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    How can I convince my doctor to do these tests, and do them at an experienced lab?**


    Scott Adams

    Vijay Kumar, M.D., Research Associate Professor at the University of Buffalo and President and Director of IMMCO Diagnostics: Convincing the doctor initially depends upon the patient. However, the laboratory to which the test is sent should be available to answer questions the doctor may have. Our laboratory always encourages such questions.


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    Karoly Horvath, M.D., Ph.D., Associate Professor of Pediatrics; Director, Peds GI & Nutrition Laboratory; University of Maryland at Baltimore: Lot of physicians in the USA did not get appropriate training to recognize the protean manifestations of celiac disease. However, if the classical symptoms are present--chronic diarrhea, weight loss, protuberant abdomen, foul-smelling stools, etc.--it is absolutely indicated to test the patients serum for antigliadin and antiendomysium antibodies.

    Professionals participating in this discussion group are educating physicians on an almost daily basis. Generally, it is useful to supply the physician with a review article or a textbook chapter describing the values of serological tests and protean manifestations of celiac disease. If that does not help, you can ask the help of professionals participating in the Cel-Pro list. They have helped several patients by calling physicians and convincing them about the necessity of serological testing.

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    Guest titanic

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    I am fighting all the systems of this and after reading this I hope my doctor will get me tested for this. I've lost so much weight and this diarrhea is getting bad so I hope my doctor will get me better soon.

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  • Related Articles

    Scott Adams
    There is no typical celiac. Individuals range from having no symptoms (asymptomatic or "latent" forms of the disease) to extreme cases where patients present to their physicians with gas, bloating, diarrhea, and weight loss due to malabsorption.
    In between these two extremes lie a wide variety of symptoms that include:
    Diarrhea Constipation Steatorrhea (fatty stools that float rather than sink) Abdominal pain Excessive gas Any problem associated with vitamin deficiencies Iron deficiency (anemia) Chronic fatigue Weakness Weight loss Bone pain Easily fractured bones Abnormal or impaired skin sensation (paresthesia), Including burning, prickling, itching or tingling Edema Headaches* Peripheral Neuropathy* (tingling in fingers and toes)
    Individuals have reported such varied symptoms as:
    White flecks on the fingernails Fuzzy-mindedness after gluten ingestion Burning sensations in the throat
      In children, the symptoms may include:
    Failure to thrive Paleness Querulousness, irritability Inability to concentrate Wasted buttocks Pot belly with or without painful bloating Pale, malodorous, bulky stools Requent, foamy diarrhea   In addition to all of these, dermatitis herpetiformis, a disease in which severe rashes appear (often on the head, elbows, knees and buttocks) is related to celiac disease.
    Reactions to ingestion of gluten can be immediate, or delayed for weeks or even months.
    The amazing thing about celiac disease is that no two individuals who have it seem to have the same set of symptoms or reactions. A person might have several of the symptoms listed above, a few of them, one, or none. There are even cases in which obesity turned out to be a symptom of celiac disease.

    Scott Adams
    Traditionally, gluten is defined as a cohesive, elastic protein that is left behind after starch is washed away from a wheat flour dough. Only wheat is considered to have true gluten. Gluten is actually made up of many different proteins.
    There are two main groups of proteins in gluten, called the gliadins and the glutenins. Upon digestion, the gluten proteins break down into smaller units, called peptides (also, polypeptides or peptide chains) that are made up of strings of amino acids--almost like beads on a string. The parent proteins have polypeptide chains that include hundreds of amino acids. One particular peptide has been shown to be harmful to celiac patients when instilled directly into the small intestine of several patients. This peptide includes 19 amino acids strung together in a specific sequence. Although the likelihood that this particular peptide is harmful is strong, other peptides may be harmful, as well, including some derived from the glutenin fraction.
    It is certain that there are polypeptide chains in rye and barley proteins that are similar to the ones found in wheat. Oat proteins have similar, but slightly different polypeptide chains and may or may not be harmful to celiac patients. There is scientific evidence supporting both possibilities.
    When celiac patients talk about "gluten-free" or a "gluten-free diet," they are actually talking about food or a diet free of the harmful peptides from wheat, rye, barley, and (possibly) oats. This means eliminating virtually all foods made from these grains (e. g., food starch when it is prepared from wheat, and malt when it comes from barley) regardless of whether these foods contain gluten in the very strict sense. Thus, "gluten-free" has become shorthand for "foods that dont harm celiacs."
    In recent years, especially among non-celiacs, the term gluten has been stretched to include corn proteins (corn gluten) and there is a glutinous rice, although in the latter case, glutinous refers to the stickiness of the rice rather than to its containing gluten. As far as we know, neither corn nor glutinous rice cause any harm to celiacs.

