Found this site to be very informative..in relation to gluten and collagenous colitis...
http://www.bcm.edu/gastro/DDC/grandroun ... 9-DISC.HTM
ive copied here...for a quick scan...to view the visuals u need to go to the site...
Final Diagnosis: Celiac sprue with collagenous colitis
1. What is the pathogenesis of celiac sprue and what is gluten?
Celiac Disease is an inflammatory disease of small intestinal caused by ingestion of wheat gluten or related proteins from rye or barley. There is the characteristic villous atrophy of the small intestinal mucosa, rapid improvement clinically and histologically after adherence to a strict gluten-free diet, and clinical relapse when gluten is reintroduced.
The prevalence of celiac disease was estimated to be approximately 1 case in every 250 in one study screening blood donors.(1) This is likely an underdiagnosed entity (prevalence in the US is 1:4500 in the clinical setting), and the average length of time it takes for a symptomatic person to be diagnosed with celiac disease in the U.S. is 11 years.(2) A significant number of patients present with iron deficiency anemia or bone disease in the absence of gastorintestinal pathology. In a study by Fasano et al., only 35% of newly diagnosed pateints had chronic diarrhea, thus showing that diarrhea does not have to be present to diagnose celiac disease. From the same study, 41% of adults diagnosed were asymptomatic.(3) The risk in first degree relatives is 10-20%.
Diagnosis is made with a combination of small intestinal biopsy and serologic tests (IgA endomysial antibody (IgA EMA), IgA tissue transglutaminase antibody (IgA tTG), IgA antigliadin antibody (IgA AGA), and IgG antigliadin antibody (IgG AGA)). These tests should be done while the patient is on a non-gluten-free diet as antibodies may disappear when individuals are gluten free. Intestinal biopsy remains the gold standard for diagnosis.
"Gluten" encompasses the prolamins and the glutenins. The prolamins in wheat are called "gliadins". Prolamins from other cereals are also considered to be gluten and are named according to their source (secalins from rye, hordeins from barley, avenins from oats, and zeins from nontoxic corn).(4) (Visual 1)
From a genetics standpoint, HLA-DQ2 (heterodimer) has been found in 95% of sprue patients and HLA-DQ8 in the remaining. After gluten is absorbed, antigen presenting cells that express HLA-DQ2 or DQ8 present gliadin peptides to gluten-specific T-cells.(5)
The mechanism behind celiac sprue is not an "allergy". A true allergy to an ingested protein (such as milk or soy) leads to an IgE-mediated response. In celiac sprue, plasma cells produce IgA and IgG, with little or no IgE involvement.(1)
Endomysium is the connective tissue structure surrounding smooth muscle and tTG is contained within the endomysium. Ingested gliadin peptides bind with tissue transglutaminase in enterocytes, which deamidates glutamine residues, forming glutamic acid. Deamidation enhances immunogenicity of gliadin, by creating epitopes that are recognized as foreign by host cell-mediated immunity. Plasma cells produce IgA and IgG that are directed against a variety of antigens, such as tTG, endomysium, gliadin, and reticulin. An intense local inflammatory response follows, leading to the destructive changes seen in the mucosa of the small bowel.(1)(6) (Visual 2)
Gliadin is broken down into four fractions (alpha, beta, gamma, omega). Prolamins from wheat, rye, and barley are rich in glutamine (>30%) and proline (>15%), whereas the nontoxic prolamins of rice and corn have a lower glutamine and proline content.
Recently, a 33-amino acid peptide (alpha-gliadin, peptide 56-89) was discovered that has features suggesting that it is the primary initiator of the inflammatory response to gluten in celiac sprue patients. It was shown that this peptide could be completely degraded by enterocytes in controls but only partly in celiac patients. It was stable toward breakdown by all gastric, pancreatic, and intestinal brush-border membrane proteases. Homologs of this peptide were found in all food grains that are toxic to sprue patients, but are absent from all nontoxic food grains. The amount and location of proline residues are what seem to be crucial in creating the resistance that the peptide has to gastrointestinal breakdown. Preliminary in vitro studies have shown that a prolyl endopeptidase could catalyze breakdown of this 33-mer gliadin peptide, thus decreasing its toxic effects. This suggests a possible future strategy for oral peptidase supplemental therapy (7). A second peptide (31-49) appears to have toxic effects and behaves similarly (8). Several other short peptide sequences have since been discovered.
Normal villous height to crypt depth ratio is 3-5:1. There are many causes of villous atrophy.(9) (Visual 3)
There is clear association with other autoimmune disorders. Nutrient malabsorption leads to many extraintestinal manifestations.(1)(5) (Visual 4) (Visual 5)
2. How does one get started on a gluten-free diet?
The primary treatment for celiac disease is complete removal of gluten from the diet. Most propose strict gluten avoidance because even a small re-introduction can lead to mucosal damage and prevent remission. Vitamin supplementation may also be necessary. Many suggest bone density studies and women of childbearing age should be supplemented with folate to prevent neural tube defects.
The best way to counsel your patient is to encourage them to follow a step-by-step process to beginning a gluten-free lifestyle (10):
Step 1: Eliminate obvious sources of gluten from your diet.
This includes any foods containing wheat, rye, and barley. Avoid all oats initially (due to contamination with gluten containing substances).
Step 2: Analyze all the foods you normally eat to determine where gluten-free substitutions may be made.
Find substitutions for your favorite foods (i.e. there are many commercial sources for gluten-free bread, pasta, flour, cereal, etc.). Soybean or tapioca flours, rice, corn, buckwheat, and potatoes are safe.
Step 3: Start slowly using fresh food.
Start with unprocessed fresh foods, such as fresh fruit, vegetables, plain meats, and poultry. Add in new foods one at a time every 2-3 days.
Step 4: Keep a food diary.
Write down everything you put into your mouth, including food, liquids, and medications, as well as your body's reactions. You may see a pattern indicating other food sensitivities.
Step 5: Become a label reader.
Most labels do not spell out gluten. Many ingredients one cannot identify. It is important to learn what these are. The "Cooperative Gluten-Free Commercial Products Listing" is available from the CSA/USA. For example, HVP (hydrolyzed vegetable protein), HPP (hydrolyzed plant protein), and TVP (texturized vegetable protein) may contain wheat. "Modified food starch", "modified starch", and gelatinized starch" should be investigated. Labels on vitamins and medications should be read for active and inactive ingredients. "Starch" on medications can mean any starch. Avoid products with malt or malt flavoring.
Many manufacturers replace fat in "Non-Fat" or "Low-Fat" products with starch of indeterminate source.
Step 6: Go the extra mile to check out items you might never consider.
Any product that comes into contact with your body must be considered. Many non-food items contain gluten: toothpaste, mouthwash, chewing gum, breath mints, lips stick, suntan lotion, postage stamps/envelope glue. Also beware of cross-contamination: butter dishes or family toaster with crumbs, from grills in restaurants, or using the same utensils, for example.(10) (Visual 6)
Other key points:
If in doubt, leave it out!
Approx. 70% of symptomatic patients report an improvement in intestinal symptoms within 2 weeks of starting the gluten-free diet.(11)
Wait 2-4 months to use milk products. Lactose intolerance occurs frequently in celiac patients in the active stages of disease. The lactase enzymes needed to digest lactose are produced on the tips of the intestinal villi. Damage to villi leads to a decreased ability to generate lactase enzymes. As the gut heals, most patients recover their ability to digest milk-products. Some patients are able to tolerate Lactaid milk, but Lactaid pills can contain gluten. Soy or rice milk may be a suitable alternative. (10) (Visual 7)
Anecdotally, other alternative products have been used by celiac patients. For example, whey protein is thought to provide a good source of protein supplement. (Visual 8)
It is important to recognize the emotional burden that patients endure when they have to change their lifestyle, especially for kids. Patients may feel that they are being perceived as 'different' because they cannot eat like everyone else.
From a physician's standpoint, besides following the patient symptomatically, the best test to use is the IgA antigliadin Ab assay. A baseline value prior to treatment should be obtained. A normal baseline value is usually achieved in 3-6 months. It is debateable whether following these levels is necessary. The other serologic tests are not used because: IgG antigliadin declines more gradually, anti-endomysial is expensive and less easier to quantify, and there is little experience with regards to tTg levels.(12)
Why treat patients who are aymptomatic?
1. Despite feeling well, may patients have deficiencies in specific nutrients and vitamins that may eventually cause symptoms (i.e. anemia from iron deficiency, bone loss from vitamin D deficiency).
2. Untreated celiac disease is associated with an increased risk of cancer (eg. lymphoma, and carcinoma of the oropharynx, esophagus, and small intestine).
3. The likelihood of celiac patients developing other immune disorders may be related to the duration of exposure to gluten.
4. Pregnant women with untreated celiac disease are at increased risk for having low birth weight newborns.(13)
3. What support aids are available?
National Support Groups:
Celiac Sprue Association ("CSA/USA") -- patients receive a handbook and other newsletters, and gluten-free products list from the "Commercial Product List". www.csaceliacs.org
Gluten Intolerance Group -- www.gluten.net
Celiac Disease Foundation -- www.celiac.org
American Celiac Society Dietary Support Coalition -- AmerCeliacSoc@netscape.net
The American Dietetic Association
Local Groups:
Houston Celiac Support Group -- meetings four times per year, chapter newsletter: "Houston Celiac Perspective"
Houston R.O.C.K. (Raising Our Celiac Kids)
Publications:
Many information books, journal articles, newsletters, and cookbooks are available. (14)(15)(16)(17)(Visual 9)
Medications:
www.glutenfreedrugs.com
"Celiac Disease: A Guide Through the Medicine Cabinet" by M. Milazzo
On-line "grocery-stores"
www.glutensolutions.com
www.glutenfreemall.com
www.gluten-free.net
www.gluten-free-supermarket.com
www.authenticfoods.com
American Celiac Task Force:
July 20, 2004 -- the "Food Allergen Labeling and Consumer Protection Act (S.741)" was passed by the House of Representatives stating that the top 8 food allergens: milk, eggs, peanuts, tree nuts, fish, shellfish, wheat, and soy, are to be listed on labels under their common name. This bill also requires that the FDA issue final regulations defining "gluten-free" by January 2008. These rules would set out guidelines for the voluntary labeling of products as 'gluten-free'.(10)
