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Celiac.com 05/20/2013 - A team of researchers recently looked at the influence of various proteins on the quality of gluten-free bread formulas. Specifically, the team looked at the influence of different concentrates or isolates of protein on the structure, properties and aging of gluten-free bread. The research team included Rafał Ziobroa, Teresa Witczakb, Lesław Juszczakc, and Jarosław Korusa. They are affiliated with the Department of Carbohydrates Technology, the Department of Engineering and Machinery for Food Industry, and the Department of Analysis and Evaluation of Food Quality, at the University of Agriculture, in Krakow, Poland. For their study they made gluten-free breads from dough that included albumin, collagen, pea, lupine or soy protein. They then analyzed the rheological properties of the dough, and found that bread made with added test proteins showed major differences in its visco-elastic properties. Different flours had different effects on specific volume of the loaves. Soy protein and collagen reduced bread volume, while lupine and albumin significantly increased bread volume. In each case, the added proteins had a noticeable impact on the color and textural properties of bread crumbs. Most of the protein preparations significantly decreased hardness and chewiness of the crumb compared to the control sample. Overall, the dough that contained pea protein yielded bread with the most acceptable qualities. The study demonstrated that pea protein created the most acceptable flavor, color, smell and bread crumb in the final product. Soy protein proved to be the least acceptable of those tested, as it produced loaves with smaller volume and a compact structure. The results of this study show that adding pea protein can improve bread quality, and help to slow staling of starch based bread. Source: Science Direct -
Celiac.com 04/22/2016 - To label a beer 'gluten-free' it must contain no gluten ingredients from start to finish. But, without wheat or barley, how does a brewer create the foundation for the beer? One problem gluten-free beers have is that, because they are brewed without wheat and/or barley, they are technically not beers under German beer laws, whatever their legal status here. Another issue is that since purely gluten-free beers must be brewed with all gluten-free ingredients, they have been often regarded as lackluster in the taste department, especially by beer connoisseurs, gluten-free or not. In an effort to provide a genuine, high quality beer for those suffering from celiac disease, and get beyond the taste limitations of totally gluten-free beers, a new generation of beer makers are using traditional ingredients and innovative methods of to remove up to 99.99 percent, or more, of the gluten molecules from the brew before bottling. The result is a beer that tests under 20ppm gluten levels, and which tastes like a genuine traditionally brewed wheat- or barley-based beers. One of the latest and perhaps best of the gluten-reduced beers on the market is Glütiny Pale Ale from Colorado's New Belgium Brewery. It's sited beer, Glütiny Pale Ale, isn't bad either. To make Glütiny, New Belgum uses a special enzyme during the brewing process that breaks down the gluten to well under the FDA standards for gluten-free products. According to Tim Dohms, of Hopjacks Pizza Kitchen and Taproom, "where most American pale ale is more floral with muted citrus notes, Glütiny showcases a big, dynamic flavor profile." Source: pnj.com
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Celiac.com 06/26/2017 - Designed to reduce or eliminate symptoms of gluten contamination in gluten-sensitive individuals, the product known as AN-PEP, marketed in the U.S. as Tolerase G, is a prolyl endoprotease enzyme, derived from Aspergillus niger, that has shown promise in breaking down gluten proteins. The latest news comes in the form of a small study that shows the enzyme to be effective in the stomach itself, where harshly acidic conditions render many enzymes ineffective. Speaking to an audience at Digestive Disease Week (DDW) 2017, lead investigator Julia König, PhD, of Sweden's Örebro University, said that the enzyme was special, because…[t]here are a lot of enzymes on the market, but this functions in the stomach where the pH is acidic. Often enzymes don't work in this environment." König was also quick to caution that "you cannot use this enzyme to treat or prevent celiac disease." The enzyme is not intended to replace a gluten-free diet for celiac patients. The enzyme is designed to provide some protection against cross-contamination for people with gluten-sensitivity by breaking down modest amounts of gluten to reduce or prevent adverse immune reaction. A previous study showed that AN-PEP breaks down gluten after an intra-gastrically infused liquid meal in healthy volunteers (Aliment Pharmacol Ther. 2015;42:273-285). In the latest randomized placebo-controlled crossover study, Dr König and her colleagues assessed the ability of AN-PEP to degrade gluten after a normal meal in people with gluten sensitivity. The research team looked at 18 people with self-reported gluten sensitivity, and with no confirmation of celiac disease. On three separate visits, investigators collected gastric and duodenal aspirates with a multilumen nasoduodenal-feeding catheter. Participants then consumed a porridge containing gluten, approximately 0.5 g, in the form of two crumbled wheat cookies. They also consumed a tablet containing AN-PEP at either 160,000 PPi or 80,000 PPi), or placebo. Investigators collected stomach and duodenal aspirates over the following 3 hours. In both the high- and low-dose AN-PEP groups, gluten concentrations in the stomach and in the duodenum were substantially lower than in the placebo group. This study shows that AN-PEP does break down gluten in the stomach, where many enzymes fail. If successfully tested and commercially released, AN-PEP could help people with gluten sensitivity, including those with celiac disease, to reduce or eliminate symptoms associated with casual gluten contamination. Source: Medscape -
Celiac.com 07/13/2016 - A really interesting study about gluten-free diets in mice just popped up over at the medical journal Diabetes, that has implications for both diabetes and celiac disease. The study found that a maternal gluten-free diet reduces inflammation and diabetes rates in the offspring of non-obese diabetic mice. The study was conducted by a research team that included Camilla H.F. Hansen, Åukasz Krych, Karsten Buschard, Stine B. Metzdorff, Christine Nellemann, Lars H. Hansen, Dennis S. Nielsen, Hanne Frøkiær, Søren Skov, and Axel K. Hansen. They are variously affiliated with the Department of Veterinary Disease Biology, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg, Denmark, the Department of Food Science, Faculty of Science, University of Copenhagen, Frederiksberg, the Bartholin Institute, Rigshospitalet, Copenhagen, Denmark, the Division of Toxicology and Risk Assessment, National Food Institute, Technical University of Denmark, Søborg, Denmark, and the Department of Biology, Faculty of Science, University of Copenhagen in Copenhagen, Denmark. Researchers have known for some time that early life interventions in the intestinal conditions have been shown to influence diabetes rates in mice. For example, a gluten-free diet in known to decrease type 1 diabetes incidence. Their team hypothesized that a gluten-free diet for pregnant mice only during pregnancy and lactation period would protect offspring mice against development of diabetes. The team fed pregnant non-obese diabetic (NOD) mice either a gluten-free or a standard diet, until all mice pups were weaned to standard diet. The early gluten-free mice showed significantly lower rates of diabetes and insulitis. Gut microbiota analysis by 16S rRNA gene sequencing showed significantly increased Akkermansia, Proteobacteria, and TM7 between both mothers and their offspring in the gluten-free diet group. Moreover, the gluten-free offspring showed increased pancreatic FoxP3 regulatory T cells, along with an increase in M2 macrophage gene markers and tight junction-related genes in the gut, coupled with lower intestinal gene expression of pro-inflammatory cytokines. Higher numbers of T cells in the pancreas expressing the mucosal integrin α4β7 suggests that the mechanism involve increased trafficking of gut-primed immune cells to the pancreas. This study supports the conclusion that a gluten-free diet during fetal and early postnatal life reduces development of diabetes. This may be due to changes in gut microbiota and better inflammatory and immunological conditions in the gut and pancreas. So, could it be that human mothers who eat a gluten-free diet through weening can impart the same kind of protection against diabetes? Clearly more studies need to be done until we can know for sure, but following a gluten-free diet while pregnant probably wouldn’t cause any harm to the mother or the baby. Source: Diabetes 2014 Apr; DB_131612.
