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    Progress at Stanford University School of Medicine's Celiac Management Clinic


    Scott Adams

    Celiac.com 05/12/2006 - Dear Colleagues in the Celiac Community: We would like to provide you with a progress report of the Celiac Management Clinic (CMC) at Stanford Medical Center. Realizing that many physicians and gastroenterologists have a limited understanding of the frequency of Celiac Sprue in the population and the subtlety of the clinical manifestations of this disease, we instituted the CMC at Stanford Medical Center in January 2005. This clinic is staffed by Dr. Gail Pyle and myself. A large number of patients who carried the diagnosis of Celiac Sprue have chosen to be seen in consultation--the majority of these did have Celiac Sprue, as estimated from blood antibody tests and the small intestinal (duodenal) biopsy. For many of these patients, comprehensive emphasis on gluten exclusion has been very effective in eliminating symptoms and the malabsorption of nutrients.


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    However, both in this patient group and in those healthy gluten-free Celiac volunteers who participated in the trial supported by the Celiac Sprue Research Foundation in collaboration with the Palo Alto Medical Foundation on pre-treatment of grocery store gluten with a special peptidase(1) there was a surprising discovery. Fully half (~50%) of those presumed to be in remission from the disease had malabsorption of important nutrients. This major finding was a surprise, and it gives us pause concerning Celiac Sprue therapy.

    Is gluten exclusion not optimal or is it insufficient therapy for this large proportion of Celiac Sprue patients?

    The concerns about the effectiveness of long-term dietary therapy in Celiac Sprue have prompted us to reassess our approach to this disease. For those of you who reside within reach of Stanford Medical Center, we invite you to visit us at the Celiac Management Clinic for an up-to-date assessment of the status of your Celiac condition. If you are the one out of every two healthy Celiacs with malabsorption, we will take a comprehensive approach to determine the reasons and to facilitate your return to complete remission.

    If strict gluten exclusion is insufficient to achieve this, we offer other approaches. Indeed, by the end of this year or the beginning of 2007 in collaboration with the Celiac Sprue Research Foundation, we expect to be able to determine the effect of an oral pill therapy for those who continue with malabsorption of nutrients.

    Stanford accepts most PPO insurance and MediCal and MediCare outpatient coverages. Those who suspect they have Celiac Sprue based on symptoms or blood antibody tests will be seen by Dr. Gray, and those with biopsy-verified disease will be seen by Dr. Pyle. For an appointment, call 650-723-6961, and please state that you wish to see us at the Celiac Management Clinic.

    Sincerely,

    Gary M Gray, M.D.
    Professor of Medicine, Emeritus
    (Gastroenterology)

    References:

    • Pyle GG, Paaso, B Anderson, BE, Allen D, Marti T, Chaitan Khosla C, Gray, GM. Low-dose Gluten Challenge in Celiac Sprue: Malabsorptive and Antibody Responses. Clinical Gastroenterology and Hepatology, 3: 679-686, 2005.
    • Pyle GG, Paaso, B Anderson, BE, Allen D, Marti T, Li Q, Matthew Siegel, M, Khosla C, Gray, GM. Effect of Pretreatment of Food Gluten With Prolyl Endopeptidase on Gluten-Induced Malabsorption in Celiac Sprue Clinical Gastroenterology and Hepatology, 3: 687-694, 2005.
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  • Related Articles

    Scott Adams
    Dig Dis Sci 1999;44:2344-2349.
    Celiac.com 04/10/2000 - Dr. Carme Farre, of Hospital Sant Joan de Deu, in Barcelona, Spain, and his multi-center colleagues, report in the November issue of Digestive Diseases and Sciences that both serologic markers and the human lymphocyte antigen class II extended DQ2 (HLA-DQ2) haplotype are useful markers for screening first-degree relatives of patients with celiac disease for the disorder. These markers are more reliable predictors of celiac disease than other clinical features, which are absent from one third of relatives of people with celiac disease.
    The researchers examined the usefulness of serologic markers, HLA-DQ2 haplotype, and clinical features common to celiac disease in the diagnosis of the disorder in 675 first-degree relatives of celiac disease patients. The diagnosis was confirmed by intestinal biopsy. Their results showed that 5.5% of the subjects were diagnosed with celiac disease, which is significantly higher than what was observed in the general public in a previous study. Serum IgA-class anti-endomysium antibodies (IgA-AEA) and IgA-class anti-gliadin antibodies (IgA-AGA) were observed in 5.8% and 1.9% of the relatives, respectively.
    According to the researchers: Our results show that IgA-AEA is the most useful marker, since all but one IgA-AEA-positive relative showed histological findings of [celiac disease]. Further, the measurement of IgA-AGA would have missed 66% of the affected relatives. The researchers also concluded that the HLA-DQ2 haplotype also appeared to be a more useful indicator to determine which first-degree relatives had an increased genetic susceptibility to celiac disease, because the marker was detected in 93% of first-degree relatives found to have celiac disease, and 18% of those without it. The four most common clinical symptoms for celiac disease, diarrhea, anemia, food intolerance and growth retardation, were not found in one third of the relatives of patients with celiac disease.
    The researchers conclude: Although the definitive diagnosis of [celiac disease] relies upon the intestinal biopsy, it should be preceded by a noninvasive, inexpensive and easy-to-perform screening technique. Their findings indicate that using blood serum IgA-AEA measurements is a useful screening tool for noninvasive screening, and HLA-DQ2 assessment may delineate a very high risk population with a particular genetic susceptibility to [celiac disease].

