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The way I'm understanding it is that the body is autoimmune to gluten, so by putting gluten in the system it kicks off an autoimmune reaction which in turn destroys the tiny villi in the colon, and because of the destroyed villi the body is not able to pull water and nutrients from the colon which in turn causes the D.
So to me it sounds like it takes a while of gluten eating for the villi to eventually become damaged. Here is my big question....
A person with MC didn't become that way overnight, because it takes a while for the villi to flatten. And if a person avoids gluten, the villi will eventually heal. So if a person with MC gets him/herself to remission and heals that villi, why then do they have a sudden reaction to a slip up? I mean if the villi have healed and they accidentally eat a bite of gluten, how does the mechanics of that work?...why do they have D just from that one bite of gluten? Just one slip up isn't enough to flatten the villi, or is it?
Help me understand the mechanics of MC
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IDreamInColor
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Hi IDream,
If you were to substitute "small intestine" for "colon", your description is accurate for celiac disease. It's not a description of what happens with MC, however. While some people with MC do experience some degree of villus atrophy in the small intestine, many/most do not. For most of us, if the small intestine is involved at all, the inflammation is due to lymphocytic infiltration, but the damage never reaches the point where the villi begin to atrophy. In the colon, the same issue causes the inflammation, an increased presence of lymphocytes between the enterocytes lining the surface of the mucosa, (along with increased collagen band thickening, in the case of CC).
If the villi are flattened in the small intestine, then, of course, that can cause D, because with major villus atrophy, nutrients will be malabsorbed, and when the electrolyte levels increase in the fecal stream, the presence of increased sodium and potassium levels tends to induce D. This is the cause of chronic, osmotic diarrhea, which takes place after the damage becomes so extensive that the intestines can no longer support normal digestive processes. However, that's an end-stage reaction, and not the primary cause of the reactions we experience in response to ingesting a food to which we are sensitive, particularly after achieving remission.
For the reaction to be so prompt, as you pointed out, it has to be in response to an immune system increase in the production of antibodies. Once we become sensitized to an allergen, the immune system continues to produce a low level of antibodies, in order to maintain all the necessary components on the "alert". This allows the immune system to respond quickly, if a threat is detected. Once a threat is detected, antibody production is immediately escalated, and it is this sudden increase in antibody production that triggers the familiar response, (D).
If we are in remission, then this response is usually faster, and much more easily noticed, (more severe), than it would have been if it had occurred during a period of chronic D. Here's why:
Before we are able to reach a state of remission, even though we are carefully following a GF diet, the immune system continues to produce a relatively high level of antibodies, in an ongoing, (chronic), reaction. It may not matter that we are not even ingesting any gluten at the time, because the immune system will continue to produce antibodies to gluten at a very high level, for a very long period of time, after we stop ingesting gluten. Enterolab can reliably detect gliadin, (gluten), antibodies in stool samples for at least a year after gluten has been completely removed from the diet. In fact, they can still detect low levels of gluten antibodies in the stool for up to 2 years after gluten is totally withdrawn from the diet. Until the production of antibodies decays to below a certain threshold level, (which probably varies by the individual), we will continue to react.
Once we stop reacting, there are still a lot of antibodies being produced, but they are below the level at which a reaction is automatically triggered, (so we are in a state of remission). If we accidentally eat some gluten, though, since there is already a significant level of antibodies in circulation, when the immune system begins to ramp up the production again, it very quickly surpasses the threshold level at which a reaction is triggered, so we have a prompt, major reaction.
Once we are in remission long enough, then the "routine" production of antibodies will slowly decay to the point at which it takes a larger amount of ingested gluten, to boost the antibody level over the threshold required to trigger a reaction, and if a reaction is triggered, it will die down much faster, because a large, "chronic" volume of antibodies are not already being produced on a steady-state basis.
Do you see what I'm trying to say? It's the sudden increase in antibody production that causes "new" reactions, but "new" reactions can only occur if the level of antibody production is allowed to drop below the threshold for triggering a reaction, in the first place. IOW, if we are already reacting to a high steady-state production of antibodies to gluten, then we won't even notice when more gluten is ingested, because once the antibody production level is above that threshold level, anything else that happens is a moot point. We can experience a "new" reaction, only after the antibody level falls enough to drop below the threshold level for triggering a reaction. That's why it's virtually impossible to tell that we are sensitive to gluten, unless we remove it from our diet long enough to allow at least partial healing. Most newbies think that if they stop eating gluten for a few days, (or a week or so), and the D continues, then that means that they are not sensitive to gluten. Nothing could be further from the truth. That trial proves nothing, because they will continue to react to the antibodies already in circulation, for a long time, probably for months after they withdraw gluten from their diet. It's a cruel, and very insidious disease.
The bottom line is, villus damage is an important marker for celiac disease, but for MC, it has no real significance, (not as far as either the laboratory symptoms, or the clinical symptoms are concerned, anyway).
I hope this helps.
Tex
If you were to substitute "small intestine" for "colon", your description is accurate for celiac disease. It's not a description of what happens with MC, however. While some people with MC do experience some degree of villus atrophy in the small intestine, many/most do not. For most of us, if the small intestine is involved at all, the inflammation is due to lymphocytic infiltration, but the damage never reaches the point where the villi begin to atrophy. In the colon, the same issue causes the inflammation, an increased presence of lymphocytes between the enterocytes lining the surface of the mucosa, (along with increased collagen band thickening, in the case of CC).
If the villi are flattened in the small intestine, then, of course, that can cause D, because with major villus atrophy, nutrients will be malabsorbed, and when the electrolyte levels increase in the fecal stream, the presence of increased sodium and potassium levels tends to induce D. This is the cause of chronic, osmotic diarrhea, which takes place after the damage becomes so extensive that the intestines can no longer support normal digestive processes. However, that's an end-stage reaction, and not the primary cause of the reactions we experience in response to ingesting a food to which we are sensitive, particularly after achieving remission.
For the reaction to be so prompt, as you pointed out, it has to be in response to an immune system increase in the production of antibodies. Once we become sensitized to an allergen, the immune system continues to produce a low level of antibodies, in order to maintain all the necessary components on the "alert". This allows the immune system to respond quickly, if a threat is detected. Once a threat is detected, antibody production is immediately escalated, and it is this sudden increase in antibody production that triggers the familiar response, (D).
If we are in remission, then this response is usually faster, and much more easily noticed, (more severe), than it would have been if it had occurred during a period of chronic D. Here's why:
Before we are able to reach a state of remission, even though we are carefully following a GF diet, the immune system continues to produce a relatively high level of antibodies, in an ongoing, (chronic), reaction. It may not matter that we are not even ingesting any gluten at the time, because the immune system will continue to produce antibodies to gluten at a very high level, for a very long period of time, after we stop ingesting gluten. Enterolab can reliably detect gliadin, (gluten), antibodies in stool samples for at least a year after gluten has been completely removed from the diet. In fact, they can still detect low levels of gluten antibodies in the stool for up to 2 years after gluten is totally withdrawn from the diet. Until the production of antibodies decays to below a certain threshold level, (which probably varies by the individual), we will continue to react.
Once we stop reacting, there are still a lot of antibodies being produced, but they are below the level at which a reaction is automatically triggered, (so we are in a state of remission). If we accidentally eat some gluten, though, since there is already a significant level of antibodies in circulation, when the immune system begins to ramp up the production again, it very quickly surpasses the threshold level at which a reaction is triggered, so we have a prompt, major reaction.
Once we are in remission long enough, then the "routine" production of antibodies will slowly decay to the point at which it takes a larger amount of ingested gluten, to boost the antibody level over the threshold required to trigger a reaction, and if a reaction is triggered, it will die down much faster, because a large, "chronic" volume of antibodies are not already being produced on a steady-state basis.