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Celiac.com 02/18/2011 - In their search for a deeper understanding of the connections between celiac disease and Crohn’s disease, scientists have begun to focus on genetic variants that trigger inflammation in the gut. A research team examining associations between celiac disease and Crohn’s disease has now confirmed four common genetic variations between the two diseases. Their discovery may help to explain why people with celiac disease suffer Crohn’s disease at higher rates than the general population. Better understanding the genetic connections will likely pave the way for new treatments for symptoms common to both conditions, such as inflammation. The study used a new method of analysis called a genome-wide association study, or GWAS. This allows researchers to look at hundreds of thousands of genetic variations, called single nucleotide polymorphisms, or SNPs, that may be involved in any one disease. The research team compared 471,504 SNPs, representing the genomes of about 10,000 people, some of whom had Crohn’s disease, some of whom had celiac disease, and others who were healthy. They found four genes that seemed to raise the risk for both diseases. Two of these genes, IL18RAP and PTPN2, had already been associated with each disease. Another, called TAGAP, had previously been identified as a risk factor in celiac disease, but was newly associated with Crohn’s disease. The fourth gene, PUS10, had been previously been tied to Crohn’s disease, celiac disease, and ulcerative colitis. Three of the four genes seem to influence immune system response to perceived threats. “The first three we can say are involved in T-lymphocyte function,” Rioux says. “They seem to have a role to play in how these cells respond to a given stimulus.” In celiac disease, gluten-induced intestinal inflammation causes damage that prevents the intestine from absorbing nutrients in food. This can cause a wide range of problems, from anemia to osteoporosis to lactose intolerance. In Crohn’s disease, inflammation of the digestive tract often causes the bowel to empty frequently, resulting in diarrhea, among other problems. Some research shows that people with one condition are more likely to have the other. One study, for example, found that more than 18.5% of people with Crohn’s disease also have celiac disease. The study has “completely changed the way we can identify genetic risk factors,” says study co-author John D. Rioux, PhD, an associate professor of medicine at the University of Montreal, in Quebec, Canada. “There are sequence differences at the genetic level that get translated down to the protein levels,” Rioux notes. “And these differences may really nudge a person toward inflammation." He adds that "we’re just in the beginning, but we hope they may elucidate a common pathway and one day help us discover treatments that correct the underlying genetic changes.” Source: Jan. 27 issue of PLoS Genetics -
Survey of Tea Shows Limits of Gluten-Screening Procedures
Jefferson Adams posted an article in Additional Concerns
Celiac.com 09/30/2015 - In 2013, a team from the U.S. Food and Drug Administration conducted a survey of white and green teas, commercially available in the northeastern United States, for the presence of gluten in the form of undeclared wheat. The survey team included EA Garber, R Panda, and KF Shireen. They are variously affiliated with the Office of Regulatory Science, U.S. Food and Drug Administration, Center for Food Safety and Applied Nutrition, and the Office of Compliance, U.S. Food and Drug Administration, Center for Food Safety and Applied Nutrition in College Park, Maryland, USA. Initially, none of the test results show the required concurrence between the RIDASCREEN gliadin (R5) enzyme-linked immunosorbent assay (ELISA) and the Morinaga Institutes of Biological Science (MIoBS) wheat protein ELISA. So, just based on that, it would appear that none of the 20 products included in the survey tested positive for wheat, rye, barley, or gluten. Moreover, eight of the teas generated responses indicative of the presence of gluten with the RIDASCREEN gliadin (R5), AgraQuant gluten G12, and Aller-Tek (Skerritt) sandwich ELISAs. Five of the eight teas generated responses indicative of >20 ppm of gluten using the RIDASCREEN and AgraQuant ELISA test kits, and all eight had ≥ 20 ppm based on the Aller-Tek ELISA. Extracts prepared using the RIDASCREEN validated protocol and the MIoBS validated sodium dodecyl sulfate plus β-mercaptoethanol (overnight) protocol were analyzed using both test kits. The extracts prepared using the RIDASCREEN protocol tested positive for gluten with both test kits. Western blot analyses of the two sets of extracts using the R5 and MIoBS antibodies to visualize the bands revealed the presence of antigenic proteins in both sets of extracts, although the profiles and band intensities were different and inconsistent with the ELISA results. Right now, there's no need for alarm. The researchers are not saying that these types of tea contains gluten. Technically these teas are not failing a gluten test. What the researchers are saying is that there needs to be a review of gluten screening procedures and how the observation of a homologous antigenic element is defined, so that the tests are accurate and reliable. Source: J Food Prot. 2015 Jun;78(6):1237-43. doi: 10.4315/0362-028X.JFP-14-575. -
Celiac.com 03/30/2011 - A team of medical researchers set out to compare gut permeability and mucosal immune gene expression in celiac disease and gluten sensitivity. The research team included Anna Sapone, Karen M Lammers, Vincenzo Casolaro, Marcella Cammarota, Maria T Giuliano, Mario De Rosa, Rosita Stefanile, Giuseppe Mazzarella, Carlo Tolone, Maria I Russo, Pasquale Esposito, Franca Ferraraccio, Maria Carteni, Gabriele Riegler, Laura de Magistris and Alessio Fasano. People with celiac disease suffer an adverse autoimmune reaction when they consume gluten. People with gluten-sensitivity cannot tolerate gluten and may develop gastrointestinal symptoms similar to those in celiac disease. However, for people with gluten intolerance, the overall clinical picture is usually less severe, and is not accompanied by the concurrence of tissue transglutaminase autoantibodies or autoimmune comorbidities. By examining and comparing mucosal expression of genes associated with intestinal barrier function, along with innate and adaptive immunity the team sought to better understand the similarities and differences between celiac disease and gluten sensitivity. For their study, the team enrolled a group of subjects with celiac disease, a group with gluten sensitivity, and a control group of healthy, gluten-tolerant individuals. They assessed intestinal permeability using a lactulose and mannitol probe, and collected mucosal biopsy specimens to study the expression of genes involved in barrier function and immunity. They found that gluten sensitivity, unlike celiac disease, is not associated with increased intestinal permeability. In fact, subjects with gluten sensitivity showed significantly reduced intestinal permeability compared with controls (P = 0.0308). This was accompanied with significantly increased expression of claudin (CLDN) 4 (P = 0.0286). Relative to controls, subjects with celiac disease expressed higher levels of adaptive immunity markers interleukin (IL)-6 (P = 0.0124) and IL-21 (P = 0.0572), while those with gluten sensitivity showed no higher levels. Subjects with gluten intolerance showed increased expression of the innate immunity marker Toll-like receptor (TLR) 2, but subjects with celiac disease showed no such increase (P = 0.0295). Finally, subjects with gluten intolerance showed significantly reduced expression of the T-regulatory cell marker FOXP3 relative to controls (P = 0.0325) and celiac subjects (P = 0.0293). This study supports the existence of gluten sensitivity and celiac disease as two clinically different gluten-associated disorders. The study also supports the characterization of gluten sensitivity as a condition associated with prevalent gluten-induced activation of innate, rather than adaptive, immune responses in the absence of detectable changes in mucosal barrier function. Source: BMC Medicine 2011, 9:23 doi:10.1186/1741-7015-9-2
