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Celiac.com 02/19/2024 - A recent study presented at the 2023 annual meeting of the American College of Gastroenterology has raised concerns about the increasing incidence of enteropathy-associated T-cell lymphoma (EATL) – a rare and aggressive form of T-cell, non-Hodgkin lymphoma. This alarming trend has prompted researchers to explore the possible connection between EATL and celiac disease, shedding light on the risks faced by individuals with this autoimmune condition. Lead investigator Dr. Isabel Hujoel, Clinic Director of the Celiac Disease Center at UW Medical Center, Seattle, highlighted the strong association between EATL and celiac disease. While EATL is rare, most cases are observed in patients with celiac disease, suggesting a potential link between the two conditions. The study, utilizing data from the Surveillance, Epidemiology, and End Results (SEER) program database, identified 463 cases of EATL between 2000 and 2020, with an age-adjusted incidence rate of 0.014 per 100,000 people. Alarmingly, the incidence of EATL increased by 2.58% annually over this 20-year period. Despite advancements in medical treatment, the prognosis for EATL remains poor, with a median survival of approximately six months. Findings from the study revealed that most cases were treated with a combination of surgery and chemotherapy. However, survival outcomes did not improve over the study period, underscoring the urgent need for more effective treatment strategies. Dr. Sophia Dar, a gastroenterology fellow at Southern Illinois University School of Medicine, emphasized the importance of early detection and treatment. While chemotherapy showed promising results, the overall mortality rate remained high, highlighting the challenges in managing this aggressive cancer. Researchers emphasized the need for further investigation into the factors contributing to the high mortality rate associated with EATL. Understanding these factors could pave the way for more efficient treatment plans and improved outcomes for patients. Debra Silberg, MD, PhD, Chief Scientific Officer of the nonprofit Beyond Celiac, emphasized the rarity of EATL and the need for targeted screening. Screening for EATL should be considered in cases of refractory celiac disease or when there is suspicion of complications related to celiac disease. The rise in cases of EATL serves as a sobering reminder of the potential complications associated with celiac disease. Heightened awareness, early detection, and improved treatment options are crucial in addressing this rare but deadly cancer among individuals with celiac disease. Read more at gastroendonews.com

Celiac.com 08/18/2020 - In the last decade or so, cases of celiac disease have been on the rise globally. Is the disease itself becoming more common, or are more people being diagnosed? A recent podcast by The People's Perspective on Medicine explores the potential surge of celiac disease with guests, Dr. Joseph Murray, MD, and Leonardo Trasande, MD, MPP. The episode also covers Covid-19, and its risks and effects in those with celiac disease, Show 1221 is called: What Explains the Recent Increase in Celiac Disease? The program explores the dramatic increase in celiac disease in the last decades, and the rise may be explained by the fact that many more people are now aware of the condition and eating gluten-free, or other facts. Dr. Murray is with the Division of Gastroenterology and Hepatology at the Mayo Clinic in Rochester, Minnesota. Dr. Murray directs a celiac disease research and clinical program focused on epidemiology, complications and mouse models of gluten sensitivity. Dr. Trasande is a professor in pediatrics, environmental medicine, and population health at New York University. He serves as Director of the Division of Environmental Pediatrics and Vice Chair for Research in the Department of Pediatrics at NYU School of Medicine. The podcast covers the topic from numerous angles, including: What Is Celiac Disease?; Diagnosing Celiac Disease; Who Gets Celiac Disease?, and Environmental Pollutants and the Increase in Celiac Disease. COVID-19 and Possible Risks Associated with Celiac Disease At about the 30 minute mark Dr. Murray discusses how COVID-19 infection can present as GI symptoms, such as diarrhea, abdominal pain, bloating, and loss of appetite. Those with celiac disease should not assume that their GI symptoms are from gluten exposure, and should consider getting tested for COVID-19. It has been shown that those with celiac disease patients have an immune system that is less responsive to vaccines, which also creates a concern about whether this will also be an issue when a COVID-19 vaccine becomes available. According to Dr. Murray, celiac disease patients also have a higher risk of pneumonia, which is of concern if it develops as a complication of COVID-19, and they also have a higher risk of shingles (herpes zoster), which might be triggered by a COVID-19 infection. Because of the additional COVID-19 risk factors mentioned, those with celiac disease should be more careful than others. Celiac disease is not considered as high a risk factor as diabetes, hypertension, and being over age 65, but those with it should consider themselves at somewhat high risk and take additional precautions, for example: Wear a mask in indoor public places at all times; Don't make unnecessary trips outside your home; Don't go into crowded shopping areas if you don't have to; Minimize your contact with people outside your household. The initial broadcast took place on July 25, 2020. The show can now be streamed online, or downloaded for free. To listed to the show: Show 1221: What Explains the Recent Increase in Celiac Disease? Join our Forum discussion on this podcast.

