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Found 93 results

  1. Celiac.com 12/29/2010 - A team of researchers recently conducted a prospective study the etiology of lymphocytic duodenosis. Among their findings are that sixteen percent of patients with lymphocytic duodenosis have celiac disease. The research team was made up of I. Aziz, K. E. Evans, A. D. Hopper, D. M. Smillie, and D. S. Sanders. They are affiliated with the Department of Gastroenterology at Royal Hallamshire Hospital in Sheffield, UK. The study came in response to earlier retrospective studies that have suggested different connections with lymphocytic duodenosis, indicating that patients with this condition should not be diagnosed with celiac disease, solely by histology. Lymphocytic duodenosis is marked by normal villous architecture and less than 25 intraepithelial lymphocytes (IELs) per 100 enterocytes. For their study, the team thoroughly evaluated one hundred patients with lymphocytic duodenosis for celiac disease and other aspects associatedwith lymphocytic duodenosis by using initial celiac blood screens, and excluding the presence of infection. Of thirty-four patients with unexplained lymphocytic duodenosis, twenty-nine underwent repeat duodenal biopsies following a gluten challenge. Biopsy results showed that 16% of patients with lymphocytic duodenosis had celiac disease. Once celiac disease was accounted for, the factors most commonly association with lymphocytic duodenosis were as follows: drugs were a factor in twenty-one percent of lymphocytic duodenosis patients; infection was a factor in nineteen percent, immune dysregulation was a factor in four percent, inflammatory bowel disease and microscopic colitis in two percent each, sarcoidosis and IgA deficiency in one percent of cases, respectively. Of thirty-four patients with no known associations, eighteen showed symptoms of irritable bowel syndrome (IBS). Of twenty-nine patients examined with repeat duodenal biopsies, the IEL count returned to normal in twenty-two patients. The study results show that known associations can be found in sixty-six percent of cases of lymphocytic duodenosis. Importantly, sixteen percent will have celiac disease. In cases of lymphocytic duodenosis with no apparent cause, there may be a connection with IBS. In such cases the IEL count returns to normal on repeat biopsy in seventy-six percent. Source: Aliment Pharmacol Ther. 2010 Dec;32(11-12):1392-7.
  2. Celiac.com 12/26/2010 - Should everyone with symptoms of celiac disease go on a gluten-free diet? Current practice allows many patients with symptoms of celiac disease, but no gut damage, and thus no official diagnosis, to forgo a gluten-free diet. In a new study, researchers found that people with celiac disease symptoms have the same distinctive metabolic fingerprint as patients with full-blown disease, and who must follow a gluten-free diet to avoid permanent damage to the gut. The new study, by Ivano Bertini and colleagues, is stirring up the discussion about just which patients with symptoms of celiac disease should follow a gluten-free diet. Their research shows that people currently diagnosed as "potential" celiac disease patients and not advised to follow a gluten-free diet may not be "potential" patients at all. Celiac disease is widely regarded as undiagnosed or misdiagnosed. For their study, the researchers used magnetic resonance metabolic profiling to analyze the biochemical markers in the blood and urine of 61 patients with celiac disease, 29 with potential celiac disease, and 51 healthy people. The researchers found that people with unproven celiac disease largely shared the same profile as those with confirmed celiac disease and that the biochemical markers in both groups differed sharply from those of healthy individuals. The researchers conclude that their findings "demonstrate that metabolic alterations may precede the development of small intestinal villous atrophy and provide a further rationale for early institution of gluten-free diet in patients with potential celiac disease, as recently suggested by prospective clinical studies." The authors do note receiving funding from Boehringer Ingelheim Italy. Source: American Chemical Society Journal of Proteome Research
  3. Celiac.com 08/25/2010 - The revolution in genetic studies continues to drive discoveries about the genetic triggers for celiac disease. In recent developments, a genome-wide association study (GWAS) has nearly doubled the number of single-nucleotide polymorphisms (SNPs) associated with celiac disease from 14 to 27, most of which contain genes related to immune functions. Doctors have known for some time now that people with genetic markers DQ2 and DQ8 are more susceptible to celiac disease than those without those gene markers. This fact points to the importance of histocompatibility complex presentation of gluten antigens to immune cells. In 2007, a landmark study established 14 celiac-associated SNPs. Recently, a team of researchers conducted a comprehensive follow-up to that study. The study team included P. C. Dubois, G. Trynka, and L. Franke. The resulting GWAS used six times more genetic samples than the 2007 study, including five European case-control data sets comprised of 4,533 celiac disease patients and 10,750 controls. In all, the team tested nearly 300,000 genes. Based on low P values (P < 5 × 10-8) and biological likelihood of candidate SNPs being related to immune function, the team selected a total of 131 single-nucleotide polymorphisms (SNPs) for replication in an independent cohort of 4918 cases and 5684 controls. Their data identify 13 additional regions associated with celiac disease. To determine the trigger gene for each potential locus, the team used three complementary, objective methods. They first used a computerized algorithm, known as GRAIL, that searches PubMed for specific terms related to various gene features. They next employed what is called expression quantitative trait locus mapping, which isolates variations that may influence the expression of the gene, rather than its protein structure and function. Lastly, they looked for co-expression of gene clusters in suspect candidate genes relative to known susceptibility loci. Each of these methods shed additional light on the association between suspect SNPs and celiac disease susceptibility. However, the authors of the study go out of their way to note that, ultimately, the authors categorized loci and predicted causal genes using their "own knowledge of celiac disease pathogenesis.” This fact, they point out, emphasizes the crucial role played by knowledgable scientists exercising their insights to reap the most benefit from ‘objective’ advanced genomic data mining technologies. This study involved genetic assessment in a very large cohort, replication in a similarly large cohort, and multiple independent approaches at refining candidate SNPs. As a result, the number of known loci of celiac disease susceptibility genes has increased from 14 to 27. Their findings also identify several new pathways of celiac disease pathogenesis that merit further investigation. The study team also notes that these findings only account for 20% of the variance in celiac disease heritability. This, they say, points to a need for additional studies regarding genetic triggers for celiac disease. Source: Nature Genetics 42, 295 - 302 (2010). doi:10.1038/ng.543
  4. 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
  5. GUT 2002;50:332-5 Celiac.com 03/19/2002 - According to a long term study conducted by Dr Matti Uusitupa and colleagues from the University of Kuopio, Kuopio, Finland, long-term ingestion of a moderate amount of oats in an otherwise gluten-free diet is safe for adult patients with celiac disease. In a previous study Dr. Uusitupa found no harmful effects from oats after patients ate them for 12 months, which was reflected by the patents symptoms, nutritional status, duodenal villous architecture, and mucosal mononuclear cell infiltrate, as seen in celiac patients who are in remission. The earlier study also showed that ingestion of oats did not delay recovery of mucosal damage in newly diagnosed celiacs. Dr. Uusitupas first study compared the effects of a gluten-free diet and a gluten-free diet that included oats with a randomized trial involving 92 adult celiac patients: 45 in the oats group whose intake averaged approximately 34 grams per day, and 47 patients in the control group. Patients in the oats group were allowed to eat oats freely in conjunction with an otherwise gluten free diet. After five years 35 patients in the original oats group, 23 of whom were still eating oats at least twice a week, and 28 in the control group that was on a conventional gluten free diet were examined. The results confirmed that eating oats did not cause ANY duodenal mucosal damage to the adult celiac patients in the study. Further, the patients were also examined using histological, histomorphometric, and immunological methods, and AGA, ARA, and EMA serological test results of those in the oat group showed no negative effects that could be linked to eating oats. According to Dr. Uusitupa, the high antibody levels that appeared in some of the patients that were in both groups are most likely explained by poor compliance to a gluten free diet, and the reason why celiac patients can tolerate oats must be based on structural differences between the proteins of oats, wheat, barley, and rye. The toxic portion of the harmful gluten protein lies in the ethanol soluble fraction called gliadins, whose toxicity remains after digestion. With oats, however, it is possible that the absence of specific amino acid sequences that are found in wheat gliadin but are not found in oat avenin allow oats to be tolerated by celiacs. Last, the researchers note that taking oats off of the list of forbidden cereals might improve patient compliance to the gluten-free diet by giving them more food choices.
