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    New Blood Tests Can Spot Gluten Sensitivity Among Enteropathy Patients Who Test Negative for Anti-Tissue Transglutaminase


    Jefferson Adams
    Image Caption: New Blood Tests for Celiac Disease

    Celiac.com 04/20/2010 - A team of researchers recently set out to determine whether new serology assays can detect gluten sensitivity among enteropathy patients seronegative for anti–tissue transglutaminase.


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    Emilia Sugai, Hui Jer Hwang, Horacio Vázquez, Edgardo Smecuol, Sonia Niveloni, Roberto Mazure, Eduardo Mauriño, Pascale Aeschlimann, Walter Binder, Daniel Aeschlimann and Julio C. Bai comprised the research team.

    They are variously affiliated with the Small Bowel Section of the Department of Medicine at C. Bonorino Udaondo Gastroenterology Hospital in Buenos Aires, Argentina, the Matrix Biology and Tissue Repair Research Unit at the Cardiff University School of Dentistry in Cardiff, UK, and with INOVA Diagnostics, Inc., of San Diego, California.

    Some patients with celiac disease may not show a normal positive reaction to the test most commonly used for IgA anti–tissue transglutaminase (anti-tTG) antibodies.

    The research team set out to determine the usefulness of newer assays incorporating synthetic deamidated gliadin-related peptides (DGPs), or other TG isoenzymes as antigen, for detecting gluten sensitivity in IgA anti-tTG–seronegative patients.

    The team tested blood samples drawn at diagnosis from 12 anti-tTG–seronegative patients with a celiac-like enteropathy, from 26 patients with skin biopsy–proven dermatitis herpetiformis (DH) and, lastly, from 26 patients with IgA anti-tTG–positive celiac disease.

    All patients showed typical levels of total IgA. On each patient, the team conducted intestinal biopsy and serum testing for detection of IgA and IgG isotypes of both anti-DGP and anti-tTG in a single assay (tTG/DGP Screen; INOVA Diagnostics). They also tested each patient for simultaneous detection of both IgA and IgG anti-DGP antibody isotypes (DGP Dual; INOVA Diagnostics). Lastly, they tested each patient for the detection of antibodies to transglutaminase 3 (TG3) or transglutaminase 6 (TG6).

    All patients who showed positive anti-tTG results also tested positive in anti-DGP assays.

    The tTG/DGP Screen caught six of the 19 anti-tTG seronegatives (31.6%), while anti-DGP Dual produced caught five of these cases (26.3%). Whereas both assays detected 2 anti-tTG–negative DH patients with partial villous atrophy, they were positive in only 2 of the 5 cases with no histologically discernible mucosal damage. Testing for antibodies to TG3 and TG6 caught seven of the 19 anti-tTG–negative patients (36.8%), five of whom also tested positive for anti-DGP.

    From these results, the team concludes that using tTG/DGP Screen, or anti-DGP Dual, to detect anti-DGP improves diagnostic sensitivity of gluten sensitive patients with non–IgA- deficiency, or anti-tTG–seronegativity, and celiac-like enteropathy. The same enhancement is also achieved by detecting antibodies to other TG isoenzymes.

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    Interesting! I tested negative to tTG and total Iva was normal, yet I was five times above positive marker on GDP IgA test! Still infesting phase and waiting for biopsy to see if I have celiac. Thanks for posting this!

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  • Related Articles

    Scott Adams
    The following article was published in The Sprue-nik Pres, Volume 9, Number 1 January 2000, Published by the Tri-County Celiac Sprue Support Group, a chapter of CSA/USA, Inc. serving southeastern Michigan. Members receive this newsletter, a shopping guide, and a new member packet full of articles and useful information. Mail-in subscriptions are welcome. For subscription information, send a note to tccssg@yahoo.com.
     
    Ann gave us TIPS: Five food tips, five health tips, five quickie tips, and five things to look forward to, always in a Lets Be Positive mode.
    Food Tips:
    Concentrate on what you CAN eat, not what you cant. Try not to blow the gluten-free (gluten-free) diet out of proportion. If you take processed foods out of the equation, you can eat almost anything: fruits, vegetables, beans, meat, fish, rice, corn, etc. When you eat plain food, you start to really taste food the way you never tasted before. What we can eat is good for us. Get used to the fact that you have to do more cooking and baking. Turn this factor into an asset and become a good gluten-free cook. Eat
    simply. For breakfast Ann eats eggs, yogurt, fruit, Jowar (sorghum) Jo Crisps Cereal, or even vegetables. For lunch you can eat leftovers. Leftover rice mixed with a vegetable is always a good idea; you can keep bags of frozen peas,
    corn, or broccoli in the freezer. One of Anns favorite lunches is to put plain peanut butter on a rice cake and slice apples on top.
    For snacks try fruit, Jell-O, or home-popped popcorn, all of which can be quickly prepared.
    In a restaurant, first check the menu to see what you can eat without question, what you might be able to eat if you ask questions, what youd better stay away from, and what you might want to look into a little bit. Try not to make an issue of it and dont be embarrassed or afraid to ask questions. Ann says she figures whatever the gathering is for, its not to discuss her diet
    Forget about getting dietary advice from your doctor. A gastroenterologists primary job is to diagnose your illness and then send you on to a dietitian and a support group. Please dont get mad at doctors for not knowing all the details of the gluten-free diet. Dietitians, too, may not know a lot about the gluten-free diet. We celiacs need to partner with dietitians to get them up to speed and help those we educate teach other dietitians. There are many pieces of the celiac pie that need to be improved, and adopting and educating dietitians is an important step toward getting more reliable
    information to more people.
    Join a support group. The best place to get information about the disease and the gluten-free diet is from a support group because the leaders and members deal with diet issues every day. Celiacs need to support their group leaders and volunteer assistance. Ann says she feels strongly about all of us giving something back to society for the richness that we have managed in our own personal lives. So if you are really interested in making celiac disease your thing, you can volunteer to work with a support group
    Accept that there are very few absolutes and very many points of disagreement about what is and is not gluten-free or what is and is not appropriate for celiacs. We know with certainty that the things we should not eat are wheat, barley, rye, oats, spelt, triticale and kamut. The next thing we need to find out is where those grains actually are, not necessarily where they might be. We should have a basic diet we can rely on before we waste valuable time and effort looking for needles in haystacks. In her research Ann has discovered that a lot of the things we celiacs believe but have
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    Celiacs need to eat dairy products because they are a prime source of calcium. Calcium, which has such a strong connection with osteoporosis, is one of the most malabsorbed nutrients in celiac disease. Some celiacs have difficulty eating dairy products because of associated lactose intolerance, but it is extremely important to get dairy products into your body in whatever way works. Of all the dairy products available, one of the best is yogurt; its low fat, easily digested (even for some who are lactose intolerant), and readily available.
    Have an annual physical exam that includes a complete blood count (CBC) and stool testing, according to Dr. Joseph Murray of the Mayo Clinic. He thinks you should have thyroid testing every other year, but if you already have thyroid disease, more frequent testing might be advantageous. The experts also say you should have serology antibody testing once a year to test for compliance with the gluten-free diet. A positive result almost always means some gluten has been inadvertently ingested. Dr. Murray says you then have to: Check your diet, check your diet again, and check your diet a third time. He also recommends taking one good multi-vitamin a day that includes 100 percent of the recommended
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    Encourage your first-degree relatives to get screened for celiac disease. Usually these relatives are not comfortable with your request because they dont want to follow your diet, but 10% of them will probably have celiac disease, and of the 10% who have it, 50% will have no symptoms but will have flat intestinal villi. How can we get our relatives tested? First of all, dont make an issue of your diet around them. Make them drool over the delicious gluten-free dishes you are eating. Keep the current complexities about the diet to yourself. And dont nag!
    If you can, send donations to the University of Maryland Prevalence Study, which is testing first-degree relatives (and others) to try to find out what the true prevalence of celiac disease is in the United States. If it turns out that celiac disease is not rare, then the FDA and food manufacturers will have to pay more attention to our problems. Please make checks payable to the UM Foundation, Inc. Center for Celiac Research, Attn: Pam King, 700 W. Lombard St., Room 206, Baltimore, MD 21201. These funds are administered by the University of Maryland Foundation, Inc.
    The very best thing you can do for yourself is to have a life beyond celiac disease. Dont let having this disorder stop you from doing anything! Make sure you have other interests. Make sure you exercise. Make sure you get out and eat with gluten-eating people. Make sure you travel. Make sure you stay all-around healthy.
    Five Quick Tips:
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    Buy a bread machine. When you bake your own bread, it is ultimately cheaper than any ready-made bread. Plus it usually tastes better.
    Not everyone can do this, but it helps to avoid processed food. Even when you investigate products over the phone or get a letter from the manufacturers or consult some of the commercial product listings that are available, you are still not totally sure the product is safe. Life is simpler and safer when you avoid processed foods--or eat them as infrequently as possible.
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    Scott Adams
    Lancet 2002;359:945-946.
    Celiac.com 04/12/2002 - According to a report published in the March 16th issue of The Lancet, a new anti-transglutaminase antibody test developed by Dr. Luis Sorell and colleagues from the Centre for Genetic Engineering and Biotechnology in Havana, Cuba can accurately diagnose people with celiac disease in less than 10 minutes. The assay consists of a nitrocellulose strip that is placed in serum or plasma specimens, and it detects both IgA and IgG antibodies to transglutaminase, which prevents misdiagnosis of patients who have IgA deficiency, a trait that is frequently seen in people with celiac disease. If two dots appear it indicates a positive result. To determine the assays accuracy Dr. Sorell and colleagues evaluated 50 patients with untreated celiac disease along with 40 patients who had other gastrointestinal disorders. The results showed that the assay was 100% accurate, all of the patients with diagnosed celiac disease tested positive, and all of the patients with other disorders tested negative. Ultimately the assay could be used for an inexpensive mass-screening program for celiac disease.