    Dr. Ron Hoggan, Ed.D.
    This article appeared in the Autumn 2005 edition of Celiac.coms Scott-Free Newsletter.
    Celiac.com 01/11/2006 - There is an abundance of stories about people who begin a gluten-free diet, find that they feel better then decide they want a firm diagnosis of celiac disease. They are facing several problems. First, they may be gluten sensitive without the intestinal lesion of celiac disease. This is very likely since about twelve percent of the population is gluten sensitive, but only a little more than one percent of the general population has celiac disease. Another problem faced by gluten-free individuals who want a diagnosis is that it can take more than five years after returning to a regular gluten-containing diet before the characteristic damage of celiac disease can be seen on a biopsy1. Simply put, after beginning a gluten-free diet, only a positive biopsy is meaningful. A negative biopsy does not rule out celiac disease.
    A variety of opinions have been offered regarding how much gluten, for how long, should result in a definitive biopsy. The reality is that no such recommendation is consistent with the medical literature1-4. Some people with celiac disease will experience a return of intestinal damage within a few weeks of consuming relatively small amounts of gluten. Such brief challenges are valuable for these individuals. However, many people with celiac disease or dermatitis herpetiformis will require much larger doses of gluten, over much longer periods, to induce characteristic lesions on the intestinal wall. Unfortunately for these latter individuals, a negative biopsy after a brief gluten challenge can, and often is, misinterpreted as having ruled out celiac disease. Blood tests can compound this problem. If, as seems likely, celiac patients who are slow to relapse are also the ones who develop milder intestinal lesions, they are the very celiac patients for whom blood tests are very unreliable5. Claims to have ruled out celiac disease based on brief challenges with small quantities of gluten is a mistake that could lead to serious, even deadly, consequences.
    We may forget that gluten consumption by a person with celiac disease can lead to deadly cancers and a variety of debilitating autoimmune diseases. Any recommendation of a gluten challenge should be accompanied by a clear warning that the process may overlook many cases of celiac disease. The absence of such warnings is inexcusable.
    And what about non-celiac gluten sensitivity? The absence of an intestinal lesion does not rule out gluten induced damage to other tissues, organs, and systems. Evidence and research-based information in this area is sadly lacking but we do know that undigested or partly digested gliadin can damage a wide range of human cells6. Thus, one need only be consuming gluten and experience increased intestinal permeability for gluten-induced damage to be a factor in an almost infinite number of ailments.
    There are several partial answers to this problem. One, which Ive raised before, is to employ Dr. Michael N. Marshs rectal challenge for the diagnosis of celiac disease, particularly when the individual has already begun a gluten-free diet. This test permits a definitive diagnosis of celiac disease for up to six months after beginning a gluten-free diet. That would catch a great number of celiac patients who have found relief through a gluten-free diet and now want a diagnosis. Another piece of this puzzle is to test for IgG anti-gliadin antibodies. Although these antibodies are considered "non-specific," they inarguably identify an immune response to one of the most common foods in a regular North American diet. Although these individuals may experience improved wellness on a gluten-free diet, we just dont know enough about non-celiac gluten sensitivity to do more than recommend that they continue on this diet since it makes them feel better.
    Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be ordered at Celiac.com. Rons Web page is: www.DangerousGrains.com.
    References:
    Kuitunen P, Savilahti E, Verkasalo M. Late mucosalrelapse in a boy with coeliac disease and cows milk allergy.Acta Paediatr Scand.1986 Mar;75(2):340-2. Bardella MT, Fredella C, Trovato C, Ermacora E, Cavalli R, Saladino V, Prampolini L. Long-term remission in patients with dermatitis herpetiformis on a normal diet. Br. J. Dermatol. 2003 Nov;149(5):968-71. Shmerling DH, Franckx J. Childhood celiac disease: a long-term analysis of relapses in 91 patients.J Pediatr Gastroenterol Nutr. 1986 Jul-Aug;5(4):565-9. Chartrand LJ, Seidman EG. Celiac disease is a lifelong disorder. Clin Invest Med. 1996 Oct;19(5):357-61. Rostami K, Kerckhaert J, von Blomberg BM, Meijer JW, Wahab P, Mulder CJ. SAT and serology in adult coeliacs, seronegative coeliac disease seems a reality.Neth J Med. 1998 Jul;53(1):15-9. Hudson DA, Cornell HJ, Purdham DR, Rolles CJ. Non-specific cytotoxicity of wheat gliadin components towards cultured human cells.Lancet. 1976 Feb 14;1(7955):339-41.

