My Enterolab results

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IDontGiveA
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My Enterolab results

Post by IDontGiveA »

Thought I would share my test results as this board was a determining factor in deciding to go with enterolab. Also, I dont understand them. Specifically it seems to me that the Fecal Anti-gliadin IgA result and the explanation are in conflict. If the result is correct and the explanation wrong, I guess it means no more tofu sandwiches. Any input would be great, and no I dont mind if my results are added to any database....

Thanks!





A) Gluten Sensitivity Stool and Gene Panel Complete *Best test/best value
Fecal Anti-gliadin IgA 302 Units (Normal Range is less than 10 Units)

Fecal Anti-tissue Transglutaminase IgA 134 Units (Normal Range is less than 10 Units)

Quantitative Microscopic Fecal Fat Score 299 Units (Normal Range is less than 300 Units)

Fecal Anti-casein (cow’s milk) IgA 7 Units (Normal Range is less than 10 Units)

HLA-DQB1 Molecular analysis, Allele 1 0301

HLA-DQB1 Molecular analysis, Allele 2 0301

Serologic equivalent: HLA-DQ 3,3 (Subtype 7,7)

C) Egg, Yeast, and Soy Food Sensitivity Stool Panel
Fecal Anti-ovalbumin (chicken egg) IgA 4 Units (Normal Range is less than 10 Units)

Fecal Anti-saccharomyces cerevisiae (dietary yeast) IgA 4 Units (Normal Range is less than 10 Units)

Fecal Anti-soy IgA 24 Units (Normal Range is less than 10 Units)

Acute/Chronic Colitis Stool Test
Fecal lactoferrin Negative (Normal - Negative)

Interpretation of Fecal Anti-gliadin IgA: Intestinal antigliadin IgA antibody was below the upper limit of normal, and hence there is no direct evidence of active gluten sensitivity from this test. However, because 1 in 500 people cannot make IgA at all, and rarely, and some people can still have clinically significant reactions to a food antigen despite the lack of a significant antibody reaction (because the reactions primarily involve T cells), if you have a syndrome or symptoms known to be associated with gluten sensitivity, a gluten-free diet may help you despite a negative test. If you have no syndrome or symptoms associated with gluten sensitivity, you can follow a gluten-containing healthy diet and retest in 3-5 years; or you may opt to go gluten-free as a purely preventive measure.

Interpretation of Fecal Anti-tissue Transglutaminase IgA: You have an autoimmune reaction to the human enzyme tissue transglutaminase, secondary to dietary gluten sensitivity.

Interpretation of Quantitative Microscopic Fecal Fat Score: Provided that dietary fat is being ingested, a fecal fat score less than 300 indicates there is no malabsorbed dietary fat in stool indicating that digestion and absorption of nutrients is currently normal.

Interpretation of Fecal Anti-casein (cow’s milk) IgA: Levels of fecal IgA antibody to a food antigen greater than or equal to 10 are indicative of an immune reaction, and hence immunologic “sensitivity” to that food. For any elevated fecal antibody level, it is recommended to remove that food from your diet. Values less than 10 indicate there currently is minimal or no reaction to that food and hence, no direct evidence of food sensitivity to that specific food. However, because 1 in 500 people cannot make IgA at all, and rarely, some people can still have clinically significant reactions to a food antigen despite the lack of a significant antibody reaction (because the reactions primarily involve T cells), if you have an immune syndrome or symptoms associated with food sensitivity, it is recommended that you try a strict removal of suspect foods from your diet for up to 12 months despite a negative test.

Interpretation Of HLA-DQ Testing: Although you do not possess the main HLA-DQB1 genes predisposing to celiac sprue (HLA-DQB1*0201 or HLA-DQB1*0302), HLA gene analysis reveals that you have two copies of a gene that predisposes to gluten sensitivity (any DQ1, DQ2 not by HLA-DQB1*0201, or DQ3 not by HLA-DQB1*0302). Having two copies of a gluten sensitive gene means that each of your parents and all of your children (if you have them) will possess at least one copy of the gene. Two copies also means there is an even stronger predisposition to gluten sensitivity than having one gene and the resultant immunologic gluten sensitivity may be more severe.

Interpretation of Fecal Anti-ovalbumin (chicken egg) IgA: Levels of fecal IgA antibody to a food antigen greater than or equal to 10 are indicative of an immune reaction, and hence immunologic “sensitivity” to that food. For any elevated fecal antibody level, it is recommended to remove that food from your diet. Values less than 10 indicate there currently is minimal or no reaction to that food and hence, no direct evidence of food sensitivity to that specific food. However, because 1 in 500 people cannot make IgA at all, and rarely, some people can still have clinically significant reactions to a food antigen despite the lack of a significant antibody reaction (because the reactions primarily involve T cells), if you have an immune syndrome or symptoms associated with food sensitivity, it is recommended that you try a strict removal of suspect foods from your diet for up to 12 months despite a negative test.

Interpretation of Fecal Anti-saccharomyces cerevisiae (dietary yeast) IgA: Levels of fecal IgA antibody to a food antigen greater than or equal to 10 are indicative of an immune reaction, and hence immunologic “sensitivity” to that food. For any elevated fecal antibody level, it is recommended to remove that food from your diet. Values less than 10 indicate there currently is minimal or no reaction to that food and hence, no direct evidence of food sensitivity to that specific food. However, because 1 in 500 people cannot make IgA at all, and rarely, some people can still have clinically significant reactions to a food antigen despite the lack of a significant antibody reaction (because the reactions primarily involve T cells), if you have an immune syndrome or symptoms associated with food sensitivity, it is recommended that you try a strict removal of suspect foods from your diet for up to 12 months despite a negative test.

Interpretation of Fecal Anti-soy IgA: Levels of fecal IgA antibody to a food antigen greater than or equal to 10 are indicative of an immune reaction, and hence immunologic “sensitivity” to that food. For any elevated fecal antibody level, it is recommended to remove that food from your diet. Values less than 10 indicate there currently is minimal or no reaction to that food and hence, no direct evidence of food sensitivity to that specific food. However, because 1 in 500 people cannot make IgA at all, and rarely, some people can still have clinically significant reactions to a food antigen despite the lack of a significant antibody reaction (because the reactions primarily involve T cells), if you have an immune syndrome or symptoms associated with food sensitivity, it is recommended that you try a strict removal of suspect foods from your diet for up to 12 months despite a negative test.

Interpretation of Fecal lactoferrin: A negative fecal lactoferrin test indicates you have no neutrophilic inflammation in your stool typical of acute and/or chronic colitis. This essentially rules out ulcerative colitis and Crohn’s colitis, however it does not completely rule out microscopic colitis.
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tex
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Post by tex »

WOW! You're Right! Someone was sound asleep when they picked that first explanation, (about anti-gliadin antibodies). Most likely they accidentally hit the wrong key on a computer keyboard, and then failed to proofread it and catch their mistake. 302 is a very high result, so you are very, very gluten-sensitive. If you question that number, an e-mail, or a phone call should provide a quick verification. I've never heard of them making a mistake such as that, but I suppose it only proves they're human. :lol:

Lucky you, you're not sensitive to dairy products, yeast, or eggs, and your sample didn't show any evidence of Crohn's or UC, but soy is clearly a problem, (in addition to gluten). Also, the fact that you have double DQ3 genes suggests that you might have other intolerances, and/or you might have above normal sensitivities to gluten and/or soy. (Double DQ genes almost always link with above normal numbers of food intolerances, and/or an above normal difficulty in achieving remission - we don't know why, we have just noticed the implications).

Thanks, I'll add these results to our database.

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 mbeezie »

I Don't Give A . . .

I'm wondering if you had CD testing for antbodies to rule our celiac disease? Just asking becasue when I met Dr. Fine last year he talked about Enterolab values over 300 being highly suspicious of celiac, not just gluten sensitivity (no confirmation, just suspected). Anyway, treatment is the same.

Mary Beth
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Post by Ginny »

Mary Beth, that is pretty interesting what Dr. Fine has stated. My Fecal Anti-gliadin IgA was over 400. I have had every test for CD and everythings is negative except for one blood test that came back positive. Maybe this is the reason I am struggling. I finally switched to the Paleo diet except for rice and potatoes (too much weight loss). Hopefully the more months that go by I will improve. Ginny
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Post by mbeezie »

I just looked at your gene profile - you don't have the main celiac genes. It's possible, but unlikely I guess. Anyway, your values are very high and I'm just relating his comment. What blood test came back positive? Did you have an endoscopy?

Mary Beth
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Post by tex »

Mary Beth,

Either I made a mistake transferring Ginny's gene data, or you must have accidentally looked at the wrong profile, because according to my gene test results list, she does have the most common celiac gene, HLA-DQ2. I also note that her other gene allele, 0602, is protective of type I diabetes, but confers a heightened susceptibility to narcolepsy, which might be something to keep in mind. (IOW, with the 0602 gene, narcolepsy may be triggered by a certain peptide, similar to the way that celiac disease is triggered by the presentation of the alpha gliadin peptide).

http://www.ncbi.nlm.nih.gov/pubmed/14769912

I agree with you, if she had even just one positive celiac blood test result, she almost certainly has CD, especially with a stool gliadin antibody count that high.

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 mbeezie »

I was responding to I Don't Give A, not Ginny. I Don't Give A doesn't have main celiac genes - I didn't look up Ginny's. But either way, those are very high antobody values.

Mary Beth
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Post by Ginny »

Tex, I don't want to take aways from I Don't Give A's situation but thanks for answering. I did have the endoscopy done and it was okay. The doc wouldn't buy that I had CD from that one blood test until he did the endoscopy. I will start a new subject and ask more questions later. Thanks for all your valuable help. Ginny
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Post by mbeezie »

Quick comment Ginny - CD can be patchy and unless the GI was incredibly skilled he could have missed it and biopsied the wrong spot. Exactly what blood test came back positive?

Mary Beth
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Post by tex »

Mary Beth,

Sorry if I jumped to the wrong conclusions - I was just going by the fact that Ginny was the one who had mentioned a positive blood test, and I didn't notice where IDontGiveA had mentioned one. :oops:

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 tex »

Ginny,

With all due respect to your GI doc, for the reason that Mary Beth mentioned, your doc probably took biopsy samples from the wrong locations, and totally missed your villus damage, in your small intestine. The same type of mistake sometimes causes some GI docs to misdiagnose MC, because they don't now where to take the biopsy samples, and they miss the areas with inflammation. I really believe that some GI docs assume that the entire colon should be inflamed, if MC is present, but that is totally incorrect. It is almost always present in random "splotches" in the colon. The same distribution pattern sometimes exists in the small intestine, with celiac disease, but some GI docs incorrectly assume that the damage will always be widespread, (and often it is widespread, but certainly not in every case).

One does not receive a positive result to a celiac blood test for no reason. Those tests are notorious for false negatives, but not false positives.

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 Ginny »

Thanks Tex and Mary Beth for your response. My GI was pretty thorough in taking 20 biopsies of the colon but the small intestine, I don't know. I am seeing him in a week and will reaffirm about the villus damage in the small intestine. When I showed him the results from Enterolab, he did mention again that I showed positive on one test and that the D would be the last to improve...............well what do you expect when they only see you for 10-20 minutes!! BUT I also have many other intolerances :sad: to deal with as well. Hopefully as each day passes things will keep improving. Ginny
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Post by IDontGiveA »

I received a response from enterolab, they apologised profusely, and told me that a computer glitch caused the wrong explanation, and that the result values are indeed correct.

@Marybeth
That is indeed an interesting comment from Dr.Fine. From the enterolab site:

' However, the amount of antibody present is not a measure of clinical severity, but rather, the amount of antibody being produced by the plasma cells in the intestine in response to gluten at that site'

So that is interesting that the higher level does actually mean something. I did the blood test for IgA about the same time I did the enterolab test, which was after about 4 months GF. It came back negative. I am considering the biopsy, but I do have some doubts. I dont know how invasive a proceedure it is, Im starting to really feel better and I dont want to do anything to trigger another relapse. My Fecal Fat Score was in the normal range as well, does this mean I have no intestinal damage (hard for me to believe) and so nothing would show on the biopsy? If I understand correctly, the main difference between full CD and 'intolerance' is damage to the villi, so maybe the fecal fat score rules me out for CD as well? Also I dont know how much more confirmation I need, especially if I can trust the enterolab results.

