Collagenous Gastritis / Gastritis in Antrum

[katinchatt]

Hi,
I am seeing my GI tomorrow and I have a list of a few things I want to ask him, but need help with this one. When I had my Colonoscopy/Endoscopy on 10/1, I was given a few pics of each procedure. One pic - Antrum, states "Gastritis" under it. Biopsies were done during the Endoscope, primarily to rule out being Celiac, which were Neg.

Question ~ Does any one know if Pathologists look for MC in areas other than the colon? I ask because I found this;

"Collagenous gastritis also seems to have the same spectrum of associated clinical findings as collagenous colitis, including frequent coexistence of celiac sprue, watery diarrhea syndrome, and female predominance."

If anyone has any experience with MC in areas, other than the colon, I would appreciate hearing your thoughts, I understand it is possible. Just curious what treatment would be if found in the stomach and or small intestine, since I am on Entocort for colon CC. This appears to be extremely rare, I think I'm just more curious if the pathology differs in what they look for, or if it would it be an obvious finding.

Thanks in advance for any and all help,
Kat

Since my appt. is tomorrow I just wanted to get this out there. I may have missed something obvious in an earlier post, as I am still researching all of this tonight ;)

This is the article if you are interested;
http://www.nature.com/modpathol/journal ... 0101a.html

[tex]

Question ~ Does any one know if Pathologists look for MC in areas other than the colon?

Okay, that's a trick question, because pathologists only look for MC in the lab, under a microscope - IOW, they can only examine the biopsy samples that are presented to them by a patient's GI doc. LOL.

Normally, GI docs never peek into the opposite end, when searching for MC. By definition, MC is diagnosed by examining under a microscope, biopsies taken from the colon, to search for certain distinct "markers" of MC, namely, intraepithelial lymphocytes, and/or sub-epithelial thickened collagen bands, subsequent to an otherwise unremarkable colonoscopy. There are other forms of MC, though, where other markers are present, as in "giant cell" MC, for example. Note that the other IBDs, may also show some of the markers of MC, but they always have other, rather obvious markers, not associated with MC, such as gross lesions in the epithelia, and sub-epithelia, crypt damage, etc.

While it's true that MC can affect any part of the GI system, typically, cases such as the one described in that article, are extremely rare, very advanced cases. They are advanced, because they have gone uncontrolled for so many years. You will note that the case described, involved celiac disease, which later evolved to UC, suggesting that the patient was not eliminating gluten from her diet, thus opening the door for other complications, (or maybe she was asymptomatic). When inflammation, (and the accompanying LGS), is allowed to continue indefinitely, eventually, additional organs can become chronically inflamed.

Interestingly, the white coats have chosen to define gastritis associated with thickened collagen bands as "collagenous gastritis", while referring to "plain vanilla, unenhanced" gastritis, as simply "gastritis". In fact, ordinarily gastritis is almost surely lymphocytic gastritis, (if we apply the same criteria that identify lymphocytic colitis). Many of us occasionally experience that condition, during our reactions, so it is probably a lot more common than they realize, but for me, at least, it always presented as an acute phenomenon, not a chronic condition. I would assume that it would have to be a chronic condition, in order to segue into collagenous gastritis.

Most of us, I believe, (though not all of us, of course), experience MC in our small intestines. If we didn't, then we couldn't have a malabsorption problem, and a fecal fat test at Enterolab wouldn't show evidence of residual intestinal damage, (since the phenomenon of fat malabsorption has to occur in the small intestine, not in the colon). The colon doesn't absorb anything, but water, for all practical purposes. Those of us who are bothered by mouth sores, that refuse to heal, during reactions, are experiencing the effects of MC in the mouth. So yes, many/most of us have experienced MC in many areas of the GI tract, other than the colon, whether we realize it or not.

The treatment is the same - if you resolve your colonic symptoms, your other symptoms will also disappear. Entocort EC may not work directly on the stomach, (since the EC stands for Enteric Coating, which prevents it from activating until it reaches at least the ilium), but chances are that the 10 % of it that becomes systemic, will take care of the upper-GI-tract inflammation. If it doesn't, the diet always works, if it's properly fine-tuned.

