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Found 1,261 results

  1. 12/13/2018 - Is wine gluten-free? Wine Spectator recently weighed in on gluten and wine. The article is worth a read, and there’s a link at the bottom of this page. Meantime, here’s a quick rundown of the basics of wine and gluten. Wine is generally regarded as gluten-free and safe for people with celiac disease and other gluten-related sensitivities. That said, there are a couple of ways that wine could come to contain gluten; but they are mostly due to old and discontinued wine making practices. First, in the old days, barrel makers used to seal barrels with with wheat paste, which contains gluten. Wine aged in these barrels could contain trace amounts of gluten. However, these days, nearly every winery in the world now uses non-gluten-based wax products to seal their barrels. Even if barrels commonly contained wheat paste, a 2012 test run by Tricia Thompson, founder of GlutenFreeWatchdog.org, found that gluten levels of two different wines finished in wheat paste–sealed barrels contained under 5ppm gluten—thus meeting the FDA gluten-free standard. So, that method of possible contact with gluten is unlikely to be a problem for most people with celiac disease or a medical gluten-sensitivity. Another way wine could be exposed to gluten is if wheat gluten is used for a process called ‘fining.’ However, these days, the use of wheat gluten in fining is practically nonexistent. And even if wheat gluten were used for fining, it is unlikely to be an issue. A 2011 study published in the Journal of Agricultural and Food Chemistry found that wines fined with gluten contained either extremely low, or undetectable, levels of gluten. Furthermore, "even if any traces of gluten would accidentally enter a wine—let's say the winemaker falls into a tank holding a whole-wheat sandwich—as a protein, gluten would react with [wine's] phenolics," said Dr. Christian Butzke, a professor of enology at Purdue University. So, the vast majority of wines are gluten-free and likely safe for with celiac disease or a medical gluten-sensitivity. One thing for consumers to watch for is any wine or wine product that contains added colors or flavors, or that is made from barley malt, such as bottled wine coolers," says Marilyn Geller, CEO of the nonprofit Celiac Disease Foundation. Bottom line: Check the label. If the product is a straight red or white or rosé wine, then it is almost certainly gluten-free. Watch out for coolers or wine with added ingredients. Read labels. If you still have questions, do not hesitate to contact the winery directly. Read more at: WINESPECTATOR.COM
  2. Celiac.com 12/12/2018 - In a step that health officials say could provide immediate relief to the estimated eight million Indians who suffer from celiac disease, the Indian government is assessing a plan to require drugmakers to declare any gluten ingredients on medical labels. India’s chief drug advisory body will discuss the issue at its meeting scheduled in early December, said people with knowledge of the plan. The Drug Technical Advisory Board’s decision to address the issue of gluten-free labels for drugs and medicine comes on the heels of an active recommendation by the department of physical medicine and rehabilitation at the All India Institute of Medical Sciences (AIIMS). In addition to clear gluten-warnings on all medical labels, experts at AIIMS have proposed changing the law to force drug makers to actively avoid gluten-containing ingredients in drugs or medicine. The proposal aligns with guidelines drafted by the US Food and Drug Administration (FDA) in 2017. Those guidelines call for drug makers to properly label medications that contain gluten. The FDA also recommends that drug makers include a voluntary statement that indicates that the product contains no gluten, or any ingredient made from wheat, barley, or rye. Proper labeling of drugs and medicines is getting a great deal of attention from regulatory bodies over the last couple of years. Look for that trend to continue and for new guidelines to drive new labeling practices for medicines containing gluten ingredients. Overall, this is an extremely positive development for anyone with celiac disease or a medical gluten-sensitivity. Until such new guidelines make it to the pharmacy, be sure to check with your pharmacist about any drug or medicine you think might contain gluten. They are in a strong position to help, and can usually get answers to such questions. Lastly, stay tuned for more news on the official labeling decision by India's Drug Technical Advisory Board. Read more at: LIVEMINT.COM
  3. Celiac.com 12/06/2018 - The growing popularity of gluten-free foods has led to numerous new products for consumers, but it has also led to some problems. One recent study showed that up to one-third of foods sold as gluten-free contain gluten above 20ppm allowed by federal law. Other studies have shown that restaurant food labeled as “gluten-free” is often contaminated with gluten. The problem of gluten in commercial food labeled gluten-free is not isolated to the United States. Recent studies abroad show that the problem exists in nearly every gluten-free market in every country. In Australia, for example, researchers from the Walter and Eliza Hall Institute in Melbourne found detectable gluten in almost 3% of 256 commonly purchased “gluten-free” manufactured foods, a study published in the Medical Journal of Australia on Monday says. Furthermore, the study shows that nearly 10% of restaurant dishes sold as "gluten-free" contain unacceptable levels of gluten. Now, the Australians have a stricter standard than nearly anyone else, so look for them to be on top of potential problems with gluten contamination in gluten-free products. The study did not name the food manufacturers responsible for the contaminated products, but did note that better, more frequent gluten testing by manufacturers would make gluten-free foods safer for people with celiac disease. In a related study, the same researchers found in May that nearly one in ten samples of “gluten-free” dishes from restaurants within the City of Melbourne contained gluten levels in excess of the official Food Standards Australia New Zealand definition of gluten-free. “It’s troubling to think that these foods could be hindering the careful efforts of patients trying their best to avoid gluten,” an author of the study, Dr Jason Tye-Din, said. A spokeswoman from Coeliac Australia said the organization was taking the findings seriously. “The research team that conducted this study has liaised with the food companies and is following up the positive samples with further retesting to ensure the issue is resolved,” she said. In addition to urging consumers to be diligent in reading labels, and to report any suspect products, “Coeliac Australia advises all people with coeliac disease to have regular medical check-ups as they do have a serious autoimmune condition and medical assessment is important to determine that their gluten-free diet is going well and no complications are developing.” Read more at: TheGuardian.com
  4. Celiac.com 12/11/2018 - In most people without celiac disease or other gluten sensitivities, the gut does a pretty good job of processing gluten, and helps to prevent local inflammatory and immune responses. However, in about one percent of the population, gluten proteins from wheat and related cereals trigger an HLA DQ2/8‐restricted TH1 immune and antibody response, which triggers celiac disease. A team of researchers recently set out to assess the role of the cystic fibrosis transmembrane conductance regulator (CFTR) in orchestrating gliadin activities in celiac disease. The research team included Valeria R Villella, Andrea Venerando, Giorgio Cozza, Speranza Esposito, Eleonora Ferrari, Romina Monzani, Mara C Spinella, Vasilis Oikonomou, Giorgia Renga, Antonella Tosco, Federica Rossin, Stefano Guido, Marco Silano, Enrico Garaci, Yu‐Kai Chao, Christian Grimm, Alessandro Luciani, Luigina Romani, Mauro Piacentini, Valeria Raia, Guido Kroemer, Luigi Maiuri. Researchers understand that epithelial stress and innate immune activation are necessary for overcoming oral tolerance to the gluten gliadin. However, exactly how gliadin subverts host intestinal mucosal defenses is poorly understood. In their study, the research team shows that the α‐gliadin‐derived LGQQQPFPPQQPY peptide (P31–43) reduces the activity of cystic fibrosis transmembrane conductance regulator (CFTR), an anion channel pivotal for epithelial adaptation to cell‐autonomous or environmental stress. P31–43 binds to, and reduces ATPase activity in, the nucleotide‐binding domain‐1 (NBD1) of CFTR, thus interferes with CFTR function. This process creates epithelial stress, tissue transglutaminase and inflammasome activation, NF‐κB nuclear translocation and IL‐15 production, all of which can be blocked by potentiators of CFTR channel gating. The CFTR potentiator VX‐770 reduces gliadin‐induced inflammation and increases tolerance in gluten‐sensitive mice and cells from celiac patients. The team’s study shows that CFTR plays a central role in orchestrating gliadin activities, and presents potentially powerful new treatment direction for celiac disease. Source: The EMBO Journal (2018) DOI 10.15252/embj.2018100101 | Published online 29.11.2018 The researchers are variously affiliated with the European Institute for Research in Cystic Fibrosis, San Raffaele Scientific Institute, Milan, Italy; the Department of Comparative Biomedicine and Food Science, University of Padova, Padova, Italy; the Department of Molecular Medicine, University of Padova, Padova, Italy; the Department of Health Sciences, University of Eastern Piedmont, Novara, Italy; the Department of Experimental Medicine, University of Perugia, Perugia, Italy; the Pediatric Unit, Department of Translational Medical Sciences, Regional Cystic Fibrosis Center, Federico II University Naples, Naples, Italy; the Department of Biology, University of Rome “Tor Vergata”, Rome, Italy. Department of Chemical, Materials and Production Engineering, Federico II University Naples, Naples, Italy; the Department of Food Safety, Nutrition and Veterinary Public Health, Istituto Superiore di Sanità, Roma, Italy; the University San Raffaele and IRCCS San Raffaele, Rome, Italy; the Department of Pharmacology and Toxicology, Faculty of Medicine, University of Munich (LMU), Munich, Germany; the Institute of Physiology CH, University of Zurich, Zurich, Switzerland; the National Institute for Infectious Diseases IRCCS “L. Spallanzani”, Rome, Italy; the Centre de Recherche des Cordeliers, Equipe labellisée Ligue Nationale Contrele Cancer, Paris, France; the Centre de Recherche des Cordeliers, INSERM U, Paris, France; the Université Paris Descartes, Paris, France; the Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, Villejuif, France; the Pôle de Biologie, Hôpital Européen Georges Pompidou, AP‐HP, Paris, France; and the Department of Women's and Children's Health, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
  5. Celiac.com 12/05/2018 - Everyone with celiac disease has their war stories. Stories of uncomfortable of painful symptoms. Stories of tough, slow diagnosis. Of accidental gluten ingestion. Picture the worst case of celiac disease you can imagine with bad symptoms and a seemingly endless quest for a diagnosis. Now imagine you’re ten years old and that worst case is you. That’s the story of 10-year-old Lillian Bordoni, whose positive attitude is helping her to recover from the worst case of Celiac Disease that Children’s Hospital Colorado has ever seen, and inspiring even the doctors she credits with saving her life. Bordoni’s book, “Cecilia the Celiac Superhero,” tells the story of her long and complicated fight with celiac disease, and she prevailed via a diagnosis, a gluten-free diet, and eventually, a change of location. She hopes to someday share her story with others. It’s a story that starts when Lillian was around four years old and living with her family in Kansas. Lillian suffered from what were, in retrospect classic symptoms of celiac disease. However, a diagnosis remained elusive. The family saw numerous doctors until they found a doctor who tested her for celiac disease and made a formal diagnosis. Even after the whole family cut out gluten, Lillian will still unable to keep food down, and lacked the energy to play outdoors. Eventually, the Bordonis traveled to the celiac clinic at Children’s Hospital Colorado, where Dr. Edward Hoffenberg helped them to figure out that Lillian’s problems were being aggravated by the fact that the family lived “in the heart of wheat country,” said Lillian’s mom, Miriah Bordoni. “There was wheat farming all around us. There were four of the largest grain elevators within blocks of our house that were processing wheat 365 days a year.” Breathing gluten every day was not an option, so the family moved to Colorado. Ever since then, Lillian has been healthy. Her experience has inspired her to write a book about her challenges with celiac disease. Of her book, Lillian says “It’s about Cecilia which is this girl here, and she has to beat gluten and cross contamination, which I had to beat too, but I turned it into like a superhero story so that it would be fun and interesting for all kids.” Lillian is in the beginning stages of having her book published. Once that happens, Children’s Hospital Colorado will distribute copies to all newly diagnosed celiac patients. Read more.
  6. Celiac.com 11/19/2018 - People with celiac disease cannot reliably determine whether they ate gluten or not based on symptoms, however severe those symptoms may be, according to research presented by Amanda K. Cartee, MD, of the Mayo Clinic, and her colleagues, at the American College of Gastroenterology Annual Meeting in Philadelphia. Because there is presently no FDA-approved test to confirm gluten exposure, celiac patients commonly rely on the presence or absence of gastrointestinal or other symptoms as an indicator of gluten exposure. But how reliable is that method? Not very reliable at all, says Dr. Cartee. Now, the study was small, but it was also rigorous. Dr. Cartee and her associates developed a double-blind, placebo-controlled gluten challenge to identify the rapid onset of symptoms after gluten ingestion, and to figure out if celiac patients could really tell whether they had been exposed to gluten. Researchers recruited 14 patients with celiac disease and 14 healthy controls for the trial. They then randomly assigned each patient to receive either a 6 g gluten suspension or placebo. Each patient completed a 100 mm visual analog questionnaire to assess their symptoms at baseline, every 30 minutes to 60 minutes for 6 hours and then daily for 3 days. The researchers also asked patients at each time point if they believed they received gluten. During the study, only two of the seven celiac patients who received gluten were able to correctly identify the gluten suspension. Cartee said it took a full day for one patient to come to that conclusion, while another gave varied responses sporadically throughout the study. Nausea and abdominal pain were the most common symptoms for celiac patients. Interestingly, there was no statistical difference in symptoms in the gluten celiac disease group compared with the placebo celiac disease group. That is, celiac disease patients receiving the placebo reported symptoms that the same rate as those who received actual gluten. So, not only could the celiac patients not tell when they got gluten, they also couldn’t tell when they got a placebo. Dr. Cartee said because physical symptoms are subjective and non-specific, they are largely unreliable for self-diagnosing gluten exposure. Dr. Cartee is calling for the development of a better, more objective way to identify gluten-related symptoms, especially in celiac patients with ongoing gastrointestinal symptoms. Do you have celiac disease? Would you welcome an easy reliable way to determine gluten exposure? How would you find it helpful? Source: Healio
  7. Celiac.com 12/07/2018 - What do hypertension, obesity, smoking and celiac disease have in common? They’re all important risk factors for coronary heart disease (CHD), a disease that kills more than a half a million people annually in the U.S. alone.(1) Based on emerging research, celiac disease may be a major contributor to heart disease in the Western world –making celiac disease an even greater public health threat than is currently understood. CHD and Celiac Disease: A Brief History The connection between CHD and celiac disease has a 35-year history. It began with a 1976 study conducted by Southampton University Hospital researchers, who found that there was an “… apparent protective effect of coeliac disease on CHD risk which “…might result from malabsorption of dietary lipids.”(2) However, this study had a number of significant flaws including a small sample size of only seventy seven. The most significant confounder in this study was the mortality rate of young subjects, which precluded them from the privilege of living long enough to develop CHD. Additionally, our understanding of CHD has undergone a paradigm shift since the low-fat 1970’s. CHD is not the result of excess dietary fat consumption, but instead is a manifestation of prolonged inflammation.(3) Based on this study and two others published around the same time period which found no link between CHD and celiac disease, researchers largely stopped investigating the heart health of people with celiac disease. The assumption was that celiac disease provided protection or, at the very least, was benign in terms of CHD risk. Then came a paper published in the July 2003 Archives of Internal Medicine which reported that celiac disease patients had a sixty percent increased risk of CHD death.(4) More recently, in a January 2011 Circulation paper, Swedish researchers published eye-catching results from an investigation of more than 15,000 individuals with celiac disease.(5) The key finding from this research was an approximately twenty percent increased risk of CHD death in people with celiac disease. While this research remains in its infancy, the biological connections between celiac disease and CHD are crystal clear, bolstering the epidemiological findings that people with celiac disease are at heightened CHD risk. CHD Today Before delving into the physiological link between CHD and celiac disease, it’s crucial to understand the pathogenesis of atherosclerosis, or narrowing of the heart’s arteries. Atherosclerosis begins with an injury to the endothelial lining of the coronary artery. A hyperactive response by immune cells, particularly macrophages and inflammatory cytokines, causes macrophage cells to become lodged inside the injured endothelium. Through a complex cascade of cell signaling, “trapped” macrophages transform into what are known as foam cells. These foam cells take in circulating blood lipids, especially low density lipoproteins (LDL). Over time this LDL/foam cell mishmash transforms into the arterial plaque most people are familiar with.(6) Inflammation fuels atherosclerosis from start to finish –from the initial injury to the development and accumulation of plaque. The Inflammation Connection Unfortunately, inflammation is something that people with celiac disease have more than enough of. Serum C-reactive protein (CRP) is a commonly used parameter for celiac disease diagnoses –suggesting that nearly all uncontrolled celiac disease patients have elevated inflammation levels.(7) CRP also happens to be a more sensitive indicator of impending heart disease risk than serum cholesterol. Cleveland Clinic cardiologist Eric Topol claims that “…in the past, people talked about their cholesterol levels. In the next decade everyone will need to know their C-reactive protein level (a marker of inflammation).”(8) Other inflammatory mediators –such as IL-6 and TNF-a—are also present in greater amounts in celiac disease patients compared to the general population. In addition to the inflammatory response to ingested gluten, a March 2009 genetic analysis found that individuals with celiac disease were more likely to have polymorphisms that promote inflammatory cytokine production. (9) Other Links in the Chain And, there’s more to this celiac disease/CHD story than inflammation. People with celiac disease tend to have comorbidities that compound celiac disease’s damage to the cardiovascular system. Fat Malabsorption Dietary fats are a heart-health double edged sword. Excessive intake of trans fats are strongly linked to dyslipidemia and heart disease. However, a recent American Journal of Clinical Nutrition meta-analysis which included over 340,000 research subjects in its analysis found no connection between saturated fat and heart disease. (10) Monounsaturated and polyunsaturated fats are protective against atherosclerosis. Omega-3 fats appear to confer a particularly strong cardiovascular disease prevention benefit.(11) Adequate intake and absorption of fats is crucial for CHD prevention. Indeed, a low-fat dietary pattern was shown to increase heart disease risk in a large-scale randomized control trial involving more than 48,000 subjects.(12) Absorption of dietary fats is severely impacted by celiac disease due to villous atrophy, pancreatic insufficiency and dysbiosis. Lewis et al found that untreated celiac disease patients had approximately twenty one percent lower serum cholesterol levels compared to the general population, suggesting severe fat malabsorption.(13) Based on this research and others it’s conceivable that many celiac disease patients don’t absorb the dietary fats required to combat heart disease. Vitamin Malabsorption Suboptimal nutrient absorption is a near-universal issue in celiac disease patients – even for individuals consuming a gluten free diet. Fat soluble vitamin absorption is particularly affected by celiac disease.(14) Poor absorption of fat soluble vitamins E and D has been tied to increased heart disease risk in several studies. (15) Homocysteine Homocysteine is an amino acid that becomes elevated in cases of vitamin B6, folic acid or vitamin B12 deficiency. Poor B-complex vitamin absorption is common in both newly diagnosed celiac disease and in celiac disease patients following a gluten free diet.(16) An October 2002 Meta-analysis found that homocysteine levels twenty five percent above normal levels boosted heart attack risk by eleven percent.(17) Due to its strong correlation with heart disease, the American Heart Association suggests that individuals with malabsorption symptoms, including celiac disease, should be screened for homocysteine.(17) Simone Saibeni, MD and her University of Milan colleagues justified this recommendation by finding that celiac disease patients were 3.5 times more likely to have elevated hyperhomocysteinemia than the general population.(16) Type 1 Diabetes (DM1) Approximately five percent of people with celiac disease also suffer from DM1.(18) Hyperglycemia promotes inflammation, endothelium stiffness and arterial plaque formation. Rheumatism Symptoms of rheumatism, especially Sjogrens syndrome and unexplained joint pain, are common symptoms of undiagnosed celiac disease. Lubrano et al found that twenty five percent of individuals with celiac disease also have arthritis.(19) A 2008 population study discovered that people with rheumatoid arthritis have double the heart attack and stroke risk of the general population.(20) Whole Grain Intake Whole grain intake is strongly associated with a decreased risk of CHD.(21). Avoidance of fortified whole grains by people with celiac disease may impact dietary intake of B-vitamins, dietary fiber and antioxidants. How People With Celiac Disease Can Fight CHD Preventing CHD in the celiac disease population isn’t dramatically different from what’s typically recommended to the general population. Maintaining a healthy body weight, eating adequate amounts of dietary fiber, staying physically active, avoiding trans fats and consuming monounsaturated fats regularly are the keys to cardiovascular health whether or not one has been diagnosed with celiac disease. However, there are a few important heart health caveats that those with celiac disease should keep in mind. Gluten-Free Diet The importance of a 100 percent gluten free diet for CHD risk reduction and overall health cannot be emphasized enough. Not only is it the most effective treatment for celiac disease, but it is also critical for limiting the inflammatory response that promotes atherosclerosis.(22,23) Additionally, a strict gluten free diet allows the intestine to heal and recover, boosting absorption of nutrients necessary for cardiovascular health. Multivitamin Supplementation Multivitamin/Multimineral supplementation is standard treatment for celiac disease today.(24) Supplementation helps partly compensate for malabsorption and suboptimal intake of vitamins and minerals. A multivitamin supplement for CHD prevention should include at least 100 percent of the RDA for folic acid, vitamin B12, vitamin B6, and fat-soluble vitamins D and E. Dietary Fats “Fat is the most commonly and severely affected nutrient in celiac disease,” reports Jay W. Marks, M.D., of Baylor University College of Medicine.(25) Individuals with celiac should aim to consume at least twenty five percent of their calories in the form of dietary fat. Healthy monounsatured and polyunsatured fat sources such as extra virgin olive oil, nuts, legumes, fatty fish, and seeds should form the foundation of a heart healthy celiac disease diet. Pancreatic enzymes may be used to aid lipid absorption and reduce gastrointestinal symptoms like diarrhea and bloating. Omega-3 Fats Omega-3 fats reduce inflammation, increase HDL cholesterol and make cardiovascular arteries resistant to injury. Zhang et al discovered that habitual fish consumption was associated with a forty percent reduction in CHD mortality in healthy populations.(26) Omega-3 fatty acids may have additional benefits for celiac disease patients, especially acceleration of intestinal healing. Celiac disease patients should consume fatty fish like mackerel and salmon at least twice weekly. Conclusion Celiac disease needn’t be an automatic CHD death sentence. Although the connection between heart disease and celiac disease is very real, lifestyle changes can dramatically reduce the chances that someone with celiac disease will develop CHD. Simply eating a gluten-free diet, supplementing with vitamins, minerals and pancreatic enzymes and consuming omega-3 fats –four measures that those with celiac disease should be doing anyway – will shield the cardiovascular system from much of the celiac disease-derived damage that can lead to CHD. In fact, this new link can ultimately become a net positive for many celiac disease patients as it can motivate them to become more proactive and aggressive in their self-care. References: 1. Centers for Disease Control and Prevention; Heart Disease Facts; Available at: https://www.cdc.gov/heartdisease/facts.htm. Accessed April 18th 2011. 2. Whorwell PJ, Foster KJ, Alderson MR, Wright R. Death From Ischaemic Heart-Disease and Malignancy in Adult Patients With Celiac Disease. Lancet 1976;113-114. 3. Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease, application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation [serial online].2003;107:499-511 4. Peters U, Askling J, Gridley G, et al. Causes of death in patients with celiac disease in a population-based Swedish cohort. Arch Intern Med. 2003;163:1566–1572. 5. Ludvigsson JF, James S, Askling J, Stenestrand U, Ingelsson E. Nationwide cohort study of risk of ischemic heart disease in patients with celiac disease. Circulation. 2011 Feb 8;123(5):483-90 6. Gotta A, Farmer F. Atherosclerosis: Pathogenesis, Morphology, and Risk Factors. Cardiovascular Medicine. 3rd Edition, Springer, London, pp. 1593-1613. 7. Lahat N, Shapiro S, Karban A, et al. Cytokine profile in coeliac disease. Scand J Immunol 1999;49:441–446 8. Role of inflammation-Growing proof inflammation is a major risk factor for heart disease. Available at: http://www.clevelandclinic.org/heartcenter/pub/news/hot/inflammation8_02.asp?firstCat=1&secondCat=429&thirdCat=524. Updated 8/02. Accessed April 18th 2011. 9. Dema B, Martínez A, Fernández-Arquero M, The IL6-174G/C polymorphism is associated with celiac disease susceptibility in girls. Hum Immunol 2009;70:191-4 10. Siri-Tarino SW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr [serial online]. 2010;91:535-546. 11. Perez-Jimenez F, Lopez-Miranda J, Mata P. Protective effect of dietary monounsaturated fat on arteriosclerosis: beyond cholesterol. Atherosclerosis 2002;163:385–98 12. Howard BV, Van Horn L, Hsia J, et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA. 2006; 295:655-66 13. Lewis NR, Sanders DS, Logan RF, Fleming KM, Hubbard RB, West J. Cholesterol profile in people with newly diagnosed coeliac disease: a comparison with the general population and changes following treatment. Br J Nutr. 2009 Aug;102(4):509-13 14. Hallert C, Grant C, Grehn S, Granno C, Hulten S, Midhagen G, Strom M, Svensson H, Valdimarsson T. Evidence of poor vitamin status in coeliac patients on a gluten-free diet for 10 years. Aliment Pharmacol Ther. 2002;16:1333–1339 15. Sesso HD et al.Vitamins E and C in the prevention of cardiovascular disease in men: the Physicians’ Health Study II randomized controlled trial. JAMA. 2008 Nov 12;300(18):2123-33 16. Saibeni S, Lecchi A, Meucci G, et al. Prevalence of hyperhomocysteinemia in adult gluten-sensitive enteropathy at diagnosis: role of B12, folate, and genetics. Clin Gastroenterol Hepatol 2005;3:574e80 17. Malinow MR, Bostom AG, Krauss RM. Homocyst(e)ine, diet, and cardiovascular diseases: a statement for healthcare professionals from the Nutrition Committee, American Heart Association. Circulation. 1999;99:178–182 18. Ludvigsson JF, Olsson T, Ekbom A, Montgomery SM. A population-based study of coeliac disease, neurodegenerative and neuroinflammatory diseases. Aliment Pharmacol Ther 2007; 25:1317 19. Lubrano E, Ciacci C, Ames PR, et al. The arthritis of celiac disease: prevalence and pattern in 200 adult patients. Br J Rheumatol 1996;35:1314-8 20. Dhawan SS, Quyyumi AA. Rheumatoid arthritis and cardiovascular disease. Curr Atheroscler Rep. 2008;10:128-133 21. Jensen MK, Koh-Banerjee P, Hu FB, et al. Intakes of whole grains, bran, and germ and the risk of coronary heart disease in men. Am J Clin Nutr. 2004;80(6):1492-1499 22. Meresse B, Cerf-Bensussan N. Celiac disease: from oral tolerance to intestinal inflammation, autoimmunity and lymphomagenesis. Mucosal Immunol. 2009;2:8e23 23. Popa C, Netea MG, van Riel PL, van der Meer JW, Stalenhoef AF. The role of TNF-a in chronic inflammatory conditions, intermediary metabolism, and cardiovascular risk. J Lipid Res. 2007;48:751–62 24. See J, Murray JA. Gluten-free diet: the medical and nutrition management of celiac disease. Nutr Clin Pract. 2006;21(1):1-15. 25. Marks, J. “Celiac Disease (Gluten Enteropathy)”Available at: https://www.medicinenet.com/celiac_disease_gluten_enteropathy/article.htm. Accessed April 29th 2011. 26. Zhang J, Sasaki S, Amano K, et al. Fish consumption and mortality from all causes, ischemic heart disease, and stroke: an ecological study. Prev Med. 1999; 28: 520–529.
  8. Celiac.com 11/26/2018 - Many people with celiac disease suffer from headaches. A team of researchers recently set out to more thoroughly explore the relationship between celiac disease and headaches. The research team included Panagiotis Zis, Thomas Julian, and Marios Hadjivassiliou. They are variously affiliated with the Academic Department of Neurosciences, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield S10 2JF, UK, and the Medical School of the University of Sheffield in Sheffield, UK. The team's goal was to establish the relationship between headaches and celiac disease, and vice versa, to explore the role of a gluten-free diet, and to describe the imaging findings in celiac patients affected by headaches. For their systematic review and meta-analysis, the team reviewed 40 articles published in the the PubMed database between 1987 and 2017. They included information regarding study type, population size, the age group included, prevalence of celiac disease among those with headache and vice versa, imaging results, the nature of headache, and response to gluten-free diet. They found that the average pooled rate of headaches in celiac patients was 26% (95% CI 19.5–33.9%) in adult populations and 18.3% (95% CI 10.4–30.2%) in pediatric populations. The headaches usually resemble migraines. Children with headaches of unknown origin, have celiac disease rates of 2.4% (95% CI 1.5–3.7%). There is presently no good data for adult populations. In such cases, brain imaging can be normal, but can also reveal cerebral calcifications with CT, white matter abnormalities with MRI, and deranged regional cerebral blood flow with SPECT. The good news is that a gluten-free diet seems to be an effective treatment. Up to 75% of celiac patients saw their headaches resolve when they followed a gluten-free diet. Celiac patients have high rates of idiopathic headache (that is, headaches of unknown cause), and patients with such headaches have higher rates of celiac disease. Therefore, patients with headache of unknown origin should be screened for celiac disease, since they may gain symptom relief from a gluten-free diet. Source: Nutrients 2018, 10(10), 1445; doi:10.3390/nu10101445
  9. Celiac.com 11/28/2018 - Patients with gluten ataxia without enteropathy have lower levels of antigliadin antibodies (AGA) compared to patients with celiac disease. Magnetic Resonance Spectroscopy (NAA/Cr area ratio) of the cerebellum improves in patients with gluten ataxia following a strict gluten-free diet, and is associated with an improvement in symptoms. A team of researchers recently set out to present their experience of the effect of a gluten-free diet in patients with ataxia and low levels of AGA antibodies measured by a commercial assay. The research team included Marios Hadjivassiliou, Richard A Grünewald, David S Sanders, Panagiotis Zis, Iain Croall, Priya D Shanmugarajah, Ptolemaios G Sarrigiannis, Nick Trott, Graeme Wild, and Nigel Hoggard. They are variously affiliated with the Academic Departments of Neurosciences and Neuroradiology; the Departments of Gastroenterology, the Departments of Dietetics; the Departments of Immunology, Sheffield Teaching Hospitals NHS Trust, in Sheffield, UK. The team conducted MR spectroscopy on 21 consecutive patients with ataxia and serum AGA levels below the positive cut-off for celiac disease, but above a re-defined cut-off in the context of gluten ataxia, at baseline and after a gluten-free diet. Of the 21 included patients with gluten ataxia, the team found that ten were on a strict gluten-free diet with elimination of AGA, 5 were on a gluten-free diet, but continued to have AGA, while 6 patients did not follow a gluten-free diet. The NAA/Cr area ratio from the cerebellar vermis increased in all patients on a strict gluten-free diet, increased in only 1 out of 5 patients on a gluten-free diet with persisting circulating AGA, and decreased in all patients who did not follow a gluten-free diet. From these results, the team concludes that patients with ataxia and low levels of AGA benefit from a strict gluten-free diet. The results suggest an urgent need to redefine the serological cut-off for circulating AGA in the diagnosis of gluten ataxia. Read more in Nutrients 2018, 10(10), 1444; doi:10.3390/nu10101444
  10. Celiac.com 11/23/2018 - The complex factors that lead to the development of celiac disease in a given individual are the subject of much research. The immune system, genetics and the environment (meaning factors in an individual’s life that would influence the development of disease) all play an important part in this process. Current research on celiac disease focuses on the immune system; scientists are working to understand the exact chain of events that occur in the gut when gluten is introduced for the first time. Understanding these events could yield insight into treatments for celiac disease that interrupt this process. Celiac disease is the only autoimmune disorder where the trigger is known: gluten. Researchers use celiac disease as a model for studying the pathogenesis of other autoimmune diseases. Other researchers are examining the role of environmental factors and the added risk they bring to an individual who already is at risk for celiac disease. These factors include the influence of breastfeeding, the timing of the introduction of cereals, intestinal infection as a precursor to celiac disease, cultural factors, geography, and more. Genetic research has determined that there are two genetic haplotypes that are necessary for the development of celiac disease; an affected individual need only to have one of these genetic haplotypes to be at risk. These factors are HLA DQ2 and HLA DQ8. HLA stands for Human Leukocyte Antigen. Antigens are substances that produce an immune response—we have many antigens in our bodies that are supposed to do that. HLA are molecules that present on the surface of cells to help the immune system to distinguish antigens that are supposed to be in the body, versus antigens that aren’t. While other genes may play a role in the process, we can conclude with virtual certainty that an individual who tests negative for DQ2 or DQ8 will not develop celiac disease. We also know that 30% of the US population has the genetic makeup for celiac disease. While it is encouraging to see a surge of interest in celiac disease research, people with celiac disease have to make choices every day that affect their health, and knowing a bit more about the immune system may make this process easier. Myths about what it means to have an autoimmune disorder are common. Knowledge about this area can help one sort out the myths and find the facts about what it means to have celiac disease. What Does the Immune System Do? The immune system provides the human body with several levels of defense from foreign invaders like bacteria and viruses. The first layer of protection is our skin. If an invader finds its way into the body, however, the second level of defense mobilizes to destroy the invader before it can replicate. Some types of invaders already replicate and invade surrounding cells before the immune system can destroy them—and there is a sophisticated type of immune response to eliminate these types of invaders. The most important decision that the immune system makes when it encounters an “invader” is to determine whether or not it is “self” (is it supposed to be in the human body?) or “non-self” (is this a virus or bacteria that will cause illness?). HLA helps the immune system by tagging cells as “self” or “non-self” to allow the immune system to attack the true invaders. In the case of celiac disease, HLA tags the antigen presenting cell as non-self, when it should be tagged as self. The human body as a house Think of the human body as a house. The exterior of the house (the roof, the brick, the door, and the windows) is like the skin of a human body, protecting everything inside. The house has an alarm system, to detect invaders. The alarm system is the body’s immune system. There is a cat inside the house, sleeping on the couch. How is the immune system supposed to work? If a burglar (who is not supposed to be in the house) comes to the side window and tries to break in, there may be a broken window, but the alarm sounds and the burglar runs away. Everything inside the house is safe. How does the immune system work when someone has celiac disease? The cat wakes up from its nap and gets a drink of water. The alarm goes off, when it’s not supposed to. The cat sets off the alarm every time it moves, but other than this, the alarm works perfectly, keeping out all of the true invaders. In other words, the immune system of an individual with celiac disease is healthy and normal in every respect, save one. The presence of gluten, and only gluten, causes a malfunction of the immune system. In our example, the cat represents gluten—it is supposed to be in the house, yet every time it moves the alarm goes off. This means that removing gluten from the diet of a person with celiac disease returns their immune system to a normal and healthy state, equal to that of someone who does not have celiac disease. Many people with celiac disease feel that they are immune compromised, which is not the case. If the house in our example represented someone with an immune compromised condition, the alarm would rarely if ever go off (invaders could enter the body without any resistance). For this reason, flu shots for people with celiac disease do not represent a concern (unless you are allergic to eggs) and people with celiac disease should receive the shot with the general population, and not the special populations who are immune compromised (the elderly, children, etc.). When should gluten be introduced to a child at risk for celiac disease? When a person with celiac disease has a baby, there is a great deal of concern regarding the child’s potential for developing celiac disease—this is understandable. One of the most troubling questions facing parents is when to introduce gluten to their child. It is a common recommendation to delay the introduction of gluten until one year of age. Unfortunately, this recommendation is based on wheat allergy, and not autoimmunity. Fortunately, recent research published in the Journal of the American Medical Association has affirmed earlier research from Finland on this subject as well as what has been a common practice throughout Europe. A protective window Researchers at the University of Colorado recently announced the results of a 10 year study on the introduction of cereals in children at risk for celiac disease. Their study demonstrated that infants who received cereals containing gluten between four to six months of age were not as likely to develop celiac disease by the age of five as were children who received gluten containing cereals at younger and older ages. The infants who received cereals between one and three months of age were five times as likely to develop celiac disease, and children who received cereals after six months of age had an elevated risk for developing celiac disease, but not to the extent of the youngest age group. Is it a gluten response? Many parents are concerned about whether or not their child will have an autoimmune response to gluten when introduced to cereals. It may help to know that it typically takes six to nine months for a child to mount an autoimmune response to gluten—if celiac disease is to occur early in their life. Therefore, a response (such as diarrhea or vomiting) shortly after cereals are introduced or eaten is usually not related to celiac disease. What about breast milk? A mother with celiac disease needs to remain on the gluten-free diet throughout pregnancy and breast-feeding. However, it is a common misconception that breast-feeding moms who are not celiac should go on a gluten-free diet while nursing. Microscopic amounts of gluten are carried in breast milk, but it is not enough to harm a child. In fact, research from Finland shows that breast milk has a protective effect in the gut when gluten is introduced to a child. This research recommends that when introducing gluten between four and six months of age, breast feeding should continue during this time to confer an added immune benefit. Understanding a bit more about the immune system may be helpful as you make decisions about your health, and the health of your family. It can be reassuring to know that the immune system of a person with celiac disease on the gluten-free diet is as healthy as an average person without celiac disease.
  11. Celiac.com 11/13/2018 - Ubiquitin is highly conserved across eukaryotes and is essential for normal eukaryotic cell function. The bacterium Bacteroides fragilis is part of the standard human gut microbiome, and the only bacterium known to encode a homologue of eukaryotic ubiquitin. The B. fragilis gene sequence points to a previous horizontal gene transfer from a eukaryotic source. The sequence encodes a protein (BfUbb) with 63% identity to human ubiquitin, which is exported from the bacterial cell. Is molecular mimicry of human ubiquitin by gut microbe linked to autoimmune diseases like celiac disease? A team of researchers recently set out to determine if there was antigenic cross‐reactivity between B. fragilis ubiquitin and human ubiquitin and also to determine if humans produced antibodies to BfUbb. The research team included L. Stewart, J. D. M. Edgar, G. Blakely and S. Patrick. They are variously affiliated with the School of Biological Sciences, University of Edinburgh, Edinburgh, UK; the School School of Biological Sciences, Queen’s University Belfast, Belfast, UK; the Regional Immunology Laboratory, Belfast Health and Social Care Trust, Belfast, UK; and the Wellcome‐Wolfson Institute for Experimental Medicine, Queen’s University Belfast, Belfast, UK. Molecular model comparisons of BfUbb and human ubiquitin predicted likely structural similarity with 99.8% confidence. The team used linear epitope mapping to identify cross-reacting epitopes in BfUbb and human ubiquitin. Also, at least one epitope of BfUbb does not cross‐react with human ubiquitin. The team used enzyme‐linked immunosorbent assay to compare the reaction of human serum to BfUbb and human ubiquitin from 474 subjects among four groups: (1) newly autoantibody‐positive patients, (2) allergen‐specific immunoglobulin (Ig)E‐negative patients, (3) ulcerative colitis patients and (4) healthy volunteers. The team’s data show that the exposure to BfUbb into the human immune system triggers the creation of IgG antibodies. Patients referred for first‐time autoimmune disease testing are more likely to have a high levels of antibodies to BfUbb than are healthy volunteer subjects. From this, the team concludes that molecular mimicry of human ubiquitin by BfUbb could be a trigger for autoimmune disease. Finding and understanding potential triggers for autoimmune conditions helps to take us one step further to understanding and potentially curing celiac disease. Stay tuned for further developments in their arena. First published: 04 August 2018 https://onlinelibrary.wiley.com/doi/full/10.1111/cei.13195
  12. Celiac.com 11/12/2018 - Here’s an uplifting celiac story. Now, this happened a while back, but it's all just coming to light in the way that so many warm and fuzzy family stories do. It starts like this: Once upon a time, a simple check for celiac disease opened the door to parenthood for couple. Just over ten years ago, AnnMarie Bradley from Celbridge, Co Kildare, thought she’d never become a mother. After two devastating miscarriages over a decade, Bradley, who is 47 years old, and her husband Christopher (48) were at wit’s end. "I was just heartbroken,” said Ms Bradley. Then, a simple visit to her doctor changed everything. A blood test indicated she might have celiac disease, which further evaluation confirmed. She began a gluten-free diet, and less than a year later, Bradley was pregnant with her son, Cameron. “Being a mother had been everything I'd wanted," she said. Cameron is nearly 16 now, and has an 11-year old sister, Emily. And they all lived happily and gluten-free ever after. In the UK, the Coeliac Society advises women struggling to conceive to consider celiac testing. Read more at: Independent.ie
  13. The following was written by Dr. Joseph Murray, one of the leading USA physicians in the diagnosis of celiac disease (celiac disease) and dermatitis herpetiformis (DH). Dr. Murray (murray.joseph@mayo.edu) of the Mayo Clinic Rochester, MN, is a gastroenterologist who specializes in treating Celiac disease: In response to your questions about DH, The following represents my views about this curious and very itchy condition. In general DH is a severely itchy skin condition that often starts abruptly, affecting the elbows knees buttocks and scalp and the back. It usually starts as little bumps that can become tiny blisters and then are usually scratched off. It can occur in one spot only but usually occurs in many different areas. The condition is related to the deposit under the skin of IgA deposits. These occur in response to the ingestion of gluten in the diet. However, once deposited there, they are only slowly cleared by the body even when the individual is gluten free. While most individuals with DH do not have obvious GI symptoms almost all have some damage in their intestine. They the potential for all of the nutritional complications of celiac disease. The diagnosis is made by taking a skin biopsy and performing immunoflorescence studies on it (a specialized type of stain in major laboratories) The test is usually reliable but it takes a significant dedication to detect early cases where there is a short history of rash rather than years or months of rash. It is unusual to develop DH after the start of a GFD for celiac disease. About 5 % of celiac disease patients will develop DH usually in the first 6-12 months. This probably reflects the long lasting nature of the deposits under the skin. Treatment for DH is twofold. (1) Remove the cause: gluten. (2) Suppress the skin response with drugs such as Dapsone or some other sulphones. The latter is the most common treatment used as it is rapidly relieves the itch. However there are some side effects associated with these medications and they need to be taken under medical monitoring with blood tests to detect side effects. It is my practice that DH should be treated with a gluten-free diet for life and use of drugs to get immediate relief in the short term. It is usually possible to get patient off the Dapsone after several months of a strict gluten-free diet. The most common complication of DH is scarring which usually fades with time. Occasionally there can be secondary infection from scratching. There is probably a slightly increased chance of malignancy in those with DH who are not on a gluten-free diet. Several physical triggers are known to set off an attack of DH, especially exposure to iodides and bromides which are contained in household cleaners. A very good reference for DH is available from the GIG in Washington.
  14. The following detailed explanation of serological tests for celiac disease was written by Tom Ryan, Technical Service Specialist, INOVA Diagnostics, Inc. There has been a lot of discussion about serological testing for celiac disease recently, specifically regarding tTG (tissue Transglutaminase) testing. I will try to answer some of the many questions that have appeared on this list about all of the tests. First, and this applies to any of the blood tests, you must currently be on a gluten containing diet for the tests to be accurate. Antibodies are produced by the immune system in response to substances that the body perceives as threatening. The immune response that your body produces is its response to being exposed to gluten in the diet and its subsequent effect on the intestinal mucosa. If there is no gluten in the diet, then there is no response that we can measure. A brief change in diet will not have a noticeable effect. If you have been gluten free for a week or so, it will not make any great difference. The response might be marginally less but the difference is insignificant because the body has not had time to respond to the change. Conversely, if you have been gluten free for a protracted period of time and decide to be tested, a brief challenge of a couple of weeks is not enough to elicit a response and get an accurate test. There are several steps that take place to generate an immune response and it takes time both for the positive reaction when gluten is present and to clear the antibodies when gluten is eliminated. There has been a great deal of discussion about how much and how long a challenge should be and there is no consensus. Talk with your Doctor. My personal feeling is that the minimum is 2 slices of bread per day for 6 weeks to get an accurate test but I would not try to second-guess the Doctor. There are basically four tests that can be performed to aid in diagnosing celiac disease. Notice that I say they will aid in diagnosing celiac disease. Immunology is fairly accurate but it is far from being an exact science. All of the lab tests, regardless of the type or source, are presented as aids to diagnosis. They should not be used alone as a basis for diagnosis but rather are intended to be considered in conjunction with the physical examination of the patient as well as the reported symptoms, etc. by a trained physician. There has been a great deal of confusion about what the tests are and I hope to alleviate some of the misunderstandings. There are many terms that we hear. tTG, IgA, IgG, ELISA, etc. What are all of these? Some contributors to the list make reference to the IgA or IgG test or to the ELISA test. These labels are incomplete for our purposes and could be referring to any number of different tests. We all have, within our bodies, a family of closely related although not identical proteins which are capable of acting as antibodies. These are collectively referred to as immunoglobulins. Five major types of immunoglobulins are normally present in the human adult. They are IgG, IgA, IgM, IgE and IgD. Each of these is a shorthand way of writing immunoglobulin gamma G (or A or M, etc.) and they each perform a different function in our systems. IgG is the principal immunoglobulin in human serum. It is important in providing immunity in a developing fetus because it will pass across the placental barrier. IgA is the principal immunoglobulin in secretions from respiratory and intestinal mucosa. IgE is a gamma globulin produced by cells lining the intestinal and respiratory tracts. It produces the antibodies associated with most hypersensitivity (allergic) responses. It is associated with asthma, hay fever, etc. IgM is a globulin formed in almost every immune response in the early part of the reaction. IgD is a rare protein present in normal sera in a tiny amount. These designations refer to the type of protein that is carrying the antibody in question. Both IgG and IgA subtypes of anti-gliadin antibody are produced, hence we refer to them as IgG gliadin or IgA gliadin. Collectively they are anti-gliadin antibodies. Anti-Gliadin Antibodies: Both IgA and IgG anti-gliadin antibodies (AGA) are detected in sera of patients with gluten sensitive enteropathy (celiac disease). IgG anti-gliadin antibodies are more sensitive but are less specific markers for disease compared with IgA class antibodies. IgA anti-gliadin antibodies are less sensitive but are more specific. In clinical trials, the IgA antibodies have a specificity of 97% but the sensitivity is only 71%. That means that, if a patient is IgA positive, there is a 97% probability that they have celiac disease. Conversely, if the patient is IgA negative, there is only a 71% probability that the patient is truly negative for celiac disease. Therefore, a positive result is a strong indication that the patient has the disease but a negative result does not necessarily mean that they don not have it. False positive results are rather uncommon but false negative results can occur. On the other hand, the IgG anti-gliadin antibodies are 91% specific and have an 87% sensitivity. This means that they will show positive results more readily but there is not as strong a correlation with celiac disease. It is less specific. Patients with other conditions but not afflicted with celiac disease will occasionally show positive results. IgG anti-gliadin antibodies are detectable in approximately 21% of patients with other gastrointestinal disorders. This test might yield false positive results but is less likely to yield false negative results. A sensitive testing protocol includes testing for both IgA and IgG anti-gliadin antibodies since a significant portion of celiac patients (approx. 2-5%) are IgA deficient. This combined IgA and IgG anti-gliadin antibody assay has an overall sensitivity of 95% with a specificity of 90%. The type of test used to detect the anti-gliadin antibodies is called an ELISA. This is an acronym and it stands for Enzyme Linked Immuno-Sorbent Assay. ELISA is not a test in itself. It is a method of testing and it is a relatively simple test to perform. It involves putting a measured amount of diluted patient serum into the wells of a specially constructed and prepared plate and incubating it for a period of time with various chemicals. The end result is a color change, the intensity of which is dependent upon the concentration of anti-gliadin antibody (or other protein being measured) in the patient serum. The ability of this colored solution to absorb light at a particular wavelength can be measured on a laboratory instrument and mathematically compared with solutions that contain a known amount of anti-gliadin antibody to arrive at a number for the amount of antibody present. The sample can then be classified as negative, (0-20 units); weak positive, (21-30 units); or moderate to strong positive if greater than 30 units. The purpose of testing for anti-gliadin antibodies includes, in addition to diagnosis of gluten sensitive enteropathy, monitoring for compliance to a gluten free diet. IgA gliadin antibodies increase rapidly in response to gluten in the diet and decrease rapidly when gluten is absent from the diet. The IgA anti-gliadin antibodies can totally disappear in 2-6 months on a gluten free diet, so they are useful as a diet control. By contrast, IgG anti-gliadin antibodies need a long time, sometimes more than a year, to become negative. The reverse is also true. That is, a patient with celiac disease who has been on a gluten free diet and tests negative for IgA anti-gliadin antibodies, will show a rapid increase in antibody production when challenged by gluten in the diet. Approximately 90% of challenged patients will yield a positive IgA anti-gliadin result within 14-35 days after being challenged. The IgG antibodies are somewhat slower. Endomysial Antibodies: IgA class anti-endomysial antibodies (AEA) are very specific, occurring only in celiac disease and DH. These antibodies are found in approximately 80% of patients with DH and in essentially 100% of patients with active celiac disease. IgA endomysial antibodies are more sensitive and specific than gliadin antibodies for diagnosis of celiac disease. Antibody titers (dilutions) are found to parallel morphological changes in the jejunum and can also be used to reflect compliance with gluten-free diets. Titers decrease or become negative in patients on gluten free diets and reappear upon gluten challenge. The test for anti-endomysial antibodies is more subjective and more complicated for the lab to perform than the anti-gliadin assays. It involves serially diluting some of the patients serum, that is, diluting it by ½ then ¼, 1/8, 1/16, etc. and putting these dilutions on a glass slide that has some sort of tissue affixed to it. The slide is then processed with various solutions and examined under a fluorescent microscope to determine if any of that serum binds to any of the proteins in the tissue. If so, then that patient is confirmed as having antibodies to that particular protein. This method of testing is called an IFA or sometimes IIFA. It stands for Indirect Immuno-Fluorescent Assay. The selection of which tissue slide to use is determined by what specific protein, hence which antibody, you are specifically looking for. Endomysial antibodies react with the endomysium, which is a sheath of reticular fibrils that surround each muscle fiber. Therefore, to detect endomysial antibodies, you would want to use a tissue substrate that contains a lot of muscle tissue. The substrate used most often for this assay is distal sections of the esophagus. These are very thinly sliced and fixed to the slide. They contain muscle fibers and not much else so there is a lot of endomysium available to react with the anti-endomysial antibodies. Reading this test involves viewing the reacted slides with a fluorescent microscope to make the determination. This requires a highly skilled and trained eye and, of necessity, is somewhat subjective. You are looking for a green fluorescence in the endomysium covering the muscle fibers. The test is reported as the titer or final dilution in which the fluorescence can still clearly be seen. As you can imagine, this is very subjective. There are no standardized values and it is up to the judgment of the particular technician what the endpoint titer is. Recently, (1998) the endomysial antigen targeted by the anti-endomysial antibodies was identified as the protein cross-linking enzyme known as tissue transglutaminase (tTG). This has enabled the production of an antigen specific ELISA assay incorporating tTG as a reliable and objective alternative to the traditional and subjective Immunofluorescence based assays. In clinical trials, the correlation with the endomysial IFA assay has been shown to be close to 100%. This is a test that has been very well received in the professional community. It is an ELISA, like the anti-gliadin antibody test and, as such, is not subject to interpretation like the IFA. That is the greatest advantage to this new test! With this or any ELISA, the response is measured on an instrument that calculates the amount of light of a particular wavelength that is absorbed by the solution and prints out a numerical result. There is no chance of human error skewing the results because there is no judgment call involved. The ELISA plate, regardless of what you are testing for, is processed with at least three control sera (sometimes as many as eight) in addition to the unknown sample being tested. There is a negative serum and at least two positive sera containing different levels of the antibody being tested. There are specific requirements for the absorption levels of these three controls. That is, each of them has a minimum or maximum (or both) number that must be seen by the instrument in order for it to be a valid test. If there is any variance from these expected numbers, it is an indication that something went wrong and the test results are discarded and the test repeated. There is therefore no way the technician could report inaccurate results, (assuming they diluted the sample correctly). Either the test was valid, and you can rely upon the accuracy of the result, or the test is invalid, and the entire result discarded. If any error was made during the processing of the ELISA plate, it would result in the control sera numbers being out of range and the entire test result would be thrown out. In summary, the tTG ELISA is measuring the same thing that the endomysial IFA is measuring but with a method that is more sensitive and specific and not subject to interpretation. IgA class Reticulin antibodies are found only in Celiac disease and dermatitis herpetiformis. These antibodies are found in approximately 60% of celiac disease patients and 25% of DH patients. This test is falling into disuse because of the limited utility and the availability of better tests. It is an IFA performed on a tissue substrate with all the attendant problems that go along with it. The development of all of these serum assays has tremendously simplified the diagnosis of celiac disease and improved the accuracy as well. The original criteria for diagnosis according to the European Society for Pediatric Gastroenterology and Nutrition, (ESPGAN), involved a year of arduous studies with: An initial positive gut biopsy; 6 months on a gluten free diet; A second, negative gut biopsy; A gluten challenge for 6 months and; A third, positive gut biopsy. The revised ESPGAN criteria call for positive results in two of the serological tests confirmed by a single positive biopsy. In practice, many gastroenterologists are utilizing the serologies in conjunction with a controlled diet and the clinical presentation to form a basis for diagnosis without the need for the invasive procedure. Through the auspices of the Celiac Disease Foundation and others, a professional symposium and workshop was organized earlier this year in Marina Del Rey, California with participants from Europe as well as the U.S. to establish standards for reporting test results. This should improve testing and diagnosis even more. At the conclusion of this conference a Celiac Disease Standardization Committee was formed to investigate and make recommendations on a standardized method of reporting results.
  15. Celiac.com 10/08/2018 - A new population based study reveals that celiac disease is associated with a wide range of medical conditions, including liver disease, glossitis, pancreatitis, Down syndrome, and autism, according to a database study of more than 35 million people. Moreover, people with autism have celiac disease at rates almost 20 times higher than in those without autism, reported lead investigator Daniel Karb, MD, a second-year resident at University Hospitals Case Medical Center in Cleveland. That raises the question of whether people with autism should be screened for celiac disease, and whether they might benefit form a gluten-free diet. "If you have a patient who is autistic and they have all these unusual symptoms, you might want to screen them for celiac disease," Dr. Karb told the World Congress of Gastroenterology last year. It is known that there are unusual symptoms of celiac disease, which include anything outside the classic symptoms of malabsorption, steatorrhea, malnutrition, abdominal pain, and cramping after eating, "but this is putting numbers to it," said Dr Karb. For their study, Karb and his fellow researchers used the Explorys database to pull health record data from 26 major integrated healthcare systems in the United States. Their search covered the period from 2012 to 2017. Of 35,854,260 people in the database, they found 83,090 with diagnosed celiac disease. Overall, the age-adjusted prevalence of celiac disease in that group was 0.22%, which is much lower than the 1% to 2% range previously estimated. Those numbers are not unusual, said Dr. Karb says that the researchers “don't think there are fewer people with celiac disease, just that it may be under-diagnosed.” The rates are, he says, “what you might expect when you screen asymptomatic people." Overall, the team found a significant connection between celiac disease and 13 other autoimmune disorders, such as type 1 diabetes, Crohn's disease, and ulcerative colitis. Moreover, celiac disease is associated with every autoimmune disease the team looked at, except for primary biliary cholangitis, Dr Karb says. This is some pretty startling study data. We knew that celiac disease was linked to other autoimmune conditions, and there has been some surprising data about gluten-free diets helping patients with autism, but these numbers are enlightening. It seems that people with autism should definitely be screened for celiac disease, and placed a gluten-free diet, if tests confirm celiac disease. Stay tuned for more information on this important celiac disease topic. Source: World Congress of Gastroenterology 2017
  16. Celiac.com 11/06/2018 - Autoimmune pancreatitis is a rare disorder whose association with celiac disease (celiac disease) has never been investigated, although celiac patients show high rates of both endocrine and exocrine pancreatic affections. To address this lack of information, a team of researchers recently set out to evaluate the frequency of celiac disease in patients with autoimmune pancreatitis and in further medical pancreatic disorders. The research team included G De Marchi, G Zanoni, MC Conti Bellocchi, E Betti, M Brentegani, P Capelli, V Zuliani, L Frulloni, C Klersy, and R Ciccocioppo. They are variously affiliated with the Department of Medicine, the Department of Pathology and Diagnostics, the Gastroenterology Unit, the Immunology Unit, and the Pathology Unit of the Department of Pathology and Diagnostics; and the Gastroenterology Unit of the Department of Medicine, AOUI Policlinico G.B. Rossi, University of Verona in Verona, Italy; the Clinica Medica I, Department of Internal Medicine, IRCCS Policlinico San Matteo Foundation in Pavia, Italy; and the Clinical Epidemiology & Biometry Unit, IRCCS Fondazione Policlinico San Matteo; Pavia, Italy. They screened for celiac disease by looking for tissue transglutaminase (tTG) autoantibodies in the blood of patients retrospectively enrolled and divided in four groups: autoimmune pancreatitis, chronic pancreatitis, chronic asymptomatic pancreatic hyperenzymemia (CAPH), and control subjects with functional dyspepsia. In patients with borderline or positive anti-tTG values, the team also looked at anti-endomysium autoantibodies. They offered duodenal biopsy to all patients with positive results. They found just one patient out of 72 (1.4%) with autoimmune pancreatitis who had already been diagnosed with celiac and was following a gluten-free diet, while one case out of 71 (1.4%) with chronic pancreatitis and one out of 92 (1.1%) controls were found to have celiac disease. They found no celiac disease in the CAPH group. By contrast, a high prevalence of cases with ulcerative colitis was found in the AIP group (13.8%). Despite an alleged connection between celiac disease and several autoimmune disorders, the data in this study do not support celiac screening for autoimmune pancreatitis patients. Celiac screening may be useful in other pancreatic disorders, but further study is needed to make a determination. Source: Nutrients. 2018 Aug 24;10(9). pii: E1157. doi: 10.3390/nu10091157.
  17. Celiac.com 06/13/2012 - In general, doctors and researchers know a good deal about how celiac disease works, and they are finding out more all the time. However, they know very little about non-celiac gluten sensitivity (NCGS). In an effort to learn more about non-celiac gluten sensitivity, a team of researchers recently carried out a study to measure the presence of somatization, personality traits, anxiety, depression, and health-related quality of life in NCGS individuals, and to compare the results with celiac disease patients and healthy control subjects. They also compared the response to gluten challenge between patients with non-celiac gluten sensitivity and those with celiac disease. The research team included M. Brottveit, P.O. Vandvik, S. Wojniusz, A. Løvik, K.E. Lundin, and B. Boye, of the Department of Gastroenterology at Oslo University Hospital, Ullevål in Oslo, Norway. In all, the team looked at 22 patients with celiac disease and 31 HLA-DQ2+ NCGS patients without celiac disease. All patients were following a gluten-free diet. Over a three day period, the team challenged 17 of the celiac disease patients with orally ingested gluten. They then recorded the symptoms reported by those patients. They did the same with a group of 40 healthy control subjects. The team then had both patients and healthy control subjects complete questionnaires regarding anxiety, depression, neuroticism and lie, hostility and aggression, alexithymia and health locus of control, physical complaints, and health-related quality of life. Interestingly, patients with non-celiac gluten sensitivity reported more abdominal (p = 0.01) and non-abdominal (p < 0.01) symptoms after the gluten challenge than patients with celiac disease. The increase in symptoms in non-celiac gluten sensitivity patients was not related to personality. However, the two groups both reported similar responses regarding personality traits, level of somatization, quality of life, anxiety, and depressive symptoms. Responses for both groups were about the same as for healthy controls. The results showed that patients with non-celiac gluten sensitivity did not show any tendencies toward general somatization, as both celiac disease patients and those with non-celiac gluten sensitivity showed low somatization levels. Source: Scand J Gastroenterol. 2012 Apr 23.
  18. Celiac.com 10/10/2018 - The Technical University in Vienna has announced a new remedy for celiac disease symptoms that they say can “alleviate or even completely eliminate the symptoms of celiac disease.” It should be available commercially in only a few years. Because most current efforts to treat celiac disease affect the immune system, possible side effects must therefore be fully assessed. This means years of study, and a long approval process. However, the TU Wien research team worked in collaboration with the industrial partner Sciotech Diagnostic Technologies GmbH to create a different approach. Their team based its approach for a celiac disease treatment on using only the part of the antibody that binds to gluten, which allowed them to create a product that works extremely well, but does not rely on triggering an immune response. Instead of a drug that works on the immune system, TU Wien created a simple medical product that directly attacks the gluten molecules to render them harmless. This makes the approval process much simpler, meaning that the product should be available in ordinary pharmacies as early as 2021. According to Professor Oliver Spadiut, head of the Integrated Bioprocess Development Research Group at TU Wien, “bodies produce antibodies that fit intruding antigens precisely, like a key to a lock. This immune response makes these antigens harmless.” He goes on to say that “If a new antibody fragment is found and produced that docks to and blocks the invading gluten molecule without triggering the immune system, the symptoms of celiac disease can be suppressed." The goal of their research project was to produce a complex of two such antibody fragments that envelop the gluten molecule at a molecular level, so that it can no longer have any further effects in the intestines. The result is a groundbreaking treatment for celiac disease and gluten intolerance. The process is complicated, and requires the team to re-program certain bacteria so that they produce exactly the desired antibody fragment. The full process took a while to iron out, but, says Spadiut, it “can be easily reproduced, can be scaled up to industrial application and delivers a very good yield of the desired product." This is very exciting news. Aside from efforts toward an outright vaccine, this is the first news of a potential treatment that can negate the effects of gluten without affecting the immune system itself. If all goes well, Spadiut says, the product “will be available in ordinary pharmacies in a few years.” Stay tuned for news about ongoing developments of this interesting treatment for celiac disease. Read: Additional scientific information Source: TUWien.ac.at
  19. Celiac.com 03/27/2017 - A number of researchers are looking to provide alternative or adjunct treatments to the gluten-free diet in celiac disease. Meanwhile, a number of companies are currently developing a wide variety of such options, ranging from various kinds of enzyme therapies, to treatments that eliminate celiac disease reactions, even to vaccines to inoculate celiac sufferers against their condition, perhaps allowing for full recovery and a return to non-gluten-free eating habits, as desired. At least, that's one dream. More likely will be the development of enzymes or other treatments that offer celiacs varying degrees of protection from gluten ingestion. Most likely, such treatments would be designed to augment an existing gluten-free diet, and to provide protection against moderate gluten-contamination when eating out. One particular enzyme that shows strong potential in breaking down toxic peptides in A-gliadin, the main culprit in celiac reactions, is caricain. A recent paper discusses the scientific principles behind the use of caricain for enzyme therapy. The paper is based on a recent study, in which a team of researchers set out to review the structures of the toxic peptides in A-gliadin for key sequences of amino acids or motifs related to toxicity, especially with respect to digestive difficulties, or immunogenicity. The research team included Hugh J. Cornell and Teodor Stelmasiak. They are affiliated with the RMIT University, School of Applied Sciences, Melbourne, Australia, and with Glutagen Pty Ltd, Maribyrnong, Victoria, Australia. For their study, they first evaluated structures of synthetic A-gliadin peptides shown to be toxic in the fetal chick assay, both before and after digestion with duodenal mucosa from patients in long remission. They also measured synthetic peptides corresponding to the undigested residues, and compared the key amino acid sequences, to see if they might be related to direct toxicity and immunogenicity of the peptides. They found that the smallest toxic peptides from celiac mucosal digestion were octa-peptides, which they found in greater amounts than similar products from normal digestion. One of those peptides corresponded to residues 12-19 of A-gliadin and contained the key motifs PSQQ and QQQP of De Ritis et al., while the other corresponded to residues 72-79, and contained the key motif PYPQ (extending to PYPQPQ). These key motifs have been noted by other workers, especially those investigating immunological activity over the past two decades. They are present in undigested residues from celiac mucosal digestion These motifs, along with the greater prevalence of these residues, as compared with residues from normal digestion, supports the basic notions underpinning enzyme therapy for celiac disease. This study also supports the basic scientific merits of research and development of the enzyme caricain to break down gliadin peptides with two different types of toxicity, and thus to potentially benefit people with celiac disease. Source: International Journal of Celiac Disease. Vol. 4, No. 4, 2016, pp 113-120. doi: 10.12691/ijcd-4-4-2 Previous study: NCBI
  20. Celiac.com 12/03/2014 - It is important for pregnant women seeking medical consultation to get good, evidence-based information. This is especially true for pregnant women with celiac disease, who might wonder whether they face an increased risk of adverse birth outcomes and pregnancy complications as a result of their disease. So, does celiac disease increase a woman’s risk for pregnancy complications and adverse birth outcomes? Until now, there hasn’t been much good, solid data to give women a clear answer. With that in mind, a research team in England recently conducted a population-based study on pregnancy outcomes and adverse birth conditions in women with celiac disease. The research team included Alyshah Abdul Sultan PhD, Laila J Tata PhD, Kate M. Fleming PhD, Colin J. Crooks PhD, Jonas F. Ludvigsson PhD, Nafeesa N. Dhalwani PhD, Lu Ban PhD, and Joe West PhD. They are variously affiliated with the Division of Epidemiology and Public Health, City Hospital Campus at the University of Nottingham, Nottingham, UK; the Department of Medical Epidemiology and Biostatistics at the Karolinska Institute in Stockholm, Sweden; and with the Department of Paediatrics at Örebro University Hospital in Örebro, Sweden. The team used linked primary care data from the Clinical Practice Research Datalink and secondary care Hospital Episode Statistics data to assess all singleton pregnancies between 1997 and 2012. They used logistic/multinomial regression to compare pregnancies of women with and without celiac disease for risks of pregnancy complications (antepartum and postpartum hemorrhage, pre-eclampsia, and mode of delivery), and for adverse birth outcomes (preterm birth, stillbirth, and low birth weight). They stratified risk levels based on whether women were diagnosed or undiagnosed before delivery. They found 363,930 pregnancies resulting in a live birth or stillbirth, 892 (0.25%) of which were among women with celiac disease. Women with diagnosed celiac disease showed no increased risk of pregnancy complications or adverse birth outcomes compared with women without celiac disease. However, pregnant women with diagnosed celiac disease did show a higher risk of postpartum hemorrhage and assisted delivery, with an adjusted odds ratio (aOR) of 1.34. Importantly, the team found no increased risk of any pregnancy complication among those with undiagnosed celiac disease. In all, they found just a 1% absolute excess risk of preterm birth and low birth weight among mothers with undiagnosed celiac disease, which corresponds to aOR=1.24 (95% confidence interval (CI)=0.82–1.87) and aOR=1.36 (95% CI=0.83–2.24), respectively. Overall, the results of this study offer some good news to pregnant women with celiac disease. Whether diagnosed or undiagnosed during pregnancy, celiac disease is not associated with a significantly higher risk of pregnancy complications and adverse birth outcomes. Source: Am J Gastroenterol. 2014;109:1653-1661.