  6. Celiac.com 06/10/2010 - New research is currently underway in Ireland, as researchers test "pseudo-cereals" to determine the quality of replacements for glutenous grains such as, wheat, rye and barley. Many celiacs, especially those with delayed diagnosis', suffer from malabsorbtion and malnutrition. It is therefore more important for celiacs to ingest grains that are vitamin fortified than it is for non-celiacs. Researchers at Teagasc Food Research Ashtown are attempting to address the nutritional concerns for gluten-free products. They are working to formulate gluten-free bread products that are tasty, and have higher nutritional properties. Doctor Eimear Gallagher, of Teagasc Food Research Ashtown, is leading the current research project which primarily focuses on using “pseudo-cereals” such as amaranth, quinoa and buckwheat, to replace gluten containing grains, also known as wheat, rye and barley. Dr. Gallagher suggests that the demand for new and improved gluten-free bread products is growing rapidly due to greater public awareness of celiac disease, and the rise in positive celiac diagnoses'. Celiac affects approximately 1 percent of the population. Which means that 1 percent of the population must look for alternatives to favored grain products such as bread, pizza and cereals to name a few. While there is a large variety of gluten-free products on the market, many gluten-free products are described as being crumbly, brittle, bland and often rendered inedible. Gluten-free products are not only considered inferior in texture and taste to their wheat counterparts, but they are also criticized for having inferior nutritional value. Most mainstream breads and grains are vitamin fortified and therefore contain many essential nutrients, vitamins, and fiber. However, most gluten-free grains are typically made with starches and refined flours such as rice, corn and potato starches, which are low in nutrients and are not usually fortified. Dr. Gallagher and researchers are studying characteristics of pseudo-cereals to replace wheat in grain products. Amaranth, quinoa and buckwheat are naturally high in nutritional values with high levels of protein and dietary fiber, which make them excellent grain alternatives for celiacs. Dr. Gallagher's findings showed that all of the pseudo-cereal breads revealed a significant increase in antioxidant and polyphenol activity, compared to the gluten-free control group. Teagasc food researchers are also working hard to create a dairy-based ingredient that can produce the same properties in bread as gluten does. So far researchers have discovered that casein aggregates and forms a protein network which can retain gas in gluten-free dough. The reactions are similar to gluten containing wheat dough, but this is a work in progress and more studies are needed. Dr. Gallagher's studies have revealed significant information on ingredients, formulations and technologies used to make gluten-free products, which will help provide edible and healthy alternatives to gluten-free products. Source: ScienceDaily (May 26, 2010)
  7. Celiac.com 05/18/2010 - A research team recently concluded a clinicopathologic and array comparative genomic hybridization study on enteropathy-associated T-cell lymphoma. The team included Young Hyeh Ko MD, PhD; Sivasundaram Karnan; Kyeong Mee Kim MD, PhD; Cheol Keun Park MD, PhD; Eun Suk Kang MD, PhD; Young Ho Kim MD, PhD; Won Ki Kang MD, PhD; Seok Jin Kim MD, PhD; Won Seog Kim MD, PhD; Woo Yong Lee MD, PhD; Ho Kyung Chune; Masao Seto MD, PhD. The are associated variously with the Department of Pathology, the Department of Laboratory Medicine, the Division of Gastroenterology, Hemato-oncology of Internal Medicine, the Department of General Surgery of Samsung Medical Center at Sungkyunkwan University in Seoul, Korea and the Division of Molecular Medicine of the Aichi Cancer Center Research Institute in Nagoya, Japan. The latest World Health Organization classification system recognizes 2 types of enteropathy-associated T-cell lymphoma. The first, EATL type 1, is strongly associated with celiac disease, and makes up most EATL cases in Western countries. The second, EATL type 2 has no associations with celiac disease. To properly classify enteropathy-associated T-cell lymphoma types in Korea, the team conducted clinicopathologic and immunophenotypic analyses of 8 Koreans with enteropathy-associated T-cell lymphoma, and investigated genomic profile via array comparative genomic hybridization. Five patients presented tumors in the small intestine, while three presented tumors in the colorectum. Two patients carried an HLA DQB1âŽ0302 allele that corresponds to HLA DQ8. None of the patients suffered gluten-sensitive malabsorption syndrome. The team found intraepithelial lymphocytosis in all patients. In seven patients showed small, or small-to-medium, tumor cells. One patient presented with a medium-to-large tumor. Tumor cell immunophenotypes were CD4−CD8+CD56+ in 4 cases, CD4−CD8+CD56− in 1 case, CD4−CD8−CD56+ in 2 cases, and CD4−CD8−CD56− in 1 case. Using array comparative genomic hybridization analysis to spot recurring genomic alterations, the team found chromosome 9q33-q34.1 gain in four of five patients, chromosome 6p21.1-21.31 gain in three of five (60%), chromosome 6p21.1-21.31 gain in three of five (60%), and chromosome 3p12.1-p12.2 and 3q26.31 loss in two out of five (40%). These results show type 2 enteropathy-associated T-cell lymphoma to be the most prevalent type in this geographic region, and that associated genetic changes are similar to those in Western countries. Source: Human Pathology (2010) doi:10.1016/j.humpath.2009.11.020
  8. Celiac.com 02/16/2010 - A team of German clinicians recently noted a case that indicates that tumors may influence immunologic reactions. The team included F. Mühr-Wilkenshoffa, M. Friedricha, H.-D. Fossb, M. Hummelb, M. Zeitza, and S. Dauma. They are associated with the Medical Clinic I, Gastroenterology, Rheumatology and Infectious Diseases, and with the Department of Pathology, Charité at University Medicine Berlin. They recently reported on the case of a 72-year-old patient who suffered from celiac disease that had been diagnosed in his early fifties. The patient had not followed a gluten-free diet. Rather, he had eaten a normal diet. However, he showed no evidence of enteropathy or celiac-associated antibodies. Still, the patient developed a jejunal T-cell lymphoma. Due to perforation, the team performed a resection, and added four courses of IMVP-16. The patient switched to a strict gluten-free diet. After two years, he presented with weight loss and a clonally divergent refractory sprue type II with loss of antigen (CD8; T-cell receptor-β) expression in intraepithelial lymphocytes. At that point, even though he remained on a strict gluten-free diet, he showed elevated blood levels of celiac-associated antibodies. The team notes several interesting facets to the case. First, the lack of enteropathy under a gluten-containing diet supports the notion that malignant diseases, especially non-Hodgkin lymphoma, trigger immune suppression. Secondly, the fact that, while still on a strict gluten-free diet, the patient developed an early form of a second independent T-cell lymphoma (refractory sprue type II), coupled with the celiac-associated antibodies, raises the question whether the clonal intraepithelial lymphocytes might be stimulating antibody production. Thus, taken alone, the detection of celiac-associated antibodies in patients with celiac disease is not sufficient to prove noncompliance with gluten-free diet. Source: Digestion 2010;81:231-234 (DOI: 10.1159/000269810)
  9. Celiac.com 02/12/2010 - A recent study to research thepredominance of celiac disease in healthy school children in IrbidCity, Jordan was conducted using ELISA, a common serological test forthe presence of EmA antibodies which are associated with celiacdisease. Serum samplesfrom the children were analyzed for the presence of IgA anti-tissuetransglutaminase antibodies (tTG). Samples that tested positive fortTG, were then analyzed for IgA anti-endomysium antibodies (EmA).Positive EmA results indicated the presence of celiac in thechildren. Using 868 boys &1,117 girls ages 5.5 to 9.5, the study measured the positiveserology of the children's weight and height, Body Mass Index (BMI)as well as blood samples from the children to determine theprevalence of celiac disease. The researchers found that 16 of the 1,985 children tested, had positive EmAantibodies, and were also positive for celiac disease. The resultsfurther indicated that both boys and girls with positive EmAantibodies also showed significant height reduction compared tochildren without the presence of the antibodies. However, only boyswith positive antibodies showed significant weight reduction. The studyconfirmed that celiac disease is widespread among Jordanschool children. It also concluded that children with celiac diseaseare prone to lower height, weight and BMI compared to children withnegative EmA antibody results. Sources: http://7thspace.com/headlines/334475/serological_screening_for_celiac_disease_in_schoolchildren_in_jordan_is_height_and_weight_affected_when_seropositive.html
  10. Celiac.com 05/30/2007 - The results of a study recently published in the Scandinavian Journal of Gastroenterology shows that patients with celiac disease can consume oats with no risk of adverse immunological effects. An international research team made up of doctors Tarja Kemppainen (1); Esko Janatuinen (2); Kati Holm (3); Veli-Matti Kosma (4); Markku Heikkinen (5); Markku Mäki (3); Kaija Laurila (3); Matti Uusitupa (1); Risto Julkunen (5), set out to evaluate local cellular immune response after 5 years of oat consumption by adult celiac patients. The doctors looked at a group of 42 celiac patients who had previously participated in a 6-12 month oats intervention study. 22 of these patients already incorporated oats as part of their gluten-free diet. During the 5-year follow-up study, 10 patients who were concerned about the safety of long-term oat consumption stopped eating oats. The 12 remaining patients consumed oats for the whole 5-year period. The remaining 20 celiac patients formed the control group, and followed a strict, conventional, gluten-free diet that excluded oats. The team conducted biopsies and counted Intraepithelial CD3, TCR (IEL) and TCR (IEL) T cells to determine corresponding densities. No Adverse Effects for Celiac Disease Patients Who Eat Oats The results showed no differences in the densities of CD3, IEL and IEL T cells between the oat and the control groups. The researchers concluded that the mucosa of the small intestine show no immunological response in celiac patients who consume oats over a long period of time. Scandinavian Journal of Gastroenterology, Volume 42, Issue 1 2007 , pages 54 - 59 Participating Institutions: Department of Clinical Nutrition, University of Kuopio and Kuopio University Hospital. Kuopio. Finland Department of General Medicine, Al Mafraq Hospital. Abu Dhabi, U.A.E. Medical School, University of Tampere and Tampere University Hospital. Tampere. Finland Department of Pathology and Forensic Medicine, University of Kuopio and Kuopio University Hospital. Gastroenterological Unit, Department of Medicine, Kuopio University Hospital. Finland About the Author: Jefferson Adams is a freelance health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
  11. BMJ. 2004 Jul 21 Celiac.com 08/09/2004 – In a study designed to quantify the malignancy and mortality risks associated with celiac disease, British researchers examined 4,732 celiac disease patients and compared them to 23,620 matched controls. The researchers found that 134 (2.8%) of those with celiac disease had at least one malignancy, and 237 (5.0%) had died. In the general population, the overall hazard ratios were as follows: for any malignancy 1.29 (95% confidence interval 1.06 to 1.55), for mortality 1.31 (1.13 to 1.51), for gastrointestinal cancer 1.85 (1.22 to 2.81), for breast cancer 0.35 (0.17 to 0.72), for lung cancer 0.34 (0.13 to 0.95), and for lymphoproliferative disease 4.80 (2.71 to 8.50). The researchers conclude that there is a modest increase in the rates of malignancy and mortality during the first year following a diagnosis of celiac disease. After one year, however, most of that increase quickly diminishes to a level that is only slightly higher than that of the normal population, presumably due to the effects of a gluten-free diet. In an unexpected finding the researchers also found a significant reduction in incidence of breast cancer in those with celiac disease, which warrants further study, as it could provide insight into the cause of the disease.
