The Gray Zone / Stool Testing

The Gluten File


 


It is important to note that many people suffer wide ranging symptoms of gluten sensitivity without meeting the stringent diagnostic criteria for Celiac Disease.


In some cases, these individuals may actually be in early stages of Celiac Disease before severe damage has occurred. They may eventually progress to total villous atrophy if they continue eating gluten.

In other cases, individuals may be suffering from a gluten sensitivity that will never show as villous atrophy. This is sometimes called non-celiac gluten sensitivity.


Unfortunately, our doctors usually only recommend a gluten free diet to those with full blown Celiac Disease, because they think the diet is "too difficult". This leaves many people suffering a life time with debilitating symptoms because our doctors are thinking they are doing us a favor???  I think, at least, our doctors need to be telling patients who have any hint of gluten sensitivity that we may improve on a gluten free diet. Many of us who have chosen this path have found the benefits of the diet far outweigh any inconveniences.


One of several doctors who recognizes that gluten sensitivity without evidence of celiac disease can cause serious chronic illness is
Dr. Kenneth Fine. His research is showing that those with a non-celiac gluten sensitivity are subject to many of the same risks and complications as those with celiac disease, including nutritional deficiency and possibly an increased risk of developing other autoimmune disease.


Dr. Fine has developed a stool test that

detects gluten related antibodies in the stool long before they may be detected in the blood, and can uncover a ‘hidden’ gluten sensitivity in some individuals that is not being realized by traditional blood testing.  Because this is not a mainstream test,  many doctors are reluctant to accept the results as meaningful. On the other hand, you will find that many patients who have eliminated gluten based on the result of the stool test are very pleased with the results..

 
Studies that support fecal antibody testing

METHODS: This study investigated 22 relatives of patients with CD genetically predisposed to gluten intolerance but negative for both serum anti-TG2 antibodies and intestinal abnormalities.
CONCLUSIONS:
A new form of genetic-dependent gluten intolerance has been described in which none of the usual diagnostic markers is present. Symptoms and intestinal anti-TG2 antibodies respond to a gluten free-diet. The detection of intestinal anti-TG2 antibodies by the phage-antibody libraries has an important diagnostic and therapeutic impact for the subjects with gluten-dependent intestinal or extraintestinal symptoms. Clinical trial number NCT00677495. 
Cryptic genetic gluten intolerance revealed by intestinal antitransglutaminase antibodies and response to gluten-free diet.
PMID 21471568  Nov 2011

Twenty-five percent of patients with IBS have FH. These patients had increased levels of fecal ECP and tryptase, indicating that they might cause inflammation in patients with IBS. Fecal assays for ECP could be used to identify FH in patients with IBS.
Fecal assays detect hypersensitivity to cow's milk protein and gluten in adults with irritable bowel syndrome.

PMID:21839707  Nov  2011

Hypersensitivity to Cow's Milk Protein and Gluten in Adults with Irritable Bowel 
Syndrome. 
PMID: 21839707 Aug 2011