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Celiac.com 06/24/2015 - The Danish National Patient Registry records about 50 cases of celiac disease per 100,000 persons. This is much lower than the celiac rates reported in other Nordic countries, and many doctors have suspected that the condition is being under-diagnosed. So, how common is under-diagnosis of celiac disease? A team of researchers recently set out to answer that question by conducting a population-based study of Danish adults. The research team included A. Horwitz, T. Skaaby, L.L. Kårhus, P. Schwarz, T. Jørgensen, J.J. Rumessen, and A. Linneberg. They are affiliated with the Research Centre for Prevention and Health, The Capital Region at the University of Copenhagen in Copenhagen, Denmark. They screened a total of 2,297 adults aged 24-76 years living in the southwestern part of Copenhagen for celiac disease via immunoglobulin (Ig)A and IgG antibodies to transglutaminases and deamidated gliadin. They invited IgA/IgG-positive participants to a have a clinical evaluation, including biopsies, by a gastroenterologist. Of 56 invited participants, 40 underwent a full clinical evaluation, 8 of whom were diagnosed with celiac disease. Experts considered 2 of the 16 persons who declined the clinical evaluation to be likely positive for celiac disease. None of the above 56 participants had a known history of celiac disease or a recorded diagnosis of celiac disease in National Patient Registry. By combining the 8 cases of biopsy-proven celiac disease, the 2 cases of probable celiac disease, and 1 registry-recorded case of celiac disease, the team calculated 11 celiac cases out of 2,297 study participants. From this number, the team estimated celiac disease rates to be 479 per 100,000 persons, for the general population (95% CI: 197-761). This figure is 10 times higher than the registry-based prevalence of celiac disease. Of 11 participants diagnosed with celiac disease in our screening study, 10 were unaware of the diagnosis prior to the study. Thus, the team suggests that celiac disease is profoundly under-diagnosed in Danish adults. Source: Scand J Gastroenterol. 2015 Jul;50(7):824-31. doi: 10.3109/00365521.2015.101057.
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Celiac Disease Drug Shows Some Promise, But Offers No Cure
Jefferson Adams posted an article in Latest Research
Celiac.com 10/14/2014 - A new drug designed to prevent gluten uptake in the gut is showing some promise for the treatment of celiac disease. The drug, larazotide acetate, significantly reduced symptoms in a large double-blind, placebo-controlled trial. The drug prevents gluten uptake by closing tight junctions in the gastrointestinal (GI) tract. The drug is intended to supplement, rather than replace, the gluten-free diet that makes up the standard celiac disease treatment. Specifically, the drug is designed to help patients who continue to experience symptoms despite efforts to avoid gluten, and will not allow celiac patients to eat gluten with impunity. Some experts are cautioning celiac disease patients against high expectations. Joseph A. Murray, MD, of the Division of Gastroenterology and Hepatology at Mayo Clinic, in Rochester, Minnesota, said that, even if the drug is approved, it would not be a cure for celiac disease, but just another way to control symptoms for those already on a gluten-free diet. Daniel Leffler, MD, director of research at the Celiac Center of Beth Israel Deaconess Medical Center, in Boston, called the news “exciting.” Dr. Leffler predicted that, if approved, the drug would be a useful addition to standard celiac disease treatment. Source: Gastroenterology and Endoscopy News. SEPTEMBER 2014 | VOLUME: 65:9 -
Celiac.com 11/30/2011 - Researchers have been talking about it for some time, raising the hopes of the celiac community: a drug to help relieve us from the harmful effects of gluten exposure. Celiac patients are closer than ever to having such a drug on the market, as Alvine Pharmaceuticals has announced that their drug ALV003 has shown promise in a clinical trial by reducing gluten-triggered harm in people with celiac disease. Celiac disease is an autoimmune reaction triggered by exposure to gluten, a protein found in wheat, barley, and rye, that causes the immune system to attack the small intestine, interfering with the absorption of nutrients and leading to malnutrition and a variety of other symptoms. The disease currently has only one treatment, which is non-drug: the gluten-free diet. By eliminating gluten completely from the diet, most celiac patients can heal their small intestine. There is currently no other drug on the market that can help relieve the symptoms of celiac disease or the intestinal damage it can cause. Now Alvine Pharmaceuticals, which is focused on developing biopharmaceuticals for autoimmune inflammatory diseases such as celiac disease, has reported favorable results for a trial with their drug ALV003, which was developed to lessen mucosal injury in the intestine caused by gluten exposure in well-controlled celiac patients. A control group study was conducted that collected data from 34 celiac patients. After both the active drug group and placebo group ingested two grams of gluten on a daily basis for six weeks, "The group with the placebo reported higher incidence of 'non-serious adverse events' (code for GI symptoms)," Triumph Dining reported. "They also had significantly more mucosal injury in their small intestines, as measured by biopsy data." ALV003 works by breaking down the gluten molecule into nontoxic parts. (Alvine Pharmaceuticals explains more specifically how the drug works on their website, AlvinePharma.com.) The drug is intended to help alleviate the gastrointestinal and other symptoms associated with cross-contamination, incorrect or misleading "gluten-free" labeling, and exposure to gluten caused by carelessness or imprudence. Even when celiac patients take care to maintain a strict gluten-free, it's difficult to stay completely away from gluten. That's why, according to coordinating investigator of the latest ALV003, Markku Maeki, M.D., chair and professor of pediatrics at the University of Tampere and Tampere University Hospital in Finland, "New non-dietary treatment options that can either eliminate, or meaningfully reduce the gluten present in an attempted gluten-free diet are needed." Currently celiacs have no drug options to help alleviate their symptoms. "These results are groundbreaking," said Professor Maeki, "as they demonstrate for the first time, in a controlled clinical trial, that a drug has the potential to diminish gluten-induced injury in celiac disease patients." According to Triumph Dining, "After Phase 3 trials, so long as results remain promising, ALV003 will enter Phase 2b trials soon; after that come Phase 3 trials and (hopefully) submission to the FDA for approval." The release of ALV003, should results remain favorable, will no doubt bring relief to many members of the celiac community. -
Celiac.com 07/16/2014 - Information about the number of cases and and overall rates of celiac disease and dermatitis herpetiformis in the UK have not been well studied over time, either by region or by age. Yet, this type of information is essential for determining potential causes and quantifying the impact of these diseases. To provide this information, a team of researchers recently conducted a population-based study to assess incidence and prevalence of celiac disease and dermatitis herpetiformis in the UK over two decades. The researchers included J. West, K.M. Fleming, L.J. Tata, T.R. Card, and C.J. Crooks. They are variously affiliated with the Division of Epidemiology and Public Health, City Hospital Campus, The University of Nottingham, the NIHR Biomedical Research Unit in Gastrointestinal and Liver Disease at Nottingham University Hospitals NHS Trust, and the Division of Epidemiology and Public Health at the City Hospital Campus of The University of Nottingham in Nottingham, UK. They used the Clinical Practice Research Datalink to identify patients with celiac disease or dermatitis herpetiformis between 1990 and 2011, and calculated incidence rates and prevalence by age, sex, year, and region of residence. They found a total of 9,087 incident cases of celiac disease and 809 incident cases of dermititis herpetiformis. From 1990 to 2011, the incidence rate of celiac disease rose from 5.2 per 100,000 (95% confidence interval (CI), 3.8-6.8) to 19.1 per 100,000 person-years (95% CI, 17.8-20.5; IRR, 3.6; 95% CI, 2.7-4.8). During that same period, incidence of dermatitis herpetiformis decreased from 1.8 per 100,000 to 0.8 per 100,000 person-years (average annual IRR, 0.96; 95% CI, 0.94-0.97). The absolute incidence of celiac disease per 100,000 person-years ranged from 22.3 in Northern Ireland to 10 in London. Celiac disease showed large regional variations in prevalence, while dermatitis herpetiformis did not. The team found a fourfold increase in the incidence of celiac disease in the United Kingdom over 22 years, with large regional variations in prevalence. This contrasted with a 4% annual decrease in the incidence of dermatitis herpetiformis, with minimal regional variations in prevalence. These contrasts could reflect differences in diagnosis between celiac disease (serological diagnosis and case finding) and dermatitis herpetiformis (symptomatic presentation) or the possibility that diagnosing and treating celiac disease prevents the development of dermatitis herpetiformis. Source: Am J Gastroenterol. 2014 May;109(5):757-68. doi: 10.1038/ajg.2014.55. Epub 2014 Mar 25.
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Study Shows Quinoa Safe for Celiac Patients
Jefferson Adams posted an article in Gluten-Free Grains and Flours
Celiac.com 02/26/2014 - Quinoa is a highly nutritious plant from the South America that is often recommended by doctors as part of a gluten-free diet. However, some laboratory data suggests that quinoa prolamins can trigger innate and adaptive immune responses in celiac patients, and thus might not be safe for celiacs to eat. To better examine this issue, a team of researchers set out to evaluate the real-life effects of quinoa consumption in adult patients with celiac disease. The research team included Alberto Caminero, Alexandra R. Herrán, Esther Nistal, Jenifer Pérez-Andrés, Luis Vaquero, Santiago Vivas, José María G. Ruiz de Morales, Silvia M. Albillos, and Javier Casqueiro. They are variously affiliated with the Instituto de Biología Molecular, Genómica y Proteómica (INBIOMIC), and the Instituto de Biomedicina (IBIOMED) Campus de Vegazana at the Universidad de León, the Área de Microbiología, Facultad de Biología y Ciencias Ambientales at the Universidad de León, the Departamento de Inmunología y Gastroenterología of the Hospital de León, and the Instituto de Biotecnología (INBIOTEC) de León, all in León, Spain. The researchers looked at 19 treated celiac patients who ate 50 g of quinoa every day for 6 weeks as part of their regular gluten-free diet. The team evaluated diet, serology, and gastrointestinal parameters, and made histological assessments of 10 patients, bot before and after they consumed quinoa. The team found normal gastrointestinal parameters. They also noticed that the ratio of villus height to crypt depth improved from slightly below normal values (2.8:1) to normal levels (3:1), surface-enterocyte cell height improved from 28.76 to 29.77 μm and the number of intra-epithelial lymphocytes per 100 enterocytes decreased from 30.3 to 29.7. Results for all the blood tests remained within normal ranges, although total cholesterol (n=19) decreased from 4.6 to 4.3 mmol/l, low-density lipoprotein decreased from 2.46 to 2.45 mmol/l, high-density lipoprotein decreased from 1.8 to 1.68 mmol/l and triglycerides decreased from 0.80 to 0.79 mmol/l. The results show that quinoa is well tolerated by celiac patients and does not worsen the condition. In fact, patients saw a general improvement histological and serological results, along with a mild reduction in blood pressure. Overall, this is the first clinical data to indicate that celiac patients can safely tolerate up to 50 g of quinoa daily for 6 weeks. However, the team points out the need for further studies to determine the long-term effects of quinoa consumption. Source: Am J Gastroenterol. 2014 Feb;109(2):270-8. doi: 10.1038/ajg.2013.431. Epub 2014 Jan 21. -
Celiac.com 01/09/2014 - Not much is known about costs associated with celiac disease. A team of Israeli researchers recently studied the costs in patients diagnosed with celiac disease. The research team included A.D. Heymann, M. Leshno, R. Endevelt, and R. Shamir of the Medical Division at Maccabi Healthcare Services in Tel Aviv, Israel. They conducted a retrospective case control study covering the period 2003-2006 in a large Israeli Health Maintenance Organization with over two million members. Their study group included 1,754 patients with celiac disease and a control group of 15,040 non-celiac patients. They calculated costs individually for each member, and aggregated costs according to main cost-branches. They conducted a linear step wise regression with costs as the dependent variable and age, gender and the presence of celiac disease as the independent variables. They then compared costs for patients with celiac disease with costs for patients suffering from other chronic diseases. The team found that the total costs of celiac disease patients were significantly higher than those for the control group for hospital admission, medications, laboratory and imaging. The overall hospital admission rate of celiac patients was 7.98% as opposed to 7.1% for the control group (p = 0.06). However, compared with other chronic illnesses, the costs of patients with celiac disease were similar to those of patients with diabetes and hypertension. This study does conclude that celiac disease patients do use more medical services than the general population, at rates likely higher than previously thought. Source: Health Econ Rev. 2013 Nov 7;3(1):23. doi: 10.1186/2191-1991-3-23.
