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Found 91 results

  1. 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.
  2. Celiac.com 07/22/2013 - Celiac disease is known to be caused by a combination of genetic and environmental factors. The genetic markers are fairly well established by now, but the environmental factors that are associated with celiac disease are still pretty foggy. A recent study suggests that antibiotic use might be one such factor. In a population-based case-control study analyzing Swedish population data, antibiotic use was compared against diagnosis of celiac disease. 2,933 people with celiac disease diagnoses were linked to the Swedish Prescribed Drug Register, in order to provide a history of antibiotic use. 2,118 people with inflammation (early celiac disease) and 620 people with normal mucosa but positive celiac disease blood test results were also compared. The control group consisted of 28,262 individuals matched for age and sex from the general population. The results of the study significantly suggest that antibiotic use is associated with celiac disease, at an odds ratio of 1.4 (1.27-1.53 confidence interval). Early celiac disease was also connected, with an odds ratio of 1.90 (1.72-2.10 confidence ratio), as well as positive celiac disease blood tests, at 1.58 odds ratio (1.30-1.92 confidence interval). Even when antibiotic use in the last year was ruled out, the results were very similar at 1.30 odds ratio (1.08-1.56 confidence interval). When ruling out patients with additional diseases, which could potentially be factors, the results were also very similar at 1.30 odds ratio (1.16-1.46 confidence interval). What does all that mean? A 1.4 odds ratio basically means that people who had a history of antibiotic use were 1.4 times as likely as those who had not taken antibiotics to develop celiac disease. The fact that inflammation associated with early celiac disease was also highly connected suggests that antibiotics' role in disrupting the biology of the GI tract could in some way cause celiac disease. There is still some question of causality, but it would seem that antibiotics could very likely be a culprit in the development of celiac disease, and should be avoided when possible. Source: http://www.biomedcentral.com/1471-230X/13/109/abstract
  3. 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.
  4. Celiac.com 03/31/2014 - Celiac disease is an autoimmune disorder that occurs in genetically susceptible individuals who carry the genetic markers HLA DQ2 or DQ8. About one in three people carry these genetic markers, while researchers estimate that the global prevalence of celiac disease is somewhere between one- and two-percent. A gluten-free diet remains the only treatment for celiac disease, but researchers are looking into new therapies aimed at gluten modification. A team of researchers have reviewed a number of promising new celiac disease therapies aimed at gluten modification. The researchers include S. Stoven, J.A. Murray, and E. Marietta, of the Division of Gastroenterology and Hepatology, Department of Internal Medicine at the Mayo Clinic in Rochester, Minnesota. Their review in Clinical Gastroenterology & Hepatology discusses gluten-based therapies including wheat alternatives and wheat selection, enzymatic alteration of wheat, oral enzyme supplements, and polymeric binders as exciting new therapies for treatment of celiac disease. Unfortunately, the full study is only available to subscribers, but anyone with the inclination to subscribe can read it online. Source: Clin Gastroenterol Hepatol. 2012 Aug;10(8):859-62. doi: 10.1016/j.cgh.2012.06.005.
  5. Celiac.com 03/26/2008 - According to the results of a recent study,adults with diet-treated celiac disease show no elevation inanti-avenin IgA by oats. Celiac disease is effectively treated with agluten-free diet that is free of wheat, rye, barley and related grains. Whileit is well known that wheat, rye and barley trigger the disease, fordecades there has been controversy about the safety of oats. Recentevidence from a number of studies has supported the idea that oats aresafe for people with celiac disease. In several countries, oats are nowon the list of safe foods for people with celiac disease. The studieson oats and celiac disease have had various designs, but most have beensmall, and often with high patient drop-out rates. To date, there hasonly been a single randomized and double-blinded study measuring the effects of oats on celiac patients. The studies have been nearly unanimous in concluding that consumption of oats is safe to celiac disease patients. Mostof these clinical studies have assessed blood histology in reaction tooats, or measured normalization after patients had been diagnosed withceliac disease and were already following gluten-free diets. Threelarge studies from Finland have investigated the effect of dietary oatsand their influence on antibody levels to wheat gluten and to tissuetransglutaminase. Previous studies have shown that people withuntreated celiac disease show elevated IgA antibodies in reaction oatavenins. However, only one study on treated celiac disease patients hasinvestigated IgA antibodies to oats. Researchers know of justthree confirmed cases of active celiac disease flaring up again inadults after these people ingested oats, which indicates thatintolerance to oats among celiacs may be rare, but also may in facthave some role to play in celiac disease. It also points to the need for clinical monitoring of celiac disease patients who eat oats. Aresearch team made up of Vigdis Guttormsen, Astrid Løvik, Asta Bye;Jorunn Bratlie, Lars Mørkrid, and Knut E. A. Lundin recently conducteda small study to determine whether treated adult celiac diseasepatients who ate oats showed elevated levels if IgA. The research team compared blood samples of 136 adult patients with treated celiac disease against 139 controls. The team used ELISA to test the blood samples to measure IgA against oats avenin, wheat gliadin and tissue trans-glutaminase. Eighty-two of the celiac disease patients had been eating oats as part of their gluten-free diet for 6 months or more. Both the oats-eating and non-oats-eating celiac disease patients showed no significant differences in IgA against oats. However, both groups did show elevated levels of IgA against wheat, oats and tissue tTG compared to healthy controls. Thegroups also showed a significant positive correlation betweenanti-avenin and antigliadin IgA (pB0.0001), and between anti-avenin andanti-tissue transglutaminase IgA (p 0.0012). The researchersconcluded that eating oats does not cause increased levels of IgA inadult celiac disease patients on a gluten-free diet. The findings support the notion that most adult celiac disease patients can tolerate oats. Scandinavian Journal of Gastroenterology, 43:2, 161 - 165.
  6. 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.
  7. 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.
  8. Celiac.com 10/15/2013 - Most case reports suggest an association between autistic spectrum disorders (ASDs) and celiac disease (celiac disease) or positive celiac disease serologic test results, but larger studies are contradictory. A team of researchers recently set out to examine the association between ASDs and celiac disease according to small intestinal histopathologic findings. The research team included Jonas F. Ludvigsson; Abraham Reichenberg; Christina M. Hultman; and Joseph A. Murray. They are variously affiliated with the Department of Medicine, Clinical Epidemiology Unit, and the Department of Medical Epidemiology and Biostatistics at the Karolinska Institutet in Stockholm, Sweden, with the Department of Pediatrics at Orebro University Hospital, Orebro University in Orebro, Sweden, with the Division of Gastroenterology and Hepatology of the Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, with the Department of Psychosis Studies at the Institute of Psychiatry at King’s College in London, United Kingdom, and with the Department of Psychiatry at the Mount Sinai School of Medicine in New York, New York. For their nationwide case-control study, the researchers used 28 Swedish biopsy registers to gather data on approximately 26,995 individuals with celiac disease, which they defined as the presence of villous atrophy, Marsh stage 3. They found 12,304 patients with inflammation (Marsh stages 1-2), 3719 patients with normal mucosa (Marsh stage 0), but positive celiac results for IgA/IgG gliadin, endomysium, or tissue transglutaminase. They then compared these results against and results for 213,208 age- and sex-matched control subjects. The team used conditional logistic regression to estimate odds ratios (ORs) for prior ASD diagnosis according to the Swedish National Patient Register and then conducted a second analysis, using Cox proportional hazards regression to estimate hazard ratios (HRs) for future ASDs in individuals undergoing small intestinal biopsy. They found that previous ASD was not associated with celiac disease (OR, 0.93; 95% CI, 0.51-1.68) or inflammation (OR 1.03; 95% CI, 0.40-2.64). However, they did finds that previous ASD was associated with a sharp higher risk of having normal mucosa but positive serologic test result for celiac disease (OR, 4.57; 95% CI, 1.58-13.22). Once the team restricted the data to individuals without no diagnosis for ASD at the time of biopsy, they found that celiac disease (HR, 1.39; 95% CI, 1.13-1.71) and inflammation (HR, 2.01; 95% CI, 1.29-3.13) were both connected with slightly higher risks of later ASDs, compared against the HR of 3.09 (95% CI, 1.99-4.80) for later ASDs in individuals with normal mucosa but positive celiac disease serologic test results. Even though this study showed no connection between previous ASD and celiac disease or inflammation, it did show that individuals with normal mucosa, but positive blood screens for celiac disease, have a much higher risk of ASD. Source: JAMA Psychiatry. Published online September 25, 2013. doi:10.1001/jamapsychiatry.2013.2048
  9. 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.
