Why Most GI Docs Are Totally Confused About MC

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tex
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Why Most GI Docs Are Totally Confused About MC

Post by tex »

Hi All,

A member recently sent me a PM, asking me why I thought that malabsorption could be due to MC, when obviously, malabsorption is an issue with the small intestine, not the colon, and her doctors have assured her that the small intestine and the colon are two entirely separate organs, and what happens in one, does not affect what happens in the other. IOW, her doctors claim that her weight loss and malabsorption are entirely unrelated to her MC, simply because the small intestine and the large intestine act as seperate organs, in which one doesn't affect the other.

After writing a response to her question, it dawned on me that this is probably at the core of why most GI docs are totally confused about MC, so I thought it might be important enough to post for all the world to see. Who knows, maybe a GI doc somewhere in the world may see this, and the light bulb may come on. LOL. I'm not holding my breath, however.

It's their own fault, of course, for being so short-sighted that they named the disease in such a way, that the name can only refer to the colon, (as our favorite doctor, Polly, has pointed out - colitis means inflammation of the colon), and apparently, "the powers that be" are either too lazy to rename it, or they feel that it doesn't matter.

Because of that misstep right out of the chute, doctors cannot logically understand that MC is similar to Crohn's disease, in that it can affect any part of the GI tract, from mouth to anus. They are bound by the name, to view MC as a disease of the colon. Period. Of course, I respectively suggest that they are totally wrong in their opinion that what happens in either the colon or the small intestine, does not affect the other organ. Obviously, that claim flies in the face of the facts, and I am embarrassed for them, that they would even suggest such a thing, let alone argue that it's true.

Obviously, though, this is not only a convoluted way of viewing the disease, but it's just plain wrong, because exactly the same lymphocytic infiltration that is the marker of MC in the colon, can often be found in the small intestine, the stomach, and even in the mucosa of the mouth, in many MC patients. It is "exactly" the same type of inflammation found in the colon. Even the thickened subepithelial collagen bands that mark CC in the colon, can be found in the small intestine, stomach, etc., of patients who have CC.

Not everyone has small intestinal involvement, of course, but a high percentage of us do. It is easy to check. A stool test at Enterolab, to check for fecal fat absorption, will detect fat malabsorption, due to damage to the small intestine. Since vitamins are fat soluble, if you have a fat malabsorption problem, then you will have a nutrient malabsorption problem. It most definitely is not an unrelated issue, because I can absolutely guarantee you that if/when you control the inflammation in your colon, you will simultaneously eliminate the inflammation in your small intestine, and any other areas where it might initially be present, (including mouth sores that are triggered for some patients with MC).

I went untreated for several years, due to my GI doc not bothering to even look for MC. There was so much damage to my small intestine, that over three years after I adopted the GF diet, (and two years after I was in remission), a fat malabsorption test still showed a significant amount of residual damage to my small intestine.

As to the common claim by GI docs, that the inflammation in the colon cannot affect the small intestine - in fact, the most likely scenario is that rather than the small intestine being affected because of the inflammation in the colon, it's the other way around. The colon is inflamed because of the inflammation in the small intestine. Proof of this can be seen in surgical intervention that has demonstrated that in most cases, if an MC patient undergoes an ileostomy, so that the fecal stream is totally diverted from the colon, subsequent biopsies will show that the histology of the colon will return to normal, and the clinical symptoms of MC, will resolve. If the surgical procedure is subsequently reversed, then the MC will return, as described by the research project documented at the following site.

http://www.ncbi.nlm.nih.gov/pubmed/7615 ... t=Abstract

I believe that pretty well proves my point, beyond a shadow of a doubt. Frankly, I doubt that many GI docs would accept this explanation, though, since most GI docs are very defensive about their professional knowledge, (or lack of it), and as a group, they don't seem to be very open minded. In fact, most of them seem to be offended, when confronted by a patient who appears to know more than they do, about a disease.

The bottom line is, the reason why they seem to be flummoxed, when confronted with MC, may be due to that regrettable indiscretion, (read that "poor judgment"), that was initially made when this disease was originally described and named. :lol: :lol: IOW, they keep stumbling over their own nomenclature.

Tex
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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.
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Post by Polly »

WOW! Lots of good ideas there, Tex.

Once an inflammatory response begins (let's say because of MC), it can affect everywhere in the body, and not just the GI tract. Researchers are now learning that inflammation underlies many of our diseases. They have found, for example, that people with periodontal disease are more likely to have heart disease. And we know that those chemicals that are released in the inflammatory processes of MC can cause fever, joint/muscle aches, fatigue, etc.

My only major comment here would be to remember that the inflammation in the small intestine is thought to be due primarily to GLUTEN. The colitis affects the large intestine, yes, but the gluten sensitivity that goes along with MC is what causes the damage (blunting of villi, malabsorption) in the small intestine. Thus, there are different causes for the damage that occurs in the large vs. small intestine.

Love,

Polly

P.S. To be more specific, it is not the gluten itself that damages the small intestine, it is the antigen-antibody complexes that are formed when the body makes antibodies to the gluten and attach to it. (In the large intestine, it is the overgrowth of "bad" bacteria that causes inflammation, which damages the cells that reabsorb water in the colon...... thus leading to that good old diarrhea).
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Post by tex »

Polly wrote:My only major comment here would be to remember that the inflammation in the small intestine is thought to be due primarily to GLUTEN. The colitis affects the large intestine, yes, but the gluten sensitivity that goes along with MC is what causes the damage (blunting of villi, malabsorption) in the small intestine. Thus, there are different causes for the damage that occurs in the large vs. small intestine.


But that's conventional medical thinking, and it's quite correct, when applied to celiac disease, of course. Most MC patients, however, do not present with villous blunting, and therefore, cannot be diagnosed as celiacs. Even so, typically, they do suffer from a malabsorption condition. My point is that the malabsorption problem does not relate to villous atrophy, but rather to lymphocytic infiltration, just as it does with Crohn's disease. IOW, contrary to conventional thinking, I'm suggesting that the small intestine is subject to the same type of reaction as the colon. We have to remember that MC is indeed an inflammatory bowel disease, and the primary distinction between Crohn's disease and MC, is that with Crohn's disease, lymphocytic infiltration and granulomatous inflammation involve the full thickness of the intestinal wall, whereas with MC, the primary issue is lymphocytic infiltration, which involves only the epithelia. Of course, with CC, sub-epithelial collagen thickening also occurs, but I doubt that issue has any significant bearing on mucosal inflammation. Granulomatous inflammation, as used in this context, refers to tightly packed "balls" of macrophages, (macrophages are another, special, type of white blood cells).
Polly also wrote:P.S. To be more specific, it is not the gluten itself that damages the small intestine, it is the antigen-antibody complexes that are formed when the body makes antibodies to the gluten and attach to it. (In the large intestine, it is the overgrowth of "bad" bacteria that causes inflammation, which damages the cells that reabsorb water in the colon...... thus leading to that good old diarrhea).
Remember that theories about the cause, (or causes), of Crohn’s disease, are pretty much the same as with MC, but of course, none of those theories have been proven. The problem may lie with bacteria, or with the immune system mistaking bacteria, foods, and other substances as foreign invaders, and improperly attacking them. We do know for a fact, that the net result of the process, is an accumulation of white blood cells, in the lining of the intestines, producing chronic inflammation, which, in the case of Crohn's disease, leads to ulcerations and severe bowel injury, and in the case of MC, leads to microscopic inflammation, confined to the epithelia, of whatever part of the digestive tract is affected.

