Hmmmmmmmm. I believe that your test results are the first to turn up here, with all negative results.
If those results are accurate, then you apparently don't have any food intolerances. The odds of that being the case, however, (assuming that you do have MC), are extremely slim. That suggests that you probably have selective IgA deficiency. You should get your doctor to measure your serum immunoglobulin concentrations. If you are IgA deficient, then no matter how severely you might react to an allergen, your immune system would not be capable of producing the antibodies necessary to cause a positive test result, (for IgA antibodies).
An IgA deficiency will make more one more prone to recurrent infections, allergies, chronic diarrhea, or autoimmune diseases. Note that it can also cause endocrine issues. This site offers a pretty decent explanation of the situation:
It appears that, regardless of the test results, (since they are invalid, if your doctor can confirm that you are IgA dificient), you will almost surely need to cut gluten, and probably casein, out of your diet. Until you get checked out for IgA deficiency, though, this is all guesswork.
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.
Thanks Tex. I was sure someone here would know more about this. I do have confirmed MC, so that is why the results doubly shocked me. I really think I am sensitive. If I go on a gluten binge during the right time of the month, I'll get achy joints. If I drink milk, it makes me hurt in my side. Yogurt takes longer to affect me, but it does. (The 24h yogurt I was using has less casein in it from the fermentation process. It doesn't break it all down, but it does some, so that could explain the slowed rxn to it).
So, If one has Selective IgA deficiency would that making taking Entocort more dangerous? Would it also mean that the other tests from Dr. Fine would be invalid for me? The IgG delayed allergy tests may help me some but that would mean that it's the food diary slow way for on IgA rxns right? I'm calling my GP today to draw for this test. Do I need to have the IgG and IgM for comparison for the result to show what I need?
Are my genetics results very common for MC people?
I have been wondering if the fecal fat score from enterolab would be higher for a person on a high fat diet as apposed to a low fat diet. IOW does quantity of fat effect the ff score?
I'm no doctor, nor am I an expert on the immune system, but it would seem highly likely that any immune system suppressants would make IgA deficient individuals more vulnerable to infections, just as they would virtually anyone else. Even if you are diagnosed to be IgA deficient, of course, most of your immune system components should still be in proper working condition. IgA is sort of the first line of defense against the invasion of pathogens into the body because it's concentrated in body fluids, such as tears, saliva, and the secretions of the respiratory tract and the digestive tract. IOW it's job is to guard the entrances into the body. With that line of defense missing, pathogens have a much better chance of gaining a "foothold" in the body, before an effective immune system response is launched.
I forgot to address the question you asked earlier, about T cells. The inflammation with IBDs is primarily due to a T cell response. There are several types of T cells, but the ones that do most of the actual destruction of foreign invaders, are called Killer T cells, (or cytotoxic T lymphocytes - CTLs, for short). These cells directly attack other cells carrying certain foreign or abnormal molecules on their surfaces. To understand how these T cells perform, in order to attack "aggressors" in our GI tract, and how budesonide, (Entocort), interacts with them, it's necessary to review a little background information on how these components of the immune system work.
T cells do not recognize free-floating antigens. Rather, their surfaces contain specialized antibody-like receptors that see fragments of antigens on the surfaces of infected, (or cancerous), cells. T cells contribute to immune defenses in two major ways - some types direct and regulate immune responses, while others directly attack infected or cancerous cells.
IOW, some T cells are helper cells, while others are killer cells. CTLs, for example, are especially useful for attacking viruses, because viruses often hide from other parts of the immune system while they grow inside infected cells. CTLs recognize small fragments of these viruses peeking out from the cell membrane and launch an attack to kill the cell.
In most cases, T cells only recognize an antigen if it is carried on the surface of a cell by one of the body’s own major histocompatibility complex, (MHC), molecules. MHC molecules are proteins recognized by T cells for distinguishing between self and non-self. Virtually every cell in the body is covered with MHC proteins, but each person has a different set of these proteins on his or her cells. If a T cell recognizes a non-self MHC molecule on another cell, it will destroy the cell.
Helper T cells, or Th cells, coordinate immune responses by communicating with other cells. Some stimulate nearby B cells to produce antibody, others call in microbe-gobbling cells called phagocytes, still others activate other T cells.
Natural killer, (NK), cells are another kind of lethal white cell, or lymphocyte. Like killer T cells, NK cells are armed with granules filled with potent chemicals. But while killer T cells look for antigen fragments bound to self-MHC molecules, NK cells recognize cells that lack self-MHC molecules. Therefore, NK cells have the potential to attack many types of foreign cells. Both kinds of killer cells kill on contact.
To get to the "punch line", budesonide decreases inflammation by acting within cells to prevent the release of certain chemicals that are important in producing immune and allergic responses. By decreasing the release of those chemicals in the gut, inflammation is reduced, but at the expense of a weakened immune response capability, obviously. Budesonide, (and other corticosteroids, of course), suppress peripheral blood natural killer cell activity, by decreasing the numbers of NK cells in the circulation. Obviously, the suppression of that line of defense, should significantly raise the risk of infection. There may be other ways that budesonide suppresses the immune system, that I'm not aware of.
As far as I'm aware, all of Enterolab's tests, (except for the gene tests, of course), are based on detection of IgA antibodies, so yes, all of their tests would be useless for someone who is IgA deficient. As you suggested, a diary, together with trial and error testing, will probably be the only practical way to determine your food intolerances.
Your doctor will probably have his/her own ideas on how he or she prefers to go about testing for IgA deficiency, but checking IgM and IgG levels might be helpful, since IgM antibodies are the first antibodies to appear in response to an initial exposure to an antigen.
Except for that first allele of 202, your genetic results are typical of the rest of us. (Could that number actually be 201?) If 202 is correct, did they offer an explanation for it?
From what I've seen, fecal fat scores are typically seen to be just under the "magic" number. I'm not sure why that is, but it probably is due to the nature of the test itself.
I'm very curious to see what your doctor may find, regarding possible IgA deficiency.
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.
A) Gluten Sensitivity Stool and Gene Panel Complete *Best test/best value
Fecal Antigliadin IgA 6 (Normal Range <10 Units)
Fecal Antitissue Transglutaminase IgA 6 Units (Normal Range <10 Units)
Quantitative Microscopic Fecal Fat Score 287 Units (Normal Range <300 Units)
Fecal anti-casein (cow's milk) IgA antibody 6 Units (Normal Range <10 Units)
HLA-DQB1 Molecular analysis, Allele 1 0202
HLA-DQB1 Molecular analysis, Allele 2 0602
Serologic equivalent: HLA-DQ 2,1 (Subtype 2,6)
Interpretation of Fecal Antigliadin 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 Antitissue Transglutaminase IgA: The level of intestinal IgA antibodies to the human enzyme tissue transglutaminase was below the upper limit of normal, and hence, there is no evidence of a gluten-induced autoimmune reaction.
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 antibody: 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.
Thanks for that explanation. I'm gonna know a lot about immunity because of all this . It's a lot to chew on though.
Also, I'm wondering if blood levels of IgA are going to tell me if I have a problem making IgA in my gut. If it's a genetic cause, then I would think the blood levels would show a trend and that secretory IgA levels would be similary affected. However, if the cause is environmental/acquired would it only be reflected in the secretory IgA. And if so, are blood levels of secretory IgA accurate or would a saliva test be more accurate?
I'm actually ordering these tests on myself and my doc doesn't really know anything about them. I'm pretty sure my GI would roll his eyes on this one as he doesn't believe in the accuracy of fecal testing when it comes to the stool analysis test, and he hasn't heard of Dr. Fine's tests, so he probably wouldn't order any testing based on the results I got from enterolab. My GP is basically just ordering whatever I want. At this point all I know to order is a quantitative immunoglobulins (IgA, IgG, IgM).
So almost over the 300 number on fecal fat really is normal?
Going to chew on the T-cell immunity more . I really want to learn this, but it's so confusing at first.
Well, that answers my question - apparently the 202 allele is totally unrelated to celiac disease, while still being an indicator of a predisposition to gluten sensitivity.
Apparently Dr. Fine believes that you are probably IgA deficient, since he mentioned the concept at least twice in the report analysis.
I'm pretty sure that equilibrium levels of IgA, (long-term, steady-state), should be similar in most body fluids, (though probably at different levels), so a serum test should be valid. I can't answer your question about which would be more accurate, but I would suspect that it's probably easier to locate "normal" blood serum values, than it would be to locate normal IgA values for saliva, though I haven't even looked to see if that might be true. Blood serum levels for IgA deficient individuals will typically be less than about 8 mg/dl, while serum IgA in normal adults ranges from 90 to 450 mg/dl.
It's the same old story - we have to find ways to resolve our GI issues despite our GI docs "help", rather than because of his or her help. <sigh>
Shonda wrote:So almost over the 300 number on fecal fat really is normal?
That seems to fit the trend, here, for the numbers that I've seen.
Here's a good, understandable reference on the basics of the workings of the immune system, if you want to learn more:
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.
. It's a lot to chew on though. 
. I really want to learn this, but it's so confusing at first.