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Celiac.com 03/01/2010 - Common autoimmune disorders often coexist in the same subjects, and to cluster in families. A research team recently set out to quantify the risk of diagnosis of coexisting autoimmune diseases in more than 3000 index cases with clinically proven Graves' disease or Hashimoto's thyroiditis. The research team included Kristien Boelaert, PhD, Paul R. Newbya, Matthew J. Simmonds, PhD, Roger L. Holder, Jacqueline D. Carr-Smith, Joanne M. Heward, PhD, Nilusha Manjia, Amit Allahabadia, MD, Mary Armitage, DM, Krishna V. Chatterjee, PhD, John H. Lazarus, MD, Simon H. Pearce, PhD, Bijay Vaidya, PhD, Stephen C. Gough, PhD, and Jayne A. Franklyn, PhD. To establish the prevalence of coexisting autoimmune disorders, the team conducted a cross-sectional multi-center study of 3286 Caucasian subjects from UK hospital thyroid clinics. 2791 of those had Graves' disease, 495 had Hashimoto's thyroiditis. The team used a comprehensive questionnaire to obtain complete personal and parental history for each subject, including information on common autoimmune disorders, and parental history of hyperthyroidism or hypothyroidism. The frequency of other autoimmune disorders was 9.67% for patients with Graves' disease and 14.3% for those with Hashimoto's thyroiditis index cases (P=.005). Rheumatoid arthritis was the most common coexisting autoimmune disorder, striking 3.15% of patients with Graves' disease, and 4.24% of Hashimoto's thyroiditis cases. However, both conditions carried substantially higher relative risks for nearly all other autoimmune diseases (>10 for pernicious anemia, systemic lupus erythematosus, Addison's disease, celiac disease, and vitiligo). Cases of Graves' disease showed relative “clustering” among index subjects with parental hyperthyroidism, while cases of Hashimoto's thyroiditis showed relative “clustering” among index subjects with parental hypothyroidism. Relative risks for most other coexisting autoimmune disorders were markedly increased among parents of index cases. This study is one of the largest so far to quantify the risk of diagnosis of coexisting autoimmune diseases among more than 3000 index cases with clinically proven Graves' disease or Hashimoto's thyroiditis. These results emphasize the the importance of screening for other autoimmune diagnoses when patients with autoimmune thyroid disease show new or nonspecific symptoms. Source: Am. J. Med. Volume 123, Issue 2, Pages 183.e1-183.e9 (February 2010)
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Celiac.com 08/30/2012 - Rates of Open Original Shared Link, and not just in the United States, with diseases like type 1 diabetes, celiac disease and lupus being diagnosed in increasingly higher numbers. Rates of type 1 diabetes, for example, rose 23%, from 2001 to 2009, according to the American Diabetes Association, with a similar increase reported in Finland. Epidemiologists in Norway have been arguing that the rising rates are are the result of a genuine "biological change of the disease," not the result of better diagnostics. They are concerned about higher rates of autoimmunity in urban areas compared to their rural counterparts. Swedish and German researchers concur that Open Original Shared Link. Meanwhile, celiac disease also seems to be on the rise in the United States, with recent population-based data suggest a sharp increase in rates over the last several decades. As science has helped eliminate worms from our bodies, once a common intestinal parasite, the incidence of inflammatory bowel disease (IBD) has gone from 1 in 10,000 people to one in 200. Open Original Shared Link. According to a new study published in the journal Arthritis & Rheumatism, there was a Open Original Shared Link over the period from 1995 to 2006. Of those with the condition, half were African American. In fact, blacks suffer end-stage renal disease at rates six to seven times greater than whites. Dr. Frederick Miller of the National Institute of Environmental Health Sciences agrees with Ladd. He also believes that the surge in autoimmune disease diagnosis likely has an environmental component. So, what does all this mean? At the moment, there is no clear answer. Numerous researchers are busy studying the more than 80 different types of autoimmune disease, and struggling to find causes and develop treatments. According to Dr. Miller, research offers the best way to fight rising rates of autoimmune disease, by helping to understand the genetic and environmental risk factors. This will help doctors spot those at risk for developing any given disease after certain environmental exposures, and perhaps to minimize those exposures and prevent the disease from developing in the first place. In the mean time, people with celiac disease and other autoimmune conditions can only continue their own treatments, and perhaps find some small solace in knowing that they are not alone, and that science is working to provide answers. Source: Open Original Shared Link
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Celiac Disease, Autoimmune Diseases and Exposure to Gluten
Scott Adams posted an article in Latest Research
Scand J Gastroenterol. 2005 Apr;40(4):437-43. Celiac.com 07/28/2005 - In an effort to determine whether gluten exposure in those with celiac disease can cause additional autoimmune diseases, Finnish researchers evaluated the frequency of autoimmune disorders in 703 adults and children with celiac disease, and compared them with 299 controls (normal duodenal histology). For each person in the study the researchers assessed the effect of age at the end of follow-up, age at diagnosis; actual gluten exposure time; and the gender and diagnostic delay time. They then determined autoimmune disease incidence figures that were expressed as a dependent variable via logistic regression analysis (per 10,000 person-years). The researchers found that the celiac disease group had a significantly higher prevalence of additional autoimmune diseases that was not affected by exposure to gluten. Additional Comments on this Study by Roy Jamron: Autoimmune disease has a high prevalence in celiacs. The following study concludes that the duration of gluten exposure in celiacs is not a significant factor in the risk of developing autoimmune disease. One diagnosed late in life with celiac disease does not appear to be at greater risk for developing autoimmune disease. This seems counter-intuitive, but there may be a good explanation for this result. Studies in the UK and Italy have demonstrated that the prevalence of celiac disease in young children is essentially the same as in adults, meaning celiac disease begins in infancy. Infancy is the critical time period for the development of the immune system. Gluten exposure and the onset of celiac disease symptoms early in life, therefore, have a much greater and more important impact on the immune system and its development than exposure to gluten later in life. Malabsorption during infancy and early childhood can also adversely affect the crucial function of the thymus, T cell production, and T cell repertoire. So the stage is set early in life rather than later for increased risk of autoimmune disease. The timing of gluten exposure in life seems to be more critical to autoimmune disease risk rather than the overall lifetime duration of gluten exposure. It is, therefore, extremely important to diagnose celiac disease and initiate a gluten-free diet as soon as possible during infancy and young childhood to lower the risk of autoimmune disease later in life.- 1 comment
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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 02/10/2010 - A team of researchers recently set out to determine whether patients with autoimmune thyroid disease risk developing secondary autoimmune disorders, and whether such diseases tend to cluster in families. The research team included Kristien Boelaert, PhD, Paul R. Newbya, Matthew J. Simmonds, PhD, Roger L. Holderb, Jacqueline D. Carr-Smitha, Joanne M. Heward, PhD, Nilusha Manjia, Amit Allahabadia, MD, Mary Armitage, DM, Krishna V. Chatterjee, PhD, John H. Lazarus, MD, Simon H. Pearce, PhD, Bijay Vaidya, PhD, Stephen C. Gough, PhD, Jayne A. Franklyn, PhD. To properly assess the prevalence of coexisting autoimmune disorders, the team conducted a cross-sectional multi-center study of 3286 Caucasian patients at UK hospital thyroid clinics. 2791 of the patients had Graves' disease, while 495 had Hashimoto's thyroiditis. Patients completed a comprehensive questionnaire detailing personal and parental history of common autoimmune disorders, along with a history of hyperthyroidism or hypothyroidism among parents. The frequency of developing another autoimmune disorder was 9.67% in Graves' disease and 14.3% in Hashimoto's thyroiditis index cases (P=.005). Rheumatoid arthritis was the most common coexisting autoimmune disorder, striking 3.15% of those with Graves' disease and 4.24% of those with Hashimoto's thyroiditis. Relative risks of almost all other autoimmune diseases in Graves' disease or Hashimoto's thyroiditis were significantly increased (>10 for pernicious anemia, systemic lupus erythematosus, Addison's disease, celiac disease, and vitiligo). Results showed relative “clustering” of Graves' disease, and of Hashimoto's thyroiditis, among patients whose parents had hyperthyroidism. Moreover, most other coexisting autoimmune disorders showed markedly increased relative risks for patients with parental history of such disorders. This effort to quantify the risk of diagnosis of coexisting autoimmune diseases in more than 3000 index cases with well-characterized Graves' disease or Hashimoto's thyroiditis represents one of the most comprehensive studies yet completed. The elevated risks for developing multiple conditions emphasizes the importance of screening for other autoimmune diagnoses in subjects with autoimmune thyroid disease who present new or nonspecific symptoms. Source: American Journal of Medicine - Volume 123, Issue 2, Pages 183.e1-183.e9 - February 2010
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Celiac.com 02/26/2010 - Data increasingly supports an association between rs6822844 at the IL2-IL21 region and multiple autoimmune diseases in individuals of European descent. A number of autoimmune diseases share susceptibility genes, pointing to similar molecular mechanisms. A team of researchers recently set out to assess evidence for a general susceptibility locus by looking for association between rs6822844 at the Il2-Il21 region and numerous autoimmune diseases. The research team included Amit K. Maiti, Xana Kim-Howard, Parvathi Viswanathan, Laura Guillén, Adriana Rojas-Villarraga, Harshal Deshmukh, Haner Direskeneli, Güher Saruhan-Direskeneli, Carlos Cañas, Gabriel J. Tobön, Amr H. Sawalha, Alejandra C. Cherñavsky, Juan-Manuel Anaya, and Swapan K. Nath Their joint effort was underwritten by grants from the National Institutes of Health (NIH - Grant Number: 5R01-AI-063622, P20-RR-020143), Colciencias (Grant Number: 2213-04-16484), Rosario University School of Medicine, and the Colombian Association of Rheumatology. The goal of the study was to replicate the association between rs6822844 and 6 different immune-mediated diseases in non-European populations, and to conduct disease-specific and overall meta-analyses using data from previously published studies. The team evaluated case-control associations between rs6822844 and celiac disease in subjects from Argentina; rheumatoid arthritis, type 1 diabetes mellitus, primary Sjögren's syndrome, and systemic lupus erythematosus in subjects from Colombia; and Behçet's disease in subjects from Turkey. They compared allele and gene distribution between cases and controls. They conducted meta-analyses using data from the present study and previous studies. The team found significant associations of rs6822844 with systemic lupus erythematosus (P = 0.008), type 1 diabetes mellitus (P = 0.014), rheumatoid arthritis (P = 0.019), and primary Sjögren's syndrome (P = 0.033) but not with Behçet's disease (P = 0.34) or celiac disease (P = 0.98). Cases and controls from Argentina and Colombia showed little evidence of population differentiation (FST = 0.01), which suggests that association was not influenced by population substructure. Disease-specific meta-analysis shows strong association for rheumatoid arthritis (Pmeta = 3.61 × 10-6), inflammatory bowel disease (IBD; Crohn's disease and ulcerative colitis) (Pmeta = 3.48 × 10-12), type 1 diabetes mellitus (Pmeta = 5.33 × 10-5), and celiac disease (Pmeta = 5.30 × 10-3). Total meta-analysis across all autoimmune diseases supports association with rs6822844 (23 data sets; Pmeta = 2.61 × 10-25, odds ratio 0.73, with 95% confidence interval 0.69-0.78). The team concludes that an association exists between rs6822844 and multiple autoimmune diseases in non-European populations. Meta-analysis provides strong confirmation for strong association across multiple autoimmune diseases in populations of both European and non-European ancestry. Arthritis & Rheumatism; Volume 62 Issue 2, Pages 323 - 329 http://www3.interscience.wiley.com/journal/123266977/abstract?CRETRY=1&SRETRY=0
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GWAS Meta-Analysis Supports Existence of Autoimmune Clusters
Jefferson Adams posted an article in Latest Research
Celiac.com 01/27/2010 - New research indicates that the same genetic variants that make a person more susceptible for developing one set of autoimmune diseases may actually make them less susceptible to others. A Stanford University research team collaborated with a California hospital and clinical center to perform meta-analysis of genome-wide association studies on half a dozen autoimmune conditions, including type 1 diabetes and rheumatoid arthritis. The team uncovered a pattern in the grouping of specific diseases based on SNP data, with certain variables that increased risk for developing some conditions while protecting against others. SNPs are short for "single nucleotide polymorphisms — pronounced "snips." They are DNA sequence variations that occur when a single nucleotide (A,T,C,or G) in the genome sequence is altered The SNP data led the team to suggest that there may be benefits in classifying autoimmune diseases according to shared genetic factors rather than considering them a single group. "Maybe we should stop considering all autoimmune diseases in one lumped category," senior author Atul Butte, a pediatric and bioinformatics researcher at Stanford University and director of the Lucile Packard Children's Hospital's Center for Pediatric Bioinformatics, says in a statement. "It looks as if there may be at least two different kinds." The team points out that all autoimmune diseases share common disease mechanisms, but that certain autoimmune diseases share more such mechanisms than do others. Past research suggests that individuals with type 1 diabetes face greater risk of developing autoimmune diseases such as autoimmune thyroid disease, multiple sclerosis, and celiac disease. And, they added, at least one SNP has been discovered to have opposing effects under varying autoimmune conditions: the G allele of that SNP, called rs2076530, is more common in individuals with type 1 diabetes or rheumatoid arthritis whereas those with systematic lupus erythematosus typically show the A allele. Given the strong connection between celiac disease, diabetes and other auto-immune conditions, the data seem intriguing. These discoveries led Butte and his colleagues to speculate about the way in which genetic factors relate to autoimmune disease clusters. The team used meta-analysis to assess 573 SNPs in several GWAS of six autoimmune diseases — type 1 diabetes, rheumatoid arthritis, Crohn's disease, multiple sclerosis, autoimmune thyroid disease, and ankylosing spondylitis — and five non-autoimmune diseases. By looking closely at alleles associated with each disease and determining the strength of these associations, the team crafted a so-called "genetic variation score" to evaluate connections between certain alleles and diseases across multiple genotyping platforms. The team evaluated nearly 600 SNPs. They found nine SNPs in which one allele appears to raise individual risk for multiple sclerosis and autoimmune thyroid disease, while lowering the risk for rheumatoid arthritis and ankylosing spondylitis. The alternative alleles for these SNPs, meanwhile, showed the opposite effect. "What was surprising was our finding that at nine locations generally associated with autoimmunity risk, where a particular chemical unit conferred a heightened risk of certain autoimmune diseases, but reduced risk of getting certain others," noted lead author Marina Sirota, who serves in a graduate capacity in Butte's Stanford University lab. Based on their findings, the research team proposes at least two distinct groups of autoimmune diseases: one containing rheumatoid arthritis and ankylosing spondylitis and another containing multiple sclerosis and autoimmune thyroid disease. In the mean time, the team observed, type 1 diabetes appeared to have similarities with both of groups; having some characteristics of autoimmune thyroid disease, but not of multiple sclerosis. Crohn's disease, in contrast, showed no such cluster with either group. The results will likely help pave the way for a more complete understanding of the biological pathways at play in these autoimmune diseases. They may also give researchers a better sense of how to apply existing therapies, and even how to create new ones. "Several of these nine interesting SNPs we've found are located in or near genes that code for molecules found on cell surfaces," Butte said, "which makes them potentially easier targets for the drugs pharmaceutical researchers are best at producing." The team expects the number and nature of SNPs involved will likely grow as more autoimmune disease GWAS reveal new genetic variants associated with these and other diseases. "As more genomic information becomes available on increasingly advanced platforms, this sort of analysis can be done on more diseases, possibly hundreds of them," Sirota noted. Source: GenomeWeb News- 1 comment
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Celiac.com 09/17/2009 - Just after the turn of this century, researchers at the University of Maryland School of Medicine discovered that a mysterious human protein called zonulin played a key role in celiac disease and other autoimmune disorders, such as multiple sclerosis and diabetes. The situation might be likened to sailors who've an island, but not explored it. Researchers knew Zonulin existed, and some of its influences, but little else about it. Recently, a team of scientists led by Alessio Fasano, M.D., set out to isolate and decode zonulin. Their results are in, and Fasano's research team has successfully identified zonulin as a molecule called haptoglobin 2 precursor. Understanding the exact biochemistry of zonulin, the exact make-up of the protein molecule, is crucial to a comprehensive study of zonulin and its relationship to numerous inflammatory disorders. Dr. Fasano is a professor of pediatrics, medicine and physiology and director of the Mucosal Biology Research Center and the Center for Celiac Research at the University of Maryland School of Medicine. Haptoglobin is a molecule that has been known to scientists for many years. It was identified as a marker of inflammation in the body. Haptoglobin 1 is the original form of the haptoglobin molecule, and scientists believe it evolved 800 million years ago. Haptoglobin 2 is a version found only in humans. Scientists believe the mutation occurred in India about 2 million years ago, spreading gradually among increasing numbers of people throughout the world. Dr. Fasano's study showed that zonulin is the precursor molecule for haptoglobin 2 — that is, it is an immature molecule that develops into haptoglobin 2. Scientists previously believed that such precursor molecules played no role in the body other than to develop into the molecules they were destined to become. But Dr. Fasano's study reveals precursor haptoglobin 2 as the first precursor molecule to serve another function altogether; that of opening a gateway in the gut, permitting gluten to pass through. People with celiac disease suffer from a sensitivity to gluten. "While apes, monkeys and chimpanzees do not have haptoglobin 2, 80 percent of human beings have it," says Dr. Fasano. "Apes, monkeys and chimpanzees rarely develop autoimmune disorders. Human beings suffer from more than 70 different kinds of such conditions. We believe the presence of this pre-haptoglobin 2 is responsible for this difference between species." According to Dr. Fasano, the haptoglobin 2 molecule "could be a critical missing piece of the puzzle to lead to a treatment for celiac disease, other autoimmune disorders and allergies and even cancer, all of which are related to an exaggerated production of zonulin/pre-haptoglobin 2 and to the loss of the protective barrier of cells lining the gut and other areas of the body, like the blood brain barrier." "The only current treatment for celiac disease is cutting gluten from the diet, but we have confidence Dr. Fasano's work will someday bring further relief to these patients. Zonulin, with its functions in health and disease as outlined in Dr. Fasano's paper, could be the molecule of the century," says E. Albert Reece, M.D., Ph.D., M.B.A., dean of the School of Medicine, vice president for medical affairs of the University of Maryland and John Z. and Akiko K. Bowers Distinguished Professor. Dr. Fasano published his findings in the online version of the Proceedings of the National Academy of Sciences, appearing the week of September 7, 2009.
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AUTHORS: Cuoco L; Certo M; Jorizzo RA; De Vitis I; Tursi A; Papa A; De Marinis L; Fedeli P; Fedeli G; Gasbarrini G AUTHOR AFFILIATION: Department of Internal Medicine, Catholic University S.C., Rome, Italy. SOURCE: Ital J Gastroenterol Hepatol 1999 May;31(4):283-7 [MEDLINE record in process] CITATION IDS: PMID: 10425571 UI: 99354303 ABSTRACT: BACKGROUND AND AIMS - Celiac disease is associated with several autoimmune disorders such as insulin-dependent diabetes, Sjogrens syndrome, Addisons disease and thyroid diseases. The aim of our study was to evaluate the prevalence of celiac disease in patients affected by autoimmune thyroid diseases by means of anti-gliadin and anti-endomysial antibodies. PATIENTS: We studied 92 patients affected by autoimmune thyroid diseases (47 chronic autoimmune thyroiditis, 22 Hashimotos thyroiditis and 23 Graves disease). Ninety patients with non autoimmune thyroid disorders (51 multifollicular goitre, 28 solitary nodule and 11 papillary carcinoma) and 236 blood donors also took part in the study as control groups. METHODS: Total serum IgA were measured in all subjects to exclude selective IgA deficiency; then we measured anti-gliadin antibodies and anti-endomysial antibodies. In patients with anti-gliadin/anti-endomysial antibody positivity and/or with haematinic and laboratory signs of malabsorption we carried out gastrointestinal endoscopy with duodenal histological examination. RESULTS: Among the 92 patients with autoimmune thyroid disease, 4 (4.3%) showed anti-gliadin and anti-endomysial positivity and had celiac disease; among the 90 patients with non autoimmune thyroid diseases, 1 (1.1%) had celiac disease; finally, among the blood donors, 1 subject (0.4%) was anti-gliadin-anti-endomysium antibody positive and had celiac disease. Those subjects presenting with only anti-gliadin antibody positivity did not have celiac disease. CONCLUSIONS: These results show that the prevalence of celiac disease in patients with autoimmune thyroid diseases is significantly increased when compared with the general population (p = 0.009) but not with patients affected by non autoimmune thyroid disorders (p = 0.18). We suggest a serological screening for celiac disease in all patients with autoimmune thyroid disease measuring anti-endomysial antibodies, considering that early detection and treatment of celiac disease are effective in preventing its complications.
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Celiac.com 09/16/2008 - A team of researchers recently set out to examine the connection between celiac disease and primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune hepatitis. The research team was made up of Alberto Rubio-Tapia, Ahmad S. Abdulkarim, Patricia K. Krause, S. Breanndan Moore, Joseph A. Murray, and Russell H. Wiesner. The team measured the rates of occurrence for tissue transglutaminase antibodies (tTGAs) and endomysial antibodies (EMAs) in end-stage autoimmune liver disease (ESALD). They then correlated autoantibodies and the human leucocyte antigen (HLA) haplotype. Finally, they assessed the effect of liver transplantation on antibody kinetics. The team tested tTGA levels on blood samples from 488 prior to transplant. 310 of these had ESALD, and 178 had non-autoimmune disease. The team tested positive samples for EMAs, and retested at 6-12 and =24 months after transplant. They then correlated their results with the HLA type of the recipient. The results showed that 3% of ESALD patients showed evidence of celiac disease compared to 0.6% of those with non-autoimmune disease. This represents a five-fold greater risk for those with ESALD. The prevalence of tTGAs was 14.2 for ESALD patients compared to 5.4% for those with non-autoimmune disease (P = 0.0001). The prevalence of EMAs was 4.3 for ESALD patients compared to 0.78% for those with non-autoimmune disease (P = 0.01)—significantly higher for those with HLA-DQ2 or HLA-DQ8 haplotypes. After transplant, tTGAs and EMAs normalized in 94% and 100%, respectively, without gluten elimination. Also, three out of five patients with classical symptoms of celiac disease improved. The research team found two cases of intestinal lymphoma in two cases that showed no clinical signs of celiac disease. Patients with ESALD, particularly those with HLA-DQ2 or HLA-DQ8 gene haplotypes, showed greater occurrances of celiac disease-associated antibodies. Following liver transplants, both tTGA and EMA levels decreased without gluten withdrawal. The team also concluded that symptoms of celiac disease might be improved through immune suppression, but those improvements may not prevent the disease from progressing to intestinal lymphoma. The study doesn’t tell what effect, if any, early detection and treatment of celiac disease might have on rates of ESALD. It would be helpful to know if celiac disease contributes to liver disease, if liver disease contributes to celiac disease, or if some third connection links the two. Until then, we’ll just have to keep a tight eye on developments concerning celiac disease and liver disease. Liver Int. 2008; 28(4): 467-476.
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Celiac.com 06/19/08 - Today in most modern countries, children are being raised in bacteria-free environments, yet studies are seeing a rising incidence of autoimmune disease and allergies. Previous studies have found that Finnish children are six times more likely to have type 1 diabetes and a five times higher rate of celiac disease than Russian children despite equal genetic susceptibility. Over-cleanliness and life-style may be promoting the higher prevalence of these disorders. The Diabimmune study, backed by the EU with EUR 6 million in financing, is asking whether by removing all bacteria, we are not actually weakening our children's immune systems. Led by the University of Helsinki, researchers from 5 European countries will collaborate on Diabimmune, a study involving some 7000 children which will last from 2008-2013. The study will focus on the development of the intestinal bacterial flora after birth, the effect that the living environment has on the composition of the bacterial flora, the effect infections have on the maturation of the human immune system, and the operation of the white blood cells that regulate immune responses. In addition, the researchers will examine whether the protection conferred by infections against autoimmune and allergic responses is associated with the overall infection load or due to specific microbes. It is expected that the results will provide much needed insight into celiac disease, other autoimmune disorders, and allergies. For the first time, researchers will comprehensively monitor the composition of microbes populating the intestines of developing infants and study how the microbes may influence the development of allergies and autoimmune disease, including celiac disease. Finally, conclusive evidence may be found which may answer the question of whether gut bacteria is involved the pathogenesis of celiac disease. Are immune systems becoming lazy? European Research Headlines 18 June 2008 http://ec.europa.eu/research/headlines/news/article_08_06_18_en.html Researchers from five countries to test hygiene hypothesis with EU funding University of Helsinki 29 May 2008 http://www.med.helsinki.fi/english/news/20080529_DIABIMMUNE.htm
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Eur J Gastroenterol Hepatol. 2002 Apr;14(4):425-7. Related Articles, Links Celiac.com 07/30/2004 - The following abstract of a study that was done in 2002 emphasizes the importance of vitamin supplementation in the treatment of many celiacs: Dickey W. - Department of Gastroenterology, Altnagelvin Hospital, Londonderry BT47 6SB, Northern Ireland. OBJECTIVE: Although coeliac disease is a disorder of the proximal small bowel, associated vitamin B12 deficiency has been reported. This study aimed to assess the prevalence of B12 deficiency in a large series of coeliac patients, and to exclude the possibility that it is due to associated autoimmune gastritis. DESIGN: Prospective routine measurement of serum B12 in coeliac patients, with investigations for pernicious anaemia/autoimmune gastritis in B12-deficient patients. SETTING: Gastroenterology department of a large district general hospital. INTERVENTIONS: If they were not taking vitamin B12 supplements already, patients had serum B12 measured before starting dietary gluten exclusion. Those with low levels also had gastric biopsies taken and plasma gastrin and serum gastric parietal cell and intrinsic factor antibodies measured. MAIN OUTCOME MEASURES: Prevalence of low serum B12, and presence or absence of indicators of pernicious anaemia/autoimmune gastritis in patients with low serum B12. RESULTS: Of 159 patients, 13 had low serum B12 at diagnosis. A further six had been receiving B12 replacement therapy for 3-37 years before diagnosis, giving an overall prevalence of 12% (19 patients). Only 2/19 patients had gastric corpus atrophy, one with intrinsic factor antibodies and the other with hypergastrinaemia. There was no relationship between low B12 and clinical characteristics. CONCLUSIONS: Low B12 is common in coeliac disease without concurrent pernicious anaemia, and may be a presenting manifestation. B12 status should be known before folic acid replacement is started.
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Dig Dis Sci 2000;45:403-406. (Celiac.com 04/10/2000) Italian researcher Dr. Tarcisio Not, of Clinica Pediatrica, I.R.C.C.S., Trieste, and colleagues, have concluded that a relatively high percentage of patients with autoimmune thyroiditis also have celiac disease. They studied 172 patients who had autoimmune thyroid disorders, and two control groups. Their control groups were comprised of 498 patients with other diseases, and 4,000 healthy patients. The method used by the researchers was a blood test that looks for IgA-class endomysium antibodies using immunofluorescence. Their results, which were published in the February issue of Digestive Diseases and Sciences, show that the prevalence of celiac disease is 3.4% in patients with autoimmune thyroiditis, compared with 0.6% and 0.25% among the two control groups. They also found a connection between untreated celiac disease, gluten consumption, and autoimmune disorders. The researchers believe that undiagnosed celiac disease can cause other disorders by switching on some as yet unknown immunological mechanism. Untreated celiac patients produce organ-specific autoantibodies. Further, By following these subjects longitudinally, it has been seen that not only do the anti-gliadin antibodies and anti-endomysium antibodies disappear after 3 to 6 months of a gluten-free diet, but so do the organ-specific autoantibodies. In conclusion the Italian researchers suggest that patients with autoimmune thyroiditis could benefit from a screening for celiac disease, which could eliminate the symptoms and limit the risk of developing other autoimmune disorders.
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