Feel free to discuss any topic of general interest, so long as nothing you post here is likely to be interpreted as insulting, and/or inflammatory, nor clearly designed to provoke any individual or group. Please be considerate of others feelings, and they will be considerate of yours.
That would imply that MC would have to be an autoimmune disease, and strangely, it's not, while Celiac disease is.
People with collagenous colitis or lymphocytic colitis sometimes also have an autoimmune disorder, such as celiac disease, rheumatoid arthritis or scleroderma.
I'm certainly not saying that you're theory is without merit - I'm just pointing out that it would require that the medical description of MC would have to be significantly altered, in order to accommodate it.
Personally, I believe it is an autoimmune disease.
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.
Tex,
You mean in order for our immune system to be sensitized to a resident bacteria, that process would have to qualify as autoimmune? Is asthma or mast cell disease considered autoimmune in the same was as celiac? Or simply allergic in nature? I don't know. I'm beginning to think the only diseases that get autoimmune designation are those that attack a critical body function or organ. Although MC attacks some portion of the digestive tract, it's not as remarkable as losing all your villi in the process.
BTW, check out what my husband just sent.
I think I've found the solution to your stomach problems. Happy to help whenever you're ready.
Yes, non-transient gut flora and fauna are considered part of "self".
Asthma reactions follow similar pathways as autoimmune reactions, but apparently it's not listed as an autoimmune disease, nor are mast cell issues. Interestingly, Crohn's disease and ulcerative colitis are listed, but MC is not.
Hmmmmmm. Call me old-fashioned, but injecting that stuff into the stomach sounds like a risky procedure. That could lead to SIBO, (among other things). Besides, stomach acid kills a lot of beneficial bacteria.
At the rate it's beginning to be publicized these days, this may turn out to be the next "fad", (whenever the GF "fad" fades away).
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.
I think a disease is called autoimmune if an actual antibody is produced to the offending agent. That is not the case with asthma, as far as a know. I believe MC is AI too.
Hugs,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Polly, Tex and Zizzle excellent discussion. I do wonder if MC is AI in nature as I think it very well might be. Polly if MC produces an antibody do we know what it is?
A far as practical experience I have seen a dramatic improvement with the Imuran in both the MC symptomology and my over all energy levels. Granted I do have crohns as well, but he crohns is 90% gone after the surgery as far as active disease presentation goes. According to my GI doc any D that I might have now is due to the CC and that has been quite minimal on the whole over this last year.
I do wonder if AI is involved but I do know as much as i dont like them that immune suppressant are working quite well so far.
FWIW, both my GI and my rheumatologist consider LC to be auto-immune in nature, and were entirely prepared to discuss/test for other auto-immune issues. Luckily, none....yet.
I cannot believe that all of you are so well versed in all this deep physiological stuff. I read it, get an idea, but certainly can't contribute to anything in the discussion. I feel like I am at a seminar where everyone is knowledgeable, and I have to run as fast as I can just to keep up.
My brain fog makes absorption, analysis, and the ability to use the info to move on and express an opinion is, I think, impossible.
I admire you all and try to learn from your experience!
Don't worry about feeling lost. Some of us (like Tex and I) have been discussing these topics for years now. And, believe me, I could never have participated in a discussion like this when I was still brain-fogged! LOL!
Joe,
Excellent question about what antibodies are produced in MC! Of course we know that food sensitivity is almost always present in MC, and that antibodies are made to each individual food - gluten, dairy, soy, etc. They are what Dr. Fine measures in his tests. I think that other antibodies may be present in MC too. I'm not 100% sure about this, but I think that the colitis, which Dr. Fine says is the hallmark of MC and is due to an imbalance of gut bacteria, may be due to the body failing to recognize its own good bacteria and then attacking it, killing it off like it is programmed to do with its bad bacteria. I don't know if an actual antibody is made, though. Does anyone have any thoughts on this? Z., perhaps the bacterium is altered by the body so that it is then considered to be foreign, not "self". Maybe this is a question for Dr. Fine. I'll try to email him, but he is probably busy getting ready for his conference.
Love,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
Enterolab offers the anti-TTG antibody test, (anti-tissue transglutaminase antibody test), which detects a secondary auto-immune reaction to the human enzyme tissue transglutaminase, (secondary to the immunologic reaction to gluten). This test is based on IgA antibodies, like the others, and it should confirm, (theoretically, at least), that gluten sensitivity has led to the development of a secondary autoimmune reaction. IOW, a positive anti-TTG antibody test confirms that the immune system is treating a part of self, (tissue transglutaminase enzyme), as a foreign invader, and it's actively attacking it.
But, of course, the mainstream medical community doesn't recognize the validity of Enterolab stool tests, and the classic serum anti-TTG antibody tests are not accurate enough to yield a positive test result, except in the case of fully-developed celiac disease, so officially, MC is not an autoimmune disease.
Love,
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.
You may recall I have am positive for Anti-Actin/Anti-Smooth Muscle Antibody. It is closely tied to autoimmune hepatitis, which is now closely tied to celiac disease (in some cases referred to as "Celiac Hepatitis"). Over the years, experts, including Dr. Fasano, have begun to regard Anti-Actin Antibodies as an indicator of severity of mucosal damage in CD. It makes sense to me that it would also be positive in other forms of IBD, especially those sensitive to gluten. Autoimmune hepatitis seems to be an end result of long-term gluten damage.
the gluten ingestion has been reported to induce a rapid alteration of the actin network on intestinal mucosa of CD patients [9]. Gliadin rapidly increases actin polymerization leading to rearrangement of actin filaments, especially in the intracellular subcortical compartment [10]. It is likely that newly generated actin polymers may be exposed to gut-associated lymphatic tissue, causing the production of IgA antibodies against actin filaments (IgA-AAA).Previous studies have described that the presence of antibodies against actin filaments is associated with severe degrees of mucosal damage and that IgA-AAA may also contribute to exacerbate the villous' cytoskeleton damage [11-14]. It has also been suggested that the presence of IgA-AAA may, in some patients, overcome the need of the intestinal biopsy [9].
Abstract
BACKGROUND: Previous studies have demonstrated that serum anti-actin antibodies are a reliable marker of intestinal damage severity in coeliac disease.
AIMS: To validate in a multicentre study the clinical usefulness of serum IgA anti-actin antibody ELISA and its possible use in monitoring intestinal mucosa lesions during gluten-free diet.
PATIENTS AND METHODS: Four centres recruited 205 newly diagnosed coeliac disease patients with villous atrophy, 80 healthy controls and 81 "disease" controls. Twelve coeliac disease patients on gluten-free diet but with persistent symptoms underwent serum IgA anti-actin antibody assay and intestinal histology evaluation. IgA anti-actin antibody ELISA was performed with a commercial kit. All coeliac disease patients underwent intestinal histology study.
RESULTS: IgA anti-actin antibodies showed a sensitivity of 80% and a specificity of 85% in the diagnosis of coeliac disease patients with villous atrophy. The area under the receiving operator curve for anti-actin antibodies was 0.873 [95% C.I. 0.805-0.899]. Serum anti-actin antibodies values were significantly higher in coeliac disease patients than in healthy or "disease" controls (P<0.0001). Serum anti-actin antibodies were positive in 41 of the 60 coeliac disease patients with mild intestinal histology lesions (69%) and in 123 of the 145 with severe lesions (85.3%) (P<0.05). There was a significant inverse correlation between anti-actin antibody values and the villi/crypts ratio (r=-0.423; P<0.0001). In the 12 coeliac disease patients on gluten-free diet who underwent re-evaluation as they were persistently symptomatic, intestinal histology showed three cases with persistent villous atrophy: all of these were positive for serum anti-actin antibodies ELISA, whereas both serum anti-tTG and EmAs were negative. The other nine patients showed normal intestinal villi and were negative for serum anti-actin antibodies.
CONCLUSIONS: Anti-actin antibodies are a reliable marker of severe intestinal mucosa damage in coeliac disease patients and a simple ELISA technique offers an accurate method for their determination. These antibodies seem to be a very reliable marker of persistent intestinal damage in coeliac disease patients.
I can't imagine I have "severe" mucosal damage, but I've always wondered the significance of this antibody, in the abcense of any liver problems (which I test for one or two times a year). Maybe I really do have a full blown case of celiac? Or maybe Anti-Actin Antibody (AAA) is an MC/IBD autoimmune marker?