@tex
Thanks for the gene insight. I am not familiar with them and dont know all of what they really mean. For example, if I do not have the main celiac gene, does that mean I cannot be a celiac or just not likley? Would one of my parents be highly suspect for having the celiac gene as well? From the enterolab site:

'' And according to my more recent research, when DQ1,1 or DQ3,3 are present together, the reactions are even stronger than having one of these genes alone (like DQ2,2, DQ2,8, or DQ8,8 can portend a more severe form of celiac disease). ''

Does this mean that because I have the double DQ3, that Im more likely to have CD than if I had the main celiac gene?


@Ginny
Good luck with the tests, and I hope you start to improve soon...

Tony
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Post by tex »

Tony,

According to most GI docs, yes, if you do not have one of the main (two) celiac genes, (DQ2 or DQ8), then you cannot develop celiac sprue. However, they are wrong, since if you add up all of the diagnosed celiac cases with either DQ2 or DQ8 genes, and add in the number of celiac patients who have both DQ2 and DQ8 genes, you get a number of something around 98%, (IOW, I don't remember the exact number, but it is somewhere in that neighborhood). That means that roughly 2% of diagnosed celiacs have no DQ2 or DQ8 genes. Obviously, some uncatalogued gene, (or genes), predispose to celiac disease. The GI docs like to ignore that possibility, since they don't know what those genes are, so they can't test for them, (IOW, they almost always follow the KISS principle, when practicing medicine).

Neither of your parents could have one of the common celiac genes, because if they did, you would have a copy from that parent. Therefore, if you do indeed have a "rare" celiac gene, then both of your parents must have at least one copy of that gene, (because you inherit one gene in this category from each parent).

If the genes that you have, do indeed predispose to celiac disease, then yes, a double copy greatly increases your chances of developing the disease. I can't find any references that connect that gene with CD, however, that doesn't mean that no connection exists - it simply means that it hasn't been discovered and/or verified, yet, (or maybe I just didn't use the right keywords in my searches).

Regarding your question about Enterolab's Fecal Fat Score for your sample, your result is obviously right on the line. In engineering, whenever we are designing a device for a critical mission, we try to design in more capacity than will ever be needed during the mission, (on a practical level), or even redundancy, if a function is absolutely vital, and part of the existing design can be easily modified to take over another function, if the primary system should fail. The body, especially the digestive system, has a lot of that sort of "versatility" built in. IOW, the small intestine normally has far more absorptive capacity than is normally needed. You could have 10% of the villi in your small intestine totally disabled, and I doubt that you would be able to tell the difference, as far as nutrient intake is concerned, because you should have enough surplus capacity to easily handle that amount. The fecal fat score is a rough measure of the amount of fat that passes through your entire GI tract, without being absorbed. I doubt that anyone, (in the general population), has a 100% fat absorption rate, (but I'm just guessing, based on the fact that there is no such thing as a perfect process - some processes are very good, and approach perfection, but none actually reach 100% effectiveness). If that weren't true, the threshold would be a lot lower than 300, for the breakpoint on the test. So what I'm leading up to is the point that GI systems have sufficient built-in flexibility, that you could easily have some degree of villus damage, while still being able to do a "normal" job of absorbing fat from the fecal stream. Obviously, you probably don't have extensive damage, or your score would be higher, but IMO, it's high enough to be a candidate for some degree of damage. Maybe Mary Beth knows more about that issue than I do, however, and I certainly wouldn't dispute her opinion.

Consider this - my small intestine is approximately a third longer than normal. (A couple of surgeons mentioned that to me, after my recent surgery, and it was even noted in the operative report). It seems pretty clear to me that I could have a fair amount of small intestinal damage, and still not show an abnormal fat malabsorption score. Almost 3 years after I adopted the GF diet, I sent a sample to Enterolab. I specifically pointed out that I wasn't ordering any anti-gliadin, or anti-tissuetransglutaminase antibody testing, because I had already been on the diet for almost 3 years, at that point. Even so, my fecal fat score was still 294. Based on that consideration, the lab's analysis of my sample was:
Analysis of this stool sample indicates you have dietary gluten sensitivity.
How would they reach that conclusion, without basing it on the fecal fat score, because my other tests were for soy, eggs, and yeast, and they all yielded negative results? We are all different, in so many ways, from what is considered "normal" for someone in the general population.

Tex
:cowboy:

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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