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Below is a copy of Dr. Fine's talk, given in Louisville, to a Celiac Sprue Support Group, in June of 2003. He gave me permission to share this. I found it very interesting and informative. I apologize for the lengthiness. I added a few things in [ ] parentheses, and added more paragraph spaces, for better readability:

Sincerely,

Carol

fsds@rkymtnhi.com

*************************

"Early Diagnosis Of Gluten Sensitivity:

Before the Villi are Gone."

"Transcript of a talk given by Kenneth Fine, M.D. to the Greater Louisville Celiac Sprue Support Group, [June, 2003] (Initial transcription by Marge Johannemann; Edited by Dr. Kenneth Fine, with assistance by Kelly Vogt)

Dr. Fine has been an intestinal researcher and an academic and clinical gastroenterologist for 15 years. He is the Director of The Intestinal Health Institute and The EnteroLab.com Clinical Laboratory in Dallas Texas.

"Gluten sensitivity" is the process by which the immune system reacts to gluten contained in wheat, barley, rye, and oats. The reaction begins in the intestine because that is where the inciting antigen, gluten, is present (from food).

When this immunologic reaction damages the [microscopic] finger-like surface projections, the villi, in the small intestine (a process called villous atrophy), it is called celiac disease (or sometimes celiac sprue or gluten-sensitive enteropathy).

The clinical focus of gluten-induced disease has always been on the intestine because that is the only way the syndrome was recognized before screening tests were developed. The intestinal syndrome consists mainly of diarrhea, gas, bloating, nausea, vomiting, fat in the stool, nutrient malabsorption, and even constipation.

Although the small intestine is always the portal of the immune response to dietary gluten, it is not always affected in a way that results in villous atrophy.

Even though recent research has shown that celiac disease is much more common than previously suspected, affecting 1 in 100-200 Americans and Europeans, past and emerging evidence indicates that it accounts for only a small portion of the broader gluten sensitive clinical spectrum (often referred to as the "Tip of the Gluten Sensitive Iceberg").

With better understanding of how gluten triggers immune and autoimmune reactions in the body under the control of various genes, and advancing techniques of detecting these reactions, it is becoming apparent that the majority of the gluten sensitive population (the submerged "mass of the iceberg") do not manifest villous atrophy in its classic, complete form and therefore do not have celiac disease.

In these non-celiac, gluten sensitive individuals, the brunt of the immune reaction either affects the function of the intestine, causing symptoms without structural damage, affects other tissues of the body (and virtually all tissues have been affected in different individuals), or both.

This is important because the commonly used diagnostic tests of clinically important gluten sensitivity (blood tests for certain antibodies and intestinal biopsies) are only positive when villous atrophy of the small intestine is present.

But if only a small minority of gluten sensitive individuals actually develop celiac disease, the majority, who have not yet or may never develop villous atrophy, with or without symptoms, can remain undiagnosed and untreated for years.

This can result in significant immune and nutritional consequences, many of which are irreversible even after treatment with a gluten-free diet. Some of these disorders include loss of hormone secretion by glands (hypothyroidism, diabetes, pancreatic insufficiency, etc), osteoporosis, short stature, cognitive impairment, and other inflammatory bowel, liver, and skin diseases, among others [like neurological problems, etc.].

Only with early diagnosis, can these problems be prevented or reversed.

I am here to report on a scientific paradigm shift regarding early diagnosis of gluten sensitivity based on about 30 years of medical research by myself and others.

My message is that earlier and more inclusive diagnosis of gluten sensitivity than has been allowed by blood tests and intestinal biopsies must be developed to prevent the nutritional and immune consequences of long-standing gluten sensitivity.

Imagine going to a cardiologist because your blood pressure is high or you’re having chest pain, and the doctor says he is going to do a biopsy of your heart to see what is wrong. If it 'looks' O.K., you are told you have no problem and no treatment is prescribed because you have not yet had a heart attack showing on the biopsy.

You would not think very highly of the doctor utilizing this approach because, after all, isn't it damage to the heart that you would want to prevent?

But for the intestine and gluten sensitivity, current practice embraces this fallacious idea that until an intestinal biopsy shows structural damage, no diagnosis or therapeutic intervention is offered.

This has to change now because with newly developed diagnostic tests, we can diagnose the problem before the end stage tissue damage has occurred, that is "before the villi are gone," with the idea of preventing all the nutritional and immune consequences that go with it.

There are many misconceptions regarding the clinical presentation of gluten sensitivity or celiac disease: For example, that you cannot be gluten sensitive if you have not lost weight, are obese, have no intestinal symptoms, or are an adult or elderly.

However, the most widely held and clinically troublesome misconception is that a negative screening blood test, or one only showing antigliadin antibodies (without the autoimmune antiendomysial or antitissue transglutaminase antibody) rules out any problem caused by gluten at that time or permanently.

For some reason, the high "specificity" of these blood tests has been tightly embraced. Specificity means if the test is positive, you surely have the disease being tested for with little chance that the positive is a "false positive."

But sadly, a negative test does not mean you do not have the problem.

This is the biggest pitfall of all because the only thing a very specific test, like blood testing for celiac disease, can do is "rule in" the disease; it can not "rule it out."

If you’ve got very far advanced and/or long-standing celiac disease, it is likely that the test will be positive.

However, several studies have now revealed that it is only those with significant villous atrophy of the small intestine who regularly show a positive antiendomysial or antitissue transglutaminase antibody, the specific tests relied upon most heavily for diagnosis of gluten-induced disease.

When there was only partial villous atrophy, only 30% had a positive test.

More disturbing perhaps, were the results with respect to screening first degree relatives of celiacs with blood tests. Despite some biopsy-proven early inflammatory changes in the small intestine but without villi damage, all blood tests were negative.

For some reason, it’s been perfectly acceptable to celiac diagnosticians that a patient must have far advanced intestinal gluten sensitivity, i.e., villous atrophy, to be diagnosed and a candidate for treatment with a gluten-free diet.

That means from the specific testing standpoint, there’s never (or rarely) a false positive.

But what about the larger majority of gluten-affected people who do not presently have or may never get this end stage, villous atrophic presentation? They are out of luck as far as blood testing is concerned.

So the fact is that we have erroneously relied on specificity (always picks up gluten sensitivity after it has caused villous atrophy, never having a false positive) instead of sensitivity (doesn’t miss gluten sensitive people even though they might be picked up early, even before full-blown celiac disease develops).

Would a test relying on specificity rather than sensitivity be good enough for you, or your children? Consider the risk of not getting an early diagnosis versus going on a gluten free diet a few months or years prematurely.

While I do not recommend anyone to have a biopsy (especially children) for diagnosis because of the shortcomings and invasive nature of this technique, I particularly do not want someone to have a biopsy showing villous atrophy, since by that time, associated bone, brain, growth, and/or gland problems are all but guaranteed.

And here is another related problem: you have a positive blood test, but, if a small bowel biopsy comes back normal or nearly normal, you are told that the blood test must have been a "false positive" and that gluten is not your problem.

Would you believe that, especially in light of the fact that most such people would have gotten the blood test in the first place because of a specific symptom or problem?

Let’s hope not. All that means (positive blood test, negative biopsy) is that the gluten sensitivity (evidenced by antibodies to gliadin in the blood) has not yet damaged your intestines severely.

Evidence of this comes from a study that I performed. We tested 227 normal volunteers with blood tests for celiac disease. Twenty-five of these people (11%) had either antigliadin IgG or IgA in their blood versus only one (0.4%) that had antiendomysial, antitissue transglutaminase, and antigliadin IgA in the blood.

So for every one person in a population that has the antibodies that have 100% specificity for celiac disease of the intestine (antiendomysial and antitissue transglutaminase), there are 24 that have antibodies to gliadin that may not have celiac disease.

So what is going on with the 11% with antigliadin antibodies in blood? Are these false positives (rhetorically)?

You’re telling me that there is a disease called celiac disease and it is associated with antibodies to gliadin in the blood and sometimes it damages the intestine?

But people with antigliadin antibody in their blood but no other antibodies do not have a clinically significant immunologic reaction to gluten?

Do you see the problem? How can 11% be false positives? What about the 89% with none of these antibodies? You cannot equate having no antibodies at all (a negative test) with having antigliadin antibodies alone.

If you have antibodies to gliadin, something is going on here. Where there’s smoke there’s fire.

The purpose of this study was to test this hypothesis: that an antigliadin antibody alone does indicate the presence of an immune reaction to gluten that may be clinically important.

Using tests for intestinal malabsorption and abnormal permeability (i.e., tests of small bowel function, unlike a biopsy which says nothing about function), we found that 45% of people with only an antigliadin IgG or IgA antibody in blood (without either antiendomysial or antitissue transglutaminase antibody) already had measurable intestinal dysfunction, compared to only 5% of people with no antibodies to gliadin in their blood.

When we did biopsies of these people’s intestines, none had villous atrophy with only a few showing some early inflammation.

Thus, having an antigliadin antibody in your blood does mean something: that there is nearly a 1 in 2 chance that functional intestinal damage is already present even though it may not be visible structurally at the resolution attained by a light microscope assessment of a biopsy.

As mentioned at the outset, not all gluten sensitive individuals develop villous atrophy. Evidence for this has been around for a long time.

In 1980, a medical publication titled "Gluten-Sensitive Diarrhea" reported that 8 people with chronic diarrhea, sometimes for as long as 20 years, that resolved completely when treated with a gluten-free diet, had mild small bowel inflammation but no villous atrophy.

In 1996 in a paper called "Gluten Sensitivity with Mild Enteropathy," ten patients, who were thought to have celiac disease because of a positive antiendomysial antibody blood test, had small bowel biopsies showing no villous atrophy.

But amazingly, these biopsies were shown to react to gluten when put in a Petri dish, proving the tissue immunologically reacted to gluten (which was likely anyway from their positive blood tests).

Two other reports from Europe published in 2001 showed gluten sensitivity without villous atrophy (and hence without celiac disease).

In one of these studies, 30% of patients with abdominal symptoms suggestive of irritable bowel syndrome having the celiac-like HLA-DQ2 gene but no antibodies to gliadin in their blood, had these antibodies detected in intestinal fluid (obtained by placing a tube down into the small intestine).

Thus, in these people with intestinal symptoms, but normal blood tests and biopsies, the antigliadin antibodies were only inside the intestine (where they belong if you consider that the immune stimulating gluten also is inside the intestine), not in the blood. This is the theme we have followed in my research, as we are about to see.