  12. Celiac.com 05/15/2009 - Certain proteins found in the gluten of wheat, rye and barley trigger adverse responses in people with gluten intolerance and celiac disease. This happens when the offending gluten proteins encounter the immune systems of susceptible individuals, triggering a CD4+ T-cell mediated immune response, together with inflammation of the small intestine. However, a number of gluten proteins contain no T-cell stimulatory epitopes, and so trigger no such adverse immune response. So, not all gluten is equally offensive to celiacs, and some may be both well tolerated and useful for making better bread. Gluten proteins are found in multiple gene sites on chromosomes 1 and 6 of the three different genomes of hexaploid bread wheat (Triticum aestivum) (AABBDD). Gluten is the stuff that makes bread delightfully chewy, among other desirable properties, so being able to successfully incorporate non-offending gluten into bread recipes might yield better breads that are safe for consumption by folks with celiac disease. Obviously, being able to produce high-quality, celiac-safe bread on a commercial scale would be of tremendous benefit for both producers and consumers. Currently, most gluten-free bread contains no gluten, as it has been difficult or impractical to separate the offending proteins from the non-offending proteins. Recently, a team of researchers based in the Netherlands attempted to remove celiac disease-related protein from Chinese Spring wheat while maintaining the beneficial bread-baking properties. The team was made up of Hetty C. van den Broeck, Teun W. J. M. van Herpen, Cees Schuit, Elma M. J. Salentijn, Liesbeth Dekking, Dirk Bosch, Rob J. Hamer, Marinus J. M. Smulders, Ludovicus J. W. J. Gilissen and Ingrid M. van der Meer. The team used a set of deletion lines of Triticum aestivum cv. Chinese Spring to assess the results of removing individual gluten sites on both the level of the T-cell stimulatory epitope in the gluten proteome and the favorable qualities of the flour. To measure the reduction of T-cell stimulatory epitopes, the team used monoclonal antibodies that recognize T-cell epitopes contained in gluten proteins. They then clinically tested the deletion lines for their dough mixing properties and dough composition. The team's attempts to remove the alpha-gliadin site from the short arm of chromosome 6 of the D-genome (6DS) yielded in a favorable decrease in the presence of T-cell stimulatory epitopes, but also yielded a significantly loss of favorable baking properties. However, by deleting the omega-gliadin, gamma-gliadin, and LMW-GS locations from the short arm of chromosome 1 of the D-genome (1DS), researchers were able to strip offending T-cell stimulatory epitopes from the proteome while maintaining technological properties. The team concludes that their data hold important implications for lowering the quantity of T-cell stimulatory epitopes in wheat, and promoting the creation of celiac-safe wheat varieties that will potentially yield breads of higher quality than currently available. BMC Plant Biology 2009, 9:41
  13. Celiac.com 11/25/2003 - Investigators from the Celiac Sprue Research Foundation, a non-profit public charity, and the Palo Alto Medical Foundation are seeking 20 volunteers who have Celiac Sprue to participate in a study called the "Gluten Detoxification Trial". The Gluten Detoxification Trial will test the effects of consumption of an Orange Juice Mixture that has been modified by the addition of gluten pre-treated with an enzyme (PEP) that is intended to "detoxify" the gluten. If the PEP is successful in detoxifying the gluten, then the stage will be set for development of a PEP therapeutic drug, or pill, that may allow Celiac Sprue patients to consume a regular gluten containing diet. The study involves 2 two-week stages, separated by one month off. The first stage will occur during the first two weeks in December. The second stage will occur during late January 2004. Participants in this study will be randomized to consume an Orange Juice Mixture containing gluten daily for 14 days during one stage, and an Orange Juice Mixture containing gluten pre-treated with the PEP daily for 14 days during the other stage. Participants will record symptoms daily during each stage, and will have laboratory tests measured before and after each stage. Participants will undergo a screening physical exam at the beginning, and brief follow-up exams after each stage at the Palo Alto Medical Foundation. Participants in the Gluten Detoxification Trial must meet all of the following criteria: Diagnosed with Celiac Sprue by small intestinal biopsy (participants must be able to provide a copy of the biopsy report). Have had at least one abnormal Celiac antibody test (e.g. transglutaminase (ttg), endomysial (EMA), anti-gliadin) in the past. Be in remission on a gluten-free diet. Be at least 18 years of age. Pre-registration is required to participate in the study. If you can participate, please contact the Celiac Sprue Research Foundation at the above address or e-mail address and request a registration packet/consent. Please call either Dr. Gail Pyle at (408) 655-0384 or Dr. Gary Gray at (650) 327-1144 if you have any questions.
  14. Celiac.com 05/21/2009 - To better diagnose celiac disease, assess intestinal damage, and monitor treatment over the long-term, doctors are looking to develop a whole new set of non-invasive evaluation tools. One of the tools currently of interest are fatty acid binding proteins (FABPs), these are small cytosolic proteins found in enterocytes (tall columnar cells and responsible for the final digestion and absorption of nutrients, electrolytes and water). FABPs are reliable indicators of intestinal mucosal damage, and are potentially useful for non-invasive assessment of intestinal damage in celiac patients. A team of researchers in the Institute of Nutrition and Toxicology Research at Maastricht University, as well as the departments of Surgery, Pediatrics and Internal Medicine at University Hospital Maastricht, recently set out to assess the potential use of FABPs in non-invasive assessment of intestinal damage in celiac disease. The study team was made up of J. P. Derikx, A. C. Vreugdenhil, A. M. Van den Neucker, J.Grootjans J, A. A. van Bijnen, J.G. Damoiseaux, L. W. van Heurn, E. Heineman, and W. A. Buurman. They began by examining the distribution and microscopic localization of FABPs in healthy human intestinal tissue. They then checked circulating levels of intestinal (I)-FABP and liver (L)-FABP in 26 healthy control subjects, and in 13 patients with biopsy-proven celiac disease, both before and after initiating a gluten-free diet. Ten celiac subjects underwent reevaluation within a year beginning a gluten-free diet. They found that I-FABP and L-FABP are common in the small intestine, particularly in the jejunum. FABPs also show up in cells on the upper part of the villi, the part that is first to be damaged in celiac disease. They also found that people with untreated, biopsy-proven celiac disease have substantially higher circulating levels of FABPs as compared with healthy control subjects (I-FABP: 784.7 pg/mL vs. 172.7 pg/mL, P<0.001; L-FABP: 48.4 ng/mL vs. 10.4 ng/mL, P<0.001). These levels return to normal when patients adopt a gluten-free diet. According to the team, the monitoring of FABP circulating levels shows strong promise as a non-invasive means of diagnosing and assessing intestinal damage in celiac disease, as well as in long-term non-invasive monitoring of treatment and gluten-free diet compliance. Journal of Clinical Gastroenterology. 2009 Apr 6.