Therefore, my point is this: I believe that eventually, medical consensus of opinion will recognize that the effect on the small intestine is a true IBD type of inflammation, (not a gluten-specific reaction), and it can occur, whether gluten is an issue, or not, nor does it depend on villous damage, to cause a malabsorption issue. The inflammation caused by the lymphocytic infiltration itself, is sufficient to adversely affect the absorption of nutrients. One would think that someone in medical research would have noticed this by now, if it were true, but remember, the inflammation due to MC is microscopic, and as such, it will not be noticed, unless it is specifically searched for, in the proper way. The bottom line is, (IMO), that while MC may indeed be closely linked with gluten sensitive enteropathy, it is first and foremost, an IBD, and any gluten issues are secondary, (even in the small intestine). That doesn't mean that gluten issues can be ignored, of course, it just means that resolving gluten issues will not necessarily resolve MC, (which all of us already knew).

I'm probably way off base here, but that's the way I see it.

Love,
Tex
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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.
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Post by Polly »

Mornin' Tex,

I think I have a better idea of your concerns. Thanks for clarifying.

You say that you believe that the small intestine is subject to the same type of reaction as the colon. You are absolutely correct, and I don't know of any docs who would disagree. The immune system of the GI tract (from mouth to anus) reacts the same way to ANY antigen or infection that tries to invade: it sends T cells to the surface of the epithelium, deposits intraepithelial lymphocytes, and makes secretory IGA.

But this immune reaction is "non-specific" - it always occurs in the same way no matter where in the GI tract it occured or what the cause was. So YES, in early stages of gluten sensitivity, the only biopsy findings would be the intraepithelial lymphocytes in the small intestine, which certainly can cause major problems in itself. Only with continued damage from gluten would the biopsy show blunted villi and would malabsorption develop. I think all of this is explained nicely in Dr. Fine's essay about diagnosing GS early - before the villi are gone.

I guess my main concern is not with the typical non-specific immune response found anywhere along the gut, but with the fact that most docs STILL don't recognize GLUTEN as a significant cause of an immune response in the small intestine. Of course, what can we expect when we know they don't even understand the possible causes of the non-specific findings in the COLON in MC? How many can look at an MC biopsy result and immediately think of NSAIDs, proton-pump inhibitors, antibiotics, etc.? And even fewer (almost none) see the MC findings and think about an associated gluten sensitivity. That's still the crux of the problem, IMHO.
And it's a serious problem, as you know, because Dr. Fine and others tell us that untreated, longstanding gluten sensitivity can lead to permanent, irreversible problems that may not repond to the GF diet.

Another issue is that the colon is frequently biopsied, whereas the small intestine biopsy is a more invasive/complicated, and expensive procedure, so we often don't get to see those non-specific early findings in the small intestine.

Hey, it's always fun chewing the fat with you!

Love,

Polly

P.S. BTW, I did not have any evidence of malabsorption on my fecal fat test, so I was fortunate the MC was caught early.
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Post by RUBYREDDOG »

Great discussion and food for thought. The more we learn about MC the better off we all are. Heck, maybe a GI doc. will actually read one of these posts and find a new direction for a treatment. This would help even more people who have been misdiagnosed with IBS and other diseases. The mainstream medical structure is still the best way to effect the most people with MC. If we could only educate them to listen to those of us who have this disease. A daunting task indeed.

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Post by tex »

Polly,

Thanks for sharing your knowledge and your insight. Probably, you have hit the nail on the head, when you suggest that the main reason they deny the small intestinal connection with MC, is because they continue to refuse to believe that non-celiac gluten-sensitivity is even possible, let alone integrally connected with MC.

Still, I have a strong hunch that if you were to query a cohort of GI docs, (now that's a formidable visual image, isn't it? :lol: ), you would find that the consensus of opinion is that MC is a disease of the colon, and celiac sprue is a disease of the small intestine, and never the twain shall meet. IOW, the state of the small intestine is off the radar, when a GI doc is thinking about MC. In fact, excluding celiac disease, they don't even care if it is inflammed, because by definition, that inflammation can't be "colitis", so it can't be related to MC.

Am I wrong? Am I grossly misjudging them?

Love,
Tex

P S Same here - I appreciate you puttin' up with me.
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Post by Gloria »

Polly,
FWIW, I didn't have any evidence of malabsorption either.

Gloria
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