More proof that patients in these studies were [had] gluten sensitivity came from the fact that they all got better on a gluten-free diet, and developed recurrent symptoms when "challenged" with gluten.

Although the gluten-sensitive patients in these studies did not have the villous atrophy that would yield a diagnosis of celiac disease, small bowel biopsies in many of them showed some, albeit minimal, inflammatory abnormalities.

Yet, when a symptomatic patient in clinical practice is biopsied and found to have only minimal abnormalities on small bowel biopsy, clinicians do not put any stock in the possibility of their having gluten sensitivity.

As much as I would like to take credit for the concept, you can see from these studies that I did not invent the idea that not all gluten sensitive patients have villous atrophy. It has been around for at least 23 years, and reported from different parts of the world.

For many years there has also been proof that the intestine is not the only tissue targeted by the immune reaction to gluten.

The prime example of this [is] a disease called dermatitis herpetiformis where the gluten sensitivity manifests primarily in skin, with only mild or no intestinal involvement.

Now from more recent research it seems that the almost endless number of autoimmune diseases of various tissues of the body also may have the immune response to dietary gluten and its consequent autoimmune reaction to tissue transglutaminase as the main immunologic cause.

A study from Italy showed that the longer gluten sensitive people eat gluten, the more likely they are to develop autoimmune diseases.

They found that in childhood celiacs, the prevalence of autoimmune disease rose from a baseline of 5% at age 2 to almost 35% by age 20. This is a big deal if you think how much more complicated one's life is being gluten sensitive AND having an autoimmune disease.

So preventing autoimmune disease is one very important reason why early diagnosis and treatment of gluten sensitivity is important.

Early diagnosis before celiac disease develops also holds the potential of preventing other clinical problems such as malnutrition, osteoporosis, infertility, neurologic and psychiatric disorders, neurotube defects (like spina bifida) in your children, and various forms of gastrointestinal cancer.

Another reason for early diagnosis and treatment is very straightforward and that is because many gluten sensitive individuals, even if they have not yet developed celiac disease (villous atrophy), have symptoms that abate when gluten is removed from their diet.

Furthermore, from a study done in Finland, a gluten sensitive individual who reports no symptoms at the time of diagnosis can improve both psychological and physical well-being after treatment for one year with a gluten-free diet.

Despite the common sense and research evidence that early diagnosis of gluten sensitivity offers many health advantages over a diagnostic scheme that can only detect the minority and end-stage patients, until now, the limitation was still in the tests being employed.

As mentioned above, the main test used for primary (before symptoms develop) and secondary (after symptoms develop) screening for celiac disease, blood tests for antigliadin and antiendomysial/antitissue transglutaminase antibodies, are only routinely positive after damage to intestinal villi is extensive.

As shown in a 1990 publication, this is because unless you have full blown, untreated celiac disease, the IgA antibodies to gliadin are only INSIDE the intestine not in the blood.

Measuring antigliadin antibody in blood and intestinal fluid (obtained by the laborious technique of having research subjects swallow a long tube that migrates into the upper small intestine), researchers found that in untreated celiacs, antigliadin antibody was present in the blood and inside the intestine, whereas after villous atrophy healed following a year on a gluten-free diet, the antigliadin antibody was no longer in the blood but was still measurable inside the intestine in those with ongoing mild inflammation.

An important conclusion can be drawn from these results, as these researchers and myself have done: gluten sensitive individuals who do not have villous atrophy (the mass of the iceberg), will only have evidence of their immunologic reaction to gluten by a test that assesses for antigliadin IgA antibodies where that foodstuff is located, inside the intestinal tract, not the blood.

This makes sense anyway, because the immune system of the intestine, when fighting an antigen or infection inside the intestine, wages the fight right in that location in an attempt to neutralize the invading antigen, thereby preventing its penetration into the body.

It does this with T cells on the surface of the epithelium, the intraepithelial lymphocytes, and with secretory IgA made with a special component called secretory piece that allows its secretion into the intestine.

The excellent English researchers that made the discovery that they could detect the immunologic reaction to gluten inside the intestine before it was evident on blood tests or biopsies knew it was a breakthrough, testing it many times over in different ways, and further extending the clinical spectrum of gluten-induced disease to include a phase before the villi are damaged, so-called "latent celiac sprue".

Furthermore, they developed this technique of assessing the intestinal contents for antigliadin antibodies into what they viewed as a "noninvasive screening test for early or latent celiac sprue" (what others and I would simply call "gluten sensitivity").

However, this was not exactly noninvasive, nor was it simple. It still required the patient to swallow a tube, followed by a complete lavage of all their gastrointestinal contents with many gallons of nonabsorbable fluid that had to be passed by rectum and collected into a large vat to be analyzed for the presence of antigliadin antibodies.

While this was indeed a conceptual breakthrough, it practically went unnoticed by the medical community because the cumbersome procedure of washing out the intestine just could not be done in a normal clinical setting.

To this day, I am not sure how many people even know that it was not me, but rather this well known celiac research group, led by the late Dr. Anne Ferguson, who pioneered the assessment of the intestinal contents as a viable and more sensitive source of testing material for the early reactions of the immune system to gluten.

What we did in my research, is to refine and simplify the method of collecting and measuring these intestinal IgA antigliadin antibodies before they can be detected in blood.

That is, instead of washing out the antibodies from the intestine, we allow them to be excreted naturally in the stool (feces).

And so with that idea, and our ability to measure these antibodies in stool, as others before us had done for fecal IgE antibodies directed to food antigens, our new gluten (and other food) sensitivity stool testing method was born.

It was actually my research of microscopic colitis that led me to discover that stool analysis was the best way of assessing for gluten sensitivity before celiac disease develops.

Microscopic colitis is a very common chronic diarrheal syndrome, accounting for 10% of all causes of chronic diarrhea in all patients, and is the most common cause of ongoing chronic diarrhea in a treated celiac, affecting 4% of all celiac patients.

However, from my published research, despite the presence of the celiac HLA-DQ2 gene in 64% of patients with microscopic colitis, very few get positive blood tests or biopsies consistent with celiac disease.

Yet, small bowel biopsies revealed some degree of inflammation sometimes with mild villous blunting in 70%.

According to the facts and previously discussed shortcomings of celiac blood tests, antibodies to gliadin are unlikely to be detected in the blood in these patients because they lack villous atrophy.

So negative blood tests for antigliadin antibodies per se did not, in my mind, rule out the possibility that these patients with microscopic colitis, a disease that under the microscope looks like celiac disease but of the colon, and that affects many celiac patients, were not gluten sensitive themselves.

But as Dr. Ferguson's research revealed, these antibodies might be detectable inside the intestine. And since we surely were not going to perform that cumbersome intestinal lavage test in my patients, we decided to see if we could find these antibodies in the stool as a reflection of what is coming through the intestine.

Here's the first set of data that we found showing the superior sensitivity of stool testing versus blood tests for antigliadin IgA antibodies.

In untreated celiac disease patients, we found a 100% positivity in the stool versus only 76% in blood. In hundreds of microscopic colitis patients since tested, only 9% have antigliadin antibody in blood but 76% have it in stool.

And the same is true of 79% of family members of patients with celiac disease; 77% of patients with any autoimmune disease; 57% of people with irritable bowel syndrome-like abdominal symptoms; and 50% of people with chronic diarrhea of unknown origin, all of whom have only about a 10-12% positivity rate for blood tests (like normal volunteers).

Thus, when you go to the source of production of these antibodies for testing, the intestine, the percentage of any population at a higher than normal genetic and/or clinical risk of gluten sensitivity showing a positive antigliadin stool test is 5 to 7.5 times higher than would be detected using blood tests.

In normal people without specific symptoms or syndromes, the stool test is just under 3 times more likely to be positive than blood (29% vs. 11%, respectively).

That's a lot more people reacting to gluten than 1 in 150 who have celiac disease.

29% of the normal population of this country, almost all of whom eat gluten, showing an intestinal immunologic reaction to the most immune-stimulating of dietary proteins really is not so high or far fetched a percentage, especially in light of the facts that 11% of them display this reaction in blood, and 42% carry the HLA-DQ2 or DQ8 celiac genes.

Why is this so important? Because some people with microscopic colitis never get better when they're treated, and most autoimmune syndrome syndromes only progress with time, requiring harsh and sometimes dangerous immunosuppressive drugs just for disease control.

If the immune reaction to gluten is in any way at the cause of these diseases as research suggests, and if we had at our disposal a sensitive test that can diagnose this gluten sensitivity without having to wait for the intestinal villi to be damaged, then treatment with a gluten free diet might allow the affected tissues to return to normal or at least, prevent progression.

We now have that test in fecal antigliadin antibody. Just a few weeks ago [a few weeks before June, 2003] we completed the first follow-up phase of our study: what happens when a gluten sensitive person without villous atrophy goes on a gluten-free diet for one or two years.

While I am still gathering and analyzing the data, most of the subjects reported a much improved clinical status (utilizing an objective measure of symptoms and well being).

Not everybody gets well, because sadly not everyone stays on a gluten-free diet (as they sometimes admit on the surveys).

Some people have the misconception that if they don’t have celiac disease, but "I just have gluten sensitivity" then maybe they do not have to be strict with their gluten elimination from the diet.

I do not think that is the case.

Although a gluten free diet is like anything: less gluten is not as damaging as more gluten, but certainly no gluten is optimal if a gluten sensitive person desires optimal health.

Of the first 25 people with refractory or relapsing microscopic colitis treated with a gluten-free diet, 19 resolved diarrhea completely, and another 5 were notably improved.

Thus, a gluten-free diet helped these patients with a chronic immune disease of a tissue other than small bowel (in this case the colon), who have been shown to be gluten sensitive by a positive stool test in my lab.

The same may be true of patients with chronic autoimmune diseases of any other tissue, but who do not have full-blown celiac disease.

Gluten-free dietary treatment, sometimes combined with dairy-free diet as well, has been shown to help diabetes, psoriasis, inflammatory bowel disease, eczema, autism, and others.

Thus, my approach, and I believe the most sensitive and most complete approach, for screening for early diagnosis and preventive diagnosis for clinically important gluten sensitivity is a stool test for antigliadin and antitissue transglutaminase IgA antibodies (IgG is not detectable in the intestine) and a malabsorption test.

The malabsorption test we developed is special, because you no longer have to collect your stool for three days; we can find the same information with just one stool specimen.

Combining this stool testing with HLA gene testing, which we do with a cotton-tipped swab rubbed inside the mouth, is the best diagnostic approach available.

Who should be screened for gluten sensitivity? Certainly family members of celiacs or gluten sensitive people being at the highest genetic risk.

For the most part, all of the following patient groups have been shown to be at higher risk than normal to be gluten sensitive: chronic diarrhea; microscopic colitis; dermatitis herpetiformis; diabetes mellitus; any autoimmune syndrome (of which there is an almost end-less number like rheumatoid arthritis, multiple sclerosis, lupus, dermatomyositis, psoriasis, thyroiditis, alopecia areata, hepatitis, etc.); Hepatitis C; asthma; chronic liver disease; osteoporosis; iron deficiency anemia; short stature in children; Down's syndrome; female infertility; peripheral neuropathy, seizures, and other neurologic syndromes; depression and other psychiatric syndromes; irritable bowel syndrome; Crohn's Disease; and people with severe gastroesophageal reflux (GERD).

Autism and possibly the attention deficit disorders are emerging as syndromes that may improve with a gluten- free (and additionally casein-free) diet.

A diagnosed celiac might be interested in our testing to know (after some treatment period no shorter than a year) that there is no on-going damage from malabsorption, for which we have a test.

If a celiac is having ongoing symptoms or other problems, a follow-up test should be done just to be sure there’s no hidden gluten in the diet, or something else that could be present, like pancreatic enzyme deficiency which often accompanies celiac disease, especially in its early stages of treatment.

Historically, with respects to diagnostic methods for celiac disease, from 100 A.D., when celiac disease was first described as an emaciating, incapacitating, intestinal symptom-causing syndrome, to 1950, we had just one diagnostic test: clinical observation for development of the end stage of the disease.

Then in 1940 to 1960, when the discovery of gluten as the cause of celiac disease occurred, the best diagnostic test was removing gluten from the diet watching for clinical improvement.

It was during this period that the 72-hour fecal fat and D-xylose absorption tests were developed as measures of gluten-induced intestinal dysfunction/damage.

In the mid- to late 1950's, various intestinal biopsy methods were pioneered and utilized, showing total villous atrophy as the diagnostic hallmark of celiac disease.

You’ve heard the intestinal biopsy called the "gold standard"; well as you can see, it is a 50 year-old test, and thus, the "old" standard.

It was not until the 1970's and 80's (and improved upon in the 1990's) that blood tests for antigliadin and antiendomysial/antitissue transglutaminase were developed, but again these tests like all methods before, can reliably reveal only the "heart attack" equivalent of the intestinal celiac syndrome: significant villous atrophy, bad celiac disease.

We are in a new century, a new millennium, and I have built upon what my research predecessors have started; mostly on the work of researchers who laboriously put down tubes and sucked out intestinal fluid for testing for antigliadin antibody when it was not present in blood.

We now know that a stool test for antigliadin antibody is just as good and much simpler.

The wide-reaching ramifications of knowing that so many more people and patients are gluten sensitive than have ever been previously known has led me to assume a professional life of medical public service.

To do so, I started a 501

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Carol,

I have a copy of this paper. I was very impressed with the information stated in it. I had no idea as to the history of the stool testing, and I was glad to have a chance to read it. Thank you for posting it here.

God bless,

Mariann

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Hi Carol,

I'm so glad that you posted Dr. Fine's talk. I printed a copy and know that I will refer to it frequently. It's well-written, easy to understand and makes a whole lot of sense to me. I feel so much more educated now and have no doubt at all that I'm doing the right thing. (I declined the blood tests and biopsy last fall and went the Enterolab route instead.)

I hope Dr. Fine is bearing down hard on the medical community. They're so stubborn! Every doctor needs to read his talk to understand the difference between celiac disease and gluten sensitivity, to realize the importance of prevention, and to learn the history behind Dr. Fine's stool test.

I also hope everyone will take the time to read this post, especially those folks who are skeptical of Dr. Fine. I think he has our best interests at heart, unlike so many other health care providers.

Thanks, Carol. Take care, all - Toni

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Thank you both! I want to give credit to "JCC", the lady who first alerted people about Dr. Fine's innovative stool sample testing, over at the Gluten Sensitivity/Celiac Disease forum, at http://www.braintalk.com

"JCC" posts on several forums, including here, and also at the Delphi forums. She tirelessly gathers info, and shares it with others!

Carol

http://cantbreathesuspectvcd.com

P.S. The connection between my VCD website and gluten sensitivity is this: VCD/Vocal Cord Dysfunction (laryngospasms) can be caused by many different things.

One common cause of VCD is GASTRIC REFLUX. And, I had been contacted by several people whose reflux was at least partly due to as yet undiagnosed gluten intolerance! So, food sensitivities can lead to reflux, and reflux is one cause of VCD. There's the connection. So, I've added info about gluten intolerance to my website, because of this!

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Hi-

Thank you for the replies to my previous post about whether to test my 11 month old daughter. She is going in to see her pediatrician next Thursday. I have a couple questions about it.

First, am I correct to think that a biopsy (which I will NOT approve at this stage) would be worthless b/c at this age there is likely no damage to the intestine yet?

Also, blood tests (IgG and IgA) *might* be accurate, but might not? Should I bother having them done?

Sounds as though Enderolab is the most accurate for a little one. So, it says on the website that some insurance companies will pay for it. Has anyone had luck with this? I am not sure where to start. If her pediatrician says okay to enderolab and "prescribes" the test then I might have a bit of luck. Did you start with your doctor, the insurance company or say to heck with it and pay out of pocket? Any suggestions on getting this covered would be appreciated.

Thank you for your time and knowledge,

Jillian

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Hi, I don't know if a biopsy would be worthless but I DO know if it comes out negative the doctor should not rule Celiac's out, but I'm sure he/she would.

You are right about the blood-work may or may not being accurate, I think Enterolab is the way to go to get a very accurate diagnosis!!

I have no idea what insurance companies pay for this way of testing; you would probably have to call to check your coverage. I just paid out of pocket for my tests! My GI doctor was not very supportive of the Enterolab idea, he just told me to try the gluten-free diet to see if it worked or not.

I hope this helps and I hope your daughter feels better soon! :)

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I am curious about this too! I hope someone writes in that has had experience with insurance. :)

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I just got my results back from Enterolab and wondered if anyone else wanted to compare results. Here are mine:

Antigliadin IgA 16 (Normal Range < 10)

anti-TTg IgA 16 (Normal Range < 10)

Fecal Fat 425 (Normal Range <300)

anti-casein IgA 11 (Normal Range < 10)

And, I have the HLA-DQ2 gene

I would like to know what the top of the range is. I mean is 16 high or just barely positive.

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Here are my test results from last November.

Antigliadin IgA 14 Units (Normal Range <10 Units*)

Antitissue Transglutaminase IgA 13 Units (Normal Range <10 Units)

Fecal Fat Score: 54 Units (Normal Range < 300 Units)

anti-casein IgA antibody 18 Units (Normal Range <10 Units)

and I also have HLA-DQ 2.

I don't have as much damage in my intestine as you apparently do. I was fortunate in this aspect, but unfortunate in that my biopsy came back negative and I cannot get my doctor to believe I have celiac disease. Mine also said this:

*  Many people assume that a lower positive antigliadin antibody value may not be as significant as a higher positive value and inquire how their antibody result compares to the range of potential measurable values. It seems they ask this question to determine how severely they are reacting to gluten and hence, whether or not they need to be fully strict and compliant with a gluten-free diet.  Actually, this is not the case.  People with low-positive antigliadin antibody values can suffer the same health consequences as those with values of 100, 200, or higher. An analogy would be trying to use the level of antibodies to penicillin in a person who has had an allergic reaction to penicillin to determine if it is safe to take penicillin again. This obviously is not done because those with demonstrated penicillin allergy can not take penicillin without the risk of suffering severe health consequences. Although gluten sensitivity is not a true allergy like penicillin allergy, the concept is the same.  Thus, any positive antibody value to a food substance indicates that the immune system considers it foreign-enough to make antibodies against it (as if it is an infection), and continued consumption can have adverse consequences on your health. If you already have any symptoms or syndromes associated with gluten or other food sensitivities, and especially if you have intestinal malabsorption, damage to the body is already occurring and a strict gluten-free diet is imperative. If you do not have malabsorption or such symptoms/syndromes, consider yourself fortunate and strictly follow a gluten-free diet to prevent them.

Did your results say anything to this effect?

God bless,

Mariann

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Mariann,

Thanks for the info. I did not get the same quote about the penicillin analogy, but it makes sense to me. It is unfortunate that your family doctor wont give you the diagnosis, but at least you know and are taking the steps necessary to be healthy.

Thanks,

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I just got my results, 6 weeks later! When I was still under from the endoscopy, they told my dad and boyfriend I had "classic celiac." I never saw anyresults, and won't meet the GI doc face to face until next week. anyhow, these are my (incomplete?) results

Endomesial Antibody IgA 1:80 (normal <1:5)

tissue translgutaminase Iga 644 (Positve>30)

Does this seem right? the second one is off the charts! I can't find evidence of the other tests you two have on the copy in front of me

Libby

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Libby, your results are from the blood tests right? You are missing the gliadin tests, and the gliadin blood tests are out of date, so many doctors don't bother with them anymore. The tests we had done with Enterolab are stool tests. So the results read differently.

Your tissue transglutaminase test is sure high! But it is certainly not unheard of. Are you (or were you) suffering from a lot of symptoms? I've heard of people with antibodies in the hundreds and they didn't know it since they were symptoms free. I have low antibodies, yet I suffered from a lot of horrible symptoms. Go figure! That is part of the reason gluten intolerance is so hard to diagnose.

Now I just got my kids Enterolab results today. Sorry, this is long, but here are their numbers:

First my 9 year old son, who has very few symptoms at all. Asthma and a few stomachaches, very dry cracking fingers, and weak dental enamel, thats it. The high antibodies to dairy makes me think maybe that is what is causing the asthma...

Gluten Sensitivity Stool Test

Fecal Antigliadin IgA      15 Units    (Normal Range <10 Units*)

Stool Test for Autoimmune Reaction to Tissue Transglutaminase

Fecal Antitissue Transglutaminase IgA    13 Units    (Normal Range <10 Units)

Stool Test for Small Intestinal Malabsorption

Microscopic Fecal Fat Score:    55  Units    (Normal Range < 300 Units)

Stool Test for Milk Sensitivity

Fecal anti-casein IgA antibody    76  Units    (Normal Range <10 Units)

Gene Test for Gluten Sensitivity

Molecular analysis:  HLA-DQB1*0301, 0301

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

Interpretation: Analysis of this stool sample indicates you have dietary gluten sensitivity, resulting in an associated autoimmune reaction to the human enzyme tissue transglutaminase, but no small intestinal malabsorption/damage.  You also have antibodies to the main cow's milk protein, casein, and hence, you are immunologically sensitive to these foods.

Although you do not possess the main genes predisposing to celiac sprue (HLA-DQ2 or HLA-DQ3, subtype 8), HLA gene analysis reveals that you have two copies of a gene (HLA-DQ3 subtype 7) that predisposes to gluten sensitivity.

My 7 year old son who is the most symptomatic, has tons of health problems. This was interesting since he has the most amount of fecal fat (malabsorbtion). He also has an increased risk for microscopic colitis, which his Pediatric GI wants to check him for.

Gluten Sensitivity Stool Test

Fecal Antigliadin IgA  25  Units    (Normal Range <10 Units)

Stool Test for Autoimmune Reaction to Tissue Transglutaminase

Fecal Antitissue Transglutaminase IgA  24  Units    (Normal Range <10 Units)

Stool Test for Small Intestinal Malabsorption

Microscopic Fecal Fat Score:  272  Units    (Normal Range < 300 Units)

Stool Test for Milk Sensitivity

Fecal anti-casein IgA antibody    18  Units    (Normal Range <10 Units)

Gene Test for Gluten Sensitivity

Molecular analysis:  HLA-DQB1*0502, 0301

Serologic equivalent:  HLA-DQ 1,3  (Subtype 5,7)

Interpretation: Analysis of this stool sample indicates you have dietary gluten sensitivity resulting in an associated autoimmune reaction to the human enzyme tissue transglutaminase, but no small intestinal malabsorption/damage. You also have antibodies to the main cow's milk protein, casein, and hence, you are immunologically sensitive to food products containing cow's milk.

HLA gene analysis reveals that you have a genotype that predisposes to gluten sensitivity (HLA-DQ1, 3 especially that involving DQB1* 0301). This genotype also can predispose to microscopic colitis and other autoimmune syndromes.

And my 4 year old daughter, who has very weak dental enamel, lots of diarrhea, occasional vomiting for no reason, some acid reflux, and is very small for her age. She was almost diagnosed as failure to thrive at 1 year old, but the doctors knew me well enough to know that I was not underfeeding her. They figured it was genetic, well I guess it was in a way.

Gluten Sensitivity Stool Test

Fecal Antigliadin IgA      16  Units    (Normal Range <10 Units)

Stool Test for Autoimmune Reaction to Tissue Transglutaminase

Fecal Antitissue Transglutaminase IgA  14 Units  (Normal Range <10 Units)

Stool Test for Small Intestinal Malabsorption

Microscopic Fecal Fat Score:    148 Units    (Normal Range < 300 Units)

Stool Test for Milk Sensitivity

Fecal anti-casein IgA antibody    12  Units    (Normal Range <10 Units)

Gene Test for Gluten Sensitivity

Molecular analysis:  HLA-DQB1*0201, 0301

Serologic equivalent:  HLA-DQ 2,3 (Subtype 2,7)

Interpretation: Analysis of this stool sample indicates you have dietary gluten sensitivity, resulting in an associated autoimmune reaction to the human enzyme tissue transglutaminase, but no small intestinal malabsorption/damage. You also have antibodies to the main cow's milk protein, casein, and hence, you are immunologically sensitive to foods containing cow's milk.

HLA gene analysis reveals that you have the main gene that predisposes to gluten sensitivity and celiac sprue (HLA-DQ2). This genotype also can predispose to microscopic colitis and other autoimmune syndromes.

It was so funny, when I told them all that I got the results back from their tests and they all need to be gluten free and dairy free, my daughter just wanted to make sure that the boys had to also, and my older boy just said that it was fine with him. My middle boy was really happy about it because now he gets to eat mommies yummy gluten-free foods, especially that yummy gluten free chocolate cake! (He was a little disappointed to have to give up yogurt though. Now they don't even want to finish the gluten foods that are in the house! And I won't make them if they don't want to. I just want them healthy! I am hoping eventually to be able to take the boys off their asthma medicines. The whole genetics aspect is interesting. Only one of them has the Celiac gene, yet they are all gluten sensitive and casein sensitive. At least it make it easy. We all get to eat the same.

God bless,

Mariann :)

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Mariann:

I know yo uhave waiting a long time for this and I am happy that you finally have some answers!!!!!!

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Thanks Stacie. I just wanted confirmation that my kids had a problem with gluten. To know they also shouldn't have dairy is also a plus. I hope their GI will learn to accept it. Otherwise we will have to give him up, too. I would like for at least one doctor to witness their improvement on the gluten-free diet. My middle boy is the sickest, and I hope that most (if not all) of his helth problems can be eliminated. He was so happy to accept the results, he is already gulping down my almond milk, and he keeps asking for more. :) They haven't touched the milk, and it's a new gallon. I wonder if one of my friends might want it? :D

God bless,

Mariann

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marrion-

what a wonderful family situation. your kids may struggle a little with this (as we all do) but waht a gif that they can do it together. Nobidy is left out, nobody is teh "freek" and thanksgiving dinner will work for everybody. I am so happy for you. and so happy for your kids to learn this while they are young. It is cool how they have embraced what will make them feel good.

as to my tests, the results I listed were from a blood test, I suppose done before the endoscopy. I was REALLy sick then, iin the hospital and pretty out of it, so I am unclear on the sequence of events. I just had to ask the people that were with me.

