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Found 18 results

  1. Celiac.com 10/11/2017 - A Merrill Lynch broker in Denver has sued the firm in federal court, claiming that its systemic "sabotage" of his relationship with clients during and following two medical leaves have cost him hundreds of thousands of dollars. In a case filed this summer in federal court in Colorado, Kirk Kringel, a broker with Merrill since 2010, alleges that the company violated his rights under the Family Medical Leave Act by retaliating against him for taking the two medical leaves, including one that was related to celiac disease. A seasoned broker, Mr. Kringel worked previously with Morgan Stanley and Dean Witter for nearly 15 years before joining Merrill Lynch. According to the complaint, colleagues and managers at Merrill "systematically interfered with and sabotaged Kringel's relationships with his clients by failing to service some of his clients, permanently re-assigning some of his clients to other financial advisors, and providing misinformation to his clients that undermined his relationships." Kringel claims that the sabotage cost him annual income in excess of $250,000, and that the actions were taken deliberately as retaliation for Kringel's three-month leave in 2015 and an unpaid medical leave that he began in February 2017. Kringel alleges in the suit that the losses to his accounts were engineered by a former business partner and colleague who moved with him to Merrill, and is claiming that the alleged violation of federal FMLA law justifies a courtroom trial. If successful, he will avoid arbitration, which would be the standard course for such complaints. Merrill Lynch spokesman Bill Halldin disputed the allegations on behalf of the company, but offered no comment on whether it will seek to have the complaint moved to arbitration. Neither Kringel, nor his lawyers at the firm of Moye, White offered further comment. Stay tuned for more on Mr. Kringel's efforts, and on legal issues regarding celiac disease and employment, disability, and the like. Read more at Advisorhub.com
  2. Celiac.com 04/07/2008 - No, this is not some kind of April Fool’s joke.When I read this report, I just about fell off my chair. New research indicates thatbeing poor and living in squalor might actually provide some benefitagainst the development of celiac disease. A team of medicalresearchers recently set out to examine gene-environmental interactionsin the pathogenesis of celiac disease. The research team was made up ofA. Kondrashova, K. Mustalahti, K. Kaukinen, H. Viskari, V. Volodicheva,A. M. Haapala, J. Ilonen, M. Knip, M. Mäki, H. Hyöty, T. E. Group.Finland and nearby Russian Karelia have populations that eat about thesame amounts of the same grains and grain products. The two populationsalso have a high degree of shared genetic ancestry. The only majordifference between the populations of the two areas lies in theirsocioeconomic conditions. The region of Russian Karelia ismuch poorer than the neighboring areas in nearby Finland. Thesanitation levels in Russian Karelia are also distinctly inferior thanthey are in Finland. The researchers compared the prevalence of celiacdisease and predisposing human leukocyte antigen (HLA) alleles inpopulations from Russian Karelia and Finland. The team performedscreening for tissue transglutaminase antibodies (tTG) and HLA-DQalleles on 1988 school-age children from Karelia and 3654 children fromFinland. Children with transglutaminase antibodies were encouraged tohave a duodenal biopsy. Interestingly, the patients fromRussian Karelia showed tTG antibodies far less often than their Finnishcounterparts (0.6% compared to 1.4%, P = 0.005). The patients fromRussian Karelia also showed Immunoglobulin class G (IgG) antigliadinantibodies far less frequently than their Finnish patients (10.2%compared to 28.3%, P<0.0001). The researchers confirmed adiagnosis of celiac disease by duodenal biopsy in four of the eighttransglutaminase antibody-positive Karelian children, for an occurrencerate of 1 in 496 versus 1 in 107 Finnish children. In bothgroups, the same HLA-DQ alleles were associated with celiac disease andthe presence of transglutaminase antibodies. The patients from RussianKarelia showed a much lower prevalence of transglutaminase antibodiesand celiac disease than the Finnish children. The poorconditions and inferior hygienic conditions in Russian Karelia mightprovide some kind of protection against the development of celiacdisease. The value of studies like this aren’t to make us wax nostalgicfor poverty, or to encourage people to fend off celiac disease bybecoming poor and living in squalid conditions. The value of a studylike this lies in the idea that there may be more to the development ofceliac disease than simple biological factors. That environmentalconditions might play a key role in both the frequency ofceliac-related antibodies, and in the development of the disease itselfis quite intriguing and clearly warrants further and more comprehensivestudy. Ann Med. 2008;40(3):223-31.
  3. Arch Dis Child 2006;91:39-43. Celiac.com 12/08/2005 – Researchers in the United Kingdom conducted a systematic review and meta-analysis of 15 studies published between 1966 and 2004 that evaluated the association between breast-feeding and celiac disease. Their review covered more than 4,000 children and found that breast-feeding may offer protection against the development of celiac disease, especially if it is prolonged and covers the period when gluten is introduced. It was unclear, however, whether breast-feeding merely delays the onset of symptoms, or actually offers permanent protection against the disease, and more long-term prospective cohort studies will be necessary to make such a determination.