Celiac.com 06/09/2014 - Anemia is extremely common in patients with celiac disease. In some cases, anemia may be the sole manifestation of celiac disease, but there is no good data on rates of celiac disease in Indian patients with nutritional anemia. A research team recently examined rates of celiac disease among nutritional anemia patients at a care center in India. The team included A. Kavimandan, M. Sharma, A.K. Verma, P. Das, P. Mishra, S. Sinha, A. Mohan, V. Sreenivas, S. Datta Gupta, and G.K. Makharia. For their study, the team conducted positive celiac disease screens on adolescent and adult patients presenting with nutritional anemia. They also prospectively screened for celiac disease using IgA anti-tissue transglutaminase antibody (anti-tTG Ab). Subjects with positive antibody screens received upper gastrointestinal endoscopy and duodenal biopsy. In all, the team screened ninety-six patients. Of these patients, 80 had iron deficiency anemia, 11 had megaloblastic anemia, and 5 had dimorphic anemia. Seventy-three patients were receiving hematinics and 36.4 % had received blood transfusions. Nineteen patients had histories of chronic diarrhea persisting for an average of about ten years. Of those, the team found 13 patients with positive IgA anti-tTG Ab screens, 12 of whom agreed to duodenal biopsy. Ten patients showed villous atrophy (Marsh grade 3a in three, 3b in one, and 3c in six), while two patients showed no villous atrophy. In all, ten patients with nutritional anemia, defined as iron deficiency 9, vitamin B12 deficiency 1, were also diagnosed with celiac disease. Multivariate logistic regression showed age, duration of symptoms, and presence of diarrhea to be the main predictors of celiac disease. The team put all patients with celiac disease on gluten-free diet, supplemented with iron and vitamin B. All patients showed significant improvement in hemoglobin concentration. The team recommends celiac disease screening, and appropriate follow-up in all cases of unexplained nutritional anemia. Source: Indian J Gastroenterol. 2014 Mar;33(2):114-8. doi: 10.1007/s12664-013-0366-6. Epub 2013 Sep 1.

Celiac.com 10/17/2017 - Are primary care physicians under-testing for celiac disease in patients with iron deficiency anemia? A new survey of primary care doctors indicates that they are. It's fairly common for people with celiac disease to develop iron deficiency anemia (IDA), but researchers don't know much about the frequency with which primary care physicians test for celiac disease in patients with IDA. A team of researchers recently set out to describe how primary care doctors approach testing for celiac disease in asymptomatic patients with IDA. The research team included Marisa Spencer, Adrienne Lenhart, Jason Baker, Joseph Dickens, Arlene Weissman, Andrew J. Read, Seema Saini, and Sameer D. Saini. They are variously affiliated with the Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States of America; the Department of Internal Medicine, Henry Ford Health System, in Detroit, Michigan, United States of America; the Department of Statistics, University of Michigan, Ann Arbor, Michigan, United States of America; the Research Center at the American College of Physicians, in Philadelphia, Pennsylvania, United States of America; Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States of America, Ambulatory Care, Veterans Affairs Medical Center, Ann Arbor, Michigan, United States of America. For their study, the team began by electronically distributing a survey to primary care doctors who are members of the American College of Physicians. The survey asked whether doctors would test for celiac disease, either by serologic testing, referral for esophagogastroduodenoscopy [EGD], or referral to GI) in hypothetical patients with new IDA, including: (1) a young Caucasian man, (2) a premenopausal Caucasian woman, (3) an elderly Caucasian man, and (4) a young African American man. The team chose the scenarios to assess differences in testing for celiac disease based on age, gender, and race. They used multivariable logistic regression to identify independent predictors of testing. Testing for celiac disease varied significantly according to patient characteristics, with young Caucasian men being the most frequently tested (61% of respondents reporting they would perform serologic testing in this subgroup (p Interestingly 80% of doctors surveyed said they would definitely or probably start a patient with positive serologies for celiac disease on a gluten-free diet prior to confirmatory upper endoscopy, which is contrary to guideline recommendations. This survey indicates that primary care doctors are under-testing for celiac disease in patients with IDA, regardless of age, gender, race, or post-menopausal status. The majority of primary care doctors surveyed do not strictly adhere to established guidelines regarding a confirmatory duodenal biopsy in a patient with positive serology for celiac disease. Clearly, even with all of the advances in celiac disease awareness and with more refined protocols, primary care doctors have some work to do when it comes to testing IDA patients for celiac disease, and even more work to do in following proper referral guidelines before putting patients on a gluten-free diet. Source: PLOSONE

Celiac.com 04/26/2016 - Vice President Dan Quayle famously stated: "what a waste it is to lose one's mind, or not to have a mind is being very wasteful, how true that is," when speaking to people involved in the United Negro College Fund (1). While it is entertaining to read and ponder, this statement evokes some ideas I have about senility, which is increasing, along with many other modern diseases, at a frightening speed. The prospect of losing my mind, my memory, my sense of connection with friends and loved-ones, and even my sense of identity and personal hygiene is a frightening spectre. Can you separate your memories and experiences, along with what you think and feel, from who you are? I can't. I'm not sure I would want to be able to do so. My identity is tied to my memories, experiences, and how I responded and continue to respond to them. I remember looking at my son's tiny hands and feet when we first brought him home from the hospital. My daughter, born prematurely, had even smaller digits. They seemed impossibly tiny yet they were all perfectly formed and quite beautiful. It seemed miraculous to me. It still does. I can't imagine anything that I'd be willing to accept in exchange for those memories. Neither would I willingly surrender my memory of the joy I felt at my first convocation or my first car. Yet those lost memories form the prison in which many people already find themselves. It appears that many more will follow. One segment of this problem, the epidemic of Alzheimer's disease (AD), already effects 5.4 million Americans and 30 million people throughout the world (2). Parkinson's disease, which is a neurological ailment that, in its later stages is often accompanied by dementia, is a similar ailment that is rapidly increasing both in absolute numbers and as a percentage of the population (3). Vascular dementia is yet another condition in which brain mass and mental acuity wane with advancing years (4). Perhaps this trend is partly due to the large number of aging baby boomers from the World War II era. But the relevant research suggests otherwise. Although we may be living longer and that may contribute to a small part of the growth of these devastating ailments, the biggest contributors appear to be lifestyle choices that include low daily activity levels, consumption of highly glycemic and inflammation-promoting refined carbohydrates and grain products, inadequate sleep duration, and exposure to toxic substances. As most students of celiac disease have long been aware, there is a powerful and potentially devastating component of brain and neurological damage associated with this ailment as a result of gluten grain consumption. In addition to the behavioral changes identified by Gibbons in 1889 (5), attention deficits identified by Reichelt (6), Neiderhofer (7, 8), and others (9 - 11), subsequent reports have connected increased incidence of seizure disorders(12-17), reductions of brain size (17 -20), a variety of neurological movement disorders (21 -23), a range of mood disorders (24, 25), and several psychiatric ailments (26, 27) including schizophrenia (28, 29), and signs of learning disabilities have been reported to improve quite dramatically and quickly on a gluten-free diet (30). Sleep disorders are also common among people with celiac disease (31). With emerging research into non-celiac gluten sensitivity over the last two decades, we have also begun to see evidence of similar connections between gluten consumption and most of these neurological/brain ailments. This added dimension of non celiac gluten sensitivity and its impact on human neurological health, were previously obscure and, in the case of amyotrophic lateral sclerosis (ALS) (26, 32), was thought to be rapidly deadly and incurable (33). Most recently, Bredesen reported that the gluten-free diet, or a low grain diet, forms one significant part of their multi-modal protocol for reversing several dementias among a small group of those who experienced recent symptom onset, including Alzheimer's disease, objectively identified disruptions in memory function or subjective, self-reported symptoms of dementia (2). Of the ten subjects studied in this latter investigation, nine showed substantial recovery in the form of symptom reversal along with either a return to work or improved performance at work (2). Harnessing the gluten-free diet makes sense, of course, because of the many neurological dimensions of gluten's harmful impact on human neurological tissues. Over the last 20 years, Dr. Marios Hadjivassiliou and colleagues, at the University of Sheffield and the Royal Hallamshire Hospital, have been reporting a wide range of neurological ailments in association with elevated anti-gliadin antibodies ( both with and without celiac disease) afflicting a large portion of their patients with neurological diseases of unknown origin (34 -37). Further, Dr. Joe Murray and colleagues have also reported on a group of thirteen patients experiencing moderate cognitive decline, three of whom experienced stabilized or improved cognitive function on a gluten-free diet alone (38). However, the protocol reported by Bredesen is aimed at correcting a greater number and broader spectrum of converging metabolic processes that are shaped, in large part, by our modern lifestyle, and are increasingly thought to be at the root of the current epidemic of dementias, including Alzheimer's disease (2). Gluten is only an important part of the overall picture. Dr. Suzanne de la Monte and colleagues have also identified a dynamic which they call type 3 diabetes at work in the brains of many patients with Alzheimer's disease (39). Insulin resistance, in the brain and elsewhere, is also a multi-factorial condition (40) which mostly involves disrupted metabolic processes, either through depletion of insulin production or, more likely, increased cellular resistance to insulin's movement of glucose into the cell. Dr. