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Found 7 results

  1. Celiac.com 12/31/2012 - In people with celiac disease, eating wheat, barley, or rye triggers inflammation in the small intestine. Left unchecked, this inflammation causes the gut damage that is associated with untreated celiac disease. Specifically, the storage proteins in these grains (gluten) trigger an adaptive Th1-mediated immune response in individuals carrying HLA-DQ2 or HLA-DQ8 as major genetic predisposition. Researchers actually have a pretty good understanding of this aspect of celiac disease, part of a process called adaptive immunity. However, there has been some research that suggests that gluten proteins might trigger an immune response in people who do not have celiac disease, and who do not carry the HLA-DQ2 or HLA-DQ8 genetic markers that predispose them to developing celiac disease. Such a response is part of a process called innate immunity, and is far less understood than the adaptive immunity process. The innate immune system provides an early response to many microbial and chemical stimuli and is critical for successful priming of adaptive immunity. To better understand the relationship between adaptive immunity and innate immunity in celiac disease, a research team recently set out to determine if gliadin digests might induce innate immune responses in celiac and non-celiac individuals. Specifically, they wanted to know if wheat amylase trypsin inhibitors drive intestinal inflammation, and if so, by what receptor mechanism. The research team included Yvonne Junker, Sebastian Zeissig, Seong-Jun Kim, Donatella Barisani, Herbert Wieser, Daniel A. Leffler, Victor Zevallos, Towia A. Libermann, Simon Dillon, Tobias L. Freitag, Ciaran P. Kelly, and Detlef Schuppan. They are affiliated variously with the Division of Gastroenterology and the Proteomics and Genomics Center at Beth Israel Deaconess Medical Center at Harvard Medical School in Boston, with the Department of General Pediatrics and the Department of Internal Medicine I at the University Medical Center Schleswig-Holstein Kiel in Kiel, Germany, the Department of Experimental Medicine at the University of Milano-Bicocca in Milan, Italy, the German Research Center for Food Chemistry in Garching, Germany, the Hans-Dieter-Belitz-Institute for Cereal Grain Research in Freising, Germany, the Division of Molecular and Translational Medicine in the Department of Medicine I at Johannes Gutenberg University in Mainz, Germany, and with the Department of Bacteriology and Immunology at the Haartman Institute at the University of Helsinki in Finland. A number of earlier studies (Molberg et al., 1998; Anderson et al., 2000; Shan et al., 2002) have found HLA-DQ2– and HLA-DQ8–restricted gluten peptides that trigger the adaptive immune response in people with celiac disease. However, only 2–5% of individuals who show these HLAs develop celiac disease, which means that other factors, especially innate immune activation, are at play in the generation of celiac disease. Responsive innate cells are primarily macrophages, monocytes, DCs, and polymorphonuclear leukocytes that by means of their pattern-recognition receptors, such as TLRs, trigger the release of proinflammatory cytokines and chemokines, resulting in recruitment and activation of additional inflammatory cells (Medzhitov, 2007). Earlier studies (Maiuri et al., 2003) showed that peptides p31-43 or p31-49 from α-gliadin, that lack adaptive stimulatory capacity, triggered innate immune reactions by inducing IL-15 and Cox-2 expression in patient biopsies, and MHC class I polypeptide–related sequence A (MICA) on intestinal epithelial cells (Hüe et al., 2004). However, these studies have proven difficult to reproduce in cell culture, and researchers could not identify any specific receptor responsible for the observed effects. In a subsequent study, gliadin, in cell culture, reportedly triggered increased expression of co-stimulatory molecules and the production of proinflammatory cytokines in monocytes and DCs (Nikulina et al., 2004; Cinova et al., 2007). Two other studies (Thomas et al., 2006; Lammers et al., 2008) implicated the chemokine receptor CXCR3 in increased intestinal epithelial permeability upon gliadin challenge in a MyD88-dependent manner. However, those studies failed to reproducibly identify a specific gliadin peptide as the trigger. So far, no clear picture of the role of the innate immune system in celiac disease has emerged. In this study, the researchers show that members of the non-gluten α-amylase/trypsin inhibitors (ATIs), CM3 and 0.19, pest resistance molecules in wheat and related cereals, are strong triggers of innate immune responses in human and murine macrophages, monocytes, and dendritic cells. Their results show that ATIs activate the TLR4–MD2–CD14 complex and lead to up-regulation of maturation markers and elicit release of proinflammatory cytokines in cells from celiac and nonceliac patients and in celiac patients’ biopsies. They also show that mice deficient in TLR4 or TLR4 signaling are protected from intestinal and systemic immune responses upon oral challenge with ATIs. These findings define cereal ATIs as novel contributors to celiac disease. Moreover, ATIs may fuel inflammation and immune reactions in other intestinal and nonintestinal immune disorders. The findings of this study mean that the proteins in wheat may trigger immune reactions not just in people with celiac disease, but in people without celiac disease, and that these reactions may be actively contributing to the development of numerous other intestinal and non-intestinal immune disorders. That's a pretty big deal. Stay tuned to see how future studies elaborate these findings. Read the entire study in the Journal of Experimental Medicine. Source: J Exp Med. 2012 Dec 17;209(13):2395-408. doi: 10.1084/jem.20102660
  2. Celiac.com 07/27/2015 - First-degree relatives of individuals with celiac disease are at increased risk for this disorder, but little is known about their risk for other autoimmune diseases. A research team recently set out to assess the risk of non-celiac autoimmune disease in first-degree relatives and spouses of people with celiac disease. The research team included Louise Emilsson, Cisca Wijmenga, Joseph A. Murray, and Jonas F. Ludvigsson. They are variously affiliated with the Primary Care Research Unit, Vårdcentralen Värmlands Nysäter, Värmland County, Sweden, the Department of Health Management and Health Economy, Institute of Health and Society, University of Oslo, Oslo, Norway, the Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands, the Division of Gastroenterology and Hepatology, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota, the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden, and with the Department of Pediatrics, Örebro University Hospital, Örebro, Sweden. The team found individuals with celiac disease by searching computerized duodenal and jejunal biopsies, collected from 1969 through 2008, at 28 pathology departments in Sweden. The team found 29,096 patients with celiac disease based on biopsy reports of villous atrophy of Marsh grade 3 or higher and matched individuals with celiac disease with up to 5 of 144,522 non-celiac control patients based on sex, age, county, and calendar year. Through Swedish health care registries, the team identified all first-degree relatives (fathers, mothers, siblings, and offspring) and spouses of 84,648 individuals with celiac disease, and 430,942 control subjects. The team used Cox regression analysis to calculate hazard ratios (HRs) for non-celiac autoimmune disease, such as Crohn’s disease, type 1 diabetes mellitus, hypothyroidism, hyperthyroidism, psoriasis, rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus, or ulcerative colitis, within these groups. Cox analysis showed that during the follow-up period averaging just under 11 years, nearly 3333, or 4%, of the first-degree relatives of patients with celiac disease, and 12,860 relatives of controls (3.0%), had an autoimmune disease other than celiac disease. First-degree relatives of people with celiac disease had an increased risk of non-celiac autoimmune disease, compared with controls (HR, 1.28; 95% confidence interval, 1.23–1.33), as did spouses (HR, 1.20; 95% confidence interval, 1.06–1.35). Risk estimates for non-celiac autoimmune disease did not differ between first-degree relatives and spouses of individuals with celiac disease (interaction test: P = .11). Hazard Ratios for non-celiac autoimmune disease were highest in the first 2 years of follow-up evaluation. First-degree relatives and spouses of individuals with celiac disease have a significantly higher risk of non-celiac autoimmune disease. In addition to genetic factors, environmental factors and better awareness, testing and diagnosis might influence rates of autoimmune disorders in first-degree relatives of individuals with celiac disease. Source: Clinical Gastroenterology and Hepatology. DOI: http://dx.doi.org/10.1016/j.cgh.2015.01.026
  3. Neurology 2001;56:385-388. Celiac.com 02/15/2001 - According to a new study published in the February issue of Neurology, severe, chronic migraine headaches can be triggered in gluten-sensitive individuals who do not exclude gluten from their diets. The study examined ten patients who had a long history of chronic headaches that had recently worsened, or were resistant to treatment. Some patients had additional symptoms such as lack of balance. Dr. Marios Hadjivassiliou, from the Royal Hallamshire Hospital in Sheffield, UK, and colleagues tested each patient and found that all were sensitive to gluten. . The patients were tested and each was found to be gluten-sensitive. Additionally, MRI scans determined that each had inflammation in their central nervous systems caused by gluten-sensitivity. Results: Nine out of 10 patients went on a gluten-free diet, and seven of them stopped having headaches completely. The patients heightened immune responses, which are triggered by the ingestion of gluten, could be one of the factors causing the headaches. The other two patients who were on a gluten-free diet experienced significant relief, but not complete relief. Conclusion: According to Dr. Hadjivassiliou, removal of the trigger factor by the introduction of a gluten-free diet may be a promising therapeutic intervention for patients with chronic headaches. Further studies are needed to confirm Dr. Hadjivassilious preliminary findings.
  4. Celiac.com 11/04/2013 - The mechanisms of cerebellar degeneration associated to prolonged and excessive alcohol intake remain unclear. Additional or even alternative causes of cerebellar degeneration are often overlooked in suspected cases of alcohol-related ataxia. A team of researchers recently set out to investigate the prevalence of gluten-related serological markers in patients with alcohol-related ataxia, and to compare the pattern of brain involvement on magnetic resonance imaging between patients with alcohol and gluten ataxias. The research team included Stuart Currie, Nigel Hoggard, Matthew J. R. Clark, David S. Sanders, Iain D. Wilkinson, Paul D. Griffiths, and Marios Hadjivassiliou. They are variously affiliated with the Academic Unit of Radiology at the University of Sheffield, and with the Department of Gastroenterology, and the Department of Neurology of Sheffield Teaching Hospitals NHS Foundation Trust in Sheffield, United Kingdom. For their study, the team used a retrospective review of patients attending an outside clinic to identify patients diagnosed with alcohol and gluten ataxias. The team recorded HLA genotype and serological markers of gluten-related disorders. They also conducted cerebellar volumetry, MR spectroscopy and voxel-based morphometric analyses on the patients and compared the results to matched control data. Results from 904 registered patients showed 104 patients with alcohol ataxia, and 159 patients with gluten ataxia. The data also showed that 61% of the patients with alcohol ataxia, and 70% of the patients with gluten ataxia had HLA DQ2/DQ8 genotype compared to just 30% of people with healthy local blood donors. Interestingly, 44% of patients with alcohol ataxia showed antigliadin antibodies compared to 12% in the healthy local population and 10% in patients with genetically confirmed ataxias. None of the patients with alcohol ataxia and antigliadin antibodies had celiac disease, while 40% in patients with gluten ataxia had celiac disease. Patients with alcohol ataxia who had antigliadin antibodies showed patterns of structural brain abnormality that were different from gluten ataxia, but were the same as those common in alcohol ataxia. The results show that alcohol related cerebellar degeneration can trigger gluten sensitivity in certain genetically susceptible individuals. Such sensitivity might be caused directly by the cerebellar impact of alcohol, but factors other than duration and amount of exposure to alcohol may also be responsible for the resulting sensitivity to gluten. Further study is needed to nail down the exact mechanisms at work here, but this is certainly an interesting study. Source: Currie S, Hoggard N, Clark MJR, Sanders DS, Wilkinson ID, et al. (2013) Alcohol Induces Sensitization to Gluten in Genetically Susceptible Individuals: A Case Control Study. PLoS ONE 8(10): e77638. doi:10.1371/journal.pone.0077638
  5. Celiac.com 06/11/2009 - Specialty pharmaceutical and diagnostic company, Prometheus Laboratories Inc., announced new findings regarding a correlation between an important serologic marker used in the detection of Crohn's disease and particular genetic markers in patients at risk for celiac disease. Using proprietary Prometheus technology, researchers analyzed blood and serum samples from 5,406 patients at risk for celiac disease who are EMA positive. Results showed a significant correlation between antibodies to the flagellin CBir1 and HLA haplotypes DQ2.5 and DQ8. They found that an overly aggressive immune response to particular bacteria in the intestine, as in Crohn's disease, may contribute to the inflammation seen in patients with celiac disease. Relatively few susceptible individuals "actually develop the disease, despite gluten ingestion, for reasons that are not well understood," said Dr. Michelle Pietzak, a Pediatric Gastroenterologist in the Division of Gastroenterology at the University of Southern California Keck School of Medicine. Research like this is helping us figure out the answers to those questions. Source: Prometheus Laboratories, Inc.
  6. Celiac.com 11/07/2002 - The results of a recent study conducted by researchers in Sweden indicate that the overall cancer risk of people with celiac disease or dermatitis herpetiformis is higher than that of the normal population, but lower than other studies have reported. Further, the overall risk is lower in children and higher in adults, and the risk "declined with time and eventually reached unity," presumably because most of the subjects followed a gluten-free diet. Here is the Medline abstract for the study: Gastroenterology 2002 Nov;123(5):1428-1435 Links Askling J, Linet M, Gridley G, Halstensen TS, Ekstrom K, Ekbom A. Clinical Epidemiology Unit, Department of Medicine, Karolinska Institute/Hospital, Stockholm, Sweden; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland; Institute of Oral Biology, University of Oslo, Oslo, Norway; and the Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden. BACKGROUND & AIMS: Studies of cancer risk in celiac disease (celiac disease) or dermatitis herpetiformis (DH) indicate increased risks for malignant lymphoma and occasionally other neoplasms, but are characterized by small numbers, lack of systematic cancer assessment, and subjects identified from referral institutions. METHODS: By using Swedish population-based inpatient and cancer registry data, we followed-up 12,000 subjects with celiac disease or DH, and evaluated cancer incidence by using standardized incidence ratios (SIR). RESULTS: Adults (but not children and adolescents) with celiac disease had an elevated overall risk for cancer (SIR = 1.3) that declined with time and eventually reached unity. Elevated risks were found for malignant lymphomas, small-intestinal, oropharyngeal, esophageal, large intestinal, hepatobiliary, and pancreatic carcinomas. The excess occurrence of malignant lymphomas was confined to adults, decreased with time of follow-up evaluation, and decreased over successive calendar periods. Decreased risks were found for breast cancer. Subjects with DH had a slightly increased overall cancer risk (SIR = 1.2) owing to excesses of malignant lymphoma and leukemia, but no increases of gastrointestinal carcinomas. CONCLUSIONS: Albeit increased, the relative risks for lymphomas and gastrointestinal cancers in this study are lower (and declining) than in most previous reports. The overall cancer risk is only moderately increased, and non-elevated during childhood and adolescence. PMID: 12404215 [PubMed - as supplied by publisher]
  7. Vijay Kumar, M.D., Research Associate Professor at the University of Buffalo and President and Director of IMMCO Diagnostics: If the test is negative and there is a strong suspicion of celiac disease, it must be repeated after several weeks (3-4 weeks), especially after a high gluten intake. We did a study of two cases with DH who were serologically negative. However, a gluten challenge 1g/Kg body wt/day resulted in positive serology; the results became normal on a gluten free diet. If you are a relative of a celiac disease patient and are on a regular diet and the serology performed by an experienced laboratory is negative then there may not be any need for retesting until and unless clinically justified. Karoly Horvath, M.D., Ph.D., Associate Professor of Pediatrics; Director, Peds GI & Nutrition Laboratory; University of Maryland at Baltimore: There is no rule for it. If a family member with previous negative tests experiences any gastrointestinal symptoms associated with celiac disease, he/she should undergo serological testing as soon as possible. It is well known that up to 15% of the family members of a patient with celiac disease may have the asymptomatic (latent or silent) form of celiac disease, although they have positive serological tests and have the pathological changes in the upper part of the small intestine. It is also evident that there are at least three developmental stages of mucosal lesions (Marsh MN. Gastroenterology 1992;102:330-354) and celiac disease may manifest at each period of life. That is why we recommend a repeat test every 2-3 years in first degree relatives of celiac patients.
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