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Celiac.com 01/04/2021 - Researchers have long known that the common chronic skin disorder atopic dermatitis is associated with other atopic conditions. A growing body of evidence supports a connection with non-atopic conditions, including autoimmune diseases, such as celiac disease, but data are limited with respect to autoimmune conditions. To remedy the situation, a research team recently examined the connection between atopic dermatitis and autoimmune diseases. The research team included L.U. Ivert, C.F. Wahlgren, B. Lindelöf, H. Dal, M. Bradley, and E.K. Johansson. They are variously affiliated with the Dermatology and Venereology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; the unit of Dermatology, Theme Inflammation and Infection, Karolinska University Hospital, Stockholm, Sweden; the Theme Cancer unit, Karolinska University Hospital, Stockholm, Sweden; and the Dermatological and Venereal Clinic, Södersjukhuset, Stockholm, Sweden. For their case–controlled study, the team looked at the Swedish national healthcare registers, and looked at data from the entire Swedish population, aged 15 years or younger, from 1968 to 2016. The researchers matched all atopic dermatitis cases by sex and age to healthy controls; including cases with an inpatient diagnosis of atopic dermatitis from 1968, and/or a specialist outpatient diagnosis of atopic dermatitis from 2001. In all, the team found 104,832 cases of atopic dermatitis, and matched them to 1,022,435 control subjects. Adults with multiple autoimmune diseases were more likely to develop atopic dermatitis than those with just one autoimmune disease. The associations were especially strong between atopic dermatitis and autoimmune dermatological, gastrointestinal and rheumatological diseases. The study was funded by the Swedish Asthma and Allergy Association Research Foundation, Hudfonden (The Welander‐Finsen Foundation), and The Swedish Society for Dermatology and Venereology. The authors declare no conflicts of interest. These results invite further study of the relationship between atopic dermatitis and autoimmune conditions, such as celiac disease. Read more in the British Journal of Dermatology
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Celiac.com 05/11/2011 - People with multiple sclerosis and their first-generation relatives have higher rates of celiac disease than the general population, according to a report by a research team in Spain. For the study, a research team led by Dr. Luis Rodrigo of University Hospital, Central Asturias, Spain looked at rates of serological, genetic, and histological disease markers in 72 multiple sclerosis patients and 126 of their first-degree relatives. They then compared the results against data from 123 healthy control subjects. The team found rates of celiac disease among multiple sclerosis patients that are 5 to 10 times higher than rates for the general population worldwide, which average between 1% and 2%. The team found similar levels of HLA-DQ2 markers in both multiple sclerosis patients (29%) and controls (26%) (NS). They found eight multiple sclerosis patients (11.1%) who showed mild or moderate villous atrophy (Marsh III type) on duodenal biopsy. Results also showed that 26 of 126 first-degree relatives (32%) had celiac disease. Multiple Sclerosis patients also displayed increased frequency of circulating auto-antibodies such as anti-TPO in 19 (26%), ANA in 11 (15%) and AMA in 2 (3%). Source: BMC Neurology 2011, 11:31doi:10.1186/1471-2377-11-31
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Celiac.com 10/02/2017 - For anyone following the efforts by ImmusanT to develop a vaccine for celiac disease, the company's recent presentations at the 2017 International Celiac Disease Symposium (ICDS) in New Delhi, India, were welcome news. Nexvax2® is a therapeutic vaccine intended to protect against the effects of gluten exposure while maintaining a gluten-free diet in HLA-DQ2.5+ patients with celiac disease. The company announced at ICDS 2017 that it has presented data showing the immunologic basis for the early clinical effects of gluten in celiac disease. Presented in two poster presentations and an oral presentation, the company says its data show that "early cytokine changes in blood following gluten ingestion could provide the basis for a new diagnostic for celiac disease in patients on a gluten free diet with an uncertain diagnosis," said Robert