Background and objective Antitransglutaminase (anti-TG2) antibodies are synthesised in the intestine and their presence seems predictive of future coeliac disease (CD). This study investigates whether mucosal antibodies represent an early stage of gluten intolerance even in the absence of intestinal damage and serum anti-TG2 antibodies. Methods This study investigated 22 relatives of patients with CD genetically predisposed to gluten intolerance but negative for both serum anti-TG2 antibodies and intestinal abnormalities. Fifteen subjects were symptomatic and seven were asymptomatic. The presence of immunoglobulin A anti-TG2 antibodies in the intestine was studied by creating phage-antibody libraries against TG-2. The presence of intestinal anti-TG2 antibodies was compared with the serum concentration of the intestinal fatty acid-binding protein (I-FABP), a marker for early intestinal mucosal damage. The effects of a 12-month gluten-free diet on anti-TG2 antibody production and the subjects' clinical condition was monitored. Twelve subjects entered the study as controls. Results The intestinal mucosa appeared normal in 18/22; 4 had a slight increase in intraepithelial lymphocytes. Mucosal anti-TG2 antibodies were isolated in 15/22 subjects (68%); in particular symptomatic subjects were positive in 13/15 cases and asymptomatic subjects in 2/7 cases (p=0.01). No mucosal antibodies were selected from the controls' biopsies. There was significant correlation between the presence of intestinal anti-TG2 antibodies and positive concentrations of I-FABP (p=0.0008). After a gluten-free diet, 19/22 subjects underwent a second intestinal biopsy, which showed that anti-TG2 antibodies had disappeared in 12/15 (p=0.002), while I-FABP decreased significantly (p<0.0001). The diet resolved both extraintestinal and intestinal symptoms. Conclusions A new form of genetic-dependent gluten intolerance has been described in which none of the usual diagnostic markers is present. Symptoms and intestinal anti-TG2 antibodies respond to a gluten free-diet. The detection of intestinal anti-TG2 antibodies by the phage-antibody libraries has an important diagnostic and therapeutic impact for the subjects with gluten-dependent intestinal or extraintestinal symptoms.
Cryptic genetic gluten intolerance revealed by intestinal antitransglutaminase antibodies and response to gluten-free diet.
PMID:21471568  April 2011


"Our results also support the concept that coeliac
disease antibodies are deposited in the small-bowel
mucosa before mucosal deterioration, and before
they are measurable in serum. This is in accordance
with the findings that coeliac autoantibodies are
produced in the small-bowel mucosa [19] and that
mucosal samples from treated coeliac patients produce
EmA when challenged with gliadin peptides in
in vitro organ cultures [35]"


"It is foreseen that the
demonstration of small-bowel mucosal villous atrophy
with crypt hyperplasia will no longer be the gold
standard in the diagnosis of coeliac disease, when the
diagnostic criteria are widened to include ‘‘genetic gluten intolerance"
Small-bowel mucosal transglutaminase 2-specific IgA deposits in coeliac disease without villous atrophy: a prospective and randomized clinical study.  PMID: 16036509 May 2005


One patient with histologically proven celiac disease had normal serological but high fecal scIgA AGA and scIgA ATA values. This patient emphasizes the importance of fecal antibody determination for the diagnosis of celiac disease, at least in patients with suggested celiac disease and negative serum antibodies.
Comparison of different salivary and fecal antibodies for the diagnosis of celiac disease. PMID: 15481630   2004

The presence of EMAs in fecal supernatants represents the in vivo proof that intestinal mucosa is a site of EMA production. Furthermore, EMA detection in the stools could be a simple and useful additional tool to clarify diagnosis in the patchy conditions of CD.
Antiendomysial antibody detection in fecal supernatants: in vivo proof that small bowel mucosa is the site of antiendomysial antibody production. PMID: 11808976   Jan 2002


We measured serum immunoglobulin (Ig) A against gliadin and tissue-transglutaminase, and IgA and IgM against gliadin, tissue-transglutaminase (intestinal cd-associated antibodies), and the dietary proteins beta-lactoglobulin and ovalbumin in duodenal aspirate by enzyme-linked immunosorbent assay. HLA-DQ2 expression and increased intestinal cd-associated antibodies are markers that can identify latent/potential cd in a subgroup of IBS patients who consequently appear to profit from a gluten-free diet.
Celiac disease-like abnormalities in a subgroup of patients with irritable bowel syndrome. PMID: 11729112 Dec 2001

 

 

OTHER OPINIONS


Dr. Scot Lewey speaks on Enterolab stool tests 


Research of Dr. Marios Hadjivassilou, a leading researcher of gluten related neurological disease, has shown that gluten sensitivity can present soley as neurological disease, with or without biopsy evidence of Celiac Disease.


A
book released in August of 2002, "Dangerous Grains: Why Gluten Cereal Grains May Be Hazardous to Your Health" by James Braly, MD, and Ron Hoggan, MA, gives an overview about the known medical implications of gluten sensitivity and celiac disease, as well as the direction current research is going. This book also discusses non-celiac gluten sensitivity, and promotes a strict gluten free diet for those with any degree of gluten sensitivity.


 

 See more on the Gluten Sensitivity vs.Celiac Disease page