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    Scott Adams
    The following was received on March 5, 1998 from Kathryn K. Harden, Ph.D., k-harden@UIUC.EDU, Assistant Editor, The Journal of Nutrition, University of Illinois, Urbana-Champaign.
    The latest issue of the American Journal of Clinical Nutrition contains two articles concerning celiac disease. It is encouraging to see research papers concerning celiac disease in important basic research and clinical journals. The citations are:
    Reversal of low bone density with a gluten-free diet in children and adolescents with celiac disease. S. Mora, G. Barera, A. Ricotti, G. Weber, C. Bianchi and G. Chiumello. AJCN 67: 477-481, 1998. The authors conclude that in children and adolescents with low bone mineral density (BMD) due to celiac disease, a gluten free diet promotes a rapid increase of BMD that leads to a complete recovery of bone mineralization. Due to the severe consequences of low BMD, the authors emphasize the need for early diagnosis and treatment of celiac disease. Nutritional status of newly diagnosed celiac disease patients before and after the institution of a celiac disease diet - association with the grade of mucosal villous atrophy. T Kemppainen, V-M Kosma, E Janatuinen, R Julkunen, P Pikkarainen, M Uusitupa. AJCN 67: 482-487, 1998. Authors found that celiac disease patients with 3 levels of intestinal villous atrophy (partial, subtotal, total) did not differ in the nutritional status variables measured except erythrocyte folate and serum ferritin concentrations. The following was received from J.C. Trevett JCTrevett@aol.com on September 28, 1998:
    Two articles I would like to add to your list if you dont already have info.
    Journal of Pediatrics, August 1998 article entitled, Celiac disease: A Reappraisal, by David Branski, MD and Ricardo Troncone, MD. Dr. Branski is Dept. of Pediatrics, Shaare Zedek Medical Center, P. O. Box 3235, Jerusalem, Israel. It is a good five page article referring to the tip of the iceberg again - at least all the experts are in agreement all over the world that we are not diagnosing enough celiac disease. This is a good article - there is some technical stuff about the DB MOLECULE, which I will never understand, but I gave a copy to my gastroenterologist and he seemed to appreciate it. Tufts University, Medford, MA, Tufts Health & Nutrition Letter - September, 1998 - Volume 16, Number 7. Good article for average layperson on Coping with Celiac Disease - mentions CSA/USA, Inc. and its many (80) support groups throughout the country. Also mentions Gluten Intolerance Group, Energy Foods and Dietary Specialties. To quote part of the article: In one survey, 43 percent of those with the condition said that theyd been diagnosed with an assortment of ailments - such as anemia, stress, ulcers, and nerves before finding out that celiac disease was responsible for the symptoms.

    Scott Adams
    Celiac.com 01/11/2007 – Researchers in Finland have determined that many patients with untreated celiac disease show the presence of intestinal endomysial autoantibodies (EmA), even in the 10-20% of cases where their serum EmA is negative. The researchers also believe that the negative serum EmA test in these cases is an indication of more advanced and long-standing celiac disease. Normally positive serum EmA is close to 100% accurate, however there is a subset of around 10-20% of patients where the test is negative even though they do have the disease. Dr. Katri Kaukinen and colleagues at the University of Tampere looked at 177 celiac disease patients and found that 22 were serum EmA-negative. A common theme among the 22 serum EmA-negative patients was that they were older and had more abdominal symptoms and other complications that indicated a more advanced stage of celiac disease than their serum EmA-positive counterparts. The research team found that even though the EmA antibodies could not be detected in the blood of these 22 patients, they could be detected in the small bowel mucosa in all of them, and none were detected in 20 control patients. Dr. Kaukinen and colleagues believe that the use of intestinal EmA antibody detection should be used in seronegative individuals who are suspected to have celiac disease.
    This study further supports Dr. Kenneth Fines use of IgA antigliadin antibodies in the stool to detect gluten sensitivity, and one has to wonder if the EmA antibodies, if detectable in the small bowel mucosa, would not also be detectable in the patient’s stool, and if so would that not be a much better and more cost-effective way to perform such a screening?
    Gut 2006;55:1746-1753.