The white coats are not going to find MC in the stomach, unless they specifically look for it there, and they're not going to look there, unless they have a particular reason. From the patients perspective, why worry about it, and why undergo an additional invasive test? The treatment will still be the same, no matter where you find the markers of the disease. The thing is, before you can find MC anywhere else, it will always present in the colon, first, so why not look there?

At least that's the way I see it.

Tex

[katinchatt]

Morning Tex,

Yes, assuming of course they are in a lab, with a microscope, and at least one good eye looking in.

Thanks for taking the time to answer my question. Since the pics didn't really show anything obvious, I filed them away the day I received them. (not my idea of Fine Art Photography). However, while making my list I needed to know what it is I am feeling in a certain part of my stomach that has bothered me off and on for years (opposite gallbladder). So last night I pulled them back out and noticed the one marked Gastritis, and well you know, that got me started. I was actually hoping it was the area that has bothered me, at least it would help explain it anyway.
Now thinking about it, Microscopic anything means you need a microscopic. This gastritis is I supposed just gastritis, I don't see any inflammation on the pic, but then I don't have that one good eye required to make such a discovery either.

Thanks for your time, it's appreciated.
Kat

The thing is, before you can find MC anywhere else, it will always present in the colon, first, so why not look there?

. . . this I did not know. I wondered why "watery diarrhea" if in other areas and NOT the colon as well, makes sense to me now.

[tex]

Morning Kat,

Now thinking about it, Microscopic anything means you need a microscopic. This gastritis is I supposed just gastritis, I don't see any inflammation on the pic, but then I don't have that one good eye required to make such a discovery either.

Right. Sometimes, if you know what you are looking for, you can actually see the inflammation caused by MC, but it is pretty subtle. I could see it on the monitor, during my colonoscopy, but at the time, I didn't realize what I was looking at. Later, after reading what Dr. Fine has to say about it, the light bulb came on. In the colon, the inflammation will present as slightly more intensely hued splotches of pink, scattered against a background of a normal, lighter shade of pink. If anything more obvious is visable to the naked eye, (such as redish, obviously inflamed areas, or lesions, or whatever, then something else is going on, (IOW, something other than MC).

I wondered why "watery diarrhea" if in other areas and NOT the colon as well, makes sense to me now.

Actually, "watery diarrhea" can be caused by upstream inflammation, and this is often seen in Crohn's disease, when it presents as ileitis, rather than colitis, or as ileocolitis. Ileocolic Crohn's, is the version of Crohn's that affects both the terminal ileum, and the ascending colon. Actually, this is the most common form of Crohn's, and it accounts for about 50 percent of total cases. About 30 percent of cases are restricted to the ileum only, and the other 20 of cases are restricted to the colon. Since both MC and Crohn's disease can affect the entire GI tract, I often wonder if MC doesn't have a similar distribution pattern, (IOW, about half the cases affect both the small intestine and the colon, etc.), but I've never seen any research information on that concept. While we're discussing inflammation patterns, note that UC only affects the colon, and usually is concentrated in the sigmoid/rectum area. IOW, it begins in the distal colon, and spreads "northward", and it can be difficult to distinguish from Crohn's colitis, in some cases.

Anyway, the point I was trying to make, is that if upstream inflammation is present, the fecal stream will contain toxic agents, which will subsequently inflame the colon, as it passes through. This has been documented, by noting that if an ileostomy is performed, and the total fecal stream is diverted away from the colon, then the colonic inflammation will disappear, (as noted by microscopic examination of biopsy samples taken from the colon). If the ileostomy is reversed, while inflammation is still present upstream, then the colon will once again become inflamed.

Good luck with your appointment.