    Scott Adams
    The common list of forbidden grains is: wheat, rye, barley and oats.
    Unfortunately, there are variants out there that go by other names. Durum and semolina are names for certain kinds of wheat that have been bred for specific uses. Both spelt and kamut are versions of wheat. (Other names for these: spelt, Polish wheat, einkorn and small spelt). Bulgur is wheat thats been specially processed. Triticale, a grain crossbred from wheat and rye, is definitely on the toxic list.
    Though corn (maize) is one of those grains that many people -- not just celiacs -- may be allergic to, it is not a grain that is thought to cause damage to the villi in celiacs. It is tolerated by most celiacs.
    Of the common grains, rice is the favorite as it rarely troubles anyone.
    Aside from corn and rice, there is a wide variety of other grains that are used in gluten-free cooking. We even use beans and peas (legumes, pulses).
    The following can be milled into flour: amaranth*, buckwheat* (or kasha), chickpeas (garbanzos), Jobs tears (Hato Mugi, Junos Tears, River Grain), lentils, millet*, peas, quinoa*, ragi, sorghum, soy, tapioca, teff*, and wild rice. Many of these flours are available in health food stores. Some (like rice flour) may be available in grocery stores. (The products marked with an "*" are listed as grains to avoid by some physicians and celiac societies. See the discussion below about anecdotal evidence and possible contamination of flours for more information.)
    To improve the texture of gluten-free baked goods, most cooks use one or more of the following: xanthan gum, guar gum (though this sometimes has a laxative effect), methylcellulose, or a new product called Clear Gel. These can be obtained either through health food stores, specialty cooks stores, or some of the mail order sources listed below.
    Oils popular in cooking include: corn, peanut, olive, rapeseed (canola), safflower, soy, and sunflower.

    Scott Adams
    Vijay Kumar, M.D., Research Associate Professor at the University of Buffalo and President and Director of IMMCO Diagnostics: The three serological tests that are used for diagnosing celiac disease are:
    Anti-endomysial antibody (EMA) Anti-reticulin antibody (ARA) Anti-gliadin antibody (AGA) Each of these three tests provide a certain degree of reliability for diagnosing celiac disease. Of these, endomysial antibody is the most specific test. The following table is taken from our studies (Lerner, Kumar, Iancu, Immunological diagnosis of childhood coeliac disease: comparison between antigliadin, antireticulin and antiendomysial antibodies).
      % of Sensitivity % of Specificity Predictive Value % Pos Predictive Value % Neg EMA 97% 98% 97% 98% ARA 65% 100% 100% 72% IgG AGA 88% 92% 88% 92% IgA AGA 52% 94% 87% 74%  
    The following definitions related to sensitivity, specificity, positive and negative predictive values may help:
    Sensitivity is the probability of a positive test result in a patient with disease. Specificity is the probability of negative test result in a patient without disease. Positive predictive value is the probability of disease in a patient with positive test result. Negative predictive value is the probability of no disease in a patient with negative test result.
    Karoly Horvath, M.D., Ph.D., Associate Professor of Pediatrics; Director, Peds GI & Nutrition Laboratory; University of Maryland at Baltimore: The summary below shows the results of the main serological tests based on several publications including 388 patients with celiac disease, and 771 healthy subjects.
     
    SENSITIVITY- the proportion of subjects with the disease who have a positive test. It indicates how good a test is at identifying the diseased:
      Percentage of - IgA AGA Percentage of - IgG AGA Percentage of - IgA EMA Average 78% 79% 97% Range 46-100% 57-94% 89-100%


    SPECIFICITY- the proportion of subjects without the disease who have a negative test. It indicates how good a test is at identifying the non-diseased:
      Percentage of - IgA AGA Percentage of - IgG AGA Percentage of - IgA EMA Average 92% 84% 98.5% Range 84-100% 52-98% 97-100%


    POSITIVE PREDICTIVE VALUE- the probability that a person with positive results actually has the disease:
      Percentage of - IgA AGA Percentage of - IgG AGA Percentage of - IgA EMA Average 72% 57% 92% Range 45-100% 42-76% 91-94%


    NEGATIVE PREDICTIVE VALUE- the probability that a person with negative results does not have the disease:
      Percentage of - IgA AGA Percentage of - IgG AGA Percentage of - IgA EMA Average 94% 94% 100% Range 89-100% 83-99% 100%


    References:
    McMillan SA, Haughton DJ, Biggart JD, Edgar JD, Porter KG, McNeill TA. Predictive value for coeliac disease of antibodies to gliadin, endomysium, and jejunum in patients attending for jejunal biopsy. Brit Med J 1991;303:1163-1165
    Ferreira M, Lloyd Davies S, Butler M, Scott D, Clark M, Kumar P. Endomysial antibody: is it the best screening test for coeliac disease? Gut 1992;33:1633-1637.
    Khoshoo V, Bhan MK, Puri S, Jain R, Jayashree S, Bhatnagar S, Kumar R, Stintzing G. Serum antigliadin antibody profile in childhood protracted diarrhea due to coeliac disease and other causes in a developing country. Scand J Gastroenterol 1989;24:1212-1216.
    Chan KN, Phillips AD, Mirakian R, Walker-Smith JA. Endomysial antibody screening in children. J Pediatr Gastroenterol Nutr 1994;18:316-320.
    Bode S, Weile B, Krasilnikoff PA, Gdmand-Hyer E. The diagnostic value of the gliadin antibody testing celiac disease in children: a prospective study. J Pediatr Gastroenterol Nutr 1993;17:260-264.
    Calabuig M, Torregosa R, Polo P, Tom s C, Alvarez V, Garcia-Vila A, Brines J, Vilar P, Farr C, Varea V. Serological markers and celiac disease: a new diagnostic approach ? J Pediatr Gastroenterol Nutr 1990;10:435-442.

  • 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.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    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.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    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. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    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.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    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.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    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