Anderson, MBChB, Ph.D., Chief Scientific Officer of ImmusanT. The company says its results are "significant" because celiac disease sufferers often adopt a gluten-free diet prior to being diagnosed by a doctor. This can cause problems and lead to unreliable or misleading results with current diagnostic tests. ImmusanT says that their data demonstrate that early changes in circulating cytokines after a single gluten exposure may offer a clinical way to assess celiac disease activity. The company says that the data, along with the potential to differentiate between celiac disease and non-celiac gluten sensitivity (NCGS) by assessing IL-2 levels, support the science behind targeted immunotherapies such as Nexvax2®. Read more at BusinessWire.com
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Multiple Sclerosis and Celiac Disease
Scott Adams posted an article in Multiple Sclerosis and Celiac Disease
The following research was compiled by Don Wiss and posted on the Celiac Listserv news group: The MS/gluten/casein connection is mostly only anecdotal as it has never really been studied. This is what I have (much contributed by Ron Hoggan): (1) Roger MacDougall was a famous British playwright, who was diagnosed with MS in the 1950s. The doctors felt it was best to keep the information from him. They thought it was in his best interests not to tell him what he had. It was not until he was bedridden that he learned what illness he had. When he knew about it, he did some reading, and went on a gluten & casein free diet. He recovered almost totally. This is from Can a Gluten-Free Diet Help? How? by Lloyd Rosenvold, M.D., [Keats Publishing, 27 Pine Street (Box 876) New Canaan, CT 06840-0876, 1992, ISBN 0-87983-538-9]. MacDougall eventually wrote a pamphlet titled My Fight Against Multiple Sclerosis, pub 1980 by Regenics Inc, Mansfield, Ohio. Rosenvold also includes some other anecdotes in his book. (2) In the Oct. 5, 1974, Lancet, Dr. Norman A. Mathesons letter Multiple Sclerosis and Diet was published on p. 831, wherein he outlined his having been diagnosed with MS and subsequently reading Roger MacDougalls story. He then described his return to good health and ended with: I thank Roger MacDougall, whose diet made it possible to carry out these observations. (3) Ashton Embry has written an article MS - probable cause and best-bet treatment in which he discusses the dietary and food allergy links to MS. (4) In Gluten Intolerance by Beatrice Trum Hunter, Keats Publishing Inc. New Canaan, CT. ISBN 0-87983435-8 She talks about a Dr. R. Shatin in Australia who has suggested that an inherited susceptibility to multiple sclerosis is from a primary lesion in the small intestine resulting from gluten intolerance, and that the demyelination is secondary. Shatin suggested that the high incidence of multiple sclerosis in Canada, Scotland and western Ireland may be related to the predominant consumption of Canadian hard wheat, which has the highest gluten content of all wheat varieties. In contrast, the incidence of multiple sclerosis is low among indigenous Equatorial Africans who mainly consume non-gluten containing grains such as millet. (5) In Multiple Sclerosis, by Jan de Vries, Mainstream Publishing, (Thorntons?) UK it recommends absolutely no gluten and very high reduction of dairy products, refined sugar, and saturated fats. He says that one of his most successful case studies, confirm that absolutely not one pinch if flour i.e. absolutely no gluten at all... otherwise you are deceiving yourself. (6) According to Dr. Joe Murray at the University of Iowa there is the possibility that the MS patient suffers from a neurological complication of undiagnosed celiac disease. About 5% of celiac patients get nerve damage that can vary from tingling and numbness in the feet to confusion, memory loss, dizziness and loss of balance, visual abnormalities. This sometimes happen in the absence of GI symptoms. (7) Lutz, W.J., The Colonization of Europe and Our Western Diseases, Medical Hypotheses, Vol. 45, pages 115-120, 1995 Dr. Lutz argues that there is a clear, inverse relationship between civilisatory diseases and the length of time the people of a given region of Europe have had to adapt to the high carbohydrate diet associated with the cultivation of cereal grains that was begun in the Near East, and spread very slowly through Europe. I quote from the first page of the article: In over thirty years of clinical practice, I have found, as published in numerous papers and several books (3, 4), that diet works well against Crohns disease, ulcerative colitis, multiple sclerosis, heart failure, acne and other problems. Don Wiss can e-mail a copy of the article text to those requesting. (8) There is a fellow named Dave Q that has recovered with a gluten-free diet and lots of supplements. He discusses this, along with other recovery stories. (9) There is supposedly a newsgroup for those interested in Natural Recovery of MS. Its alt.support.mult-sclerosis.alternatives. Ask your system administrator to add it if you cant find it. But it seems to be hard to find. (10) A page on Milk and MS is from the Carbondale Center for Macrobiotic Studies and blames dairy for the distribution of MS. Visit: http://www.macrobiotic.org/health3.html (11) The following is a list of articles in medical journals, which were published at about the time that prednisone became popular in the treatment of MS. They appear to connect MS with celiac-like intestinal morphology. Cook, Gupta, Pertschuk, Nidzgorski Multiple Sclerosis and Malabsorption Lancet; June 24, 1978, p. 1366 Fantelli, Mitsumoto & Sebek Multiple Sclerosis and Malabsorption Lancet May 13, 1978 p. 1039-1040 Davison, Humphrey, Livesedge et al. Multiple Sclerosis Research Elsevier Scientific Publishing New York, 1975 I find it curious that the connection between malabsorption and MS stopped at about the same time that prednisone and other such steroids became the treatment of choice for MS. As Im sure you know, prednisone incites the re-growth of the villi despite the ingestion of gluten, in the celiac gut. Investigators who did endoscopies on MS patients admit that they have not asked about the patients use of such drugs. (12) Some literature from the celiac view point: Drs. Cooke & Holmes in Celiac Disease 1984; Churchill Livingstone, NY say that 10% of celiacs have neuropathic symptoms. Many appear to be associated with demyelination. Fineli et. al. echo that figure in Adult celiac disease presenting as cerebellar syndrome Neurology 1980; 30: 245-249. Cooke & Holmes come right out and express some of their frustration with neurologists for ignoring the potiential for neuropathic celiac. A new school has emerged, on the heels of the following report: Hadjivassiliou, et. al. Does cryptic gluten sensitivity play a part in neurological illness? Lancet 1996; 347: 369-371 They found that 57 percent of those with neurological problems of unknown cause also had antibodies to gliadin, which is a component of gluten. Sixteen percent of them had celiac disease, a much higher level than normally found. Most of the patients with the anti-gliadin antibodies did not have other symptoms of celiac disease such as poor absorption of vitamins. (13) There is supposedly a book on MS written by a Greg Nooney, a fellow that has cured himself with a gluten-free diet. He may be in Colorado.- 37 comments
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Celiac.com 02/24/2016 - Rosacea is a common inflammatory skin condition that shares the same genetic risk location as autoimmune diseases such as type 1 diabetes mellitus (T1DM) and celiac disease. Researchers have noted a clustering of autoimmune diseases in patients with rosacea. In fact, a recent genomewide association study found 90 genetic areas associated with T1DM, celiac disease, multiple sclerosis, and/or rheumatoid arthritis, but did not address a possible association with rosacea. A team of researchers recently set out to assess any connections between rosacea and T1DM, celiac disease, multiple sclerosis, and rheumatoid arthritis, respectively. The research team included Alexander Egeberg, MD, Peter Riis Hansen, MD, PhD, DMSci, Gunnar Hilmar Gislason, MD, PhD, Jacob Pontoppidan Thyssen, MD, PhD, DMSci, National Allergy Research Center, Department of Dermato-Allergology, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark, Department of Cardiology, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark. For their study, the team conducted a population-based case-control study in which a total of 6,759 patients with rosacea were matched with 33,795 control subjects on age, sex, and calendar time. They used conditional logistic regression to calculate crude and adjusted odds ratios (ORs) with 95% confidence intervals (CIs). After adjustment for smoking and socioeconomic status, patients with rosacea had significantly increased ORs for T1DM (OR 2.59, 95% CI 1.41-4.73), celiac disease (OR 2.03, 95% CI 1.35-3.07), multiple sclerosis (OR 1.65, 95% CI 1.20-2.28), and rheumatoid arthritis (OR 2.14, 95% CI 1.82-2.52). The connection was seen most commonly in women, while for men, only the rheumatoid arthritis connection was statistically significant. As a disclaimer, the researchers point out that they were unable to distinguish between the various sub-types and severities of rosacea. However, they did find that rosacea in general is associated with T1DM, celiac disease, multiple sclerosis, and rheumatoid arthritis in women, whereas the association in men was statistically significant only for rheumatoid arthritis. Source: Journal of the American Academy of Dermatology
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Celiac.com 05/29/2015 - On Thursday, May 7, Dateline featured Tom Brokaw's journey with multiple myeloma, a serious blood malignancy that develops in bone marrow. Now an author of a recent book on gluten and health is saying that Brokaw's cancer may be linked to adverse gluten reactions. Numerous cancers, including non-Hodgkin's lymphoma, throat/esophageal, stomach/intestinal/colon, and multiple myeloma are now being connected to gluten consumption, says Anne Sarkisian, author of "Toxic Staple: How Gluten May Be Wrecking Your Health — And What You Can Do About It!!"Â Scientific research suggests that multiple myeloma may be linked to gluten, says Sarkisian, "and thousands of scientific studies from around the world link gluten to over 300 symptoms, diseases, and associated conditions."Â "Early detection of celiac disease is vital to reducing complications such as lymphoma and many other cancers and diseases. Does this mean a gluten-free lifestyle is preventative medicine? More alternative medical experts advocate this approach,"Â says Sarkisian. Could Brokaw's multiple myeloma be related to gluten? Possibly. Sarkisian's claim sounds good, and may be true, but, at the end of the day, there's just no way to know for sure. It is true that early detection of celiac disease is vital to reducing complications such as lymphoma and many other cancers and diseases, and it is also true, as Sarkisian asserts, that "More alternative medical experts advocate this approach [a gluten-free diet],"Â for many people without celiac disease. Source: http://www.webwire.com/ViewPressRel.asp?aId=197635
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Celiac.com 04/15/2011 - Celiac disease is associated with various autoimmune and neurological diseases. A team of researchers recently completed a study on the prevalence of celiac disease in a prospective series of Multiple Sclerosis (MS) patients and their first-degree relatives. The study team included Luis Rodrigo, Carlos Hernández-Lahoz, Dolores Fuentes, Noemí Alvarez, Antonio López-Vázquez, and Segundo González. They are affiliated variously with the departments of Gastroenterology, Immunology Services and Neurology at the Hospital Universitario Central de Asturias (HUCA) in Oviedo, Spain. For the study, the team analyzed the prevalence of serological, histological and genetic celiac disease markers in 72 MS patients and 126 of their first-degree relatives. They then compared their results with data from 123 healthy control subjects. The results showed 7 MS patients (10%) with positive screens for tissue IgA-anti-transglutaminase-2 antibodies, compared with just 3 positive screens for healthy controls (2.4%) (p < 0.05). OR: 5.33 (CI-95%: 1.074-26.425). The team found no difference in HLA-DQ2 markers between MS patients (29%) and controls (26%) (NS). The team found 8 MS patients (11.1%) with mild or moderate villous atrophy (Marsh III type) in duodenal biopsies. Results also showed celiac disease in 23 of 126 first-degree relatives (32%). The data showed several other associated diseases, especially dermatitis 41 (57%) and iron deficiency anemia in 28 (39%) MS patients. MS patients also showed increased frequency of circulating auto-antibodies such as anti-TPO in 19 (26%), ANA in 11 (15%) and AMA in 2 (3%). The increased prevalence of celiac disease in MS patients and in their first-degree relatives suggests that early detection and dietary treatment of celiac disease in antibody-positive MS patients is advisable. Source: BMC Neurology 2011, 11:31doi:10.1186/1471-2377-11-31
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Celiac.com 12/26/2012 - Currently, researchers have found forty separate gene sites that they associate with celiac disease. They classify all of these sies as "low-penetrance," with the exception of the high-risk genotypes in the HLA-DQA1 and HLA-DQB1 genes, which are necessary, but not sufficient to cause the disease. So far, their efforts to find more such sites have been prevented by the strong effects from the known HLA loci and the genetically complex nature of the major histocompatibility complex (MHC). A research team wanted to test the hypothesis that additional celiac disease gene sites exist within the extended major histocompatibility complex (xMHC). The research team included Richard Ahn, Yuan Chun Ding, Joseph Murray, Alessio Fasano, Peter H. R. Green, Susan L. Neuhausen, and Chad Garner. They are variously affiliated with the Department of Epidemiology, University of California Irvine, Irvine, California, the Department of Population Sciences at eh Beckman Research Institute of City of Hope in Duarte, California, the Department of Medicine and Immunology at The Mayo Clinic in Rochester, Minnesota, the Center for Celiac Research at the University of Maryland School of Medicine in Baltimore, Maryland, and the Celiac Disease Center at Columbia University in New York, New York. To follow up on the hypothesis, they looked at a collection of single nucleotide polymorphisms, frequently called SNPs (pronounced “snips”), which are the most common type of genetic variation among people. For their study, the research team analyzed a set of 1898 SNPs for association across the 7.6 Mb xMHC region in 1668 patients with confirmed celiac disease, and 517 non-celiac control subjects. The researchers used what is called conditional recursive partitioning to create a marker of known HLA-DQA1 and HLA-DQB1 high-risk genotypes that was included in the association analysis to account for their effects. After accounting for the known effects, they used a linkage disequilibrium-based grouping procedure to estimate the number of independent celiac disease loci present in the xMHC. They found strong statistical evidence for four new independent celiac disease loci within the classic MHC region. This was the first time researchers have conducted a comprehensive association analysis of the xMHC in celiac disease that specifically accounts for the known HLA disease genotypes and the genetic complexity of the region. Source: PLoS One. 2012;7(5):e36926. Epub 2012 May 17.
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Celiac.com 04/22/2011 - A research team recently set out to examine multiple independent variants in 6q21-22 associated with susceptibility to celiac disease in the Dutch, Finnish and Hungarian populations. The study team included Elisabet Einarsdottir, Marianna R Bevova, Alexandra Zhernakova, Alienke Monsuur, Lotta LE Koskinen, Ruben van't Slot, Chris Mulder, M Luisa Mearin, Ilma R Korponay-Szabo, Katri Kaukinen, Kalle Kurppa, Juha Kere, Markku Mäki, Cisca Wijmenga and Päivi Saavalainen. Studies in Dutch, Finnish and Hungarian populations have shown that a locus on chromosome 6q21-22 carries higher susceptibility to celiac disease. This same locus has previously been associated with susceptibility to other autoimmune diseases such as Crohn's disease and type 1 diabetes. The study team conducted fine mapping on 446 independent individuals with celiac disease and 641 control subjects of Dutch origin. The team tested 872 tagging single-nucleotide polymorphisms (SNPs) in a 22 Mb region of chromosome 6. To identify risk variants in this region, the team followed up on the 12 most promising SNPs in 2071 individuals from 284 Finnish and 357 Hungarian celiac disease families. Numerous markers in the region showed strong associations with celiac disease in the Dutch material. Two SNPs, rs9391227 and rs4946111, showed strong association with celiac disease in the Finnish population. The rs9391227 connection is the strongest such connection yet found in the Finnish (P=0.003, OR 0.66), as well as the combined Dutch, Finnish and Hungarian populations (P=3.6 × 10−5, OR 0.76). The rs9391227 site is located downstream from the HECT domain and ankyrin repeat containing, E3 ubiquitin protein ligase 1 (HACE1) gene and is contained within a region of strong linkage disequilibrium enclosing HACE1. A meta-analysis of the three populations showed two additional independent, susceptibility variants in the 6q21-22 region. The team confirmed the 6q21-22 region as a celiac disease susceptibility locus; one that is independently associated with a number of other conditions, and which may implicate ubiquitin-pathways in celiac disease susceptibility. Source: European Journal of Human Genetics , (16 February 2011) | doi:10.1038/ejhg.2011.2
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Celiac.com 07/16/2010 - Advances in genetic science are allowing researchers to look more deeply into the genetic causes of auto-immune diseases, including celiac disease. One recent study showed that a particular variation, called the non-synonymous (Gly307Ser) variant, rs763361, in the CD226 gene carries a higher risk for multiple autoimmune diseases in European Caucasian populations. At the conclusion of that study, though, there was still no comparable study of shared autoimmunity with CD226 in non-European populations. An international research team set out to investigate any connection between this single nucleotide polymorphism (SNP) with autoimmune diseases in non-European populations. The team included Amit K. Maiti, Xana Kim-Howard, Swapan K. Nath, Celi Sun, and Parvathi Viswanathan; Laura Guillén and Alejandra C. Cherñavsky; Xiaoxia Qian and Nan Shen; Adriana Rojas-Villarraga and Juan-Manuel Anaya; Carlos Cañas, Gabriel J. Tobón; and Koichi Matsuda They are affiliated variously with the Genetic Epidemiology Unit of the Arthritis and Immunology Research Program at the Oklahoma Medical Research Foundation in Oklahoma City, OK, USA, the Immunogenetic Laboratory of the Hospital de Clínicas José de San Martín at the Universidad de Buenos Aires in Buenos Aires, Argentina, the Shanghai Institute of Rheumatology at Renji Hospital, JiaoTong University School of Medicine in Shanghai, P.R. China, the Centre for Autoimmune Diseases Research (CREA) at the Universidad del Rosario-Corporación para Investigaciones Biológicas in Bogota, Colombia, the Rheumatology Unit of the Fundación Valle del Lili in Cali, Colombia and the Laboratory of Molecular Medicine at the Human Genome Centre of the Institute of Medical Science at the University of Tokyo, Japan. To evaluate any connection between this single nucleotide polymorphism (SNP) with autoimmune diseases in non-European populations, the team compared case–control association between rs763361 and celiac disease (CED) samples from Argentina; SLE, RA, type-1 diabetes (T1D) and primary SS (pSS) from Colombia; and SLE samples from China and Japan. They then genotyped rs763361 and used 2-test to evaluate its genetic association with multiple auto-immune disorders. For each association, the team calculated odds ratio (OR) and 95% CI. Their results show clearly that rs763361 shares a significant association with celiac disease in Argentina (P = 0.0009, OR = 1.60). They also noted indications of possible association with Chinese SLE (P = 0.01, OR = 1.19), RA (P = 0.047, OR = 1.25), SLE (P = 0.0899, OR = 1.24) and pSS (P = 0.09, OR = 1.33) in Colombians. The team then conducted meta-analyses for SLE, using their three populations, and T1D, using their population together with three published populations. Those analyses showed a significant association with rs763361, P = 0.009 (OR = 1.16) and P = 1.1.46 x 10–9 (OR = 1.14), respectively. The team's results show clearly that the coding variation rs763361 in the CD226 gene is associated with multiple auto-immune disorders in non-European populations. Taken together, these studies show that the non-synonymous (Gly307Ser) variant, rs763361, in the CD226 gene carries a higher risk for multiple autoimmune diseases in both European Caucasian and non-European populations. Source: Rheumatology 2010 49(7):1239-1244; doi:10.1093/rheumatology/kep470
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Celiac.com 03/11/2010 - As part of an effort to investigate the possibility of multiple common variants for celiac disease influencing immune gene expression, a team of more than sixty scientists recently worked together to conduct a second-generation genome-wide association study (GWAS) of 4,533 individuals with clinically proven celiac disease, along with 10,750 control subjects. They genotyped a total of 113 selected SNPs with PGWAS < 10−4 and 18 SNPs from 14 known loci in another 4,918 confirmed celiac disease patients and 5,684 control subjects. The research team included dozens of scientists associated with a variety of major research institutions, hospitals and clinics. The GWAS included five European sample collections of celiac disease and control cases, including the celiac disease dataset reported previously. The team's stringent data quality control measures included calling genotypes using a custom algorithm on both large sample sets and, where possible, cases and controls together. The team tested 292,387 non-HLA SNPs from the Illumina Hap300 marker pool for association in 4,533 individuals with celiac disease and 10,750 control subjects of European descent. They also tested another 231,362 additional non-HLA markers from the Illumina Hap550 marker set for association in a subset of 3,796 individuals with celiac disease and 8,154 controls. All markers came from autosomes or the X chromosome. For both datasets, Genotype call rates were >99.9%. The study showed over-dispersion factor of association test statistics comparable to that observed in other GWASs of this sample size. Factoring in missing genotypes for 737 cases with celiac disease genotyped on the Hap300 BeadChip and corresponding controls did not change the findings in any meaningful way.Variants from 13 new regions reached genome-wide significance (Pcombined < 5 × 10−8); most contain geneswith immune functions, such as BACH2, CCR4, CD80, CIITA-SOCS1-CLEC16A, ICOSLG and ZMIZ1, while ETS1, RUNX3, THEMIS and TNFRSF14 play key roles in thymic T-cell selection. The data suggested associations for 13 additional regions. Expression quantitative trait meta-analysis of 1,469 whole blood samples showed that 52.6% of tested loci (20 of 38 loci) had celiac risk variants corresponding with cis gene expression (P < 0.0028, FDR 5%). Source: Nature Genetics (28 February 2010) | doi:10.1038/ng.543
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Celiac.com 07/01/2009 - Immunity to food allergens such as gliadin, or the proteins in cow's milk is central to prevention of certain diseases via an appropriate restriction diet. Detecting heightened levels immune reactions to antigen(s) in food is important because scientists have credible reports of certain health disturbances, such as celiac disease, and some pre-malignant conditions, such as monoclonal gammopathy of undetermined significance (MGUS), disappearing under a regimen of appropriate food restriction diets. Only a small number of genetically predisposed individuals show a toxic small bowel mucosa reaction to gliadin. Since levels of immunogenic gliadin may vary between different wheat species, a team of researchers first set out to assess immunogenic gliadin levels in ten bread wheat types and in three strains of commercially grown durum wheat. The team was made up of Aleksandra Konic-Ristic, Dejan Dodig, Radmilo Krstic, Svetislav Jelic, Ivan Stankovic, Aleksandra Ninkovic, Jelena Radic, Irina Besu, Branka Bonaci-Nikolic, Njegica Jojic, Milica Djordjevic, Dragan Popovic, and Zorica Juranic. They were spurred by previous studies that showed sera of some of multiple myeloma (MM) patients with elevated levels of anti-gliadin IgA, without enhanced levels of anti-gliadin IgG antibodies, as determined by commercial ELISA test. They designed their own specifically to uncover any hidden anti-gliadin IgG immunoreactivity in patient blood samples. For this reason, researchers tested blood of both MM patients and celiac disease patient for immunoreaction with native gliadin isolated from regional wheat species used for bread and pasta making. The team isolated gliadin from wheat flour by two step 60% ehanolic extraction. They determined gliadin levels by commercial R5 Mendez Elisa using PWG gliadin as the standard. Results showed immunogenic gliadin content varies between 50.4 and 65.4 mg/g in bread wheat samples and between 20 and 25.6 mg/g in durum wheat samples. Anti-gliadin IgA and IgG immunoreactivity of patients'sera in (IU/ml) was first measured by commercial diagnostic Binding Site ELISA test, and then additionally by non-commercial ELISA tests, using standardized ethanol wheat extracts -gliadin as the antigen. In both patient groups, IgA immunoreactivity to gliadin from different samples was almost homogenous and in correlation with results from commercial test, except for one IgA(lambda) myeloma patient. However, results for IgG immunoreactivity were less homogeneous. Results showed different immunogenic gliadin epitope levels in various species of wheat. They also point to a need for developing a new standard antigen, a representative mixture of gliadin isolated from local wheat species used for bread production in corresponding geographic region for ELISA diagnostic tests. Source: BMC Immunology 2009, 10:32
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