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    Screening Irritable Bowel Syndrome Patients for Celiac Disease Found to be Cost Effective


    Scott Adams

    Aliment Pharmacol Ther 19(11):1199-1210, 2004.


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    Celiac.com 06/08/2004 - Researchers at the University of California, San Francisco have determined that everyone with Irritable Bowel Syndrome (IBS) should also be screened for celiac disease. The researchers used decision analysis to estimate the number of celiac disease cases detected, quality-adjusted life-years gained, and costs resulting from screening suspected IBS patients for tissue transglutaminase antibody and antibody panel. Positive tests were followed up with an endoscopic biopsy. A gluten-free diet was initiated to improve the quality of life in those with celiac disease.

    The results of this study indicate that 3% of the 1,000 patients with suspected IBS have celiac disease. Based on these results the researchers analyzed the costs of several celiac disease screening methods used a decision analysis formula to determine whether or not the screening is cost effective. The researchers conclude that celiac disease screening in patients with suspected irritable bowel syndrome is likely to be cost-effective even at a relatively low celiac disease prevalence.

    Perhaps the researchers should have taken their analysis one step further and concluded that it would make good economic sense to screen the entire population of the USA (as well as that of other countries) for celiac disease, rather than just those with IBS, given the fact that it affects approximately 1% of the population--which is the only conclusion that I could reach after my review of their good work. -Scott Adams

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    Guest Donna Harlan

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    I have been living with IBS for 6 years now and just recently taken gluten out of my diet. Everything has changed for the better, and I now have hope. Wish I could have realized this a long time ago. My doctors never mentioned it as a possibility.

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    Guest elizabeth

    Posted

    I have been living with IBS for 6 years now and just recently taken gluten out of my diet. Everything has changed for the better, and I now have hope. Wish I could have realized this a long time ago. My doctors never mentioned it as a possibility.

    I don't know recipes for people with both IBS and celiac. Do you have any?

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  • Related Articles

    Scott Adams
    Lancet Nov 2001 Volume 358, Number 9292 1504-08 03
    Celiac.com 11/14/2001 - A recent study published in The Lancet by Dr. David S Sanders et al. of the Gastroenterology and Liver Unit, Royal Hallamshire Hospital, Sheffield, UK, explored the number of people who were diagnosed with irritable bowel syndrome but actually had celiac disease.
    The case-control study was done at a university hospital in which 300 consecutive new irritable bowel syndrome patients who met the Rome II criteria for their diagnosis were compared against 300 healthy age and sex-matched controls. Both groups were investigated for celiac disease by analysis of their serum IgA antigliadin, IgG antigliadin, and endomysial antibodies (EMA). Patients and controls with positive antibody results were offered duodenal biopsy to confirm the possibility of celiac disease.
    An amazing 66 patients with irritable bowel syndrome tested positive for the antibodies, and 14 of them or 4.6% had active celiac disease as compared with 2 or 0.66% of the non-IBS matched controls. In other words there is a sevenfold increase over the normal population in the number of people with IBS who have celiac disease. All of the patients with celiac disease in the IBS group were therefore misdiagnosed. The study did not indicate how many of the other 52 patients who had positive antibody results would eventually develop celiac disease, but this would be an interesting follow-up study. Celiac.com believes that the 4.6% with celiac disease will grow higher over time.
    Conclusion: All patients with irritable bowel syndrome should be screened celiac disease.