    Jefferson Adams
    Celiac.com 03/12/2009 - The latest antihuman tissue transglutaminase (tTG) IgA tests are reported to spot celiac disease with nearly 100% sensitivity and specificity. Also, a new generation of deamidated gliadin peptide (α-DGP) antibody tests is alleged to have sensitivity levels on par with the tTG IgA tests. However, in actual practice, sensitivity and specificity for these tests are often lower than claimed for trial conditions.
    A team of Columbia University researchers recently evaluated sensitivities and specificities of four commercial IgA tTG kits, along with three commercial deamidated gliadin peptide (α-DGP) kits. The team evaluated the results for four tTG IgA assays: A—Inova (Hu red blood cell); B—Binding site (rHu Ag); C—Eurospital (rHu Ag), D—Immco (rHu Ag) and three Inova α-DGP assays, E—α-DGP-IgA, F—α-DGP-IgG, and G—α-DGP-IgA+G.
    The research team was made up of Afzal J. Naiyer, MD; Lincoln Hernandez, MD; Edward J. Ciaccio, PhD; Konstantinos Papadakis, MD; John S. Manavalan, MD; Govind Bhagat, MD; Peter H. R. Green, MD, all associated with the Department of Medicine and Pathology, Columbia University, New York, NY.
    The team used blood samples from four different groups of celiac disease patients and controls: Group 1 consisting of 28 patients with active celiac disease; Group 2 consisting of 54 celiac patients following a gluten-free diet; Group 3 consisting of 40 healthy controls; Group 4 consisting of 57 disease controls—17 with Crohn's disease, and 40 with chronic hepatitis. In each case, the researchers used the manufacturer's own cut-off values. They found that sensitivities and specificities of different kits ranged from 71.4% to 96.4% and 87.5% to 100%, respectively.
    Compared with disease controls, sensitivity for Group 1 stayed the same, while specificity fell. All tests showed higher sensitivities for higher patient villous atrophy. The study showed that overall sensitivity was 90% or less, which is below figures reported in the literature.
    Recombinant and red blood cell antigen-based tTG assays performed similarly, while the α-DGP tests showed lower values. The bottom line was that a number of factors can influence the sensitivity and specificity for these test, and that doctors should keep these facts in mind when evaluating patients.
    Journal of Clinical Gastroenterology: Volume 43 (3) March 2009, pp 225-232


    Jefferson Adams
    Celiac.com 06/03/2010 - Clinical presentation of celiac disease can vary considerably from patient to patient. Most patients with celiac disease present atypical symptoms. Moreover, most patients who present abdominal symptoms in primary care do not have celiac disease, and so diagnostic tests for celiac disease are not necessary and should be avoided.
    A team of researchers recently conducted a systematic review of diagnostic testing for celiac disease among patients with abdominal symptoms.
    The team included Daniëlle A. W. M. van der Windt, PhD; Petra Jellema, PhD; Chris J. Mulder, MD, PhD; C. M. Frank Kneepkens, MD, PhD; and Henriëtte E. van der Horst, MD, PhD. Their article appears in the Journal of the American Medical Association.
    The goal of the research was to review and summarize evidence on the performance of diagnostic tests for spotting celiac disease in adults who present abdominal symptoms in primary care or similar settings.
    To obtain initial data, the team search MEDLINE (from January 1966  through December 2009, and EMBASE from January 1947 through December 2009. They also conducted a physical search of references for additional relevant studies.
    The team chose cohort or nested case-control diagnostic studies which included adults presenting non-acute abdominal symptoms, which featured celiac disease prevalence of 15% or less, and in which the tests included gastrointestinal symptoms or serum antibody screens.
    Two independent reviewers conducted studies tool and data extraction. They then calculated sensitivities and specificities for each study and computed pooled estimates using bivariate analysis where there was clinical and statistical homogeneity.
    In all, the team included sixteen studies encompassing 6085 cases in their review.
    Specificity, sensitivity, and confidence intervals for predicting celiac disease varied with abdominal symptoms.  For patients presenting with classic diarrhea, for example, predictive sensitivity ranged from 0.27 to 0.86, while specificity ranged from 0.21 to 0.86.
    Pool estimates for 8 studies on IgA antiendomysial antibodies were 0.90, with a 95% confidence interval [CI] (0.80-0.95) for sensitivity and 0.99, with a 95% CI (0.98-1.00) for specificity, with a positive likelihood ratio [LR] of 171 and negative LR of 0.11.
    Pool estimates for IgA antitissue transglutaminase antibodies (7 studies) were 0.89, with a 95% CI (0.82-0.94) and 0.98 at 95% CI (0.95-0.99), respectively, with a positive LR of 37.7 and negative LR of 0.11.
    IgA and IgG antigliadin antibodies showed variable results, especially for sensitivity, which ranged from 0.46-0.87 for IgA, and from 0.25-0.93 for IgG.
    One recent study using deamidated gliadin peptides showed good specificity (0.94), but the target population offered limited supporting evidence.
    For adults who present abdominal symptoms in primary care or other unscreened settings, IgA antitissue transglutaminase antibodies and IgA antiendomysial antibodies offer high sensitivity and specificity for diagnosing celiac disease.
    SOURCE:  JAMA. 2010;303(17):1738-1746. doi:10.1001/jama.2010.549


  • Recent Articles

    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

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics