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    Higher Celiac Disease Risk in Children with Certain HLA Haplotypes


    Jefferson Adams
    Image Caption: Photo: CC--Phalinn Ooi

    Celiac.com 07/21/2014 - The presence of HLA haplotype DR3–DQ2 or DR4–DQ8 is associated with an increased risk of celiac disease. In addition, nearly all children with celiac disease have serum antibodies against tissue transglutaminase (tTG).


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    Photo: CC--Phalinn OoiA research team recently set out to determine the risk of celiac disease autoimmunity and celiac disease, by age and by halpotype, in children. The research team included Edwin Liu, M.D., Hye-Seung Lee, Ph.D., Carin A. Aronsson, M.Sc., William A. Hagopian, M.D., Ph.D., Sibylle Koletzko, M.D., Ph.D., Marian J. Rewers, M.D., M.P.H., George S. Eisenbarth, M.D., Ph.D., Polly J. Bingley, M.D., Ezio Bonifacio, Ph.D., Ville Simell, M.Sc., and Daniel Agardh, M.D., Ph.D. for the TEDDY Study Group.

    The team studied 6403 children with HLA haplotype DR3–DQ2 or DR4–DQ8 prospectively from birth in the United States, Finland, Germany, and Sweden. The study’s primary end point was the development of celiac disease autoimmunity, which the team defined as the presence of tTG antibodies on two consecutive tests at least 3 months apart. The secondary end point was the development of celiac disease itself, which they defined as either a diagnosis on biopsy or persistently high levels of tTG antibodies.

    The average follow-up was 5 years, with an overall range of 46 to 77 months. A total of 786 children (12%) developed celiac disease autoimmunity. A total of 350 children underwent biopsy, and 291 of those were diagnosed with celiac disease. Another 21 children did not undergo biopsy, but showed persistently high levels of tTG antibodies.

    For children with a single DR3–DQ2 haplotype, rates of celiac disease autoimmunity and celiac disease by the age of 5 years were 11% and 3%, respectively. For those with two copies (DR3–DQ2 homozygosity) rates of celiac disease autoimmunity and celiac disease by the age of 5 years were 26% and 11%, respectively.

    The adjusted hazard ratios for celiac disease autoimmunity were 2.09 (95% confidence interval [CI], 1.70 to 2.56) among children with one gene, and 5.70 (95% CI, 4.66 to 6.97) among children with both genes, as compared with children who had the lowest-risk genotypes (DR4–DQ8 heterozygotes or homozygotes).

    Living in Sweden was also independently associated with an increased risk of celiac disease autoimmunity (hazard ratio, 1.90; 95% CI, 1.61 to 2.25). Children with the HLA haplotype DR3–DQ2, especially homozygotes, were found to be at high risk for celiac disease autoimmunity and celiac disease early in childhood.

    People in Sweden face a higher risk for celiac disease autoimmunity and celiac disease than residents of other countries. These finding highlight the importance of studying environmental factors associated with celiac disease.

    Source:

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  • Related Articles

    Jefferson Adams
    Celiac.com 03/13/2009 - A recent study confirms that celiac disease affects adults with Turner Syndrome at rates of up to 5%, compared to 1% for the general population.
    A team of researchers recently set out to assess rates of celiac disease in adults with Turner Syndrome. Led by doctor A. Frost of the Department of Endocrinology at University College Hospital in London, UK, the research team included doctors M. Band, G. Conway.
    The researchers enlisted 256 adults with clinically proven Turner Syndrome. Five turned out to have existing diagnosis of celiac disease. The team conducted IgA endomysium antibody (EMA) screening for celiac disease on the remaining 251 Turner Syndrome patients.  Eight patients (3.2%) showed positive EMA screens. Doctors offered those eight patients endoscopy with duodenal biopsy.
    Seven patients committed to duodenal biopsy, and all seven (2.8%) showed positive histological confirmation for celiac disease. Thus, the doctors reasonably estimate the rate of sub-clinical celiac disease to be between 2.8% and 3.2%. When the existing cases are factored in, the total population shows rates between 4.7% and 5.1%.
    The team conducted human leukocyte antigen (HLA) typing in the existing celiac disease cases and new EMA-positive cases. Ten of those 13 patients submitted to HLA typing. Eight showed positive results for HLA-DQ2, one for HLA-DQ8, while one showed negative results for both HLA-DQ2 and HLA-DQ8.
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    Jefferson Adams
    Celiac.com 01/25/20010 - Women with celiac disease face greater risks for adverse pregnancy outcomes. A team of researchers recently set out to examine the effects of treated and untreated maternal celiac disease on infant birthweight and preterm birth. Among their findings are that expectant mothers with celiac disease face a higher risk of underweight and early-term birth than those without celiac disease.
    The research team included A.S. Khashan, T.B. Henriksen, P.B. Mortensen, R. McNamee, F.P. McCarthy, M.G. Pedersen and L.C. Kenny. They are affiliated variously with the Anu Research Centre of the Department of Obstetrics and Gynecology at the University College Cork at Cork University Maternity Hospital in Ireland, the Perinatal Epidemiology Research Unit in the Department of Paediatrics at Aarhus University Hospital, the National Centre for Register-based Research at the University of Aarhus, Denmark, and the Biostatistics Group, University of Manchester, Manchester, UK.
    For their data, they used a population-based cohort study of all live births in Denmark between 1 January 1979 and 31 December 2004. During that period, 836,241 mothers gave birth to a total of 1,504,342 babies. Mothers with diagnosed celiac disease gave birth to 1105 of those babies, while 346 were born to women with undiagnosed celiac disease.
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    The good news is that mothers with treated celiac disease showed no increased risk of reduced mean birthweight, or of delivering SGA and VSGA infants or preterm birth compared with mothers with no celiac disease.
    From the results, the research team concluded that untreated maternal celiac disease increases the risk of low birthweight, SGA and VSGA, and preterm birth.
    Diagnosis and treatment of maternal celiac disease with a gluten-free diet seems to return the birthweight and preterm birth rate to one comparable to women without celiac disease.
    This study drives home the importance of expectant mothers with celiac disease maintaining a gluten-free diet to promote a healthy delivery.
    Source: Human Reproduction, doi:10.1093/humrep/dep409


    Jefferson Adams
    Celiac.com 09/20/2010 - People with celiac disease face increased risk of cancer and a large amount of circumstantial evidence suggests that oxidatively damaged DNA may be used to help predict future cancer development in celiac patients.
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    Anna Szaflarska-PopÅ‚awska, Agnieszka Siomek, MieczysÅ‚awa Czerwionka-Szaflarska, Daniel Gackowski, RafaÅ‚ Różalski, Jolanta Guz, Anna Szpila, Ewelina Zarakowska and Ryszard OliÅ„ski comprised the research team. They are associated with the college of medicine at Nicolaus Copernicus University, in Bydgoszcz, Poland.
    They found that children with celiac disease have higher than normal levels of the oxidative DNA damage biomarkers urinary 8-oxodG and 8-oxoGua, regardless of following a gluten-free diet.
    To measure urinary excretion of 8-oxodG and 8-oxoGua, and levels of oxidative DNA damage in the leukocytes, as well as the level of antioxidant vitamins, the team used high-performance liquid chromatography (HPLC) and HPLC/gas chromatography with isotope dilution mass detection.
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    From the results indicate that oxidative stress and/or oxidatively damaged DNA in celiac patients cannot be explained by diet alone, and that factors independent of diet play an important role.
    Supplemental vitamin A and E in celiac disease patients may help minimize the risk of cancer development.
    Source:

    Cancer Epidemiol Biomarkers Prev 2010; 19: 1960–1965

    Gryphon Myers
    Celiac.com 07/16/2012 - Between 1984 and 1996, Sweden experienced a celiac disease epidemic: celiac disease rates shot up to four times normal levels, then dropped just as abruptly ten years later. This is interesting because it shows that there is some environmental cause for the disease, but the nature of that cause is proving hard to pinpoint.
    One proposed candidate for the cause of Sweden's celiac disease epidemic is early life vaccinations. Given that vaccinations modulate the developing immune system, they could feasibly lead to immune-related diseases (like celiac disease ,whereby the immune reaction toward gluten proteins is changed).
    To test whether changes in Sweden's vaccination programs were responsible for the celiac disease epidemic, data pertaining to such vaccination program changes were gathered from the Swedish Council on Technology Assessment in Health Care and the Swedish Institute for Infectious Disease control. These data were plotted on a graph spanning 1973 to 2003 and compared against data on celiac disease rates as gathered by The National Swedish Childhood Celiac Disease Register. An incident case-referent study of infants was also performed.
    To be considered for the study, children were required to have been diagnosed with celiac disease through three biopsies (one for diagnosis, one on gluten-free diet and one after gluten challenge). 475 participants qualified and were diagnosed with celiac disease as infants. For each selected child, 2 referents were chosen based on date of birth, area of residence and gender. All participants and referents were given questionnaires regarding family characteristics, infant feeding and general health. Final inclusion in the study required complete vaccination records of participants and at least one referent. 1015 total infants qualified: 392 case children and 623 referents.
    The case-referent study and statistical analyses showed that changes in Swedish vaccination programs did not seem to correlate with the celiac disease epidemic. Introduction of the pertussis vaccine did coincide with a rise in celiac disease rates, however the infant case-referent study showed no association between the vaccine and celiac disease. Haemophilus influenzae type b and measles/mumps/rubella vaccines also showed no association. Diptheria/tetanus and polio vaccines covered 99% of participants, and were thus not feasible candidates. Vaccination against tuberculosis (BCG) actually showed possibility for some protective effect (further studies may explore this).
    The early vaccination programs enacted by Sweden in the past few decades do not seem to correlate with the celiac disease epidemic. However, we cannot generalize these findings too much, as not all vaccines are the same, and we still don't know what factors are in play here. The results of this study show that we are still a long way from understanding exactly what environmental factors contribute to celiac disease.
    Source:
    http://pediatrics.aappublications.org/content/130/1/e63.full

  • 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.
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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. 
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    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