I think I had two triggers- one that sent off chronic, low level symptoms when I was 14, and getting the flu in december (at 23). Somehow that bumped up my symptoms from feeling a little crummy all the time, to having to be supervised at all times, I was so sick. Pretty crazy how this disease can work.

So when the bood test was taken, I was having really severe symptoms.

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Every Enterolab report I've read about here anecdoctally says the person was gluten-sensitive. Maybe this is because the negative people never bother to post again. Just wondering...anyone know of a test that came back negative from them? :huh:

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Hi YankeeDB,

Anyone who tests negative would not bother to post at a Celiac message board. There are some people here(or at least on the old board) that have relatives who have tested negative. Obviously they are going to have a high number of positives since the people paying for testing are generally very symptomatic, and will have a higher rate of positives that would the general population.

God bless,

Mariann :)

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Hi. I had the enterolab testing done last July. I have been doing wonderful on the diet and have improved with my pain and nausea but still have one problem. I cannot lay on my left side or put pressure on my left side of the stomach as I get instant flareup of pain. The pain is right underneath my left rib cage and radiates right around to the back and at times is very intense and have to sleep with a heating pad to get comfortable and of course not put any type of pressure on that side whatsoever. It hasn't improved any.

I wonder if I have that much damage to my intestines or what and it is very scary to me. Can anyone offer some advice??

Gluten Sensitivity Stool Test

Fecal Antigliadin IgA 25 Units (Normal Range <10 Units*)

Stool Test for Autoimmune Reaction to Tissue Transglutaminase

Fecal Antitissue Transglutaminase IgA 28 Units (Normal Range <10

Units)

Stool Test for Small Intestinal Malabsorption

Microscopic Fecal Fat Score: 651 Units (Normal Range < 300

Units)

Thanks!!!

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Stool Test for Small Intestinal Malabsorption

Microscopic Fecal Fat Score: 651 Units (Normal Range < 300 Units)

Bikerblue,

That is a pretty high score for malabsorbtion (mine was only 54 and I had a lot of pain!), so yes, it could be just a lot of damage that will take time to heal. But it could also be something else.

Have you been tested for any type of colitis (inflammation of the colon)? That can also occur in celiacs and can cause a lot of pain and discomfort, as well as chronic diarrhea in some people. You would need a colonoscopy with biopsies to rule it out, but it might be a good idea.

God bless,

Mariann

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Thank you Mariann. I guess I should have mentioned that I have had a colonoscopy along with a CT scan and ultrasound of that area and nothing has come up. Which is fortunate but yet is troubling. It is rather frustrating because I know I am eating gluten free but yet I get these flareups like I am having now that are just miserable and sometimes quite intense and I need to take a pain pill to help me. When I do eat gluten that area becomes flared up also.

I guess I'm not sure if I just chalk it up to gluten or if I should pursue it further.

Just confused...

Tami

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Hi Tami,

Are you still eating dairy foods?? I know that I have severe inflammation in my intestines due to dairy and I get a lot of pain. Infact when I went back on gluten for a biopsy for two months I stayed dairy free and experienced much less stomach pain.

You could try cutting out dairy for a few weeks to see if it makes a difference. It certainly does for me. I also had the milk sensitivity test done on me and my three kids at Enterolab. Two of us have low positiveantibodies, my oldest boy has high positive antibodies to milk and my daughter is borderline. I now keep all of us as dairy free as is physically possible and I know that I feel much better for it. Just something you might try.

And I am very glad to know you don't have colitis. :) All my tests were negative, too, but it sure is frustrating when you have symptoms that won't go away!! It quite possibly is another food intolerance.

God bless,

Mariann

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Hi Mariann,

Yes I do some dairy but not a lot. I did have dairy cut out completely for a while but it didn't seem to make a difference for that. It could very well be an intolerance of some sort... I really dont know. It just seems strange though that pressure of any type sets the pain off though doesn't it??? That is what I really can't understand.

Tami

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Advice please....

Fecal Antigliadin IgA 33 Units (Normal Range<10 Units)

Microscopic Fecal Fat Score 592 Units (Normal Range<300 Units)

Fecal anti-casein IgA antibody 13 Units (Normal Range<10 Units)

Molecular Analysis: HLA-DQB1*0201, 0602

Serologic equivalent: HLA-DQ 2,1 (Subtype 2,6)

thank you, Paula

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I just recieved my results from Enterolab

Fecal Antigliadin IgA 102 units (Normal Range <10)

Just wondering what such a high number really reflects in terms of severity?

I do have multiple autoimmune problems as does most of my family. My daughter was also tested from Quest laboratory with some elevated IGG at 20.7. Now the gastrointerologist is going to get blood tests from Prometheus (sp?) lab. Hopefully we will find some answeres for her as well.

Thanks for any comments!

Tia

Gluten Free 2 weeks.

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I have a couple of questions for those of you who have used the enterolab.

--How long did it take for you to get your results? It has only been two weeks for me but I am getting anxious to get the results.

--Also did your insurance cover any of it? I am just wondering if anyone has had luck with the insurance. We have a high deductable so even if it could go toward that I would be thankful.

Thanks for your help,

Kayla

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