  21. Celiac.com 09/17/2018 - Her name is Hawkeye, she’s a black lab, and her mission is to detect gluten for a young man named Toby, who gets terribly sick if he eats food that contains gluten. Hawkeye is up to 98% accurate at detecting gluten with just a few sniffs. Hawkeye was also expensive, costing a princely $16,000, not including food, and vet bills. That may sound expensive, but, says Toby’s mom, Amy "when you think about it trainers are often training only one to two dogs at a time and our trainer, she only trained one dog at a time and it took a year.” In Toby’s case, the community rallied to raise the money to buy Hawkeye, who is a registered service dog, and so can accompany Toby nearly everywhere. Everyone loves Hawkeye and her role in Toby’s life. Amy calls Hawkeye a “life-giver, and says that Amy continued “she's breathed life and confidence into Toby that we haven't seen in a really long time." She adds that the family has “really seen just growth and development in him because he's not getting sick as often and he's now able to learn more. So he can now say his alphabet, learn his numbers and colors, things that just a year ago he wasn't doing." Gluten-sniffing dogs are rare, but their numbers are growing. The Mercola.com website says that Willow, a gluten-sniffing German shorthaired pointer in Michigan, can detect gluten with 95 percent to 98 percent accuracy. The website Nimasensor.com notes that “[g]luten-sniffing dogs may detect gluten in amounts as small as .0025 parts per million with 95 percent to 98 percent accuracy.” Love the idea of a gluten sniffing dog, but maybe daunted by the price, logistics or commitment? There are portable gluten sensors currently on the market, with greater accuracy than Hawkeye, for a few hundred dollars. Disclosure: Nima Labs is a paid advertiser for Celiac.com
  22. Celiac.com 09/03/2018 - Can an office-based point of care test (POCT) improve celiac disease detection and diagnosis? A team of researchers recently set out to measure the diagnostic performance of an IgA/IgG-deamidated gliadin peptide (DGP)-based POCT for celiac disease detection, patient acceptability, and inter-observer variability of the POCT results. The research team included Michelle S. Lau MBChB, Peter D. Mooney MD, William L. White MBChB, Michael A. Rees BMedSci, Simon H. Wong MBChB, Marios Hadjivassiliou FRCP, Peter H. R. Green MD, Benjamin Lebwohl MD & David S. Sanders FRCP. They are variously affiliated with the Academic Department of Gastroenterology, the Academic Department of Neurosciences and University of Sheffield, Royal Hallamshire Hospital, Sheffield Teaching Hospitals, Sheffield, UK, and with the Celiac Disease Centre at Columbia University Medical Centre in New York, NY, USA. Beginning in 2013, and running through 2017, the team recruited patients who had been referred for secondary care with gastrointestinal symptoms, anemia and/or weight loss (group 1), along with a group of patients with self-reported gluten sensitivity, but unknown celiac disease status (group 2). Every patient in the study received a POCT, tests for IgA-tissue transglutaminase (IgA-TTG), IgA-endomysial antibodies (IgA-EMA), total IgA levels, and a duodenal biopsy. A total of 500 patients completed acceptability questionnaires, and the team compared inter-observer variability of the POCT results among five clinical staff for 400 cases. Group 1 included 1,000 patients. The team saw forty-one patients (4.1%) diagnosed with celiac disease. The sensitivities of the POCT, IgA-TTG, and IgA-EMA were 82.9, 78.1, and 70.7%; the specificities were 85.4, 96.3, and 99.8%. Group 2 included 61 patients. The POCT showed 100% sensitivity, but negative predictive value in detecting celiac disease in group 2. A majority of patients preferred the POCT to a blood draw (90.4% to 2.8%). A Fleiss Kappa coefficient of 0.895 reflected good inter-observer agreement on the POCT results. The POCT had comparable sensitivity to a blood test, and accurately spotted all celiac disease cases in a gluten sensitive group. But, because its low specificity may could cause further unnecessary tests, it’s not good enough to take the place of blood testing. It turns out that spotting celiac disease is only part of the battle. Making sure to rule out people who don’t have celiac disease is equally important. That’s why it’s important that any diagnostic test be both sensitive, to spot celiac disease, and specific, to rule out celiac disease in those who don’t have it. Until we get a PCOT with high enough sensitivity and specificity to make accurate celiac diagnosis and accurate elimination of those without celiac disease, the current blood testing regime will continue. Read more at: The American Journal of Gastroenterology; volume 113, pages1238–1246 (2018)
  23. Celiac.com 10/30/2013 - Rates of celiac disease and the use of drugs to inhibit the secretion of stomach acid have both increased in recent decades. A research team recently set out to explore the association between anti-secretory medication exposure and subsequent development of celiac disease. The research team included Benjamin Lebwohl, Stuart J. Spechler, Timothy C. Wang, Peter H.R. Green, and Jonas F. Ludvigsson. They are affiliated with the Celiac Disease Center at the Department of Medicine at Columbia University College of Physicians and Surgeons in New York, NY. For their population-based case control study, the research team looked at data for celiac disease patients diagnosed at any of the pathology departments in Sweden from July 2005 through February 2008. They matched each patient by age and gender with up to 5 control subjects. They found prior prescriptions for proton pump inhibitors and histamine-2 receptor antagonists in all subjects. Using conditional logistic regression to measure the association between these prescriptions and the subsequent diagnosis of celiac disease, they also found that patients with proton pump inhibitor prescriptions were much more likely to have celiac disease (OR 4.79; 95% CI 4.17–5.51). Patients prescribed both proton pump inhibitors and histamine-2 receptor antagonists had an even higher risk for celiac disease (OR 5.96; 95% CI 3.58–9.91) than those who received proton pump inhibitors alone (OR 4.91; 95% CI 4.26–5.66) or histamine-2 receptor antagonists alone (OR 4.16; 95% CI 2.89–5.99). The data clearly show that patients who use anti-secretory medications are at much greater risk for developing celiac disease following the use of these medicines. The fact that this connection persisted even after the team excluded prescriptions for anti-secretory medicines in the year preceding the celiac disease diagnosis suggests a causal relationship. Source: Digestive and Liver Disease
  24. Celiac.com 09/11/2018 - Gluten sensitivity is the most common sign of celiac disease. Clinical celiac diagnosis usually involves a positive blood test followed by biopsy confirmation of a typical enteropathy. The body’s immune response to celiac disease involves both adaptive and innate immunity, and is marked by anti-gliadin (AGA) and anti-transglutaminase 2 antibodies (tTGA), lymphocytic infiltration in the intestinal epithelial membrane, and expression of multiple cytokines. Researchers know that long pentraxin 3 (PTX3), an acute-phase inflammatory molecule, plays an important role in innate immunity. A pair of researchers recently set out to assess the relationship between Pentraxin 3 and biopsy status in celiac patients. Roberto Assandri and Alessandro Montanelli of the Department of Clinical Pathology, Clinical Chemistry Laboratory ASST Ospedale Maggiore di Crema, Italy, and the Clinical Chemistry Laboratory, Spedali Civili di Brescia, Italy, set out to explore a possible relationship between PTX3 and celiac disease. They used Marsh Histological grade following Marsh criteria classification to dividing 108 celiac disease patients into three groups: Group 1: Marsh 0, patients with a known history of celiac disease under gluten free diet, complete remission; Group 2: Marsh 1 and Marsh 2; Group 3: Marsh 3. As a control group, they used 30 healthy age-matched individuals with no known history of celiac disease or gastrointestinal symptoms. They used sandwich ELISA on an automated platform to measure PTX3 serum levels. They found that PTX3 serum levels were substantially higher in group 3 and group 2 compared with the healthy control group. They found no statistically significant differences between group 1 and the healthy control group. They noted a strong linear correlation between PTX3 serum levels and AGA levels in group 2, and group 3, but no such correlations between PTX3 serum levels and tTGA levels. Blood tests showed that PTX3 correlated with major gastrointestinal damage in celiac patients. PTX3 is a part of the innate immune system’s humoral branch. Data from this study show that PTX3 serum levels are high in active disease patients with pathological levels of AGA. They also show that patients with normal AGA IgA levels had PTX3 serum levels compared to healthy control subjects. The team proposes that PTX3 can modulate the innate response to gliadin in celiac disease, and may also regulate the adaptive immune response. Read more at: Gastroenterology and Hepatology
  25. Celiac.com 09/05/2018 - About one out of every twenty celiac patients fails to respond to a gluten-free diet, and goes on to develop refractory celiac disease (RCD). RCD is a serious condition marked by appearance of intraepithelial T lymphocytes. Depending on the phenotype of the lymphocytes, people develop either RCD I or RCD II. Patients with RCD type II (RCDII) show clonal expansions of intraepithelial T lymphocytes, and face an especially poor prognosis. Just over half of these patients will die within five years of onset due to aggressive enteropathy-associated T-cell lymphoma. At this time, researchers don’t know whether genetic variations might play a role in the severe progression from celiac disease to RCDII. A team of researchers recently set out to try to get some answers. The team began by conducting the first genome-wide association study to identify the causal genes for RCDII, along with the molecular pathways at play in cases of RCDII. For their genome-wide association study, the team used 38 Dutch patients with RCDII, and replicated the 15 independent top-associated single nucleotide polymorphism (SNP) variants (P<5×10) in 56 independent French and Dutch patients with RCDII. The team found that, after replication, SNP rs2041570 on chromosome 7 was significantly associated with progression to RCDII (P=2.37×10, odds ratio=2.36), but not to celiac disease susceptibility. They also found that SNP rs2041570 risk allele A was associated with lower levels of FAM188B expression in blood and small intestinal biopsies. Stratifying RCDII biopsies by rs2041570 genotype revealed differential expression of innate immune and antibacterial genes that are expressed in Paneth cells. The team’s efforts resulted in the identification of a new SNP associated with the severe progression of celiac disease to RCDII. Their data suggest that genetic susceptibility to celiac disease might be unrelated to celiac progression to RCDII, and suggests that Paneth cells might play a role in RCDII progression. Source: Eur J Gastroenterol Hepatol. 2018 Aug;30(8):828-837. The research team included B Hrdlickova, CJ Mulder, G Malamut, B Meresse, M Platteel, Y Kamatani, I Ricaño-Ponce, RLJ van Wanrooij, MM Zorro, M Jan Bonder, J Gutierrez-Achury, C Cellier, A Zhernakova, P Nijeboer, P Galan, S Withoff, M Lathrop, G Bouma, RJ Xavier, B Jabri, NC Bensussan, C Wijmenga, and V Kumar. They are variously affiliated with the Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, the Department of Gastroenterology, VUMC, Amsterdam, The Netherlands, INSERM U1163, Imagine Institute and Paris Descartes University, the Department of Gastroeneterology, Georges Pompidou European Hospital, the Paris 13 University Sorbonne Paris Cité, UREN, Inserm (U557), Inra (U1125), Cnam, Bobigny, France, the scientific director of McGill University and Génome Québec Innovation Centre, Montréal, Québec, Canada, the Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital and Harvard Medical School, Boston, The Broad Institute of MIT and Harvard, Cambridge, Massachusetts, the Department of Medicine, University of Chicago, Chicago, Illinois, USA., and the K.G. Jebsen Coeliac Disease Research Centre, Department of Immunology, University of Oslo, Norway.
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