4. What is the association with collagenous colitis?
Up to one-third of patients with celiac sprue have findings suggestive of microscopic colitis (2 main subtypes: lymphocytic colitis and collagenous colitis) on colonic biopsy. 2-10% of patients with microscopic colitis have small bowel mucosal changes consistent with celiac sprue.(18) Serologic tests for celiac sprue can be positive in up to 17% of patients with microscopic colitis. So, in patients with refractory disease, the other condition should be considered. Two groups of patients have been noted. One group of untreated celiac patients with histological changes consistent with microscopic colitis, responds to a gluten-free diet and never manifests the clinical picture of microscopic colitis. The second group is diagnosed as microscopic colitis and occurs even though a gluten-free diet has been instituted. Treatment algorithm for microscopic colitis.(19) (Visual 10)
Gastroenterology (Grand Rounds )celiac and cc
Moderators: Rosie, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh, mbeezie
Hmmmmmmmm. You're right. I didn't bother to even look at the treatment algorithm visual, when I originally read it. That treatment outline totally sucks, doesn't it.
Like a lot of GI docs, the author did pretty well, until he got to the part about treating MC, and then he ran the train plumb off the tracks.
Thanks for pointing that out.
Tex
Like a lot of GI docs, the author did pretty well, until he got to the part about treating MC, and then he ran the train plumb off the tracks.
Thanks for pointing that out.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
The second group is diagnosed as microscopic colitis and occurs even though a gluten-free diet has been instituted. Treatment algorithm for microscopic colitis.(19) (Visual 10)...
well in visual 10 see here..
http://www.bcm.edu/gastro/DDC/grandroun ... VIS-10.HTM
it states....treatment...dietary modifcation... gluten free only if celiac disease..
Now theres a surprise
(not that we didnt know that already)...no wonder docs dont take us seriously when we claim gluten intolerance with mc...Iow that the majority of people who have full blown celiac probably wouldnt have got that far if only testing was done in earlier stages to check for gluten intolerance.
well in visual 10 see here..
http://www.bcm.edu/gastro/DDC/grandroun ... VIS-10.HTM
it states....treatment...dietary modifcation... gluten free only if celiac disease..
Now theres a surprise
(not that we didnt know that already)...no wonder docs dont take us seriously when we claim gluten intolerance with mc...Iow that the majority of people who have full blown celiac probably wouldnt have got that far if only testing was done in earlier stages to check for gluten intolerance.Angy ;)
I'm just going from my memory of what I read the other night, but I think the incidence was out of date as well. Didn't it say something like 1 in 250 people had the condition. Dr. Fasano's (of U of Maryland's Med School) prevalence study that's put celiac disease in the forefront all of a sudden reported about 1 in 100 people in the USA having the condition.
Remember that they are talking about the currently "accepted" way of finding these people -- through their BLOOD antibodies, so you can just imagine how many more there would be for whom a blood test wouldn't pick up their gluten sensitivity.
One of the big surprises of late is that, compared to some blood saved from soldiers in WWII, the presence of antibodies, tTg and EMA, taken to mean the donors had celiac disease, compared to blood from people of the same ages today, the incidence has gone up 4 to 5 fold in the last fifty years. This was NOT what was expected from this study as it was thought that the condition was just being missed back then. Now, what we need to ask is WHY the incidence of this disease is going up.
Anyway, the current "authorities" have changed from that old 1 in 250 position to the more recent 1 in 100 rate based on blood donors antibodies.
Yours, Luce
Remember that they are talking about the currently "accepted" way of finding these people -- through their BLOOD antibodies, so you can just imagine how many more there would be for whom a blood test wouldn't pick up their gluten sensitivity.
One of the big surprises of late is that, compared to some blood saved from soldiers in WWII, the presence of antibodies, tTg and EMA, taken to mean the donors had celiac disease, compared to blood from people of the same ages today, the incidence has gone up 4 to 5 fold in the last fifty years. This was NOT what was expected from this study as it was thought that the condition was just being missed back then. Now, what we need to ask is WHY the incidence of this disease is going up.
Anyway, the current "authorities" have changed from that old 1 in 250 position to the more recent 1 in 100 rate based on blood donors antibodies.
Yours, Luce