Tex

[tex]

Since both MC and Crohn's disease can affect the entire GI tract, I often wonder if MC doesn't have a similar distribution pattern, (IOW, about half the cases affect both the small intestine and the colon, etc.),

Okay, I've located a reference to substantiate my "speculation" that small intestinal inflammation is a very prominent feature of MC. In fact, according to this research report, fully 70% of patients with MC, have small intestinal inflammation, and presumably, this is the primary source of the colonic inflammation, (IOW, toxic agents in the fecal stream, in the colon, due to upstream inflammation):

http://www3.interscience.wiley.com/jour ... 7/abstract

IOW, for most of us, the primary problem is centered in the small intestine, not in the colon. The colonic inflammation is a direct result of the upstream inflammation, (at least initially). This suggests that the treatment should be directed toward the small intestine, rather than the colon, (resolve the symptoms in the small intestine, and the problems in the colon will also disappear). That implies that Entocort EC is not the ideal medication for such a situation, since for those of us with inflammation in the duodenum and/or jejunum, the med will not be activated soon enough to adequately treat those upper sections of the small intestine. Presumably, that's why the most severe cases are so difficult to treat with medications, and it's why Prednisone will work for a few patients, when Entocort EC will not. What is needed, is a source of budesonide, that is not encapsulated with an enteric coating, or better yet, one that has an enteric coating that breaks down at a lower pH.

One way to do this, by "shade-tree" engineering, is to drink grapefruit juice, since grapefruit juice has been documented to double systemic exposure of orally-administered budesonide. This, of course, will also double the risk of adverse side effects from the budesonide, but it might significantly improve it's effectiveness in treating proximal small intestinal inflammation.

Tex

[Polly]

Interesting discussion.

Just wanted to offer a little clarification. MC, by definition, cannot occur anywhere else in the body - the term MC means inflammation of the COLON (hence "colitis"). Of course, we have always noticed that other areas of the GI tract can suffer inflammation, too - like the stomach (gastritis) or esophagus (esophagitis). It is interesting that they have now found microscopic findings similar to those found in MC in some gastric biopsies. But it is not surprising, since those are findings of almost any kind of ongoing inflammation - white cells and collagen deposits.

Colitis is mainly a disease of bacterial imbalance in the colon - the "bad bacteria" begin to outnumber the "good" bacteria. Here is Dr. Fine's discussion of the cause of colitis from his website:

What is the cause of Microscopic Colitis?
Extensive data from animals (mainly rodents) suggest that any form of colitis is the result of the body's immune system setting up an unusual attack on the bacteria living in the colon. What makes the body suddenly recognize these bacteria as harmful and worthy of this attack is not fully understood but there are several clues based on my research. First, it is known that aspirin and other non-steroidal antiinflammatory drugs (NSAID's) can cause this reaction. Also, if the balance of less immune stimulating bacteria (we will call "good bacteria") and more immunostimulatory bacteria ("bad bacteria") favors the latter, inflammation can result. This can occur from use of antibiotics and probably from chronic consumption of certain foods that favor growth of bad bacteria. The role of yeast (for example Candida) in this process is unstudied and therefore unknown. However, whatever tips the scale toward this reaction, it appears that there is an underlying gene responsible for the predisposition to have this form of colitis. In fact, my recent studies have revealed in most cases, the gene is the same as the one known to cause celiac sprue and gluten sensitivity (explaining why some patients get both syndromes). Furthermore, it appears that colitis can cause the immune system to begin recognizing gluten as immunostimulatory and vice versa, gluten sensitivity can lead to colitis. (from www.finerhealth.com)

Thus, what damages the small intestine (and leads to malabsorption) is GLUTEN (not bacteria, although at times some of the bacteria can travel backwards from the colon into the small intestine). Apparently the same gene controls the likelihood of getting both colitis and gluten sensitivity - that's why they are often occur together.

Polly

[tex]

Polly,

You're quite correct, of course. To say that MC could occur anywhere else in the body, would be like saying that you could have an earache in your foot. I don't know why something so obvious never occurred to me, previously. Apparently I must be at an advanced stage of dementia, to not automatically recognize that. LOL.

Incidentally, the reference that I cited in the post above, is an article by Dr. Fine, written in the early part of this century.

Love,
Tex

[Polly]

Tex,

I knew what you meant, since we have always noticed how prone to any kind of GI inflammation we MCers are! It's really more of a semantics issue. And I can empathize about dementia......happens to me more and more as time goes on.

I did notice that your article had Dr. Fine as lead author. Always good to see him published.

Love,

Polly

[katinchatt]

Catching up on all of the above................;)

Back from GI ~ (he is so confused by the way)

1. Sleep, yes I will now sleep, due to script for sleep meds.
2. Gastritis in the Antrum, . . . just learned this today - Pathology: Mild Lympocytic Involvement Gastritis
3. Silly question now, which came first the chicken or the egg? (of course I would say, well, the chicken rolled over and lit a ciggy first). SERIOUSLY NOW!!

**I hear Ya Tex about the grapefruit ~ wonder if I should just dump the stuff on my tongue? Kidding of course!!

Sorry I'm a tad overwhelmed at the moment.
Like I said above, he is so confused! With the NEW information, I'm now having to re-think my healing strategy. Well not re-think, more like reconsider, since recently I began questioning Entocort's selective areas of healing. Darn it, I feel better, that has to count for something!

First of all, when I sat down with said Dr. I mainly wanted sleep meds. I haven't slept in 3 months. 1st Nocturnal D, now Entocort, it's vicious cycle and I WANT TO SLEEP!
Easy . . . but no, he said, "I'll switch you to Colazal". "No" I said, "I like what the Entocort is doing, I just want to sleep". (while Dr. is writing script for Colazal). Said Dr. looked up dazed/confused ~ "Oh you want a sleep med"? Now writes script for sleep med.
Secondly, I said, "please tell me about the gastritis found during my Endoscope". Opens laptop, looks it up, and reads the above Pathology report. I'm asking "WHAT - are these 2 not related somehow"? Dr. looks at me and says "you know Microscopic Colitis is a weird disease, we just do what ever works". DUH! Goes on and on about the auto-immune issues, and I ask him about the Gluten factor in MC, as far as sensitivities - you guessed it! He opens his laptop and freakin Googles "Gluten Microscopic Colitis". OMG!
Finally, he never answered my question about the upper lympocytic and lower collagenous connection. He did take blood for Celiac testing, as he said the biopsy did not totally rule it out. They won't find it there either,.......but I didn't tell him that.

Breathing now..............................slow, deep, breaths.

If I treat my colon with Entocort, obviously I won't treat anything above it going on. (Unless I dump it on my tongue and wash it down with a glass of grapefruit juice). I don't have a clue about Colazal, other than it's for IBD so I doubt it will help with the above issue either.

Rattled,
Kat

. . . off to research, and pull hair out. At least I'll freakin sleep tonight!

[tex]

Polly,

Speaking of semantics, IMO, we wuz robbed, when MC was originally named. Why didn't they call it Lindstrom's microscopic syndrome, or simply Lindstrom's disease? Did Dr. Lindstrom upset whoever was in charge of naming this disease, so they chose to spite him? LOL.

Consider how fortunate the Crohn's disease patients are, in this respect. They can freely talk about Crohn's colitis, Crohn's ileitis, etc., without having to worry about committing mayhem on syntax. We're stuck with trying to describe the manifestations of a disease which is improperly named, and improperly defined, and there are obviously some questions about the criteria used to diagnose it, which means that we're licked before we start. While MC is diagnosed in the colon, (by definition), it is obviously due to upstream issues, and therefore improperly categorized. Who was responsible for this mess, I wonder.

Love,
Tex

[tex]

Kat,

Well, I at least give your doctor credit for being interested enough to try to look a few things up. That's always a good sign, because the "bad" docs already know it all, so they never have to look anything up.

Colazal will basically do anything that Asacol, Rowasa, Pentasa, or Lialda will do. IOW, it should have about a 50% chance of eventually controlling MC symptoms. Like Entocort, the various 5-ASA meds have enteric coatings, and each of them has a different type of delivery mechanism, so that they work somewhat differently, for different patients. IOW, they all use different methods of delaying activation, to insure that the med is far enough down the GI tract to target it essentially at the ileum and the ascending colon, before activation. Some activate sooner than others, however. I'm thinking that colazal is the one that has a unique type of activation system that actually begins in the stomach, (but at a low rate), and then accelerates the rate of release, as it progresses down the system. If you ever want to try that, though, we really need to look that up to verify that this is true, because I might have it confused with Pentasa.

