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Gluten Intolerance Vs. Celiac Disease?


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#1 sroggio

 
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Posted 10 February 2004 - 08:09 PM

Hi all,

I'm new here, and here's my long story ...

About 18 months ago, out of the blue, I started having vaginal pain during sex (sorry to be graphic, but this is the condition that led to my discovery of a problem with gluten). After several doctors, tests and creams that didn't relieve the pain, I was referred to a specialist who diagnosed vestibulitis.

Not much is known about the cause of vestibulitis, but one theory is that it's nerve damage (infections were ruled out by other tests). So, my doctor put me on a low dose of an anti-depressant called Imipramine, intended to help reduce any pain from nerve damage. I also introduced some hygiene changes, such as switching to fragrance-free soap and laundry detergent to avoid any irritants.

The pain went down, but it didn't go away completely. About six months ago, this specialist referred me to a physical therapist who specializes in pelvic pain. She helped reduce muscle pain that had developed throughout my pelvic region, but it didn't really do anything for the vestibulitis pain. But, she's the one who suggested I see a nutritionist when I told her I was frequently constipated (she pointed out this was only adding to the overall pelvic pain, so it would be a good idea to try to solve the problem).

Through blood tests, the nutritionist determined that I had a low red blood cell count and wasn't properly absorbing calcium, magnesium and iron. I also had an abnormally high level of c-reactive protein (4.5 mg/l; normal is 0-1 mg/l), which suggests an inflammation in the body. She suggested I go on an 8-week gluten-free, yeast-free diet (including no alcohol), and had me start taking acidopholus, a multi-vitamin and magnesium supplements daily.

A few weeks into the diet, I realized that my body felt different. For the first time ever, it seemed, I started having regular BM. A number of other symptoms I had been noticing also went away -- gas, bloating, tingling in my feet. After the diet, my c-reactive protein level was 1.7 mg/l.

I decided to get a blood test for celiac disease, and went back on gluten for the next two weeks. In addition to the gas, bloating and tingling coming back, I also experienced other symptoms that I realized I'd had before -- sores on my tongue, excema on my face, muscle cramps in my legs, pain in my lower back/hips/knees. During the 8-week diet, I read a lot about gluten sensitivity, and discovered that the dental defects I have in my teeth and the fact that I've always bruised easily are also common signs of this problem.

I tested negative for celiac disease, but I decided to go back off the gluten to see how I felt. Within days, the symptoms began to disappear (except for tingling in my feet, which I get anytime I have alcohol. I've also found I get ringing in my ears after alcohol.). My husband was having a hard time believing me, and I wanted to confirm it for myself, so I decided to order a stool and gene test through Enterolab, which tests for antibodies solely in the intestines, not just in the blood.

The stool test came out positive for gluten sensitivity, with an antigliadin antibody level of 133 units. The gene test came out positive for the HLA-DQ3 gene, which Enterolab said predisposes to gluten sensitivity. They said I do not have either of the genes primarily associated with celiac disease, HLA-DQ2 or HLA-DQ8.

So ... my questions are: Has anyone else here tested positive for gluten sensitivity only, versus celiac disease? Does anyone know what this means? For example, does that mean I'm at any less risk of damaging my intestines by eating gluten than someone who's been diagnosed with celiac disease? How "gluten-free" do I really need to be? I am feeling better by not eating gluten, and I have noticed spikes in the vestibulitis pain if I accidentally eat gluten, so I think there is a connection ... although the specialist I'm seeing has never heard of one.

My primary care physician does not have the answer to my questions and has referred me to a gastroenterologist who specializes in malabsorption. But, he's not available until mid-April. I'm trying to stay as gluten-free as possible, but it's been frustrating for both my husband and me -- especially when dining out. At home, he thinks I shouldn't worry about things like toasting my gluten-free bread and his wheat bread in the same toaster. And my answer is, I don't know, but better safe than sorry.

If anyone has any insights into gluten intolerance vs. celiac disease, I'd love to hear them. I'm also curious whether any other women here also have vestibulitis/vulvodynia. A couple women on the vulvar pain listserve I'm on have the same gene I do, and we're starting to wonder whether there's a connection ... Thanks so much for reading this long post, and I promise to be more brief in the future!

Best regards,
Sarah
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#2 gf4life

 
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Posted 11 February 2004 - 08:54 AM

Hi Sarah,

Welcome to the board. :)

First off, there is a whole spectrum of levels of gluten intolerance, and research has really only touched the tip of the iceburg, so to speak. Gluten sensitivity is one of those grey areas, as far as the medical profession is concerned. Obviously you are having a reaction to gluten. Even those with clear symptoms of Celiac Disease have a hard time getting a diagnosis. I think you are very lucky to have figured it out relatively early in the symptoms. If you stay on gluten will you eventually get celiac disease? Hard to say. That is not really a question anyone can answer. You should do whatever helps you be healthy. What do your doctors say about staying gluten free?
Two weeks on gluten was probably not long enough for accurate tests following eight weeks off gluten. I'm glad you went to Enterolab. If Dr. Fine recommends staying gluten free, I would listen to him. He knows what he is talking about.