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Celiac.com 10/14/2013 - A team of researchers recently set out to assesses the safety and efficacy of Aspergillus niger prolyl endoprotease (AN–PEP) to mitigate the effects of gluten in celiac patients. For their study, the researchers included celiac patients with positive serology and subtotal or total villous atrophy on duodenal biopsies, who follow a strict gluten-free diet (GFD) resulting in normalised antibodies and mucosal healing classified as Marsh 0 or I were included. Prior to this randomized double-blind placebo-controlled pilot study, the team measured complaints, quality-of-life, serum antibodies, immunophenotyping of T-cells and duodenal mucosa immunohistology. They then had patients consume approximately 7 grams of gluten per day as toast, along with AN-PEP for a two week safety phase. The team put subjects through a two week washout phase where they followed their usual gluten-free diets. The team then randomly assigned 14 patients to receive gluten, with either AN-PEP or placebo, for a two week efficacy phase. They also collected patient questionnaires on serum and quality of life during and after the safety, washout and efficacy phase. They conducted duodenal biopsies after both the safety phase and the efficacy phase. Change in histological evaluation according to the modified Marsh classification served as the primary endpoint. In all, 16 adults participated in the study. No serious adverse events occurred during the trial and no patients withdrew during the trial. The average score for the gastrointestinal subcategory of the celiac disease quality (CDQ) was relatively high throughout the study, indicating that AN-PEP was well tolerated. In the efficacy phase, the team saw no significant deterioration in the CDQ scores of patients consuming gluten with placebo or gluten with AN-PEP, nor did they observe any other differences between the groups. During the efficacy phase, neither the placebo nor the AN-PEP group showed significant antibody titers. IgA-EM concentrations remained negative in both groups. The team excluded two patients from entering the efficacy phase because their mucosa showed an increase of two Marsh steps after the safety phase, yet with undetectable serum antibodies. A total of 14 patients were considered histologically stable on gluten with AN-PEP. Also, after the efficacy phase, the team saw no significant deterioration in immunohistological and flow cytometric evaluation in the group consuming placebo compared to the group receiving AN-PEP. Furthermore, in four out of seven patients on placebo, IgA-tTG deposit staining increased after two weeks of gluten intake compared to baseline. In the seven patients receiving AN-PEP, one patient showed increased and one showed decreased IgA-tTG deposits. AN–PEP appears to be well tolerated. However, the primary endpoint was not met due to lack of clinical deterioration upon placebo, impeding an effect of AN–PEP. The research team included Greetje J Tack, Jolanda MW van de Water, Chris J Mulder of the Department of Gastroenterology and Hepatology, VU University Medical Centre in Amsterdam, The Netherlands; Engelina MC Kooy-Winkelaar, Jeroen van Bergen, and Frits Koning of the Department of Immunohematology and Blood Transfusion, Leiden University Medical Centre in Leiden, The Netherlands; Petra Bonnet, B Mary E von Blomberg, and Marco WJ Schreurs from the Department of Pathology, VU University Medical Centre, in Amsterdam, The Netherlands; Anita CE Vreugdenhil, with Department of Paediatrics, University Hospital Maastricht in Maastricht, The Netherlands; and Ilma Korponay-Szabo, with the Department of Paediatrics, University of Debrecen in Hungary, and the Paediatric Research Centre, University of Tampere, in Tampere, Finland. Source: World Journal of Gastroenterology, 10/03/2013 -
Celiac.com 08/19/2013 - Data from blood studies suggest that about 1% or so of North Americans have celiac disease. However, there is no good screening data based on small intestinal biopsy performed during routine endoscopic evaluations. Researcher H.J Freeman recently set out to determine rates of detection of adult celiac disease via duodenal screening biopsies over a thirty year period. For his study, he looked at patients referred between January 1982 and December 2011 for evaluation of gastrointestinal symptoms that required elective investigative upper endoscopic assessment, and who underwent duodenal biopsies to determine whether changes of adult celiac disease were present. Freeman looked at a total of 9665 patients, including 4008 (41.5%) males and 5657 (68.5%) females, who underwent elective endoscopies and duodenal biopsies. Overall, 234 patients (2.4%) exhibited changes of celiac disease. That included 73 males (1.8%) and 161 females (2.8%). During the first 20 years, the number of biopsy-positive patients in five-year intervals progressively decreased, while, during the next 10 years, the number progressively increased. From this study, the team concludes that celiac disease is far more common in specialist practice than has been suggested in the evaluation of healthy populations using serological screening studies. Endoscopic duodenal biopsy is an important way to spot underlying celiac disease and should be routinely considered in all patients undergoing an elective endoscopic evaluation. They also note that the appearance of biopsy-defined celiac disease may be influenced by non-inherited factors, possibly environmental, which alter its detection over time. Source: Can J Gastroenterol. 2013 Jul;27(7):405-8.
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Study Shows Gluten Intolerance Without Celiac Disease
Jefferson Adams posted an article in Latest Research
Celiac.com 02/14/2011 - In what may seem for some like an obvious finding, a team of Australian researchers has shown that people can suffer gluten intolerance without having celiac disease. Their study is published in The American Journal of Gastroenterology. I say obvious, because many in the celiac and surrounding community have long understood and accepted the concept of gluten-intolerance as distinct from celiac disease. Surprisingly, there has been very little scientific research to establish the existence of gluten-intolerance as distinct from celiac disease. That is changing, and the recent Australian study offers some support for gluten-intolerance as distinct from celiac disease. For their study, a team of researchers led by Peter Gibson, professor of medicine at Eastern Health Clinical School at Monash University in Australia, recruited 34 people with irritable bowel syndrome, but who were clinically proven to be free of celiac disease. All participants had previously benefited from a gluten-free diet. The 34 volunteers were all fed bread and muffins, half of which contained gluten, half of which were gluten-free. Nearly 70 per cent of the volunteers who ate the gluten reported pain, bloating, toilet problems and extreme tiredness. ''Gluten is indeed a trigger of gut symptoms and tiredness,'' the researchers concluded. Professor Gibson said: ''These symptoms have a big impact on quality of life. But conservative medicine has not been so good at dealing with this because we haven't had any evidence.'' A number of the volunteers had sought help from alternative health practitioners, a fact that impaired recruitment of volunteers, as many of these folks had adopted a gluten-free diet without proving or disproving celiac disease via colonoscopy and biopsy. It was important for the team to exclude celiac disease for several reasons, including the fact that although it was safe to use gluten to test people who may have an intolerance, it could harm people with celiac disease. "If you go back on gluten while you have celiac disease - even if you only eat a few pieces of bread - you will damage your body and undo many months of healing," Professor Gibson said. For that reason, and also to prove gluten intolerance alone was the symptom cause, the team recruited people clinically proven to be free of celiac disease, and who were already on gluten-free diets. For those patients with irritable bowel syndrome, excluding celiac disease, who were symptomatically controlled on