If you should decide to try taking Entocort with grapefruit juice, please leave it in the capsule, because as far as I am aware, there has been no published information on what budesonide might do in the extremely low pH environment of the stomach. Some sort of adverse chemical reaction could conceivably occur when you travel uncharted waters, such as that.

you know Microscopic Colitis is a weird disease, we just do what ever works

Okay, I admit that that doesn't sound good, especially when coming from the mouth of your "trusted" doctor, but again, I have to give him credit, because the sad truth is: That's quite true, and when you think about, it's exactly how we go about it here on this board. (Your doctor is refreshingly candid, at the very least. LOL). We have always maintained, (at least I have, and I believe that Polly, for one, agrees with me on this), that anything that works, to allow a patient to achieve remission, is fair game, and worth considering. Isn't there an old saying that goes something like, "Anything is fair in love, and war, and treating MC"?

Tex

[katinchatt]

Tex wrote:

I'm thinking that colazal is the one that has a unique type of activation system that actually begins in the stomach, (but at a low rate), and then accelerates the rate of release, as it progresses down the system. If you ever want to try that, though, we really need to look that up to verify that this is true, because I might have it confused with Pentasa.

Since finding out about the above Lympocytic gastritis, this may be a better option ~ Sounds logical, but I'm not thinking very logical at said moment.

Tex asked nicely:

If you should decide to try taking Entocort with grapefruit juice, please leave it in the capsule, because as far as I am aware, there has been no published information on what budesonide might do in the extremely low pH environment of the stomach. Some sort of adverse chemical reaction could conceivably occur when you travel uncharted waters, such as that.

OK, Tex ~ I promise I won't. I'm thinking a baking soda and vinegar reaction might be cool as heck right about now. LOL Better yet, maybe the Large Hadron Collider team may be interested in the results..........hum? Black Holes lookout!

KABOOM
Kat

[katinchatt]

Tex & Polly,

No, I should apologize for asking about M "C" outside of the "Colon". Indeed a silly question to say the least. Thank You Tex for "catching my drift".


____________
Kat

[tex]

Kat,

Well, that was a fair question, because we tend to make that little faux pas on a somewhat regular basis around here. Fortunately, no one has ever been thrown in the dungeon here, for such a slip. (Besides, I would have been the one to have to spend some time in the dungeon, on that one.

Actually, for all I know, budesonide might be quite safe in the stomach, (as far as chemical reactions are concerned- it's just that no one knows), but it would almost surely have many of the side effects of Prednisone, if administered that way.

Okay, concerning the enteric coatings, and other time release mechanisms used by the various 5-ASA meds, read post number 3, (one of my posts), on this page:

http://www.perskyfarms.com/phpBB2/viewt ... n&start=30

As noted in that discussion, Colazal sometimes works when the other 5-ASA meds don't work, for some patients. It's also possible that Pentasa might work better, since it uses a rather interesting method of providing the time release capability. Also note that none of these meds are going to work right, if certain strains of vital gut bacteria are either missing, or compromised, because they are necessary for the decomposition of the enteric coating.

Tex

[Polly]

Hey Kat,

Your posts make me laugh (i.e. your side "editorial" comments). Very clever. You are kind to refer to your doc as "confused" - you definitely give him the benefit of the doubt. LOL. We used to refer to most GI docs as JERK docs. Altho I agree with Tex that at least he is looking things up on the computer.

You know, if I were you, I'd wouldn't worry about the gastric inflammation for now. The main thing is the MC and Entocort is an excellent treatment. Especially if you are not having any major stomach symptoms. You could have gastric inflammation from some other causes even - like a recent GI bug or a reaction to a medication. And, getting the MC under control may take care of the gastric issue. Just my 2 cents worth.

Polly