  4. Celiac.com 06/15/2010 - A clinical team conducted a functional analysis of celiac risk loci, and found that SH2B3 offers protection against bacterial infection. The team included Alexandra Zhernakova, Clara C. Elbers, Bart Ferwerda, Jihane Romanos, Gosia Trynka, Patrick C. Dubois, Carolien G.F. de Kovel, Lude Franke, Marije Oosting, Donatella Barisani, Maria Teresa Bardella, the Finnish Celiac Disease Study Group, Leo A.B. Joosten, Paivi Saavalainen, David A. van Heel, Carlo Catassi, Mihai G. Netea, and Cisca Wijmenga. Celiac disease has a fairly high morbidity, yet it is prevalent in Western populations at rates of of 1%–2%. So far, scientists don't understand why the celiac disease phenotype is so common despite its obvious negative impact on human health. This is especially true when one considers that doctors only developed a gluten-free diet to treat celiac disease in the 1950's. The research team scientists hypothesize that the high prevalence of celiac disease might suggest that the process of natural selection favors genes that trigger celiac disease, and thus, that the gene may convey some evolutionary advantage to those who inherit them. The study group included 8,154 controls from four European populations, and 195 individuals from a North African population. By examining haplotype lengths using the integrated haplotype score (iHS) method, the team looked at selection signatures for ten confirmed celiac-associated loci in several genome-wide data sets. They found consistent indications of positive selection for celiac-associated derived alleles in three loci: IL12A, IL18RAP, and SH2B3. For the SH2B3 risk allele, they also found a variation in allele frequency distribution (Fst) between HapMapphase II populations. Functional investigation of the effect of the SH2B3 genotype in response to lipopolysaccharide and muramyl dipeptide showed that carriers of the SH2B3 rs3184504*A risk allele provided more robust triggering of the NOD2 recognition pathway. This suggests that SH2B3 plays a role in protection against bacteria infection, and it provides a possible explanation for the selective sweep on SH2B3, which occurred sometime between 1,200 and 1,700 years ago. Source: AJHG - 2010, 04 May. doi:10.1016/j.ajhg.2010.05.004
  5. Celiac.com 06/02/2014 - Despite following a gluten-free diet, many people with celiac disease continue to have symptoms, and to suffer from ongoing small intestinal inflammation. Can a drug be created to alleviate such symptoms and inflammation, and protect celiacs on a gluten-free diet against small amounts of gluten contamination? San Carlos California-based Alvine Pharmaceuticals is conducting a phase 2 trial to determine whether their drug, ALV003, an orally administered mixture of 2 recombinant gluten-specific proteases can protect celiac disease patients from gluten-induced mucosal damage. For this trial, Alvine is working with researchers Marja-Leena Lähdeaho, Katri Kaukinen, Kaija Laurila, Pekka Vuotikka, Olli-Pekka Koivurova, Tiina Kärjä-Lahdensuu, Annette Marcantonio, Daniel C. Adelman, and Markku Mäki. They are affiliated with the School of Medicine and Tampere University Hospital at the University of Tampere; the Department of Gastroenterology and Alimentary Tract Surgery at Tampere University Hospital and School of Medicine at the University of Tampere, and FinnMedi Oy in Tampere, Finland; the Department of Medicine at Seinäjoki Central Hospital in Seinäjoki, Finland; Liikuntaklinikka, Oulu Diakonissalaitos; and Terveys, Oulu Diakonissalaitos, Oulu, Finland. For their Phase 2 trial, the research team first established two grams of gluten per day as the optimal challenge dose for their 6-week gluten study. They then randomly assigned 20 adults with biopsy-proven celiac disease to receive ALV003, and twenty-one to receive a placebo. Both groups also received 2 grams of gluten each day. The team conducted duodenal biopsies at baseline, and after gluten challenge, focusing on the ratio of villus height to crypt depth and densities of intraepithelial lymphocytes. A total of seven patients dropped out due to adverse reactions. Four were receiving ALV003, and three were receiving the placebo. Sixteen patients given ALV003 and 18 given placebo were eligible for efficacy evaluation. Biopsies from subjects in the placebo group showed evidence of mucosal injury after gluten challenge, with average villus height to crypt depth ratio changed from 2.8 before challenge to 2.0 afterward. (P = .0007; density of CD3þ intraepithelial lymphocytes changed from 61 to 91 cells/mm after challenge; P = .0003). However, the team saw no significant mucosal deterioration in biopsies from the ALV003 group. The two groups showed no significant differences in symptoms, though they did show substantial differences in morphologic changes, and CD3þ intraepithelial lymphocyte counts differed significantly from baseline to week 6 (P = .0133 and P = .0123, respectively). This small, but important, step means that ALV003 did provide significant protection against gluten-induced gut damage for people with celiac disease on an otherwise gluten-free diet, which means that Alvine can continue to the next phases in the development process. If successful, glutenase ALV003 will be the first drug to protect people with celiac disease against gut damage from small amounts of gluten. Source: Clinicaltrial.gov, Numbers: NCT00959114 and NCT0125569