Do you see what I'm trying to say? It's the sudden increase in antibody production that causes "new" reactions, but "new" reactions can only occur if the level of antibody production is allowed to drop below the threshold for triggering a reaction, in the first place. IOW, if we are already reacting to a high steady-state production of antibodies to gluten, then we won't even notice when more gluten is ingested, because once the antibody production level is above that threshold level, anything else that happens is a moot point. We can experience a "new" reaction, only after the antibody level falls enough to drop below the threshold level for triggering a reaction. That's why it's virtually impossible to tell that we are sensitive to gluten, unless we remove it from our diet long enough to allow at least partial healing. Most newbies think that if they stop eating gluten for a few days, (or a week or so), and the D continues, then that means that they are not sensitive to gluten. Nothing could be further from the truth. That trial proves nothing, because they will continue to react to the antibodies already in circulation, for a long time, probably for months after they withdraw gluten from their diet. It's a cruel, and very insidious disease.
The bottom line is, villus damage is an important marker for celiac disease, but for MC, it has no real significance, (not as far as either the laboratory symptoms, or the clinical symptoms are concerned, anyway).
I hope this helps.
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.
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IDreamInColor
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Yes, it's basically an inflammation of the mucosa of the colon, technically, but in reality, it can involve the entire GI tract, and it frequently involves the small intestine. All the issues other than the inflammation, (and the collagen band thickening), though, are satellite issues, and not "officially" a part of the disease.IDreamInColor wrote:So is MC just an inflammation basically?
The villus damage shown on your pathology report was in reference to your small intestine, wasn't it? That's evidence of advanced celiac disease, (by definition). Some GI specialists insist that in the absence of positive celiac blood test results, villus damage cannot be described as celiac disease, but that amounts to insisting that an arbitrary diagnostic procedure absolutely defines a disease. It does not, in many cases. Celiac disease was too restrictively defined, in the original description of the disease, just as microscopic colitis was incorrectly defined in it's original description, (it's description is also too limited).
If you will post your pathology report, I'll be happy to try to interpret it. If you've already posted it, please point me to it, (and please forgive me for having a poor memory at times).
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.
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IDreamInColor
- Adélie Penguin
- Posts: 167
- Joined: Tue Sep 14, 2010 5:20 pm
- Location: Ohio
Here it is Tex, I'm sorry for all the questions, I'm still just trying to understand this disease.
Diagnosis:
1. Ileal Mucosa with presence of ileal villi showing nonspecific chronic inflammation. No evidence of granulomas.
2. Random Colon Biopsies-Colonic glands are tubular, focally slightly crowded and surface epithelium and lamina propria show focal mild increase in lymphcytes. Evolving microscopic colitis is possible.
Note: Close follow-up for microscopic colitis is suggested.
Diagnosis:
1. Ileal Mucosa with presence of ileal villi showing nonspecific chronic inflammation. No evidence of granulomas.
2. Random Colon Biopsies-Colonic glands are tubular, focally slightly crowded and surface epithelium and lamina propria show focal mild increase in lymphcytes. Evolving microscopic colitis is possible.
Note: Close follow-up for microscopic colitis is suggested.
Never apologize for asking questions - that's how we learn, and that's why we're here.
I recognize your report, so obviously you did post it before, but I had forgotten the details. This report appears to me to describe a classic case of LC. Unfortunately, the pathologist didn't measure the thickness of the collagen bands in the lamina propria, so he did not even check for collagenous colitis, for some unknown reason. It doesn't matter whether you have LC or CC, though, because the clinical symptoms and the treatment are the same.
Tex
That says that the final section of your small intestine is inflamed, but no damage to the villi is noted, and there is no indication of Crohn's disease, or any other problems. The report doesn't specify a reason for the inflammation in the ileum, but IMO, it is almost certainly due to MC.IDreamInColor wrote:1. Ileal Mucosa with presence of ileal villi showing nonspecific chronic inflammation. No evidence of granulomas.
I recognize your report, so obviously you did post it before, but I had forgotten the details. This report appears to me to describe a classic case of LC. Unfortunately, the pathologist didn't measure the thickness of the collagen bands in the lamina propria, so he did not even check for collagenous colitis, for some unknown reason. It doesn't matter whether you have LC or CC, though, because the clinical symptoms and the treatment are the same.
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.