  10. 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
  11. Celiac.com 07/08/2013 - Right now, the only way for doctors to distinguish between the complicated and uncomplicated forms of celiac disease is to use invasive methods. In an effort to find a way other than these invasive methods to distinguish between uncomplicated and complicated forms of celiac disease, a research team set out to study serum parameters in the spectrum of celiac disease The research team included Greetje J Tack, Roy LJ van Wanrooij, B Mary E Von Blomberg, Hedayat Amini, Veerle MH Coupe, Petra Bonnet, Chris JJ Mulder, and Marco WJ Schreurs. They are variously affiliated with the Departments of Epidemiology and Biostatistics, Gastroenterology and Hepatology, and Pathology of VU University Medical Centre in Amsterdam, The Netherlands, and with the Department of Immunology, Erasmus MC at theUniversity Medical Centre in Rotterdam, The Netherlands. The team's cohort study looked at the possible use of new testing methods, including IL-6, IL-8, IL-17, IL-22, sCD25, sCD27, granzyme-B, sMICA and sCTLA-4 in patients diagnosed with active celiac disease, celiac disease following a gluten-free diet, Refractory celiac disease (RCD) types I and II, and enteropathy associated T-cell lymphoma (EATL). The results showed elevated levels of the pro-inflammatory IL-8, IL-17 and sCD25 in both active celiac disease and RCDI-II. In addition, patients with RCDII showed higher serum levels of soluble granzyme-B and IL-6 compared with active celiac disease patients. They did not find any differences between RCDI and active celiac disease, or between RCDI and RCDII. However, they did find that EATL patients had higher IL-6 levels compared with all other groups. This study document a specific series of serum parameters that show that RCDII and EATL have distinct immunological features compared with uncomplicated celiac disease and RCDI. This new method of distinguishing uncomplicated and complicated forms of celiac disease might promote the development of non-invasive procedures in the future. Source: BMC Gastroenterology 2012, 12:159. doi:10.1186/1471-230X-12-159.
  12. Celiac.com 07/03/2013 - Researchers have completed a genetic study of six autoimmune diseases, including diabetes, the largest such study of human disease genetics to date. The study will help scientists in their efforts to uncover the causes of these diseases, which include autoimmune thyroid disease, celiac disease, Crohn’s disease, psoriasis, multiple sclerosis and type 1 diabetes. While currently unknown, the underlying causes of these conditions are believed to involve a complex combination of genetic and environmental factors. In each of the six diseases, the identified genetic variants explained only a proportion of the heritability. Under one of the current major genetic disease hypotheses, the so called ‘rare-variant synthetic genome-wide association hypothesis,’ a small number of rare variants in risk genes are likely the major cause of the heritability of these conditions. In their study, the research team used high-throughput sequencing techniques, in an effort to identify new genetic variants, including rare and potentially high risk variants, in 25 previously identified risk genes taken from a sample of nearly 42,000 patients. Their data suggest that the genetic risk of these diseases more likely results from a complex interaction of hundreds of variants, each small on its own, but which, taken together impact the development of these six diseases. They estimate that rare variants in these risk genes make up only about three per cent of the heritability of these conditions that can be explained by common variants. The results, says lead study author David van Heel, suggest that "risk for these autoimmune diseases is not due to a few high-risk genetic variations." Rather, risk is likely due to a "random selection from many common genetic variants which each have a weak effect.” This could mean that it will never be possible to accurately predict a person's risk of developing any of these six autoimmune diseases, simply because there are too many variables. “However, the results do provide important information about the biological basis of these conditions and the pathways involved, which could lead to the identification new drug targets,” said van Heel. Source: Nature Genetics 42, 295–302 (2010). doi:10.1038/ng.543; and Firstpost.com.
  13. 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
  14. Celiac.com 11/08/2012 - T-cell lymphoma is a deadly type of cancer that is more common in people with celiac disease than in the general population. Currently, there is no cure for T-cell lymphoma, and no promising treatment exists for people who suffer from this condition. However, that may be set to change, as the results of a new study suggest that new treatments for T-cell lymphoma my be on the horizon. The study appears in the journal Clinical Lymphoma Myeloma and Leukemia. The study team included J.R. Bertino, M. Lubin, N. Johnson-Farley, W.C. Chan, L. Goodell, and S. Bhagavathi. They are affiliated with the Departments of Medicine, Pharmacology, and Pathology, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, New Brunswick, NJ. The team was attempting to address the fact that doctors treating T-cell lymphomas, especially types of T-cell lymphoma known as peripheral T-cell lymphoma (PTCL), angioimmunoblastic T-cell lymphoma (AITL), and anaplastic large cell lymphoma (ALCL) have limited treatment options and cannot cure the condition. Their study noted that a high percentage of PTCL, AITL, and ALCL, along with T-cell leukemia and T-cell lymphoblastic leukemia lack the enzyme methylthioadenosine phosphorylase (MTAP). Their published results also note that MTAP-deficient cells cannot cleave endogenous methylthioadenosine to adenine and 5-methylthioribose-1-phosphate, a precursor of methionine, and as a result have enhanced sensitivity to inhibitors of de novo purine biosynthesis. A recently introduced antifolate, pralatrexate, which has been shown to inhibit de novo purine biosynthesis, has been approved for treatment of PTCL and may have an increasing role in therapy. An alternative strategy involving coadministration of methylthioadenosine and high-dose 6-thioguanine has been proposed and may prove to be selectively toxic to MTAP-deficient uncommon lymphomas. As a result of these MTAP results, the team suggests that new therapies and treatments for T-cell lymphoma may be possible going forward. Source: Clin Lymphoma Myeloma Leuk. 2012 Oct;12(5):306-9. doi: 10.1016/j.clml.2012.07.001.
  15. Celiac.com 04/04/2012 - After numerous studies over several decades showing higher mortality rates in people with celiac disease, including a comprehensive study in 2009, published in Gastroenterology, news of a recent UK study, finding mortality rates for people with untreated celiac disease that are similar to the general population, has raised a few eyebrows. With diverse study data fueling differing opinions, questions regarding long-term mortality in people with celiac disease will likely take time to resolve. In the meantime, a review of scientific literature brought up this small 2007 study. In it, a research team compared long-term mortality rates in people diagnosed with celiac disease as children with rates for those diagnosed as adults. They wanted to find out how those rates might differ and if the rates might be related to the disease and the length of gluten exposure before diagnosis. To find an answer, the team gathered data for 285 children and 340 adults diagnosed with celiac disease. They continued to gather data for each until the end of 2004, excepting those who failed to follow up for other reasons. From their data, the team calculated standardized mortality ratios (SMRs) for the period starting five years after patient diagnosis. They found that adults diagnosed with celiac disease had 38% higher mortality rates (SMR 1.38, 95% CI 1.16-1.63). Children on the other hand, faced rates three-times higher (SMR 3.32, 95% CI 2.05-5.07). This excess mortality in children was mainly due to higher rates of death from accidents, suicide, and violence (seven deaths, SMR 3.22, 95% CI 1.29-6.63), cancer (five deaths, SMR 3.72, 95% CI 1.21-8.67), and cerebrovascular disease (two deaths, SMR 10.03, 95% CI 1.21-36.00). The 2007 study found that adults with celiac disease face a modest increase in mortality rates over the long-term, but that mortality rates for those diagnosed with celiac disease as children were three-times higher starting five years after diagnosis. The team proposed that the increased mortality in children from external causes may be due to behavioral changes associated with living with life-long celiac disease and its treatment. Stay tuned for further developments regarding mortality rates in people with celaic disease. Source: The American Journal of Gastroenterology. 2007;102(4):864-870.
  16. 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
  17. 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.
  18. Celiac.com 05/08/2007 - A recent news release by the American Academy of Neurology claims that results of a recent Iranian study find no link between autism in children and the development of celiac disease. The study was conducted by a team of researchers led by Dr. Samra Vazirian of Tehran University of Medical Sciences. The researchers compared blood samples from 34 children with autism and 34 children without autism. All blood samples were tested for antibodies used to detect celiac disease: anti-gliadin and anti-endomysial antibodies. Six children tested positive for these antibodies (four with autism, two without autism). These children were given intestinal biopsies to confirm the serological tests. The biopsies on all six children were negative for celiac disease. From this, researchers concluded that children with celiac disease were no more likely to develop celiac disease than children without autism. According to Dr. Samra Vazirian, the gluten intolerance suffered by people with celiac disease might have no connection to autism, but also indicates that further research into the matter will be of benefit. American Academy of Neurology, news release, May 1, 2007. **Authors note: Given the small sample of subjects in this study, and given the clinical and anecdotal evidence for autistic children responding favorably to a gluten-free diet, coupled with the difficulty of conducting a comprehensive double-blind study involving clinical responses to a gluten free diet in autistic children versus their non-autistic counterparts, the results of this test should be treated with considerable scrutiny, if not outright skepticism. It will be interesting to find out whether or not the researchers used Marsh criteria in their assessment of the biopsies. Given the fact that double the number of autistic children had celiac disease positive serology we must conclude that, at the very least, autistic children have double the rate of gluten sensitivity than their non-autistic counterparts. health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
  19. Celiac.com 09/29/2011 - Results of various studies comparing mortality in undetected celiac disease compared with the general population have been contradictory. Some studies have suggested a fourfold increase in mortality compared with the general population, while others have found no increase at all. A research team set out to clarify the matter by crafting a cohort study of Cambridge doctors that would establish all-cause and cause-specific mortality in undiagnosed celiac disease, identified by anti-endomysial antibody (EMA) positivity. The team included C. Canavan, R. F. Logan, K. T. Khaw, and J. West. They are variously affiliated with the Division of Epidemiology and Public Health at University of Nottingham in Nottingham, UK, with the NIHR Biomedical Research Unit of the Nottingham Digestive Diseases Centre at Nottingham University Hospital in Nottingham, UK, and with the Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. For their study, the team chose their subjects from a general population aged 45-76 years in 1990. They then tracked all deaths using the Office for National Statistics. They calculated mortality rates per 1000 person year, making adjustments for age, gender, smoking and socioeconomic group using multivariate Cox regression to estimate hazard ratios (HR) and 95% confidence intervals (CI). Results showed 117,914 patient years of follow-up from 7527 participants, with an average of 16.8 years. Eighty-seven patients suffered from undetected celiac disease, their all-cause mortality rate was 9.4 per 1000 person years (95% CI 5.4-16.1) compared with 12.7 (95% CI 12.1-13.4) in EMA-negative participants. The adjusted all-cause mortality hazard ratio was 0.98 (95% CI 0.57-1.69). Untreated celiac disease showed no increase in death due to cancer or circulatory diseases. Adjusted hazard ratios were 1.27 (95% CI 0.57-2.85) and 1.39 (95% CI 0.66-2.92) respectively. The research team found no higher overall mortality in people older than 45 years with undetected coeliac disease compared with the general population. They also found no increase in deaths related to circulatory disease or cancer. The team concludes that these results do not support routine screening people older than 45 years for celiac disease. Source: Aliment Pharmacol Ther. 2011 Aug 17. doi: 10.1111/j.1365-2036.2011.04811.x.
  20. Celiac.com 08/04/2011 - People who use direct-to-consumer genetic tests sold by deCODEme and 23andMe frequently receive misleading results, because these tests do not accurately predict risk factors. So say two geneticists, who conducted two studies that assessed the accuracy of test predictions relative to various known disease risks. Presenting their results from both studies at the annual conference of the European Society of Human Genetics, the scientists have gone so far as to call for a ban on the tests. The first study was conducted by Rachel Kalf, from the department of epidemiology at Erasmus University Medical Centre in Rotterdam. Using established genotype frequencies, Kalf simulated genotype data for 100,000 individuals. She then used the formulas and risk data provided by the test companies to predict risks for eight common multi-factorial diseases: age-related macular degeneration (AMD); atrial fibrillation; celiac disease; Crohn's disease; heart attack; prostate cancer; and Type 1 and Type 2 diabetes (T2D). Kalf noted that both companies assigned an increased risk to a substantial part of the test group. However, Kalf says the risk of disease in this group was often substantially lower than the risk in the rest of the study group. For example, for AMD, which has the highest predictive ability of all eight diseases, both companies assumed that the risk in the population was around 8 percent. However, among subject assigned an increased risk factor, 23andMe estimated risk at 16 percent, while deCODEme's estimated that 19 percent would develop AMD. This contrasts with a risk of about 4 percent for the rest of the study population. This means that people in the higher risk group may have a four-fold increased risk of disease, but "are still far more likely not to develop the disease at all," explains co-researcher Cecile Janssens. For T2D, using the risk levels of about 25 percent assigned by the companies, 32 percent of those in the higher risk group would actually develop T2D compared to just 22 percent in the rest of the study population. "This difference in disease risk is too small to be of relevance," says Janssens. Source: Science Blog
  21. Celiac.com 04/25/2011 - Research shows that celiac disease is associated with numerous gastric abnormalities. An international research team recently set out to examine the association between rates of celiac disease and Helicobacter pylori infection in an Iranian population of 250 patients. The research team included Mohammad Rostami Nejad BS1, Kamran Rostami MD PhD, Yoshio Yamaoka MD PhD, Reza Mashayekhi MD1, Mahsa Molaei MD, Hossein Dabiri PhD, David Al Dulaimi MD, Dariush Mirsattari MD, Homayoun Zojaji MD, Mohsen Norouzinia MD, and Mohammad Reza Zali MD FACG AGAF. The team members are variously affiliated with the Research Institute of Gastroenterology and Liver Disease, Shahid Beheshti University, M.C., in Tehran, Iran, the School of Medicine, University of Birmingham in the UK, the Department of Medicine-Gastroenterology, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine in Houston, Texas, and the Department of Gastroenterology, Alexandra Hospital, Redditch, UK. For the study, the team took topsides from the gastric antrum and duodenum. They assessed morphology and histology using the updated Sydney system and modified Marsh criteria, respectively. In order to simplify the assessment of gastric lesions, the team classified gastritis in both macroscopic and microscopic stages. They screened for anti-tissue transglutaminase antibody to determine the presence of celiac disease. Of the 250 patients, 232 (93%) showed histological evidence of Helicobacter pylori infection, while 24 patients (10%) showed histological abnormalities (Marsh I to IIIc). Of the 24 patients with histological abnormalities 20 (83%) showed Helicobacter pylori infection. Of the total 250 patients, 25 patients (10%) showed positive anti-tissue transglutaminase antibody screens, nine (3.6%) of whom showed microscopic and macroscopic enteritis (Marsh I to IIIc). Clinically, there was no way to distinguish the presentation of celiac disease from those cases infected with Helicobacter pylori. Histology, even in patients with positive antibody screens, was non-specific and not useful. The results also showed a high prevalence of Helicobacter pylori infection and chronic gastritis in the study group. However, neither was associated with celiac disease, but rather, matched average rates in Western population studies. Source: Archives of Iranian Medicine, March 2011
  22. 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
  23. Celiac.com 03/15/2011 - For celiacs, it's not really the cinnamon bun that's the enemy. Nor the pizza crust, nor the ravioli. It's the gliadin in these foods - the alcohol-soluble portion of the gluten protein - that's the real culprit. Gliadin is the "gladiator" of the human digestive tract. When we ingest gliadin, enzymes try to break it down into a form that can be absorbed by the small intestine. But gliadin resists, fighting hard to remain intact. A regular small intestine has, like any good fortress, a protective wall: the mucosal lining of the intestine. This layer of mucus normally acts as a barrier against gliadin's assaults. But in a celiac intestine, the mucosal lining is permeable. With gliadin's destructive power enhanced by its enzyme sidekick, tissue Transglutaminase (tTG), it quickly gets past this poorly-guarded layer. Scientists are working to put their finger on exactly what makes the mucosal lining of a celiac's small intestine so permeable. Now a January study by Czech researchers found at least one thing that affects the permeability of the intestinal mucosa: gut bacteria. In this study, called "Role of Intestinal Bacteria in Gliadin-Induced Changes in Intestinal Mucosa: Study in Germ-Free Rats", researchers tied off sections of rats' intestines and introduced various kinds of bacteria to each section. They wanted to measure the effect that these bacteria had on the intestinal mucus - or more specifically, on the goblet cells that produce the intestinal mucus. To ensure that the kinds of bacteria in the rats' intestines were under experimental control, the rats had been raised from birth in germ-free conditions. They found that introducing gliadin to the intestines had the effect of decreasing the mucus-producing cells, thereby eroding the intestines' protective layer. No big surprises there - gliadin is a fighter, a digestive "gladiator", after all. But when they added strains of so-called harmful bacteria, Escherichia coli (otherwise known as E coli) or Shigella, the mucus-producing cells decreased even more. The cells first secreted massive amounts of mucus, then promptly exhausted themselves and gave up. This left the intestine looking very similar to that of a person in the early stages of celiac disease, say the researchers. But the tale did indeed have a happy ending. Along came the good bacteria, Bifidobacterium bifidum (or "Biff" for short). The mucus-producing cells in the small intestine increased when Biff was present. In fact, Biff was able to partially reverse the mucus-decreasing effects of E coli and Shigella. The researchers concluded that the composition of gut bacteria has an effect on the protective mucus of the intestines: an overgrowth of bad bacteria decreases the protective layer, while the addition of good bacteria increases the protective layer. Their study may eventually lead to treatment options for human celiacs, by finding ways to protect tender intestines from the harmful effects of gliadin. Source: PLoS One. 2011 Jan 13;6(1):e16169
  24. Celiac.com 12/29/2010 - A team of researchers recently conducted a prospective study the etiology of lymphocytic duodenosis. Among their findings are that sixteen percent of patients with lymphocytic duodenosis have celiac disease. The research team was made up of I. Aziz, K. E. Evans, A. D. Hopper, D. M. Smillie, and D. S. Sanders. They are affiliated with the Department of Gastroenterology at Royal Hallamshire Hospital in Sheffield, UK. The study came in response to earlier retrospective studies that have suggested different connections with lymphocytic duodenosis, indicating that patients with this condition should not be diagnosed with celiac disease, solely by histology. Lymphocytic duodenosis is marked by normal villous architecture and less than 25 intraepithelial lymphocytes (IELs) per 100 enterocytes. For their study, the team thoroughly evaluated one hundred patients with lymphocytic duodenosis for celiac disease and other aspects associatedwith lymphocytic duodenosis by using initial celiac blood screens, and excluding the presence of infection. Of thirty-four patients with unexplained lymphocytic duodenosis, twenty-nine underwent repeat duodenal biopsies following a gluten challenge. Biopsy results showed that 16% of patients with lymphocytic duodenosis had celiac disease. Once celiac disease was accounted for, the factors most commonly association with lymphocytic duodenosis were as follows: drugs were a factor in twenty-one percent of lymphocytic duodenosis patients; infection was a factor in nineteen percent, immune dysregulation was a factor in four percent, inflammatory bowel disease and microscopic colitis in two percent each, sarcoidosis and IgA deficiency in one percent of cases, respectively. Of thirty-four patients with no known associations, eighteen showed symptoms of irritable bowel syndrome (IBS). Of twenty-nine patients examined with repeat duodenal biopsies, the IEL count returned to normal in twenty-two patients. The study results show that known associations can be found in sixty-six percent of cases of lymphocytic duodenosis. Importantly, sixteen percent will have celiac disease. In cases of lymphocytic duodenosis with no apparent cause, there may be a connection with IBS. In such cases the IEL count returns to normal on repeat biopsy in seventy-six percent. Source: Aliment Pharmacol Ther. 2010 Dec;32(11-12):1392-7.
  25. Celiac.com 12/26/2010 - Should everyone with symptoms of celiac disease go on a gluten-free diet? Current practice allows many patients with symptoms of celiac disease, but no gut damage, and thus no official diagnosis, to forgo a gluten-free diet. In a new study, researchers found that people with celiac disease symptoms have the same distinctive metabolic fingerprint as patients with full-blown disease, and who must follow a gluten-free diet to avoid permanent damage to the gut. The new study, by Ivano Bertini and colleagues, is stirring up the discussion about just which patients with symptoms of celiac disease should follow a gluten-free diet. Their research shows that people currently diagnosed as "potential" celiac disease patients and not advised to follow a gluten-free diet may not be "potential" patients at all. Celiac disease is widely regarded as undiagnosed or misdiagnosed. For their study, the researchers used magnetic resonance metabolic profiling to analyze the biochemical markers in the blood and urine of 61 patients with celiac disease, 29 with potential celiac disease, and 51 healthy people. The researchers found that people with unproven celiac disease largely shared the same profile as those with confirmed celiac disease and that the biochemical markers in both groups differed sharply from those of healthy individuals. The researchers conclude that their findings "demonstrate that metabolic alterations may precede the development of small intestinal villous atrophy and provide a further rationale for early institution of gluten-free diet in patients with potential celiac disease, as recently suggested by prospective clinical studies." The authors do note receiving funding from Boehringer Ingelheim Italy. Source: American Chemical Society Journal of Proteome Research
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