  15. Celiac.com 03/26/2009 - The recent discovery that people with celiac disease harbor antibodies that are specific for deamidated gliadin peptides (DGP), which are the product of tTG binding to gliadin peptides, offers a chance to examine the connection between the production of anti-tTG IgA and the antibodies against DGP in celiac patients. A group of researchers led by Doctors Marietta, Rashtak, and Murray from the Mayo Clinic in Rochester, MN recently set out to make just such an examination, and a report on their study appears in the February issue of the World Journal of Gastroenterology. Their data show that the blood level of anti-tTG IgA shares a significant connection with the blood level of anti-DGP of both the IgG and IgA isotypes in people with untreated celiac disease. The same data showed only a weak connection between the production of anti-tTG IgG and anti-DGP IgG/IgA. Moreover, the results show that the immune response by T and B cells to deamidated gliadin differs at the most basic level from the immune response by T and B cells to tissue transglutaminase in celiac patients. Their results also indicate, however, that the immune responses against deamidated gliadin and tTG are substantially connected, and thereby offer support for the hapten-carrier theory for the origin of anti-tTG IgA. World Journal of Gastroenterology; February, 2009.
  16. Celiac.com 06/08/2007 - This study shows that celiac disease is as common among British Columbians with Type 1 diabetes as it is in Europeans with Type 1 Diabetes. The research team was made up of doctors P.M. Gillett, H.R. Gillett, D.M. Israel, D.L. Metzger, L. Stewart, J-P. Chanoine, H.J. Freeman. The team looked at 233 children with Type1 diabetes. In a blind study, the children were screened for celiac disease using immunoglublin A endomysium antibody (EmA), and the Immunoglublin A tissue transglutaminase. Children with positive results were offered small bowel biopsies. For those confirmed with celiac disease, doctors recommended a gluten-free diet. British Columbians with Type 1 Diabetes Get Celiac Disease at Rates Comparable to their European Counterparts Nineteen children tested positive for EmA and showed elevated tTG levels. Of the 18 patients who agreed to biopsies, one was normal, three showed normal morphology with elevated Intraepithelial lymphocyte counts, and 14 biopsies showed morphological changes consistent with celiac disease. 9 of the 19 children who tested positive for EmA were asymptomatic. Seven patients showed only mildly elevated tTG levels. Of this second group, five refused biopsy and two showed normal biopsies. In addition to the four known cases, the doctors uncovered at least 14 new cases of celiac disease. The total rate of biopsy confirmed celiac disease was 18 out of 233, or 7.7%. The doctors concluded that these results confirm that celiac disease is prevalent in pediatric type 1 diabetes. The doctors say the study reinforces the importance of celiac screening for children with type 1 diabetes, and also the advisability of keeping an eye on tTg serology as part of determining the effects of and compliance to a gluten-free diet. Participating Facilities 1. Division of Pediatric Gastroenterology at British Columbias Childrens Hospital Vancouver, British Columbia. 2. Division of Endocrinology, British Columbias Childrens Hospital, Vancouver, British Columbia. 3. Division of Gastroenterology, University of British Columbia, Vancouver, British Columbia Journal of Pediatric Gastroenterology & Nutrition: Volume 29(4)October 1999p 495. About the Author: Jefferson Adams is a freelance health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
  17. Celiac.com 10/30/2007 - Many studies over the years have supported the idea that celiac disease is a permanent condition, and that those who strayed from the strict gluten-free diet that forms the core of celiac treatment risked relapsing and suffering the telltale intestinal damage associated with celiac disease. However, it was generally assumed that symptoms of celiac disease and associated intestinal degradation occurred within two years of reintroducing gluten back into the diet. The medical journal GUT recently published a paper by Matysiak-Budnik et al. concerning the natural history of celiac disease, which indicates that classic celiac damage to the intestinal lining may take years or decades to develop in some cases. A team of researchers looked at 61 adults who had been diagnosed with celiac disease as children, and who felt themselves to be asymptomatic for anywhere from 3 to 21 years, with a group average of 11 years. An exam revealed that 48 of the 61 test subjects indeed showed villous atrophy with crypt hypoplasia. The 13 other patients showed no celiac-associated intestinal damage. Strangely, 2 of the 13 patients with no signs of damage had showed such damage a short time after gluten was reintroduced into their diets, only to return to normal as they continued to consume gluten. From this, the researchers concluded that some people might actually become truly latent and tolerate gluten with no adverse effects. It’s also possible that such people actually still have celiac disease and that the intestinal damage has yet to recur, as villous atrophy occurs only at the tail end of celiac disease. In fact, delayed relapse of celiac disease after gluten reintroduction supports the notion that people with normal mucosa may in fact have celiac disease. Still, it is highly uncommon for patients with celiac disease to show no clinical symptoms on a long-term gluten-inclusive diet. The level of celiac disease+ intraepithelial lymphocytes has proven to be more useful than mucosal Marsh Type 1 lymphocytes in revealing early developing celiac disease in such cases and in general. Reliable diagnosis of celiac disease is important, as untreated celiac disease carries a broad range of associated risks including markedly higher rates of certain cancers. A recent study also suggests celiac disease may also adversely impact both the peripheral the central nervous systems. However, regarding the 13 asymptomatic patients, the original diagnosis of celiac would seem to be accurate in each case, as each had celiac-type HLA, either HLA DQ2 or DQ8, and their follow-up exam results showed that 5 of those patients had positive serum antibody results and higher densities of small bowel mucosa celiac disease+ and CD3+ intraepithelial lymphocytes than did the non-celiac control groups. Two of the 13 patients developed symptoms of a relapse during the follow-up. The study team concluded that the “2 year rule” for reintroducing gluten is invalid and supports the view that celiac disease exists beyond villous atrophy. As villous atrophy of the small intestine is only one manifestation of genetic gluten intolerance, and that the present diagnostic guidelines based on mucosal damage and ignoring early developing celiac disease and dermatitis herpetiformis is only one incarnation of celiac disease. GUT 2007; 56:1339-1340 Katri Kaukinen, Pekka Collin, Medical School, University of Tampere and Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, Tampere, Finland Markku Ma¨ki, Medical School, University of Tampere and Department of Paediatrics, Tampere University Hospital, Tampere, Finland
  18. 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
  19. Alimentary Pharmacology & Therapeutics Volume 17 Issue 4 Page 587 - February 2003 Aliment Pharmacol Ther 2003 Feb;17(4):587-94 Peraaho M, Kaukinen K, Paasikivi K, Sievanen H, Lohiniemi S, Maki M, Collin P. Departments of Medicine and Pediatrics, Tampere University Hospital, Tampere (also Medical School, University of Tampere), Bone Research Group, UKK Institute, Tampere, and Finnish Coeliac Society, Tampere, Finland. Celiac.com 3/14/2003 - BACKGROUND: : The safety of wheat-starch-based gluten-free products in the treatment of coeliac disease is debatable. Prospective studies are lacking. AIM: : To compare the clinical, histological and serological response to a wheat-starch-based or natural gluten-free diet in patients with newly detected coeliac disease. METHODS: : Fifty-seven consecutive adults with untreated coeliac disease were randomized to a wheat-starch-based or natural gluten-free diet. Clinical response, small bowel mucosal morphology, CD3+, alphabeta+ and gammadelta+ intraepithelial lymphocytes, mucosal human leucocyte antigen-DR expression and serum endomysial, transglutaminase and gliadin antibodies were investigated before and 12 months after the introduction of the gluten-free diet. Quality of life measurements were performed by standardized questionnaires and the bone mineral density was analyzed. RESULTS: : In both groups, abdominal symptoms were alleviated equally by a strict diet. There were no differences between the groups in mucosal morphology, the density of intra-epithelial lymphocytes, serum antibodies, bone mineral density or quality of life tests at the end of the study. Four patients on a natural gluten-free diet and two on a wheat-starch-based gluten-free diet had dietary lapses; as a result, inadequate mucosal, serological and clinical recovery was observed. CONCLUSIONS: : The dietary response to a wheat-starch-based gluten-free diet was as good as that to a natural gluten-free diet in patients with newly detected coeliac disease. PMID: 12622768
  20. Celiac.com 09/10/2007 - Sorghum is a cereal grain with poised for development as a major crop for human nutrition. The flour made from white sorghum hybrids is lightly colored, and offers a bland, neutral taste that leaves no trace of unusual colors or flavors when added to food products. These features make sorghum favorable for use in wheat-free food products. While sorghum is considered as a safe food for celiac patients, primarily due to its relationship to maize, no direct studies have been made regarding its safety for individuals with celiac disease and gluten intolerance. Thus, further study was warranted to clearly demonstrate the safety and tolerability of sorghum for celiac patients. A team of researchers set out to determine the safety and tolerability of sorghum flour products in adult celiac patients The team consisted of Carolina Ciacci, Luigi Maiuri, Nicola Caporaso, Cristina Bucci, Luigi Del Giudice, Domenica Rita Massardo, Paola Pontieri, Natale Di Fonzo, Scott R. Bean, Brian Ioerger and Marco Londei. Study participants who consumed sorghum-derived food product for 5 days straight experienced no gastrointestinal or other symptoms and the level of anti-transglutaminase antibodies was unchanged at the end of the 5-day medical challenge. Sorghum protein digests produced no morphometric or immunomediated alteration of duodenal explants from celiac patients. In both in vitro and in vivo challenge, sorghum-derived products show no toxicity for celiac patients. Sorghum can thus be regarded safe for people with celiac disease. Clinical Nutrition, 24 August 2007 health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
  21. Celiac.com 11/15/2007 - There’s a large body of evidence pointing to the importance of a life-long gluten-free diet for people with celiac disease. However, following a gluten-free diet is not always easy. Studies show that only 50% to 75% of all celiac patients are successful in faithfully following their gluten-free diets. But until now, very little has been published that indicates why this might be, or offers evidence as to the best way to succeed in faithfully maintaining a gluten-free diet. Recently, a team of doctors led by Dr. Daniel Leffler conducted a study of the factors that are most important in increasing the success rates for people trying to maintain a gluten-free diet. Dr. Leffler is a clinical fellow in gastroenterology at Boston’s Beth Israel Deaconess Medical Center. Dr. Leffler presented the results of that study recently at the 2007 American College of Gastroenterology’s Annual Scientific Meeting and Postgraduate Course. The results of the study indicate that support groups seem to have an important role to play. A team of doctors, dietitians, psychologists, and patients created a study questionnaire that included 155 questions designed to measure ten areas important to success in living with celiac disease, including the burden of the disease, knowledge specific to celiac, health care access, mood and stress factors, perceptions about adherence, reasons for adherence, social support, symptoms. Participants of the study were all found through biopsy to have celiac disease. A professional nutritionist assessed each of the participants for dietary adherence. Of the 154 participants, 76% were Caucasian women. Nearly 70% had at least a college-level education. The average age was 50, and they had followed gluten-free diets for an average of 5 years. Concerns over cost and changes in stress levels and shifts in mood were among the reasons that contributed not following a gluten-free diet. Being a member of a celiac support group (P=.008), the ease of eating gluten-free while traveling (P=.012), or while attending social functions were important factors in successfully following the gluten-free diet. Demographic factors like age, sex, and age at diagnosis had no bearing on successfully remaining on a gluten-free diet.
  22. Celiac.com 11/06/2007 - This study investigated the effect of screening detected celiac disease in type I diabetic children in a multi-center case-control fashion. The research team consisted of B Rami, Z Sumni, E Schober et al from Austria, Czech Republic, and Slovenia, among other European countries. The team compared 98 diabetics with silent celiac disease to 196 control diabetics without celiac matched for age, sex, diabetes duration. Mean age at diabetes diagnosis was 6.5 yrs, celiac diagnosis was 10.0 yrs. Celiac screening included yearly antibody testing and positive patients underwent biopsy. Hemoglobin A1c, hypoglycemia, ketoacidosis, insulin dosage, body-mass index, and height did not differ between cases and controls at celiac diagnosis or after a mean follow-up of 3.3 years. After diagnosis of celiac disease, weight gain was diminished in boys with celiac disease compared to their controls. Although a clear link between type I diabetes and increased risk of celiac disease is established, the benefit of a gluten-free diet is unclear in these children. This study followed 98 patients with diabetes and silent celiac for a mean of 3.3 years and compared them to 196 controls. This is the largest, best designed case-control study to date and it did not demonstrate any significant differences between the two groups, except for a decreased Body Mass Index (BMI - though still greater than non-diabetic, control children) in males after diagnosis. What is more intriguing is that at diagnosis, no significant differences in height, BMI, HbA1c, insulin need, or hypoglycemia events were seen, questioning the metabolic significance of silent celiac disease. In this study, it is difficult to estimate the duration of silent celiac disease prior to diagnosis. Although, given the fact that these patients were asymptomatic and their mean diabetes duration was 3.6 years, it likely implies that silent celiac disease was present for a few years. The data regarding the benefit of a gluten-free diet in screening detected celiac disease in type I diabetic children is scant but is slowly increasing. Numerous psychological (burden of gluten free diet in addition to diabetic diet), cost (of diet), and ethical issues (potential long-term benefits of gluten-free diet, compliance with diet) exist regarding these children and hopefully this question will be answered soon and with good, convincing data. Journal of Pediatric Gastroenterology and Nutrition, 41:317-321, 2005
  23. Celiac.com 09/28/2007 - Celiac disease is one of the most common lifelong disorders in western countries. However, most cases in North America remain currently undiagnosed, mostly because they present unusual symptoms and because of the low number of doctors who have a sound awareness of celiac disease. In a large European survey, the ratio between diagnosed and undiagnosed cases, found by mass serological screening, was as high as 1 to 7 , an effect termed the ‘celiac iceberg’. In addition to having chronic symptoms that might otherwise respond to a gluten-free diet, undiagnosed patients are exposed to the risk of long-term complications of celiac disease, such as anemia, infertility, osteoporosis, or cancer, particularly an intestinal lymphoma. Celiac Disease is diagnosed by confirming the presence of intestinal damage to the small intestine through a biopsy, along with a clinical response to the gluten-free diet. However, serological markers, e.g., the IgA class anti-tissue transglutaminase (tTG) antibodies, are useful screening tests. The sensitivity and the specificity of the IgA anti-tTG test are 94% and 97%, respectively. To address the large number of undiagnosed cases, a team of researchers recently set out to assess whether an active case-finding strategy in primary care could lead to increased frequency of celiac disease diagnosis, and to assess the most common clinical manifestations of the condition. The team was made up of Carlo Catassi, M.D., M.P.H.; Deborah Kryszak, B.S.; Otto Louis-Jacques, M.D.; Donald R. Duerksen, M.D.; Ivor Hill, M.D.; Sheila E. Crowe, M.D.; Andrew R. Brown, M.D.; Nicholas J. Procaccini, M.D.; Brigid A Wonderly, R.N.; Paul Hartley, M.D.; James Moreci, M.D.; Nathan Bennett, M.D.; Karoly Horvath, M.D., Ph.D.; Margaret Burk, R.N.; Alessio Fasano, M.D. 737 women and 239 men, with a median age of 54.3 years, who attended one of the practices participated in a multi-center, prospective study involving adult subjects during the years 2002-2004. All individuals with celiac-associated symptoms or conditions were tested for immunoglobulin A anti-transglutaminase (tTG) antibodies. Those with elevated anti-tTG were then tested for IgA antiendomysial antibodies (EMA). All who were positive for EMA were advised to undergo an intestinal biopsy and HLA typing. 30 out of 976 study subjects showed a positive anti-tTG test (3.07%, 95% CI 1.98-4.16). 22 patients,18 women, 4 men, were diagnosed with celiac disease. In these 22 cases the most common reasons for screening for celiac disease was: bloating (12/22), thyroid disease (11/22), irritable bowel syndrome (7/22), unexplained chronic diarrhea (6/22), chronic fatigue (5/22), and constipation (4/22). The prevalence of celiac disease in the serologically screened sample was 2.25% (95% CI 1.32-3.18). The diagnostic rate was low at baseline (0.27 cases per thousand visits, 95% CI 0.13-0.41) and rose sharply to 11.6 per thousand visits (95% CI 6.8-16.4, P This study shows that the diagnosis rate for celiac disease can be significantly increased through the implementation of a strategy of active case-finding. Am J Gastroenterol. 2007;102(7):1454-1460.
  24. Patients Diagnosed in Childhood Might Evolve toward Latency on a Normal Diet Celiac.com 05/23/2007 - The results of a study recently published in the journal Gut indicate that some people who suffer from celiac disease might not need to remain on a gluten free diet for their entire lives, and that some celiac patients might be able to safely introduce gluten containing foods without suffering a relapse. Previous Studies Showing Positive Response to Wheat Introduction in Patients with Celiac Disease are Promising, But Incomplete Several studies have shown that some patients diagnosed with celiac disease in childhood were able to remain on a gluten-containing diet after gluten challenge without suffering a relapse. However, most of these studies included a small number of patients, or followed the patients for only a short period after gluten was reintroduced into their diets. These previous studies also limited their evaluation largely to assessment of celiac disease serology and histology of duodenal biopsies, and did not attempt to identify what factors might predict the development of tolerance to gluten. Determining Long-term Response to Gluten Consumption in Celiac Disease Patients A research team made up of doctors Tamara Matysiak-Budnik (1), Georgia Malamut (1,2), Natacha Patey-Mariaud de Serre (3), Etienne Grosdidier (2), Sylvie Seguier (3), Nicole Brousse (3), Sophie Caillat-Zucman (4), Nadine Cerf-bensussan (1), Jacques Schmitz (5) and Christophe Cellier (1,2), set out to determine whether children diagnosed with celiac disease must follow a gluten free diet for life. To determine the effects of reintroducing gluten into the diets of celiac patients, the research team set out to monitor the clinical and physical progress of adult celiac patients who had been diagnosed as children, who underwent a gluten challenge, and who were asymptomatic. The study focused on a specific group of patients, all but two of whom were diagnosed as children and followed until adulthood in the Department of Pediatric Gastroenterology in Necker Hospital and thereafter at the Georges Pompidou European Hospital in Paris; after which, they were entered into a local register of adult celiac patients and were recruited for the study based on two criteria: celiac disease diagnosed in childhood; and adherence to a normal diet. The patients in the study were from 18 to 65 years old, and had been diagnosed with celiac disease in childhood. The research team recorded data in the following categories: biological parameters of malabsorption; bone mineral density; clinical celiac status; gluten intake; HLA genotype; serological markers of celiac disease; as well as histological and immuno-histochemical parameters in duodenal biopsies. Results Show 20% Long-term Latency in Celiac Patients who Eat Normal Diet Of those studied, 61 patients had returned to a normal diet, and were asymptomatic. 48 showed various degrees of villous atrophy (silent celiac disease), and 13 had no detectable atrophy (latent celiac disease) on duodenal biopsies. Compared to those with silent celiac disease, patients with latent celiac disease showed markedly less osteopenia/osteoporosis [1/9 (11%) versus 23/33 (70%), p<0.001)], and lower TcR- + intraepithelial T cell counts (38±20 vs. 55±15, p<0.01). Patients with latent celiac disease had a lower mean age at the time of their first gluten free diet compared to patients with silent celiac disease (14.4±5 vs 40.1±47 months, p<0.05). Compared to the seven control patients on a long-term gluten free diet, the latent patients did not differ significantly, except for a higher frequency of celiac disease-specific serum antibodies. However, a follow-up found that two of the patients with latent celiac disease had suffered a clinical and histological relapse. Results showed that of those patients who remained asymptomatic after the reintroduction of gluten, 20% showed long-term latency. The study concludes that some patients with celiac disease may not need to remain on a life-long gluten free diet, and that some may indeed be able to safely reintroduce gluten into their diets with no adverse effects. However, the latency patients may experience may be transient, and therefore a regular follow-up is necessary. Also, patients with silent celiac disease should remain on a gluten free diet. Participating hospitals: (1) INSERM, U793, Faculté de Médecine René Descartes, IFR94, Paris, France. (2) AP-HP, H&OCIRC;pital Européen Georges Pompidou, Department of Hepato-Gastroenterology, Paris, France. (3) AP-HP, H&OCIRC;pital Necker-Enfants Malades, Department of Pathology, Paris, France. (4) INSERM, Equipe Avenir, Faculté de Médecine René Descartes, Paris, France. (5) AP-HP, H&OCIRC;pital Necker-Enfants Malades, Department of Pediatric Gastroenterology, Paris, France. Gut 2006;13(10). Comments on this Study by Ron Hoggan This is dressed up like a new finding, but it isn't. There are a number of studies that show similar findings. Part of that problem lies in the interpretation of the biopsies, and part of the problem arises out of failing to recognize the variable nature of the disease. It has long been known to wax and wane for reasons beyond our ken. Samuel Gee (1888) and Gibbons (1889) both reported the cyclic nature of their patients symptoms. They cited a study to support the idea of a two year rule saying that relapse would usually occur within two years, yet Kuitunen P, Savilahti E, Verkasalo M., in Late mucosal relapse in a boy with coeliac disease and cows milk allergy. Acta Paediatr Scand. 1986 Mar;75(2):340-2. reported one patient who at 4.3 years on a normal diet showed normal villous architecture. It was not until a follow-up biopsy at more than 8 years of eating a gluten-containing diet that he showed villous atrophy. These findings, along with all the other studies that have shown long delays in some patients before relapsing, argue strongly for Michael N. Marsh's position that we should concentrate on treating any immune system that is sensitized to gluten with a gluten-free diet. His rectal challenge is an excellent tool for identifying such sensitized immune systems. Dr. Fines fecal antibody test probably fits into the same category. The underlying assumption is that the biopsy will identify all cases of intestinal lesion regardless of the possibility of patchy lesions that are well documented in the literature. They deal with increased IEL counts as if they were a feature of latent celiac disease when that is not the case. There are several other points on which this study falters. They admit that the latency can be transient. Unfortunately, they have not exchanged emails with people where they have returned to eating gluten and have developed an abdominal cancer. I exchanged emails with such a young man who blamed himself for having killed himself with his carelessness about his diet. How awful that was for him! Yet these authors seem to think it is quite acceptable for patients to indulge during their latency periods and only consider a diet if there is a relapse of intestinal lesion.
  25. Celiac.com 07/10/2007 - A study published recently in the American Journal of Gastroenterology tracks the appearance and disappearance of antibodies associated with childhood risk celiac disease, and suggests that key antibodies often disappear even when gluten is still present in the diet. A team of Finnish doctors set out to evaluate the natural history of antibodies versus tissue transglutaminase (TGA), endomysium (EMA), reticulin (ARA), and gliadin (AGA-IgG and AGA-IgA). They looked at data for children genetically at risk for celiac disease, specifically, children who carried HLA-conferred risk of celiac disease who had been monitored frequently since birth. The research team was made up of S. Simell, S. Hoppu, A. Hekkala, T. Simell, M.R. Ståhlberg, M. Viander, H. Yrjänäinen, J. Grönlund, P. Markula, V. Simell, M. Knip, J. Ilonen, H. Hyöty, O. Simell. The team looked at serum samples from 1,320 children who were genetically at risk for celiac disease. Serum samples taken between 2000 and 2003 were assessed for TGA. Samples testing positive for TGA were evaluated for all five antibodies. Also, all future samples for the given patient were similarly evaluated. Also, positive TGA patients were encouraged to have a duodenal biopsy. The assessment was completed in August 2004. At that time, the test subjects ranged in age from 1 year to 9.5 years, with a mean age of 4.1 years. In all, 49 children (3.7%) were TGA positive. 26 of these TGA positive children submitted to biopsy. Celiac disease was diagnosed by biopsy in 20 of the 26. Of the 49 children who tested TGA positive, AGA-IgA surfaced at an average age of 2 years (+/- 1.5 over a range of 0.5 to 6.6 years for subjects). Compared to AGA-IgA, TGA, EMA, and ARA all surfaced together about 1 year later (TGA at 3.2 +/- 1.5, 1.0-7.0 yr, P < 0.001). Key Antibodies Can Vanish Early in Childhood Celiac Disease Even with ongoing gluten consumption, positive TGA values disappeared in 49%, EMA values disappeared in 49%, ARA values disappeared in 43%, AGA-IgA values disappeared in 41%, and AGA-IgG in 32%. The research team concluded that there are likely potential triggers for celiac disease that are active before AGA-IgA surfaces, or about 3 months earlier on average than when the TGA-associated antibodies appear. In a significant number of children, antibodies vanish spontaneously. This indicates that in many cases, conditions allow the regulatory immune phenomena to eliminate incipient celiac disease in genetically at-risk children even when gluten is still significant part of the diet. Am J Gastroenterol 2007;102:1–10
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