ulcerative colitis involves the mucosa or the innermost lining of the colon wall whereas Chrohn's disease involves all layers of bowel and may involve any part of the gut, from mouth to anus. Like Chrohn's, having ulcerative colitis increases the risk for colon cancer.
Conventional treatment involves the use of aminosalicylates (ASA) and corticosteroids. The old Sulfa antibiotics and newer 5-ASA preparations like Asacol, Pentasa, Dipentum are still the mainstay of treatment. Acute relapses are often treated with Corticosteroids, though their long-term use has substantial toxicity. In patients requiring long-term steroids, immunosuppressive agents like imuran and 6-MP are helpful in reducing the required dose of steroids. However, these drugs may take several months to manifest their action.
Evidence suggests that patients with ulcerative colitis have elevated antibodies to opposing blood groups. This probably represents the production of blood group like substances from the mucins of the intestinal lining by bacteria in the gut. If so, it may help explain why Sulpha drugs, which work by suppressing the levels of gut bacteria, are generally effective in controlling inflammation. The intestinal microflora are known to be disturbed inflammatory bowel disease.(3) and it has been thought that ulcerative colitis patients were mounting some sort of allergic hypersensitivity to gut bacteria, so depressing the levels of bacteria reduces the immune provocation.
However, it may be specific strains of bacteria capable of degrading the mucin of colitis patients into antigens which mimic an opposing blood type are the true cause of the immune reaction in inflammatory bowel disease. For example, bacteria producing the B antigen in the mucous of a colitis patient who is type A who cause the immune system of the patient to mistake their own colon lining for a bad blood transfusion, and attack it as foreign. This has been reported in the literature, and several strains of bacteria, including species of Proteus vulgaris, a common gut bacteria, are capable of synthesizing a blood type B antigen out of colon mucous called "pseudo-B".
In one case history reported, a 27 year old man was admitted to a hospital for extensive relapse of his ulcerative colitis. He was typed as "B" and was vigorously treated with prednisolone (50 mg/day i.v.) but no response was obtained. Surgery (colectomy with ileostomy) was performed on the 22nd hospital day, and a proctosigmoidectomy (removal of the rectum and lower bowel) was performed on him six months later. At the second sugery, a preoperative blood type disclosed that his blood was not cross-matched but his ABO blood group could not be identified as "B", as determined upon admission.
Gut bacteria are capable of manufacturing large amounts of both A and B blood type antigens in the gut by degrading colon mucin. Because of this, it might be hypothesized that type O, who are the only blood type to manufacture both anti-A and anti-B, would have a greater incidence of ulcerative colitis. The literature is mildly supportive of this (1) though larger and better studies need to be done. It is true, though that type O, especially type O non-secretors, do mount a more intense immune reaction (phagocytosis) than the other types. (2) In my own practice, I have found that type O's with inflammatory bowel disease do tend to develop a more aggressive form than the other types, but do well when they follow the appropriate diet for their type.
As well have seen, many gums found in commercially processed foods can intensify the effects of dietary lectins. One gum in particular, carrageenan is used to induce ulcerative colitis like symptoms in test animals. Because carrageenan is effective at stabilizing milk proteins, it is often used in milk and diary products. However, the studies on humans are conflicting: Given large doses, no inflammatory lesions were noticed in healthy human volunteers. (5) However, it should be remembered though that milk proteins as well as gums intensify the effects of dietary lectins, so giving large does of carrageenan independant of milk products and lectin containing foods may not be sufficient to produce problems in healthy individuals.
|Special Note||Most physicians are pretty negligent about the role of blood type in the large intestine (or colon). Here the emphasis is on elimination -unlike the small intestine, where the focus is predominately on absorption. A bit of assimilation does takes place in the large intestine - principally electrolytes like sodium and potassium and a few vitamins. Large quantities of ABO blood type antigens are found in the gastrointestinal mucosa; a fact which led an editorial in the renowned journal Lancet to peripatetically suggest that they must have some function. |
Your particular blood type is an important influence on the growth of particular strains of bacteria in your intestine. Many bacteria consume blood type antigens (which when you think about it, are just another sugar). ABO blood type are extensively expressed in the human large intestine. Interestingly enough, the upper colon contains very large amounts of blood type antigens, which gradually diminish until by the very end of the colon, there is little or no blood type antigen to be found. This probably reflects their use as a food source by the colon bacteria; as debris passes through the colon, less and less nutrients can be found in it. The depletion of blood type antigens is just another aspect of this phenomenon.
The composition of the normal flora varies somewhat from individual to individual. Some bacterial species may be carried only transiently. Most are fairly permanent--animal experiments have shown that it can be extremely difficult to alter the composition of the normal flora of the gut in a healthy person. Many of the common bacteria choose to live in the colon of one blood type or another. Sometimes this is because the bacteria can mimic the blood type of their host, and so are viewed as 'self' by the host's immune system. In other circumstances, certain bacteria have a taste for one particular ABO antigen over others and prefer to nibble mucus containing that particular blood type antigen. Some bacteria more easily adhere to the mucus on one blood type over others because they themselves make lectins which they use to attach to the walls of the colon, and these lectins are usually specific for one blood type.
|References||1. Editorial. Lancet Saturday 20 September 1969|
2. Springer GF Importance of blood-group substances in interactions between man and microbes. Ann NY Acad Sci. 1970 Feb 13;169(1):134-52.
3.Variyam EP, Hoskins LC Mucin degradation in human colon ecosystems. Degradation of hog gastric mucin by fecal extracts and fecal cultures. Gastroenterology 1981 Oct;81(4):751-8
4. Springer GF. Role of human cell surface structures in interactions between man and microbes. Naturwissenschaften. 1970 Apr;57(4):162-71.
5.Chiba M, et al Anti-erythrocyte antibodies in ulcerative colitis: case report and discussion on the pathophysiology of anti-erythrocyte antibody. Gastroenterol Jpn. 1988 Oct;23(5):564-9.
6.Kesely KT. Frequency of blood groups of the ABC and Rho(D) system in patients with viral hepatitis, cirrhosis of the liver, bile stones, pancreatitis, urolithiasis and ulcerative colitis. Rev Czech Med. 1970;16(2):60-71.
7.Tandon OP, Bhatia S, Tripathi RL, Sharma KN Phagocytic response of leucocytes in secretors and non-secretors of ABH (O) blood group substances. Indian J Physiol Pharmacol 1979 Oct-Dec;23(4):321-4
8.Hentges DJ (Ed.) Human Intestinal Microflora in Health and Disease. Academic Press, New York, NY, 1983
9. Bonfils S. Carrageenan in the human gut. Lancet 1970,ii, 414