  6. Celiac.com 11/22/2012 - Cardiovascular disease has many causes, and can be influenced by so many factors. It also happens to be the main cause of death in developed countries. With regard to celiac disease and cardiovascular disease, there are two conflicting schools of thought. The first suggests that the gluten-free diet might help people with celiac disease to reduce the risk of developing cardiovascular disease. The second suggests the opposite: that a gluten-free diet may leave people with celiac disease at greater risk of developing cardiovascular disease. So far, the research has provided conflicting and data offer no clear answers. A group of researchers recently tried to figure out if a gluten-free diet protects people with celiac disease against the development of cardiovascular disease, or weather it increases their risk. The research team included Lorenzo Norsa, Raanan Shamir, and Noam Zevit, who are affiliated with the Institute of Gastroenterology, Nutrition and Liver Diseases, Schneider Children's Medical Center of Israel at Clalit Health Services in Petach Tikva, Israel, with the Sackler Faculty of Medicine at Tel-Aviv University in Tel Aviv, Israel, and with the Department of Pediatrics at San Paolo Hospital and University of Milan in Milan, Italy. The idea that a gluten-free diet may protect celiacs against cardiovascular disease hinges on the fact that eating gluten-free reduces intestinal inflammation and improves intestinal absorption. This hypothesis argues that the reduction in inflammation is important because a number of studies over the past decade have shown that a large percentage of people with acute coronary syndrome show signs of increased inflammation. Studies also show that several clinical conditions that are accompanied by persistent low grade of inflammation, such as autoimmune disorders, may result in a higher risk of cardiovascular problems. Also, researchers note that, from a nutritional point of view, improving nutritional uptake may help lipid levels return to normal, and to increase HDL-C. Better nutritional uptake may also lead to an increase in soluble vitamin absorption, which may help to lower homocysteine levels in the blood. As such, supporters of this hypothesis argue that, by helping to reduce intestinal inflammation, and to increase nutritional absorption, a gluten-free diet may thus lower the risk of cardiovascular disease in people with celiac disease. For the most part, studies suggesting that a gluten-free diet may increase the risk of cardiovascular disease tend to hinge on the idea that an unguided gluten-free diet may be more likely to be unbalanced, and to include higher fat intake, which could increase risk factors for cardiovascular disease. Supporters of this hypothesis point to a recent study that suggests that consuming saturated fatty acids increases the LDL-C concentration in plasma and has therefore been suggested to increase the risk of ischemic heart disease (IHD), or myocardial ischaemia, which is a type of heart disease characterized by reduced blood supply to the heart muscle. Furthermore, studies have shown that a gluten-free diet can increase weight and percentage of fat, which may reveal an additional risk factor for cardiovascular disease in developed countries, where the incidence of overweight and obesity are rising, both in the general population, and in celiac disease patients. Unfortunately, a recently published review of the research team's available evidence on the relationship between celiac disease, a gluten-free diet, and cardiovascular disease and its risk factors does little to provide a clear answer one way or the other. In the face of conflicting data regarding gluten-free diet and cardiovascular disease, the takeaway seems to be that it is important that people with celiac disease follow a gluten-free diet that is well-balanced, and not too high in saturated fat; a conclusion that many would likely find to be good, common sense. Source: Nutritional Therapy & Metabolism 2012; 30 (1): 1-9
  7. Celiac.com 01/08/2014 - Push-back mounts against a controversial new report alleging that genetically engineered foods may trigger gluten sensitivity and celiac disease. In the first salvo, Celiac Disease Foundation CEO Marilyn Geller derided the report, published last week by the Institute for Responsible Technology (IRT), as merely "speculative." Then followed comments by leading plant geneticist, Dr. Wayne Parrott, professor of crop science at the University of Georgia, that the report relied on "a handful of deeply flawed"studies and ignored "more than 1,000 studies that have been published in refereed journals and which show that GM crops are as safe as their counterparts." According to Geller, no one has offered scientific evidence "for a GMO/celiac disease link that is supported by the CDF Medical Advisory Board. For their part, the authors of the IRT report admit that there is no data to prove that GMO consumption causes gluten sensitivity. However, they try to hedge slightly by claiming that more and more research shows that GMO consumption may worsen celiac symptoms or lead to gluten sensitivity. Here again, they offer no good data to support their claims. Source: FoodNavigator.com
  8. Celiac.com 11/21/2013 - Gluten-free food manufacturer Against the Grain, of Brattelboro Vermont, has filed a trademark infringement lawsuit against a California company doing business as Against All Grain. Against The Grain Gourmet Foods has filed documents in the U.S. District Court for the District of Vermont asking the court to order Against All Grain to give up all claims to the name. The lawsuit, which was filed on Oct. 11, alleges the use of Against All Grain by the defendants "is likely to cause confusion, to cause mistake, or to deceive and therefore constitutes infringement of Plaintiff's federally registered trademark ..." In the court documents, attorneys for Against The Grain assert that the defendants are using a website and Facebook page and have published a cookbook of gluten-free recipes using their "Against All Grain" marks. The documents filed by Against The Grain further assert that Against All Grain's alleged infringements have devalued Against The Grain's brand and will confuse consumers, some of whom might assume there is a relationship between the two companies. Sound complicated? It is, a bit, and not just for the similarity of names. Want to read a detailed account? Check out this excellent article by Bob Audette for the Brattleboro Reformer, which does a great job of laying out the legal zigs and zags of this particular gluten-free name battle.
  9. Celiac.com 07/22/2011 - Many reports indicate a hypercoagulative state in diabetes mellitus as result of endothelial damage. Numerous researchers have reported a strong association between type 1 diabetes mellitus (DM1) and celiac disease. Clinical data indicate that vascular dysfunction can result from a cascade of biochemical events triggered by a metabolic malfunction. The net result changes the cells that line the interior surface of the blood vessels; from a surface called a thrombo-resistant surface to one called a thrombo-genic surface. A research team recently set out to determine whether celiac disease in a group of DM1 patients is connected with a different expression of certain hemostatic factors, and with a different manifestation and/or progression of microvascular complications of DM1, as compared to patients with diabetes alone. For the study, the team enrolled ninety-four adult patients with DM1, who they then screened for celiac disease. They found anti-endomysial antibodies (EMA) in 13 of 94 DM1 patients (13.8%). The team then confirmed celiac disease diagnosis by histology and organ culture. The mean age and duration of DM1 of patients also affected by celiac disease were similar to those patients with diabetes alone, but the groups showed very different parameters for metabolic control and hemo-coagulation. In DM1 patients with celiac disease those parameters include: Signiï¬cantly lower concentrations of glycosylated hemoglobin (HbA1c) (P.05), cholesterol (P.001), triglycerides (P.001), factor VII antigen (FVII:ag) (P.005), factor VII coagulant activity (FVII:c) (P.05), and prothrombin degradation fragments (F1+2) (P.001). Higher values of activated C protein (APC) (.001). DM1 patients with celiac disease showed no retinal abnormalities and no signs of renal damage.The results suggest a potential protective role of celiac disease in the pro-thrombotic state of DM1. Source: Acta Diabetol. DOI 10.1007/s00592-011-0301-1
  10. Celiac.com 03/11/2013 - People with celiac disease must follow a gluten-free diet if they want to remain healthy, but a 200-patient study conducted by Alvine Pharmaceuticals show that 90 percent of celiac patients who followed a gluten-free diet still reported symptoms of the disease. That reality is helping to drive an effort by Alvine to develop a drug that would help those people to avoid symptoms and damage that come with accidental exposure to gluten. According to a recent press release, Alvine had already raised at least $42 million for its celiac disease drug, and now has $6 million more as it works through a second phase 2 trial. The company's top drug prospect is ALV003, a mix of two recombinant gluten-specific proteases that’s designed to be used along with a gluten-free diet to prevent immune reactions associated with celiac disease. As disclosed in a recently filed U.S. Securities and Exchange Commission document, the company has raised at least $6 million in debt and other non-equity securities, and could raise up to $500K more. ALV003 is designed to be taken orally by people with celiac disease at the time of a meal. It mixes with and breaks down the gluten in food before it can reach the small intestine, where it would cause inflammatory responses. The drug is designed to prevent accidental gluten contamination, not to allow celiac sufferers to freely and safely consume large amounts of gluten. In a phase 2a study, ALV003 met its goals and reduced gluten-induced intestinal injury in celiac patients who were already following a gluten-free diet. According to clinicaltrial.gov, ALV003 is presently in a study phase with a March 2013 completion date. In the fall of 2012, Alvine received permission from the U.S. Food and Drug Administration to fast-track ALV003, which means the company can work more closely with the FDA during clinical trials, and may get a faster review if they file a New Drug Application. Alvine is a San Carlos, California-based biopharmaceutical company founded in 2006 on technology from Stanford University. Its investors include Abbott Biotech Ventures, Panorama Capital, InterWest Partners, Prospect Venture Partners, Sofinnova Ventures, Black River Asset Management and Flagship Ventures. Read more here.
  11. Celiac.com 08/16/2012 - Tests for blood antibodies against native gliadin (anti-nGli) are still often assumed to perform better in the diagnosis of celiac disease in young children than tests for antibodies to deamidated gliadin (anti-dGli), tissue transglutaminase (anti-tTG), and endomysium (EmA). A team of researchers recently set out to determine whether testing IgG and IgA antibodies Against native gliadin was best for diagnosing celiac disease in children under 2-years old. Specifically they wanted to compare the performance of assays for anti-nGli, anti-dGli, anti-tTG, and EmA in this age group. The research team included T. Richter, X. Bossuyt, P. Vermeersch, H.H. Uhlig, M. Stern, A. Hauer, K.P. Zimmer, L. Mearin, J.H. Roo, C. Dähnrich, and T. Mothes. They are affiliated with the University Children's Hospital, the Children's Hospital of the Clinical Centre, "Sankt Georg," and the Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics at University Hospital in Leipzig, Germany; with the Department Laboratory Medicine of University Hospital in Leuven, Belgium, the University Children's Hospital in Tübingen, Germany, the University Children's Hospital in Graz, Austria, the University Children's Hospital in Giessen, Germany, the Department of Paediatrics at Leiden University Medical Centre in Leiden, The Netherlands, and with EUROIMMUN Medizinische Labordiagnostika GmbH in Lübeck, Germany. For their study, they conducted a retrospective analysis of 184 children. The study group included 42 children with celiac disease under normal diet, and a control group of 142 children up to 2 years of age. The team measured immunoglobulin (Ig) A- and IgG-anti-dGli, IgA- and IgG-anti-nGli, IgA- and IgG-anti-tTG, and IgA-EmA in blood samples. They calculated areas under receiver operating characteristics curves, sensitivities, specificities, positive and negative predictive values, positive and negative likelihood ratios, as well as diagnostic odds ratios. When all the data was complete, they found that only tests for IgG-anti-dGli, IgA-anti-tTG, and IgA-EmA had high specificity (≥0.96) connected with high sensitivity (≥0.86), with high positive predictive values (≥0.52 and ≥0.69 at pretest probabilities of 0.05 and 0.1, respectively) and negative predictive values (≥0.99 and ≥0.98 at pretest probabilities of 0.05 and 0.1, respectively). These tests also showed high positive likelihood ratio (≥24) at low negative likelihood ratio (≤0.15) and high diagnostic odds ratios (≥136). From their data, the team concluded that using anti-nGli tests to diagnose celiac disease in young children was not helpful. They maintain that IgA-anti-tTG, IgA-EmA, and IgG-anti-dGli provided much more reliable results than anti-nGli in diagnosing celiac disease in young children. Source: J Pediatr Gastroenterol Nutr. 2012 Jul;55(1):21-25.
  12. Celiac.com 01/20/2012 - Candi Smithson says her 2-year-old son, Preston, has severe allergies that present him from eating certain breads and dairy items, among other things. Celiac disease prevents Preston from eating anything containing gluten, a protein found in wheat, rye and barley. Preston also is allergic to certain milk proteins, making things like butter and other dairy products hazardous to his health. Smithson claims that the local pizza Hut in Muskogee, Oklahoma discriminated against her by asking her and her son to leave the restaurant. Smithson told reporters that she was in Muskogee as part of a home-schooling group to see replicas of the Niña and Pinta ships, which had been cruising the Arkansas River in recent weeks. Smithson, another parent and four children, including Preston, stopped at Pizza Hut to have lunch. Smithson told reporters from NewsOk.com that, before going into Pizza Hut, she had first stopped at McDonald's to get Preston a hamburger without the bun, and some french fries, which is safe for Preston to eat. She brought that food with her into Pizza Hut, where she planned to order pizza for the other kids. But before the group could place an order, Smithson said a waitress told her that she could not be in the store with the McDonald's items. Smithson told reporters that she explained the situation, but that the waitress remained unmoved. “I explained why I was bringing in the food, but she said it didn't matter,” Smithson said. Smithson then asked to speak to the manager. She says that the manager, who was reportedly unavailable for comment, was also unsympathetic to the situation. According to Smithson, the manager basically said, "We can't have this food in here, so we're going to have to ask you to leave,'” Smithson said. “I was really shocked ... we bring food into restaurants all the time, and this has never happened before.” Smithson told reporters that Pizza Hut had no signs indicating a no-outside-food policy, and added that the restaurant lost out on five paying customers by demanding the hamburger and fries be discarded. Indeed, a Pizza Hut official, who spoke to reporters on the condition he remain unnamed, says he knows of no company policies that would prevent paying customers from eating outside food in a Pizza Hut restaurant. According to reporters, calls to Pizza Hut's corporate offices seeking comment on this story went unreturned. Smithson says the actions of the Pizza Hut manager violated her son's rights as a person living with a disability. She claims food allergies that interfere with “major life activities” are considered disabilities. Marca Bristo, who helped craft the original Americans with Disabilities Act during the late 1980s, agrees with Smithson. Bristo served as chairman of the National Council on Disability, a position she was appointed to by former President Bill Clinton. Bristo said the Americans with Disabilities Act, enacted in 1990, was amended in 2008 to broaden what are considered “major life activities.” She said the changes were necessary because “the courts had narrowed the definition of the law” up to that point. Eating is listed as major life activity in the amended act, which went into effect Jan. 1, 2009. When asked about Candi Smithson's ordeal, Birsto said, “I do think she is right to challenge this." There are some ambiguities in the law, but, basically, Bristo says, "…if a food allergy affects life activities, it's got to be considered a disability and should fall under the act.” Still, Smithson insists she's not looking for money. “I just want the policies changed,” she told reporters. “That way, when he gets older, he won't have to deal with things like this.” Has anything like this happened to you or anyone you know? Should restaurants be flexible when paying customers need to bring in outside food for reasons concerning allergies or food sensitivities? Let us know your thoughts. The story was originally reported by NewsOk.com. Source: http://newsok.com/oklahoma-mother-says-muskogee-pizza-hut-discriminated-against-son/article/3627995
  13. Celiac.com 10/26/2011 - In vitro and in clinical studies have shown that oxidative stress plays a role in gluten-induced toxicity, but no studies have observed this activity in living tissue. A research team set out to examine the role of nuclear factor erythroid 2-related factor2 in gliadin-mediated toxicity in human Caco-2 intestinal cells and in gliadin-sensitive human leukocyte antigen-DQ8 transgenic mice (DQ8), along with assessing the protective activity of CLA. The research team included Paolo Bergamo, Marta Gogliettino, Gianna Palmieri, Ennio Cocca, Francesco Maurano, Rosita Stefanile, Marco Balestrieri, Giuseppe Mazzarella, Chella David, and Mauro Rossi. The team had previously observed the protective role played by conjugated linoleic acid (CLA), which works by the activation of nuclear factor erythroid 2-related factor2 (Nrf2), which serves as a crucial transcription factor for the synthesis of antioxidant and detoxifying enzymes (phase 2). To assess gliadin effects in differentiated Caco-2 cells and in DQ8 mice, they fed the mice a gliadin-containing diet with or without CLA supplementation, and then combined enzymatic, immunochemical, immunohistochemical, and quantitative real-time PCR (qRT-PCR) data. In both laboratory tests, and in living tissue tests, they found gliadin toxicity accompanied by downregulation of phase 2 and elevated proteasome-acylpeptide hydrolase activity. Interestingly, in DQ8 mice intestine, gliadin did not generate severe oxidative stress extent or pathological reactions like those found in celiac patients. Moreover, the reactions that did result were mitigated by CLA. From these results, the researchers conclude that CLA offers beneficial effects against the reduction of key intestinal cytoprotective defenses. This indicates a new nutritional approach for the treatment of intestinal disease associated with altered redox homeostasis. Source: Molecular Nutrition and Food Research; Vol 55 Issue S2. DOI: 10.1002/mnfr.201100295
  14. Celiac.com 12/03/2009 - Clinicians recently described a case of severe osteoporosis with high bone turnover, in which they found neutralizing autoantibodies against osteoprotegerin to be present. They also report finding autoantibodies against osteoprotegerin in three additional patients with celiac disease. The clinical team reporting the findings was made up of Philip L. Riches, M.R.C.P., Euan McRorie, F.R.C.P., William D. Fraser, Ph.D., F.R.C.Path., Catherine Determann, B.Med.Sci., Rob van’t Hof, Ph.D., and Stuart H. Ralston, M.D. They are associated with the Rheumatic Diseases Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh (P.L.R., E.M., C.D., R.H., S.H.R.); and the Unit of Clinical Chemistry, School of Clinical Sciences, University of Liverpool, Liverpool (W.D.F.) — both in the United Kingdom. The adult patient presented severe, high-turnover osteoporosis associated with subclinical celiac disease and autoimmune hypothyroidism. The clinicians found circulating autoantibodies against osteoprotegerin. Autoantibodies against osteoprotegerin block the inhibitory effect of osteoprotegerin on signaling by the receptor activator of nuclear factor (NF)-κB (RANK). The patient's osteoporosis did not respond to celiac disease treatment of a gluten-free diet, but completely reversed with bisphosphonate therapy. Immunoglobulins purified from specimens of the patient’s serum abolished the inhibitory effect of osteoprotegerin on RANKL-induced NF-κB signaling in vitro, while those from the control serum did not, which indicates the presence of neutralizing autoantibodies against osteoprotegerin. The clinicians used immunoprecipitation assay for osteoprotegerin on non-fasting patient serum samples at several points during the course of his illness, as well as from 10 age-matched healthy male controls, 15 patients with celiac disease, and 14 patients with autoimmune hypothyroidism. They used bicinchoninic acid assay to measure protein content. Serum samples from the 10 healthy controls and the 14 patients with autoimmune hypothyroidism showed no evidence of circulating autoantibodies against osteoprotegerin, while the serum samples from 3 of the 15 patients (20%) with celiac disease did show antibodies. Autoantibodies against osteoprotegerin may be connected to the development of high-turnover osteoporosis, but whether autoantibodies against osteoprotegerin contribute to the pathogenesis of osteoporosis in celiac disease patients remains unknown. Source: N Engl J Med 2009;361:1459-65.
  15. Celiac.com 05/08/2007 - One of the strategies for developing alternative therapies for treating celiac disease centers on the identification of antagonist peptides that might inhibit the abnormal immune response caused by gliadin peptides in celiac disease. A recent study published in the journal Pediatric Research indicates that a peptide that occurs naturally in durum wheat may protect against the effects of celiac disease by acting as an antagonist against gliadin peptides associated with abnormal immune response. The study was conducted by a team of Italian researchers made up of Drs. Marco Silano, Rita DiBenedetto, Antonello Trecca, Gioachhino Arrabiato, Fabiana Leonardi, Massimo De Vincenzi. The research team set out to assess the antagonistic effects of 10mer, a decapeptide (sequence QQPQDAVQPF) from the alcohol–soluble protein portion of durum wheat, and to evaluate its prospects for preventing gliadin peptides from activating celiac peripheral blood lymphocytes. The team extracted peripheral blood mononuclear cells from children with celiac disease who tested DQ2-positive, and from a healthy control group. These samples were then incubated with the peptic-tryptic digest of bread wheat gliadin (GLP) and peptide 62-75 from [alpha]-gliadin, both alone and separately with 10mer. PBMC proliferation, release of pro-inflammatory Th1 cytokines interferon-[gamma] and tumor necrosis factor-[alpha], release of immuno-regulatory cytokine IL-10, and analysis of CD25 expression as indexes of lymphocytes activation were performed. Exposure to wheat gliadin peptide and peptide 62-75 from [alpha] gliadin both showed increased activation of lymphocytes. However, the incubation samples with 10mer showed inhibited lymphocyte action. The study indicates that naturally occurring peptide 10mer in durum wheat may protect against lymphocyte activity in patients with celiac disease, and that further study and evaluation of these findings is warranted. Pediatric Research. 61(1):67-71, January 2007.
  16. Celiac.com 06/08/2007 - On May 30th, federal judge Elaine E. Bucklo dismissed key parts of a lawsuit against McDonalds regarding the gluten-free status of their famous French fries. The case, In Re McDonalds French Fries Litigation (MDL-1784), was brought in February 2006, by two Florida plaintiffs on behalf of their autistic daughter who allegedly suffered ill effects from eating McDonalds French fries. At the time, the company claimed that the French fries were gluten-free. The lawsuit claimed in part that McDonalds "failure to disclose the fact that their French fries contained gluten constitutes deceptive, unfair, unconscionable, misleading and fraudulent trade practices," and that "McDonalds unfairly and unjustly profited from their conduct. The judge dismissed claims of fraud, breach of implied warranty, and a request for injunctive relief, but left intact two counts, breach of express warranty and unjust enrichment. In its arguments for dismissal, McDonalds claimed that most of the plaintiffs legal causes of action were barred as a matter of law. Basically, McDonalds asserted that the plaintiffs pled themselves out of court by arguing facts that undermined their own claim. The plaintiffs fraud allegations were rejected because they failed to meet the specificity required under the federal rules. McDonalds argued that the plaintiffs claim of fraud and misrepresentation failed to state how, when, or where the alleged misrepresentations took place. Federal Rule 9( of Civil Procedure requires that all claims of fraud be stated with particularity; otherwise, they face dismissal. Judge Bucklo rejected the plaintiffs claim for injunctive relief because she found there was no threat of future wrongful conduct. The company revised its web site in 2006 to show that its fries and hash browns contain gluten. Also, the publicity brought by the suit arguably eliminated any need for injunctive relief. The plaintiffs have 28 days to amend their complaint or the lawsuit will go forward based on the two remaining counts. health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
  17. Eur J Gastroenterol Hepatol. 2003 Sep;15(9):995-1000. Celiac.com 08/27/2004 - Past studies have demonstrated an association, but not a causal connection, between cigarette smoking and celiac disease. Using the Bradford Hill criteria British researchers have now established a causal connection. In a matched case-control study, the researchers utilized a questionnaire to obtain the smoking histories of 138 celiacs and 276 age-matched and sex-matched controls. The subjects were then categorized according to their pre-diagnosis cigarette exposure, and it was found that 10% of celiacs, and 30% of the controls were smokers during this time. A biological gradient was demonstrated for total, recent and current cigarette exposure, and the greatest risk reduction related to current exposure. The researchers conclude: "This study strengthens the case for a causal relationship between smoking and coeliac disease by demonstrating a strong, temporally appropriate and dose-dependent effect, thus meeting the Bradford Hill criteria. This suggests that cigarette smoking truly protects against the development of adult coeliac disease."
  18. Celiac.com 09/01/2002 - Patients with celiac disease are 20 times more likely than the general population to have epilepsy and often have associated cerebral and cerebellar calcifications imaged by CT and MRI. Depression, dementia, and schizophrenia are all also common in persons with untreated celiac disease. Cerebellar degeneration with resulting ataxia (gluten-associated ataxia) is a known entity in Europe, and the National Institutes of Health (NIH) is currently recruiting subjects with ataxia to examine them for gluten sensitivity and celiac disease. Focal white matter lesions in the brain recently have been reported to occur in children with celiac disease and are thought to be either ischemic in origin as a result of vasculitis or caused by inflammatory demyelination. Parents of children with celiac disease have reported behavioral changes such as irritability, separation anxiety, emotional withdrawal, and autistic-like behaviors that all seemed to improve on a GFD. Although not scientifically validated, the GFD is now also being advocated for children with autism by several groups. Whether or not children with autism are at a higher risk for celiac disease or celiac children have a higher incidence of autism remains to be proven. However, children with Down syndrome, who often have autistic-like behaviors, are at higher risk for celiac disease. It has been hypothesized that gluten may be broken down into small peptides that may cross the blood-brain barrier and interact with morphine receptors, leading to alterations in conduct and perceptions of reality. The serologic tests can be divided into 4 different types of antibodies: antigliadin (AGA), antireticulin, antiendomysium (AEA), and antitissue transglutaminase (tTG). Each antibody varies widely in its sensitivity, specificity, and positive and negative predictive values (Table 2). Table 2 (from Pietzak et al, 2001, compiled data from multiple studies) Test Sensitivity Specificity PPV NPD AGA IgG 57-100 42-98 20-95 41-88 AGA IgA 53-100 65-100 28-100 65-100 AEA IgA* 75-98 96-100 98-100 80-95 Guinea pig tTG† 90.2 95 Human tTG† 98.5 98 * Patients older than 2 years of age. † IgG +IgA antibodies. The AEA IgA immunofluorecent antibody is an excellent screening test for celiac disease, with both a high sensitivity and specificity. This antibody was discovered in the early 1980s and rapidly gained use as part of a screening celiac panel by commercial laboratories in combination with AGA IgG and AGA IgA. Its major drawbacks are that it may be falsely negative in children under the age of 2 years, in patients with IgA deficiency, and in the hands of an inexperienced laboratory. Also, the substrate for this antibody was initially monkey esophagus, making it expensive and unsuitable for screening large numbers of people. Recently, the human umbilical cord has been used as an alternative to monkey esophagus. However, the subjective nature of the AEA assay may lead to false-negative values and unacceptable variability between laboratories. Because tTG had been first described as the autoantigen of celiac disease in 1997, it has been used to develop innovative diagnostic tools. The tTG IgA ELISA test is highly sensitive and specific, using either the commercially available guinea pig tTG or human recombinant tTG. The tTG assay correlates well with AEA-IgA and biopsy. However, it represents an improvement over the AEA assay because it is inexpensive and rapid (30 minutes), is not a subjective test, and can be performed on a single drop of blood using a dot-blot technique. Therefore, this test is ideally suited for mass screenings and in the future could be performed in the general practitioners office, much like the now routine finger-stick hematocrit. For the reasons outlined above, the IgA class human anti-tTg antibody, coupled with the determination of total serum IgA, currently seems to be the most cost-effective way to screen for celiac disease. AEA should be used as a confirmatory, pre-biopsy test, whereas AGA determinations should be restricted to the diagnostic work-up of younger children and patients with IgA deficiency, using the guidelines in Table 3. Table 3 Probability of celiac disease based on three antibodies in combination AEA IgA AGA IgA AGA IgG Interpretation + + + Celiac disease 99% probable + - + probable + + - Celiac disease probable + - - Celiac disease probable - + + Celiac disease less likely* - - + Celiac disease less likely* - + - Celiac disease less likely - - - Celiac disease very unlikely+ * If patient is IgA sufficient: AGA IgG > 100 warrants work-up of enteropathy. + If patient is on a gluten-containing diet. Celiac disease: AEA, antiendomysium antibodies: AGA, antigliadin antibodies.
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