a gluten-free diet, the team crafted a double-blind, randomized, placebo-controlled re-challenge trial. Participants received either gluten or placebo in the form of two bread slices plus one muffin per day with a gluten-free diet for up to 6 weeks. The team evaluated symptoms using a visual analog scale and markers of intestinal inflammation, injury, and immune activation monitoring. A total of 4 men and 30 women between the ages of 29–59-years old completed the study as per protocol. Overall, 56% showed human leukocyte antigen (HLA)-DQ2 and/or HLA-DQ8. Adherence to diet and supplements was very high. Of 19 patients (68%) in the gluten-consuming group, 13 reported that symptoms were not adequately controlled compared with 6 of 15 (40%) on placebo (P=0.0001; generalized estimating equation). On a visual analog scale, patients were significantly worse within one week of consuming gluten for overall symptoms (P=0.047), pain (P=0.016), bloating (P=0.031), satisfaction with stool consistency (P=0.024), and tiredness (P=0.001). In no cases did gluten-consumption trigger anti-gliadin antibodies. Moreover, there where were no significant changes in fecal lactoferrin, levels of celiac antibodies, highly sensitive C-reactive protein, or intestinal permeability. There were no differences in any end point in individuals with the DQ2/DQ8 and those without. Gibson calls the general lack of research into gluten intolerance "almost unbelievable." He plans to now investigate the prevalence of non-celiac gluten intolerance, why it occurs and whether low levels of gluten can be eaten safely. Source: American Journal of Gastroenterology: 11 January 2011. doi: 10.1038/ajg.2010.487 -
Celiac.com 10/26/2010 - A recent study shows that, since 1974, the rate of celiac disease has doubled every fifteen years, and that celiac rates increase as people grow older, with many developing the disease in their 50s or 60s. The Center for Celiac Research led the study, which looked at 3,511 volunteers who submitted blood samples in 1974 and 1989, along with updates every two to three years until 2007. Because researchers in the study surveyed the same people over time, says Mayo Clinic gastroenterologist Dr. Joseph Murray, the study adds weight to the concept that celiac disease can emerge at any age. The study results also echo those of a 2008 Finnish study that found that elderly people had rates of celiac disease nearly two and a half times higher than the general population. The fact that celiac disease seems to be increasing among older age groups is significant because, if someone can be gluten-tolerant for 40 or 50 years before developing celiac disease, environmental factors may outweigh genetic causes for the disease, says Alessio Fasano, director of the Center for Celiac Research. Fasano says that other unknown environmental changes and changes in "the composition of bacteria in our guts" may be causing gluten autoimmunity to present itself later in life. Although researchers have identified specific genetic markers for the development of celiac disease, the exact way in which people lose tolerance to gluten remains unknown. However, it's important to understand that even people who have the genetic markers in question are not fated to develop an autoimmune disease, says Fasano. That's because recent study shows "that environmental factors cause an individual's immune system to lose tolerance to gluten, given the fact that genetics was not a factor in our study since we followed the same individuals over time," he says. If environmental factors do play a role in celiac disease, then it will be interesting to see if certain areas and regions have high celiac rates that are not due to genetic factors. More importantly, the research team notes that by identifying the environmental factors behind celiac disease, researchers may lead to better treatment and possible prevention of celiac disease and other autoimmune disorders, including type 1 diabetes, rheumatoid arthritis and multiple sclerosis. SOURCE: Annals of Medicine: October 2010, Vol. 42, No. 7 , Pages 530-538 doi:10.3109/07853890.2010.514285 -
Celiac.com 06/08/2007 -The results of a study recently published in the Alimentary Pharmacology & Therapeutics indicates that patients with celiac disease face a significant risk of polyneuropathy. Faced with inconclusive evidence of past studies linking celiac disease to various neurological conditions, doctors J. F. Ludvigsson, T. Olsson, A. Akbom, and S.M. Montgomery, set out to provide more conclusive evidence regarding the association between celiac disease and several neurological diseases. They used Cox regression to examine the risk of neurological disorders in 14,000 people who were diagnosed with celiac disease between 1964 and 2003. These patients were compared with 70,000 reference individuals matched for age, sex, calendar year and county. Celiac disease was associated with later polyneuropathy at a hazard ratio (HR) of 3.4; [95% CI = 2.3–5.1]. Results also showed prior polyneuropathy to be associated with subsequent celiac disease with an odds ratio of 5.4; [95% CI = 3.6–8.2). However, they found no statistically significant association between celiac disease and subsequent Huntingtons disease, hereditary ataxia, multiple sclerosis, myasthenia gravis, Parkinsons disease, or symptom ataxia. The actual study results are as follows: (HR = 0.9; 95% CI = 0.3–2.3), Parkinsons disease (HR = 1.2; 95% CI = 0.8–1.9), Alzheimers disease (HR = 1.5; 95% CI = 0.9–2.6), hereditary ataxia (HR = 1.3; 95% CI = 0.5–3.6), the symptom ataxia (HR = 1.9; 95% CI = 0.6–6.2), Huntingtons disease (HR = 1.7; 95% CI = 0.3–8.6), myasthenia gravis (HR = 0.8; 95% CI = 0.2–3.8) or spinal muscular atrophy. Doctors Recommend Regular Celiac Disease Screening for People with Polyneuropathy Because the connections between celiac disease and polyneuropathy indicate shared risks the doctors suggest that people with polyneuropathy undergo regular screening for celiac disease. health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
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Celiac.com 11/14/2011 - Alvine Pharmaceuticals claims that Phase 2a clinical trial of ALV003 demonstrates the drug's ability to mitigate gluten-triggered intestinal mucosal damage in serologically negative celiac disease patients who followed a gluten-free diet for one or more years. The company presented findings from the study at the 19th United European Gastroenterology Week (UEGW) in Stockholm. Alvine will present their data in an abstract, titled "ALV003, a Novel Glutenase, Attenuates Gluten-Induced Small Intestinal Mucosal Injury in Celiac Disease Patients: A Randomized Controlled Phase 2A Clinical Trial," The results are important because "up to 60 percent of adult celiac disease patients continue to experience symptoms and up to 80 percent continue to have persistent intestinal inflammation despite adhering to a strict gluten-free diet," says Markku Maeki, M.D., chair and professor of pediatrics at the University of Tampere and Tampere University Hospital in Finland, and coordinating investigator of the ALV003 Phase 2a trial. Finding a treatment that can help eliminate gut damage in celiacs who are following a gluten-free diet is an important step in improving long-term treatment of celiac disease. Doctor Peter Green, M.D., agrees. Dr. Green is director of The Celiac Disease Center and professor of clinical medicine at Columbia University College of Physicians and Surgeons. He says that a "gluten-free diet does not completely prevent exposure to gluten and does not affect the underlying cause of disease." This can potentially leave patients "vulnerable to gastrointestinal symptoms and serious long-term medical consequences," he says. Simply put, Dr. Green says, "there are currently no approved therapies for celiac disease. For the trial, 41 adults with clinically proven celiac disease, and who followed on a gluten-free diet for one or more years, received ALV003 or a placebo each day for six weeks. Test subjects also received 2g of gluten in the form of bread crumbs. Each subject received small bowel biopsy at the start of the trial, and again after six weeks of daily gluten challenge. Researchers obtained biopsy results from 34 patients. Results showed significantly less small intestinal mucosal injury in patients treated with ALV003 than in placebo-treated patients after six weeks (p=0.013). Placebo-treated patients suffered more adverse events, most commonly including abdominal distention, flatulence, eructation, abdominal pain and diarrhea. "Based on the results of this rigorously conducted trial, we believe that clinical proof-of-principle has been achieved. We are currently preparing for a Phase 2b trial of ALV003 in celiac disease patients targeted to begin in 2012," said Daniel Adelman, chief medical officer at Alvine Pharmaceuticals. Source: PRESS RELEASE Oct. 11, 2011, 8:00 a.m. EDT The full abstract (#OP050B) can found on the UEGW website: www.uegw11.uegf.org. -
Celiac.com 03/28/2011 - While rates of diagnosed celiac disease are less than 1 in 2,000 in the United States, screening studies in European and other populations have shown a much higher prevalence. A team of researchers recently set out to assess rates of celiac disease and the benefits of screening in the general adult population in certain geographically isolated areas. The research team included Kent D. Katz MD, Shahrooz Rashtak MD, Brian D. Lahr BS, MS, L. Joseph Melton III MD, Patricia K. Krause BS, MBA, Kristine Maggi PA-C, Nicholas J. Talley MD, PhD, and Joseph A. Murray MD. They are affiliated variously with the Wyoming Medical Center in Casper, Wyoming, the Department of Dermatology, the Division of Gastroenterology and Hepatology of the Department of Internal Medicine, the Division of Biostatistics, and the Division of Epidemiology in the Department of Health Sciences Research at the Mayo Clinic in Rochester, Minnesota. The team measured serum tissue transglutaminase antibodies (tTG-IgA) in adult volunteers at the annual Casper, Wyoming, Blue Envelope Health Fair blood draw. The team then checked endomysial IgA antibodies in those with positive tTG-IgA results. For those who tested positive for both screens, the team offered endoscopy with small bowel biopsy. All participants completed a short gastrointestinal (GI) symptom questionnaire. The team did blood tests on a total of 3,850 subjects, 34 of whom tested positive for both tTG and endomysial antibody (EMA) IgA. The team excluded three individuals who had been previously diagnosed with celiac disease, leaving 31 subjects, and making the total positive celiac serology in this community sample 0.8%. The team offered small bowel biopsy to those 31 subjects. They performed a total of 18 biopsies, with 17 patients (94%) showing at least partial villous atrophy. Symptoms reported by test subjects did not predict positive diagnosis. In fact, most subjects showed no symptoms, or else showed atypical symptoms. Serologic testing readily detects celiac disease in a general population. Screening results showed that undiagnosed celiac disease affects 1 in 126 individuals in this Wyoming community. Source: Am J Gastroenterol advance online publication 1 March 2011. doi: 10.1038/ajg.2011.21 -
Celiac.com 07/16/2010 - Advances in genetic science are allowing researchers to look more deeply into the genetic causes of auto-immune diseases, including celiac disease. One recent study showed that a particular variation, called the non-synonymous (Gly307Ser) variant, rs763361, in the CD226 gene carries a higher risk for multiple autoimmune diseases in European Caucasian populations. At the conclusion of that study, though, there was still no comparable study of shared autoimmunity with CD226 in non-European populations. An international research team set out to investigate any connection between this single nucleotide polymorphism (SNP) with autoimmune diseases in non-European populations. The team included Amit K. Maiti, Xana Kim-Howard, Swapan K. Nath, Celi Sun, and Parvathi Viswanathan; Laura Guillén and Alejandra C. Cherñavsky; Xiaoxia Qian and Nan Shen; Adriana Rojas-Villarraga and Juan-Manuel Anaya; Carlos Cañas, Gabriel J. Tobón; and Koichi Matsuda They are affiliated variously with the Genetic Epidemiology Unit of the Arthritis and Immunology Research Program at the Oklahoma Medical Research Foundation in Oklahoma City, OK, USA, the Immunogenetic Laboratory of the Hospital de Clínicas José de San Martín at the Universidad de Buenos Aires in Buenos Aires, Argentina, the Shanghai Institute of Rheumatology at Renji Hospital, JiaoTong University School of Medicine in Shanghai, P.R. China, the Centre for Autoimmune Diseases Research (CREA) at the Universidad del Rosario-Corporación para Investigaciones Biológicas in Bogota, Colombia, the Rheumatology Unit of the Fundación Valle del Lili in Cali, Colombia and the Laboratory of Molecular Medicine at the Human Genome Centre of the Institute of Medical Science at the University of Tokyo, Japan. To evaluate any connection between this single nucleotide polymorphism (SNP) with autoimmune diseases in non-European populations, the team compared case–control association between rs763361 and celiac disease (CED) samples from Argentina; SLE, RA, type-1 diabetes (T1D) and primary SS (pSS) from Colombia; and SLE samples from China and Japan. They then genotyped rs763361 and used 2-test to evaluate its genetic association with multiple auto-immune disorders. For each association, the team calculated odds ratio (OR) and 95% CI. Their results show clearly that rs763361 shares a significant association with celiac disease in Argentina (P = 0.0009, OR = 1.60). They also noted indications of possible association with Chinese SLE (P = 0.01, OR = 1.19), RA (P = 0.047, OR = 1.25), SLE (P = 0.0899, OR = 1.24) and pSS (P = 0.09, OR = 1.33) in Colombians. The team then conducted meta-analyses for SLE, using their three populations, and T1D, using their population together with three published populations. Those analyses showed a significant association with rs763361, P = 0.009 (OR = 1.16) and P = 1.1.46 x 10–9 (OR = 1.14), respectively. The team's results show clearly that the coding variation rs763361 in the CD226 gene is associated with multiple auto-immune disorders in non-European populations. Taken together, these studies show that the non-synonymous (Gly307Ser) variant, rs763361, in the CD226 gene carries a higher risk for multiple autoimmune diseases in both European Caucasian and non-European populations. Source: Rheumatology 2010 49(7):1239-1244; doi:10.1093/rheumatology/kep470 -
Celiac.com 06/30/2010 - Presently, the only proven treatment for celiac disease is a lifelong gluten-free diet. As part of a gluten-free diet, people with celiac disease are encouraged to avoid consuming foods containing rye, along with avoiding wheat and barley. However, there is surprisingly little evidence to document the adverse effects of rye in cases of celiac disease. To address this deficiency, a team of clinicians set out to determine conclusively whether rye should be excluded from the celiac diet. The team included S. M. Stenman, K. Lindfors, J. I. Venäläinen, A. Hautala, P. T. Männistö, J. A. Garcia-Horsman, A. Kaukovirta-Norja, S. Auriola, T. Mauriala, M. Mäki, and K. Kaukinen They are affiliated variously with the Department of Pediatrics, and the Pediatric Research Center of the Medical School University of Tampere, the Department of Gastroenterology and Alimentary Tract Surgery at Tampere University Hospital, the Department of Pharmacology and Toxicology, the Department of Pharmaceutical Chemistry at the University of Kuopio, the Division of Pharmacology and Toxicology, the Division of Pharmaceutical Chemistry at the University of Helsinki, and Technical Research Centre of Finland. The goal of the team was to determine whether rye secalin triggers toxic reactions in vitro in intestinal epithelial cell models to the same degree as wheat gliadin. Moreover, they examined whether the harmful effects of secalin can be reduced by germinating cereal enzymes from oat, wheat and barley to hydrolyze secalin into short fragments as a pretreatment. The data showed that secalin did trigger toxic reactions in intestinal Caco-2 epithelial cells in a similar manner to gliadin. Secalin triggered epithelial cell layer permeability, tight junctional protein occludin and ZO-1 distortion, and actin reorganization. High-performance liquid chromatography and mass spectroscopy (HPLC-MS), showed that germinating barley enzymes best degraded the secalin and gliadin peptides. Further in vitro analysis showed that germinating barley enzyme pretreatment ameliorated all toxic secalin-triggered reactions. From these results, the team concludes that germinating enzymes from barley offer efficient degradation of rye secalin. In future, these enzymes might be utilized as a novel medical treatment for celiac disease or in food processing in order to develop high-quality celiac-safe food products. Such enzyme treatments might pave the way for either new treatments for celiac disease, or, new methods of processing rye for production of new, celiac-safe foods. SOURCE: Clinical & Experimental Immunology DOI:10.1111/j.1365-2249.2010.04119.x -
Celiac.com 03/12/2010 - A team of researchers recently noted similar presentations of celiac disease in both elder and younger patients.The research team included Rupa Mukherjee, Ikenna Egbuna, Pardeep Brar, Lincoln Hernandez, Donald J. McMahon, Elizabeth J. Shane, Govind Bhagat, and Peter H. R. Green. They are affiliated variously with the Division of Digestive and Liver Diseases, the Division of Endocrinology, Department of Medicine, and the Department of Pathology at the Columbia University College of Physicians and Surgeons in New York, and with Columbia University Medical Center's Celiac Disease Center. It is well known that celiac disease can affect individuals of all ages. However, there have been few studies to focus solely on how celiac disease presents among elderly people. To get a better understanding of how celiac disease presents in the elderly, a research team recently set out to compare aspects of celiac disease from elderly populations with a population of young adults with celiac disease. The first step was to assemble two groups of patients, an elderly cohort over 65-years old, and a young adult cohort aged 18–30 years, with biopsy-confirmed celiac disease. They did this by reviewing a tertiary center database of celiac disease patients with celiac disease, which provided data on symptom duration, clinical presentation, small intestinal pathology, associated conditions, and the presence of bone disease. The team reviewed data on 149 young adult and 125 elderly patients with celiac disease; The elderly subjects comprised 12.4% of the patient database. Both groups showed similar duration of symptoms before diagnosis, with young adults at 5.8 ± 12 years and elderly at 6.14 ± 12.6 years, respectively (p = 0.119). The presenting symptoms were also basically the same for both groups, with diarrhea being the main presenting symptom in 49% of young adults and 50% of the elderly (p = 0.921). Both groups showed similar rates of autoimmune disease, with 19% of young adult and 26% of elderly patients having relevant autoimmune conditions (p = 0.133). Both groups showed similar presence of villous atrophy and rates of bone disease, while the elderly group showed higher rates of thyroid disease and neuropathy (p = 0.037 and p = 0.023, respectively). The team expressed surprise that, both clinically and histologically, celiac disease seems to present similarly in elderly and young adult patients. They note that since the exact causes for celiac disease at any given age remain unclear and warrant further study. Source: Dig Dis Sci DOI 10.1007/s10620-010-1142-4.
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Celiac.com 05/30/2007 - The results of a study recently published in the Scandinavian Journal of Gastroenterology shows that patients with celiac disease can consume oats with no risk of adverse immunological effects. An international research team made up of doctors Tarja Kemppainen (1); Esko Janatuinen (2); Kati Holm (3); Veli-Matti Kosma (4); Markku Heikkinen (5); Markku Mäki (3); Kaija Laurila (3); Matti Uusitupa (1); Risto Julkunen (5), set out to evaluate local cellular immune response after 5 years of oat consumption by adult celiac patients. The doctors looked at a group of 42 celiac patients who had previously participated in a 6-12 month oats intervention study. 22 of these patients already incorporated oats as part of their gluten-free diet. During the 5-year follow-up study, 10 patients who were concerned about the safety of long-term oat consumption stopped eating oats. The 12 remaining patients consumed oats for the whole 5-year period. The remaining 20 celiac patients formed the control group, and followed a strict, conventional, gluten-free diet that excluded oats. The team conducted biopsies and counted Intraepithelial CD3, TCR (IEL) and TCR (IEL) T cells to determine corresponding densities. No Adverse Effects for Celiac Disease Patients Who Eat Oats The results showed no differences in the densities of CD3, IEL and IEL T cells between the oat and the control groups. The researchers concluded that the mucosa of the small intestine show no immunological response in celiac patients who consume oats over a long period of time. Scandinavian Journal of Gastroenterology, Volume 42, Issue 1 2007 , pages 54 - 59 Participating Institutions: Department of Clinical Nutrition, University of Kuopio and Kuopio University Hospital. Kuopio. Finland Department of General Medicine, Al Mafraq Hospital. Abu Dhabi, U.A.E. Medical School, University of Tampere and Tampere University Hospital. Tampere. Finland Department of Pathology and Forensic Medicine, University of Kuopio and Kuopio University Hospital. Gastroenterological Unit, Department of Medicine, Kuopio University Hospital. Finland About the Author: Jefferson Adams is a freelance health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
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Celiac Study: Non-invasive Intestinal Evaluation Shows Promise
Jefferson Adams posted an article in Latest Research
Celiac.com 05/21/2009 - To better diagnose celiac disease, assess intestinal damage, and monitor treatment over the long-term, doctors are looking to develop a whole new set of non-invasive evaluation tools. One of the tools currently of interest are fatty acid binding proteins (FABPs), these are small cytosolic proteins found in enterocytes (tall columnar cells and responsible for the final digestion and absorption of nutrients, electrolytes and water). FABPs are reliable indicators of intestinal mucosal damage, and are potentially useful for non-invasive assessment of intestinal damage in celiac patients. A team of researchers in the Institute of Nutrition and Toxicology Research at Maastricht University, as well as the departments of Surgery, Pediatrics and Internal Medicine at University Hospital Maastricht, recently set out to assess the potential use of FABPs in non-invasive assessment of intestinal damage in celiac disease. The study team was made up of J. P. Derikx, A. C. Vreugdenhil, A. M. Van den Neucker, J.Grootjans J, A. A. van Bijnen, J.G. Damoiseaux, L. W. van Heurn, E. Heineman, and W. A. Buurman. They began by examining the distribution and microscopic localization of FABPs in healthy human intestinal tissue. They then checked circulating levels of intestinal (I)-FABP and liver (L)-FABP in 26 healthy control subjects, and in 13 patients with biopsy-proven celiac disease, both before and after initiating a gluten-free diet. Ten celiac subjects underwent reevaluation within a year beginning a gluten-free diet. They found that I-FABP and L-FABP are common in the small intestine, particularly in the jejunum. FABPs also show up in cells on the upper part of the villi, the part that is first to be damaged in celiac disease. They also found that people with untreated, biopsy-proven celiac disease have substantially higher circulating levels of FABPs as compared with healthy control subjects (I-FABP: 784.7 pg/mL vs. 172.7 pg/mL, P<0.001; L-FABP: 48.4 ng/mL vs. 10.4 ng/mL, P<0.001). These levels return to normal when patients adopt a gluten-free diet. According to the team, the monitoring of FABP circulating levels shows strong promise as a non-invasive means of diagnosing and assessing intestinal damage in celiac disease, as well as in long-term non-invasive monitoring of treatment and gluten-free diet compliance. Journal of Clinical Gastroenterology. 2009 Apr 6.
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