As for your symptoms. I was also frequently constipated (alternating with diarrhea), terrible gas, bloating, tingling in my feet, dental defects, sores on my tongue, rash on my face (and other places), muscle cramps in my legs, pain in my lower back/hips/knees and many other joints in my body ached frequently. Not to mention a multitude of other symptoms. One of which was pelvic pain and painful intercourse. I never connected it directly to the gluten intolerance, but thought it probably had to do with the inflammation in my intestines and the painful gas and bloating (as well as a prolapsed bladder, and partially tilted uterus). But I was not as fortunate as you to have doctors take me serious and run any tests. I have no idea if I have what you have with the nerve damage and such, but I do know that I hope the pain decreases being gluten free.

I also had testing done at Enterolab, after a negative blood test, and no biopsy. I tested low positives on the antibody stool tests, and positive for the main gene (HLA-DQ2) that predisposes me to celiac disease as well as many other auto-immune diseases. I have since had an intestinal biopsy and will get those results on Friday. I don't know what more to say, other than to recommend a book to read (if you haven't read it already), Danna Korn's Wheat Free, Worry Free. She talks a lot about the entire gluten sensitivity spectrum and all about why we need a gluten free/wheat free diet, no matter if we have celiac disease, gluten sensitivity, or wheat allergy.

God bless,
Mariann :)
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~West Coast-Central California~

Mariann, gluten intolerant and mother of 3 gluten intolerant children

#3 tarnalberry

 
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Posted 11 February 2004 - 11:16 AM

I have vulvar vestibulitis myself. My specialist (Dr. Willems at the Scripps Clinic in La Jolla) noted he wasn't surprised when initial testing made it likely that I had it. He said he has a lot of patients who are gluten intolerant. (He treats VVS with antihistamines, estrace, and biofeedback with physical therapy.) While my blood tests for celiac were not conclusive, my results trying the diet have been pretty obvious (I think ;) ), so I maintain a gluten-free diet. It may well have helped my VVS pain as well, but is not the only answer to that pain.
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Tiffany aka "Have I Mentioned Chocolate Lately?"
Inconclusive Blood Tests, Positive Dietary Results, No Endoscopy
G.F. - September 2003; C.F. - July 2004
Hiker, Yoga Teacher, Engineer, Painter, Be-er of Me
Bellevue, WA

#4 wdavie

 
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Posted 21 February 2004 - 07:04 PM

Hi,
I have recently read a speech by Professor Alessio Fasano, who is the Director for the Centre for Celiac Research in Maryland. That states emphatically that you cannot develop Celiac Disease unless you do carry the DQ2 or DQ8 gene.
So that leads me to believe that Celiac Disease and Gluten Intolerance/Sensitivity are 2 different things however the treatment for each is the same a Gluten Free diet. The absence of the DQ2 or DQ8 gene would indicate that you cannot go on to develop Celiac Disease, however to remain healthy and symptom free than a gluten-free diet is also the treatment for intolerance.
Wendy
P.S: I hope I have not trodden on any toes here but I am just quoting from sources and will happily try and track down further reasearch on the DQ2 and DQ8 genes.
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#5 concernedlady

 
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Posted 21 February 2004 - 10:21 PM

I posted the following talk by Dr. Fine, in a Jan 17 2004, 11:28 AM message in the "pre-diagnosis" section of this forum. Dr. Fine's talk (SEE BELOW) may help to describe the differences between CELIAC DISEASE and some types of non-Celiac GLUTEN INTOLERANCE.

To summarize, I believe that Celiac Disease (celiac disease) is one kind of gluten intolerance, among many, and with celiac disease, the microscopic finger-like projections called "villi" in the small intestine lining, are noticeably (can be seen with a regular microscope) damaged, blunted, flattened or destroyed by an auto immune reaction to eating gluten.

What can be tricky, is that a person may be genetically prone to developing celiac disease, but, if the person stops eating gluten, before celiac disease starts to develop, the celiac disease may never fully develop! So does this person have celiac disease or not? The docs might say "no" because no villous atrophy can be detected...yet. Yet, a person who is prone to getting celiac disease, but hasn't developed the celiac disease, still may have some small intestinal problems. These problems usually lessen, once the person goes on a strictly gluten-free diet.

On the other hand: The small intestine can ALSO be damaged by a reaction to gluten, in a person who has non-Celiac Disease GLUTEN INTOLERANCE, but the small intestinal damage may be on such a sub-microscopic scale, that the "villi" never get "obviously" damaged--However, as Dr. Fine describes below, the small intestinal damage in non-celiac disease gluten intolerant people, can still be considerable, even if it is "non-detectible", and even if it is not celiac disease! So, a person with non-celiac disease "gluten intolerance" can have serious small intestinal problems of indigestion and/or mal-absorption!

Also, hidden gluten can cause small intestinal problems, as can additional intolerances, to such things as casein (a protein in cow's milk), whey (another protein in cow's milk), soy, corn, etc.

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

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
http://cantbreathesuspectvcd.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 5013 not-for-profit institute called the Intestinal Health Institute, have brought these new diagnostic tests to the public on the internet (at http://www.enterolab.com ), and volunteer my time helping people with health problems by email and by lecturing.

With greater awareness and education of both the public and medical community that early diagnosis of gluten sensitivity can be achieved before the villi are gone, more of the gluten sensitive iceberg will be diagnosed and treated early, leading to far fewer gluten-related symptoms and diseases than has ever been experienced before.

With that, I thank you for your attention."

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