    Scott Adams
    Celiac.com 09/12/2006 – A recent study by researchers at Stanford University has found that barley endoprotease EP-B2 is effective at digesting gluten in rats, and should be studied further as an “adjunct to diet control” in human celiac disease patients. This new finding adds to Stanford’s growing body of work on enzyme therapy as a possible treatment for those with celiac disease, and may one day lead to a effective treatment. Effect of barley endoprotease EP-B2 on gluten digestion in the intact rat.
    J Pharmacol Exp Ther. 2006 Sep;318(3):1178-86.
    Gass J, Vora H, Bethune MT, Gray GM, Khosla C.
    Stanford University.

    Abstract:

    "Celiac Sprue is a multi-factorial disease characterized by an intestinal inflammatory response to ingested gluten. Proteolytically resistant gluten peptides from wheat, rye and barley persist in the intestinal lumen, and elicit an immune response in genetically susceptible individuals. Here we demonstrate the in vivo ability of a gluten-digesting protease ("glutenase") to accelerate the breakdown of a gluten-rich solid meal. The proenzyme form of endoprotease B, isoform 2 from Hordeum vulgare (EP-B2) was orally administered to adult rats with a solid meal containing 1 g gluten. Gluten digestion in the stomach and small intestine was monitored as a function of enzyme dose and time by HPLC and mass spectrometry. In the absence of supplementary EP-B2, gluten was solubilized and proteolyzed to a limited extent in the stomach, and was hydrolyzed and assimilated mostly in the small intestine. In contrast, EP-B2 was remarkably effective at digesting gluten in the rat stomach in a dose and time dependent fashion. At a 1:25 EP-B2:gluten dose, the gastric concentration of the highly immunogenic 33-mer gliadin peptide reduced by more than 50-fold within 90 min, with no overt signs of toxicity. Evaluation of EP-B2 as an adjunct to diet control is therefore warranted in celiac patients."

    Jefferson Adams
    Celiac.com 06/12/2009 - In a medical first, researchers at UCLA have made a connection between intestinal inflammation and systemic chromosome damage in mice, a discovery that may pave the way for early identification and treatment of human inflammatory disorders, some of which raise the risk for various kinds of cancer, according a study published in Cancer Research.
    Scientists discovered that local intestinal inflammation caused DNA damage to lymphocytes of the peripheral blood circulating throughout the body. So, contrary to conventional medical wisdom, chromosome damage is not limited to the immediate intestine, but involves body tissues far away from the actual inflammation. Their results showed single- and double-strand DNA breaks in the blood, and chromosome damage in peripheral blood indicating systemic genetic damage.
    Inflammatory diseases have been linked to some lymphomas and abdominal, liver and colorectal cancers, said Robert Schiestl, lead author, and professor of pathology, radiation oncology and environmental health sciences and a Jonsson Cancer Center scientist.
    Finding inflammation early – before any symptoms surface - and treating the associated causes quickly may prevent the damage that eventually triggers these cancers, he said. Before the study, researchers had no knowledge that "intestinal inflammation causes damage that can be found throughout the body,” said Schiestl, adding that this "may help explain how inflammation leads to these cancers.”
    Intestinal inflammation can be caused by such maladies as Crohn’s disease, inflammatory bowel disease, ulcerative colitis and Celiac disease. Nearly 1.5 million Americans, and 2.2 million Europeans currently suffer from inflammatory bowel diseases and global incidence is on the rise, Schiestl said.
    The discovery opens up the possibility of using chromosome damage in the peripheral circulating blood as a biomarker to spot intestinal inflammation before any symptoms surface.
    Researchers were able to detect chromosome damage in the blood of specially bred mice before the onset of colitis, said Aya Westbrook, a graduate student of the UCLA Molecular Toxicology Interdepartmental Program and the paper's first author. Westbrook added that disease severity correlated directly with higher levels of chromosome damage in the blood.
    Chromosome damage, according to study author Dr. Jonathan Braun, professor and chairman of the Department of Pathology and Laboratory Medicine at UCLA, may be the “earliest detectable indicator” of intestinal inflammatory disease. Currently, the only way to diagnose patients with inflammatory bowel disease is through full endoscopic exam, which is both invasive and costly. In theory, Braun said, a biomarker blood test might replace the invasive endoscopic exam and allow physicians to identify early inflammatory disease before it develops fully.
    Spotting disease and being able to ward it off early is one of the Holy Grails of all medicine. This breakthrough could “change the natural history of these diseases,” Braun said. For the first time, doctors might have a tool that can actually help spot inflammation, the earliest precursor to multiple kinds of cancer, at its earliest stages, long before any actual disease develops. This could lead to the prevention of tens of thousands of cancers.
    UCLA researchers have launched a clinical trial to confirm their findings in humans, Schiestl said. They’re focusing on patients with Crohn’s disease and ulcerative colitis. They're hoping the discovery will permit them to test new strategies for treating smoldering disease, which we’ve never been able to identify before,” Schiestl said, adding that they might be able to assess new drugs for treating early inflammatory disease.
    The research may also show why some patients with inflammatory disease develop cancers, while others endure chronic inflammation for decades, yet remain cancer-free. Researchers suspect that some unknown molecular mechanisms might work to protect some patients and not others. Finding such mechanisms might lead to tests for predicting which patients with intestinal inflammatory diseases are predisposed to cancer.
    Cancer Research: June 1 2009, Volume 69, Issue 11 

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
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    Read more at: Sciencedaily.com

    Jefferson Adams
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    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
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    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
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    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
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    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
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    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023