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    Abnormal T-Lymphocytes in Refractory Celiac Detected Outside Small Intestinal Intraepithelia


    Jefferson Adams

    Celiac.com 01/17/2010 - A team of researchers based in the Netherlands and in Germany recently found that abnormal T-Lymphocytes in refractory celiac disease may occur beyond small intestinal intraepithelia. The research team was made up of W.H.M. Verbeek, B.M.E. von Blomberg, V.M.H. Coupe, and S. Daum, C.J.J. Mulder, and M.W.J. Schreurs.


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    The team members are associated with the Departments of Gastroenterology, Pathology, Epidemiology and Biostatistics at VU University Medical Centre, Amsterdam, The Netherlands, and with the Department of Medicine I, Gastroenterology, Infectious Diseases & Rheumatology at Charite Universitatsmedizin, Campus Benjamin Franklin, in Berlin, Germany.

    Refractory celiac disease (RCD) is characterized by persistent mucosal pathology despite a strict gluten free diet. Patients with RCD type II show phenotypically abnormal (CD71CD3-CD4/8-cytoplasmicCD31) T-lymphocytes within the intraepitelial lymphocyte (IEL) population in the small intestine, with 50–60% of these patients developing an enteropathy associated T-cell lymphoma (EATL).

    The goal of the study was to determine whether abnormal T-lymphocytes in RCD II can be detected in other parts of the small intestinal mucosa besides the intraepithelial compartment. Additionally, the presence of aberrant
    T-lymphocytes was analyzed in two RCD II patients that developed atypical skin lesions.

    Researchers conducted multi-parameter flow cytometric immunophenotyping on both IEL and lamina propria lymphocyte (LPL) cell suspensions, isolated from small bowel biopsy specimens of RCD II patients (n 5 14), and on cutaneous lymphocytes isolated from skin-lesion biopsy specimens of RCD II patients (n 5 2). They also carried out immunofluorescence analysis of frozen RCD II derived small intestinal biopsies.

    The results clearly show that abnormal T-lymphocytes may develop in both the IEL and the LPL compartments of RCD II derived small intestinal biopsies.

    Indeed, even though the highest percentages are always found in the IEL compartment, abnormal LPL can exceed 20% of total LPL in half of patients with RCD II.

    Interestingly, cutaneous lymphocytes isolated from atypical skin lesions that developed in some RCD II patients showed a similar abnormal immunophenotype as found in the intestinal mucosa.

    In RCD II, the abnormal T-lymphocytes may also manifest in the sub-epithelial layer of the small intestinal mucosa, in the lamina propria, or even in locations completely outside the intestine, including the skin.

    Whether this finding indicates a passive overflow from the intestinal epithelium or active movement towards other anatomical locations remains to be determined.

    Source: Cytometry Part B (Clinical Cytometry) 76B:367–374 (2009)

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  • Related Articles

    Scott Adams
    Arch Intern Med. 2003;163:1566-1572.
    Ulrike Peters, PhD, MPH; Johan Askling, MD; Gloria Gridley, MS; Anders Ekbom, MD, PhD; Martha Linet, MD
    Celiac.com 07/30/2003 - The following abstract paints a fairly bleak picture for those of us with celiac disease; however, after taking a closer look at it I believe that it has some serious limitations that should not be overlooked, and have likely produced skewed or irrelevant results. For example, the study does not indicate whether or not the patients in it followed a strict gluten-free diet. Other studies have shown that the mortality risk for celiacs decreases to that of the normal population when a gluten-free diet is followed for at least five years, and that it is also affected by how soon the diagnosis is made and how soon treatment begins. It is well known that not following a gluten-free diet will increase a celiacs risk of death by many causes to many times that of the normal population, which is precisely why it is so important to include such information in studies of this type. In my opinion doing a study like this and not including such data is like doing a study on diabetes where perhaps half or more people in the study do not take insulin but ought to, and then publishing the ultra-high mortality rate that would be its outcome: "Conclusion: Diabetics have a 20-fold mortality rate over the normal population." The conclusion would clearly not be true for those who took their insulin.
    Additionally the time period that is covered by this study, 1964-1993, could be considered the dark ages of celiac disease, even in Europe (we actually may be just entering the Renaissance age for celiac disease here in the USA, but this could be argued!). Many doctors during this time did not stress enough to their patients the importance of following a strict gluten-free diet, just as many still do not even do this day. My doctor didnt. He just diagnosed me and said I shouldnt eat gluten (as opposed to telling me that it could kill me if I kept eating it), and he didnt even explain to me HOW to avoid it! Is it possible that some of the folks in this study, diagnosed as far back as 1964, might have had similar experiences with their doctors? I would be willing to bet that at least 50% of the people in this study (if not more) were not following a strict gluten-free diet, or were not following the diet at all. If this is true, it is kind of like studying a group of diabetics whose only treatment was to be told by their doctors that they should avoid sugar, which seems absurd if you think about it.
    Last, the study has considerable bias in that it recruited only hospitalized celiacs, presumably because they were already significantly ill, and those who never made it into a hospital were excluded. It reports findings of auto-immune diseases and small bowel/lymphomaexcesses--these are already well known--but what other researchers may disagree with is the scale of the excess--SMR is always a very crude method ofexpressing this in such studies. - Scott Adams (special thanks to Dr. Geoff Helliwell for his comments on this study)

    Abstract
    :
    "Background: Patients with celiac disease have an increased risk of death from gastrointestinal malignancies and lymphomas, but little is known about mortality from other causes and few studies have assessed long-term outcomes."
    "Methods: Nationwide data on 10,032 Swedish patients hospitalized from January 1, 1964, through December 31, 1993, with celiac disease and surviving at least 12 months were linked with the national mortality register. Mortality risks were computed as standardized mortality ratios (SMRs), comparing mortality rates of patients with celiac disease with rates in the general Swedish population."
    "Results: A total of 828 patients with celiac disease died during the follow-up period (1965-1994). For all causes of death combined, mortality risks were significantly elevated: 2.0-fold (95% confidence interval [CI], 1.8-2.1) among all patients with celiac disease and 1.4-fold (95% CI, 1.2-1.6) among patients with celiac disease with no other discharge diagnoses at initial hospitalization. The overall SMR did not differ by sex or calendar year of initial hospitalization, whereas mortality risk in patients hospitalized with celiac disease before the age of 2 years was significantly lower by 60% (95% CI, 0.2-0.8) compared with the same age group of the general population. Mortality risks were elevated for a wide array of diseases, including non-Hodgkin lymphoma (SMR, 11.4), cancer of the small intestine (SMR, 17.3), autoimmune diseases (including rheumatoid arthritis [sMR, 7.3] and diffuse diseases of connective tissue [sMR, 17.0]), allergic disorders (such as asthma [sMR, 2.8]), inflammatory bowel diseases (including ulcerative colitis and Crohns disease [sMR, 70.9]), diabetes mellitus (SMR, 3.0), disorders of immune deficiency (SMR, 20.9), tuberculosis (SMR, 5.9), pneumonia (SMR, 2.9), and nephritis (SMR, 5.4)."
    "Conclusion: The elevated mortality risk for all causes of death combined reflected, for the most part, disorders characterized by immune dysfunction."


    Jefferson Adams
    Celiac.com 09/06/2010 - Celiac disease rates have risen some 400% in the last fifty years. Some of that is due to advances in diagnostic technology, and increased awareness, but scientists also consider increased wheat and gluten consumption to be a major cause.
    Proper celiac disease diagnosis takes over a decade for about one in four sufferers, so clearly a significant portion of that increase reflects an alarming rise in celiac disease rates over the last decades.
    According to a new study by a team of plant researchers from The Netherlands, it's possible that modern wheat breeding habits have promoted an increase in celiac disease epitopes, and thus a proliferation of celiac disease.
    The research team set out to compare the presence of celiac disease epitopes in modern and old hexaploid wheat varieties. The team included H. C. van den Broeck, H. C. de Jong, E. M. Salentijn, L. Dekking, D. Bosch, R. J. Hamer, L. J. Gilissen, I. M. van der Meer, and M. J. Smulders, all affiliated with Plant Research International, Wageningen, The Netherlands.
    It's well-known that gluten proteins from wheat can induce celiac disease in genetically susceptible individuals. This happens when antigen presenting cells expose gluten-sensitive T-cell lymphocytes to specific gluten peptides.
    To analyze whether wheat breeding contributed to the increase of the prevalence of celiac disease, the team compared genetic diversity of gluten proteins for the presence of two celiac disease epitopes (Glia-alpha9 and Glia-alpha20).
    They examined samples of 36 modern European wheat varieties and 50 older varieties grown up to the beginning of the 20th century. Glia-alpha9 is a major (immunodominant) epitope that triggers sensitivity in most celiac disease patients. The minor Glia-alpha20 is included as a technical reference.
    Generally, the modern wheat varieties showed higher levels of Glia-alpha9 epitope, and lower levels of Glia-alpha20 epitope compared to the older varieties.
    This indicates that modern wheat breeding methods may have promoted an increase in celiac disease epitopes, and thus a proliferation of celiac disease.
    On  more positive note, there are both modern and older varieties that are known to have relatively low contents of both epitopes.
    The team conceives a scenario in which such varieties serve as breeding stock for farmers to one day breed wheat specifically designed to eliminate proteins and other substances that promote and trigger celiac disease. On a large-scale, such varieties might help to reduce fast-increasing rates of celiac disease.
    Source:

    Theor Appl Genet. 2010 Jul 28. PMID: 20664999

    Diana Gitig Ph.D.
    Celiac.com 07/18/2011 - People with celiac disease are relatively lucky; a simple change in diet, without any drugs, can completely reverse all symptoms in most patients and causes no side effects. But maintaining a gluten free diet is, of course, far from simple. A number of treatment options are in varying stages of development, but no one has asked celiac patients what kind of treatment they would prefer to a gluten free diet, or if they would even prefer one at all. A recent study in the UK did just that. It found that over 40% of celiac patients are dissatisfied with the gluten free diet.
    Aziz et al. gave a questionnaire to 310 celiac patients and 477 controls. The first section measured their satisfaction with the gluten free diet; the second measured their use of complementary or alternative medicine by asking if they took popular oral supplements (multivitamins, kava, Echinacea, etc.); and the third assessed their views of novel therapies being developed to treat celiac disease. These include a vaccine that would be injected and would allow the consumption of unlimited gluten; peptidases or zonulin antagonists that would enzymatically degrade gluten or inhibit intestinal permeability, respectively, and would be taken orally in case of accidental or periodic ingestion of gluten; and genetic modification of wheat to reduce its toxicity.
    Although more than 40% of celiac patients were unhappy with the gluten free diet, they did not use complementary or alternative medicines with more frequently than controls. This suggests that they do not view these as viable alternative treatments to a gluten free diet. Most celiac patients - 42% - said that they would be interested in a vaccine that would allow them to eat unlimited gluten, while 35% said they would prefer anti-zonulin and 23% said they would like peptidases. Both of these latter therapies would not necessarily allow for healing of the small bowel mucosa like a gluten free diet does, but either could be taken as an adjuvant or to protect against minor or occasional ingestion of gluten. Of the potential novel treatments, all patients ranked genetic modification of wheat as their lowest preference.
    Adherence to dietary advice is among the lowest of all kinds of guidance given by doctors. Among celiac, strict adherence to a gluten free diet varies from 96% all the way down to 36% among different populations. As these British researchers demonstrated and noted in their conclusions, "patients with coeliac [sic] disease are keen to consider novel therapies."
    Source:

    Aziz I, Evans KE, Papageorgiou V, Sanders DS. Are patients with coeliac disease seeking alternative therapies to a gluten-free diet? J Gastrointestin Liver Dis 2011; 20(1) 27-31.

    Jefferson Adams
    Celiac.com 06/17/2013 - To investigate the prevalence of human leukocyte antigen (HLA) DQ2/8 alleles in Southern Italians with liver and gastrointestinal (GI) diseases outside of celiac disease, a team of researchers recently looked at human leukocyte antigen DQ2/8 prevalence in non-celiac patients with gastrointestinal diseases.
    The research team included Daniel DiGiacomo, Antonella Santonicola, Fabiana Zingone, Edoardo Troncone, Maria Cristina Caria, Patrizia Borgheresi, Gianpaolo Parrilli, and Carolina Ciacci. They are variously affiliated with the Gastrointestinal Unit of University Federico â…¡ in Naples, Italy, the Department of Medicine, Celiac Disease Center of Columbia University in New York, in the United States, The Celiac Center of Loreto Crispi Hospital in Naples, Italy, the Celiac Center, Gastrointestinal Unit in San Giovanni di Dio e Ruggi d’Aragona Hospital at the University of Salerno, and the Department of Medicine and Surgery, Campus di Baronissi at the University of Salerno Medical School in Baronissi, Italy.
    The team assessed HLA DQ2/8 status in 443 patients from three ambulatory gastroenterology clinics in Southern Italy. The clinics were located at the University of Federico â…¡ and Loreto Crispi Hospital in Naples, and Ruggi D’Aragona Hospital in Salerno.
    The team grouped patients according disease status for pre-post transplant liver disease, esophageal/gastric organic and functional diseases, irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD), along with DQ2/8 alleles, which correspond to a celiac disease genetic risk scale.
    They then compared allele frequencies in the test subjects with healthy Italian control subjects. Out of 443 subjects, the team found that 196 subjects (44.2%), tested positive for DQ2/8. The average age of DQ2/8 positive subjects was 56 years, and 42.6% were female.
    Overall, the team found that 86/188 (45.7%) patients with liver disease were HLA DQ2/8 positive, 39/73 (53.4%) with functional upper GI diseases and 19/41 (46.3%) with organic upper GI diseases were positive.
    Moreover, 38/105 (36.2%) patients with IBS and 14/36 (38.9%) with IBD were HLA DQ2/8 positive (P = 0.21). Additionally, people with functional upper GI diseases disorders had rates of DQ2/8 positivity that were nearly double those of healthy control subjects. Those with liver disease had rates of DQ2/8 positivity that were 1.3 percent higher than controls, though this rate is not statistically significant. People with IBS and IBD had a lower rates of DQ2/8 positivity compared to healthy controls.
    Compared to general population estimates, the percentage of individuals who were HLA DQ2/8 positive is higher in those with liver/upper functional GI disease and lower in IBS/IBD.
    Source:
    World J Gastroenterol 2013 April 28; 19(16): 2507-2513. ISSN 1007-9327 (print) ISSN 2219-2840 (online). doi:10.3748/wjg.v19.i16.2507

  • 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.
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    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.
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    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