    Tina Turbin
    This article originally appeared in the Autumn 2010 edition of Journal of Gluten Sensitivity.
    Celiac.com 01/10/2011 - As an author, researcher, and gluten-free advocate, I work hard to raise awareness for celiac disease and gluten issues, particularly when it comes to increasing the diagnosis rate. Part and parcel of improving diagnosis is proper testing. Evidence is mounting that indicates that blood testing may not be the most effective way to test for celiac disease, and I would recommend that people who suspect they have celiac disease to check with their doctors about other testing options.
    Celiac disease, which is essentially an autoimmune reaction to gluten, a protein found in wheat, barley, and rye, affects approximately three million Americans, but according to estimates, only three percent of them have been properly diagnosed with the disease. Once celiac disease is diagnosed, treatment is simple—following a gluten-free diet. With so many American celiacs going without a diagnosis,  this painful and potentially fatal autoimmune disorder, with its easy method of treatment, attention needs to be focused on effective, efficient testing.
    Although awareness of celiac disease and gluten-free living is increasing in the various medical fields, accurate and reliable testing has not been definitively tackled or uniformly implemented by medical practitioners. Currently a popular method of testing is a blood test, but some people with celiac disease can get blood testing many times and the results will nevertheless be negative.
    Although blood testing has been successful in diagnosing some people with celiac disease, this method is inaccurate at least 80 percent of the time, according to Dr. Datis Kharrazian, Blood Chemistry Seminar instructor and the formulator for Apex Energetics, Inc. supplements. To understand how blood testing works, a basic grasp of the workings of the immune system is essential. Antibodies are part of the immune system and designed to attack specific antigens, or invaders, of the body. Tests can be conducted that find an increase of antibodies in the system, which are on the prowl for certain foreign invaders. Specifically, anti-gliadin, or anti-gluten antibodies, can be tested for; when these exist in the system in large amounts, it is a sign of the autoimmune disorder, celiac disease. Although this may sound workable in theory, in practice blood testing is insufficient and inaccurate due to the fact that the autoimmune response doesn’t occur in the blood stream, but in the small intestine, as the immune system attacks this organ’s absorptive finger-like structures called villi which line the inside. Thus, for the sake of reliability, this suggests that testing should be focused on the gut.
    So what method can we turn to? Fortunately, there is another method apart from an intestinal biopsy, which is an invasive as well as expensive procedure. It turns out that the immune cells which surround the gut also can be located in large numbers in the stool, making a stool anti-gliadin antibody test a reliable alternative to blood testing.
    Stool testing may be more accurate than blood testing and is more convenient. One doesn’t need a doctor’s prescription for the test, which can be conducted in the privacy of one’s own home with an online-ordered kit from EnteroLab, which according to its website, is “a registered and fully accredited clinical laboratory specializing in the analysis of intestinal specimens for food sensitivities.”
    Enterolab offers the Anti-Gliadin Antibodies Stool Test as well as additional tests which can be ordered may be important diagnostic tools for people who have celiac disease or gluten-sensitivity. These additional tests include the Tissue Transglutaminase Stool Test, which tests whether gluten is actively attacking the intestine and other tissues, the Malabsorption Test, used to determine whether the intestine is malabsorbing nutrients due to the autoimmune reaction to gluten, or the Celiac and Gluten-Sensitivity Gene Test. The lab also offers a Milk Sensitivity Test, which tests for reactions to casein, a milk protein
    With millions of celiac Americans living with their disease undiagnosed, we can’t afford to waste time with inaccurate and inefficient testing. The anti-gliadin antibodies stool test, so easily available to the public, is a great stride forward for the celiac community.
    Talk with your health care provider today about this alternative to celiac blood testing.


    Jefferson Adams
    Celiac.com 01/26/2015 - Celiac disease occurs along a spectrum, which includes cases where patients have only minor histological abnormalities, or, what is called "potential celiac disease."
    Can a scientific equation based on immunohistochemical analysis of duodenal biopsies help to better diagnose celiac disease and cases of potential celiac disease? A team of researchers recently set out to assess the potential of immunohistochemical analysis of duodenal biopsies to aid in the diagnosis of gluten-related minor enteropathy.
    The research team included A. Tosco, M. Maglio, F. Paparo, L. Greco, R. Troncone, and R. Auricchio. They are affiliated with the Department of Translational Medical Science, Section of Pediatrics, and the European Laboratory for the Investigation of Food Induced Diseases at the University Federico II in Naples, Italy.
    For their analysis, the team looked at duodenal biopsies from 56 untreated celiac patients and 56 control subjects, and assessed patients based on CD3 and γδ intraepithelial lymphocytes number, γδ /CD3 ratio, and density of CD25+ lamina propria cells. 
    To help them blindly evaluate 61 more biopsies with normal villous architecture, the team used a discriminant equation, that is, an equation that allows them to determine whether the patient has celiac disease based on the four factors noted above. Both celiac patients and control subjects showed widely variable immunohistochemical ranges, and no single parameter showed sufficient specificity for celiac disease. However, by combining parameters for all four markers, the team was able to produce an accurate discriminant equation.
    The result of the team’s discriminant equation is a score called a Dscore. Their equation is as follows: Dscore = (CD3 x 0.06) - (γδ x 0.119) + (CD25 x 0.012) + (γδ /CD3 x 0.131) - 4.709.
    Under the team’s system, patients’ Dscores could be used to correctly point to celiac disease in 97.3% of cases.
    When the team applied this equation to a validation set of 61 patients with normal villous architecture and unknown diagnosis, 92.9% of those with a positive score turned out to be potential celiac patients. However, a normal score did not exclude celiac disease.
    In certain cases, immunohistochemistry can be helpful for diagnosing celiac disease, but, because it lacks sensitivity, it can miss some potential celiac cases.
    Source:
     J Pediatr Gastroenterol Nutr. 2014 Dec 14.

  • 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