    Scott Adams
    Celiac.com 09/30/2002 - The Canadian Medical Association Journal (Hoey, 2002;166:479-80) published the following, Irritable Bowel Syndrome: Could it be Celiac Disease?, as excerpted below. This was an analysis of a Lancet article (Sander et al, 2001;358:1504-8) called, Association of Adult Coeliac Disease with Irritable Bowel Syndrome: A Case-Control Study in Patients Fulfilling Rome II Criteria Referred to Secondary Care.
    Here are the CMAJ excerpts:
    Irritable Bowel Syndrome is found in 10% to 20% of people with the use of standard diagnostic tools such as the Rome II criteria. Rome II criteria is specified below: At least 12 weeks, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that has 2 out of 3 features:
    Relieved with defecation Onset associated with a change in frequency of stool Onset associated with a change in form (appearance) of stool Symptoms that cumulatively support the diagnosis of irritable bowel syndrome:
    Abnormal stool frequency (more than 3 bowel movements per day or fewer than 3 bowel movements per week) Abnormal stool form (lumpy/hard or loose/watery stool) Abnormal stool passage (straining, urgency or feeling of incomplete evacuation) Passage of mucus Bloating or feeling of abdominal distention Question: What proportion of patients who meet the Rome II criteria for irritable bowel syndrome have celiac disease?
    Case subjects: The article cites that 300 people (214 women, 86 men ranging in age from 18 to 87, (mean 56 years)) met the Rome II criteria out of 686 new patients who were referred by a family physician to a university hospital gastroenterology clinic. Control subjects were healthy people without irritable bowel syndrome. Also, most control subjects were companions of the patients who were matched to case subjects by age (within 1 year) and sex, as well as questioned in the same manner as case subjects.
    All case and control subjects underwent a wide range of baseline investigations, including full blood count, measurement of erythrocyte sedimentations rate, blood urea nitrogen and serum electrolyte levels, and thyroid function tests. In addition, they were investigated for celiac disease by analysis of serum levels of IgG antigliadin, IgA antigliadin and endomysial antibodies. Most of the case subjects, particularly those older than 45, underwent colonoscopy or sigmoidoscopy and barium enema. Case and control subjects with positive antibody test results were offered duodenal biopsy to confirm the possibility of celiac disease.
    Of the 66 case subjects who had positive antibody test results,
    49 had elevated levels of only IgG antigliadin
    4 of only IgA antigliadin and
    6 of only endomysial antibodies
    Fourteen of the 66 were subsequently found to have histologic evidence of celiac disease; 11 of the 14 were positive for endomysial antibodies. Nine of the of 66 case subjects were lost to follow-up or refused duodenal biopsy; 1 of them was positive for endomysial antibodies.
    Of the 44 control subjects who had positive antibody test results,
    41 had elevated levels of only IgG antigliadin
    1 of only IgA antigliadin and
    2 of IgG antigliadin and endomysial antibodies
    Only the last 2 subjects elected to undergo duodenal biopsy, and both were found to have histologic evidence of celiac disease.
    Commentary: The authors found that a high proportion of patients (about 5%) who were referred to a university hospital gastroenterology clinic and who met the Rome II criteria did have celiac disease. In addition, the clinic specialists uncovered other organic abnormalities in almost 20% of the referred patients.
    The study had several weaknesses. For instance, although most of the case subjects underwent extensive investigations of the lower gastrointestinal tract, the control subjects did not. Thus, some of the case subjects who were lost to follow-up or refused investigation and many of the age-matched control subjects might have been found to have irritable bowel disease, celiac disease or other gastrointestinal abnormalities.
    The authors conclude from their findings that patients who meet the Rome II criteria for irritable bowel syndrome and who are referred to a secondary care centre should be investigated routinely for celiac disease.
    In an editorial accompanying the Lancet article, a gastroenterologist cautioned that more studies are needed. He noted an earlier study in which 121 consecutive patients were referred for investigation of irritable bowel syndrome. Using Rome I criteria and similarly extensive investigation, the researchers detected no cases of celiac disease.
    Because of the findings from the Lancet study, the editorialist has decided to further lower his threshold for screening for celiac disease among patients referred for investigation of irritable bowel syndrome. Perhaps other gastroenterologists would be wise to do the same.
    I verified the five percent as cited in the CMAJ as 14 out of the 300 patients who met the Rome II criteria also had celiac disease. The CMAJ also cites the following, Studies in Europe have shown that up to 1% of the adult population may have celiac disease. We can make our own conclusions from this study in Lancet and we might agree that 1% may be understated but further studies have to be performed to corroborate a higher percentage of undiagnosed celiacs; I hope this definitely encourages closer scrutiny of IBS patients like myself who was diagnosed with IBS in 1997 with only a symptom of left side tenderness below my rib cage and a sigmoidoscopy which revealed no abnormalities except a hemorrhoid. Then, in the summer of 2001, I was diagnosed with lactose intolerance and IBS once more before discovering from medical research and my food dairy taken since May 2001, along with corroboration by an allergist in October 2001, that it may be celiac disease, as my malabsorption symptoms grew worse.
     

    Scott Adams
    Mayo Clin Proc 2004;79:476-482. Celiac.com 05/25/2004 - The results of a study conducted by Dr. G. Richard Locke III and colleagues at the Mayo Clinic College of Medicine in Rochester, Minnesota do not show an association between irritable bowel syndrome (IBS) and celiac disease. The case-control study was based on the respondents of a bowel disease questionnaire that was sent to random Olmsted County residents who were 20 to 50 years old. The researchers evaluated 150 subjects, 72 of whom reported having symptoms of IBS and dyspepsia, and 78 controls with no gastrointestinal symptoms. In the group with symptoms they found that 50 had IBS, 24 had dyspepsia and 15 had both conditions. Serological screening of both groups for celiac disease showed no significant difference between them—two controls, two IBS subjects and two people with dyspepsia tested positive for celiac disease. The researchers conclude that celiac disease alone cannot explain the presence or IBS or dyspepsia in the subjects.
    The results of this study are interesting, but probably not large enough to be statistically significant. The total number of people with celiac disease in each group was astounding:
    2 out of 50 with IBS (4%)
    2 out of 24 with dyspepsia (6%)
    2 of the 78 controls (2.6%)
    These findings do not necessarily contradict previous IBS/celiac disease studies that looked at hospital outpatients who are more likely to have more severe and prolonged symptoms than a group that selects itself from the general public by responding to a questionnaire. Additionally most of the earlier studies that concluded that there was a connection between celiac disease and IBS were conducted before more recent epidemiological studies that have shown just how high the incidence of celiac disease in the general population is--now estimated between 0.8% and 1.3%--this study suggests 2 -3%. These recent epidemiological studies have also shown that a large percentage of celiacs have little or no symptoms, perhaps due to the length of time or the severity of the disease.
    A 1 in 20 diagnosis of celiac disease in patients with IBS/dyspepsia is consistent with other studies, and is still high and suggests that testing for celiac disease should be done routinely on these patients. No studies have ever suggested that all or even most IBS patients have celiac disease, just that the incidence is higher than that of the normal population.
    I propose that if this study had been done on exactly the same people several years from now, the 2 people in the control group who were found to have celiac disease may well develop symptoms that would put them in either the IBS or dyspepsia group, which would create a statistically significant result that would contradict this studys result. Last, perhaps the results of this study really support a more broad conclusion: Everyone ought to be screened for celiac disease, not just those with symptoms.

    Jefferson Adams
    Celiac.com 02/25/2013 - Patients with celiac disease often report symptoms compatible with irritable bowel syndrome (IBS). However, there haven't been any systematic studies regarding how adherence to a gluten-free diet might affect rates of irritable bowel syndrome-type symptoms in patients with celiac disease.
    To better answer that question, a research team conducted a meta-analysis of celiac disease patients to determine rates of irritable bowel syndrome-type symptoms, and how those symptoms relate to a gluten-free diet.
    The research team included A. Sainsbury, D.S. Sanders, and A.C. Ford, of the Leeds Gastroenterology Institute at St James's University Hospital in Leeds, United Kingdom.
    For their analysis, the team searched MEDLINE, EMBASE, and EMBASE Classic to identify cross-sectional surveys or case-control studies reporting prevalence of IBS-type symptoms in adult patients (≥16 years old) with established celiac disease.
    The team used case or control status and adherence to a gluten-free diet to determine the number of individuals with IBS symptoms.
    The team analyzed data from 7 studies with 3383 participants.
    They then calculated pooled prevalence and odds ratios (ORs), with 95% confidence intervals (CIs).
    They found that pooled prevalence of IBS-type symptoms in all patients with celiac disease was 38.0% (95% CI, 27.0%-50.0%).
    People with celiac disease had higher pooled odds ratios for IBS-type symptoms than did control subjects (5.60; 95% CI, 3.23-9.70).
    In patients who did not follow a strict gluten-free diet, the pooled odds ratios for IBS-type symptoms, compared with those who were strictly adherent, was 2.69 (95% CI, 0.75-9.56).
    Patients who did not adhere to the gluten-free diet had higher odds ratios for IBS-type symptoms compared with controls (12.42; 95% CI, 6.84-11.75).
    Such patients also had higher odds ratios compared with that observed for celiac disease patients who followed a strict gluten-free diet or controls (4.28; 95% CI, 1.56-11.75).
    The results show that patients with celiac disease suffer IBS-type symptoms more frequently than control subjects, and that following a strict gluten-free diet might help to reduce those symptoms.
    Source:
    Clin Gastroenterol Hepatol. 2012 Dec 13. pii: S1542-3565(12)01491-7. doi: 10.1016/j.cgh.2012.11.033.

  • 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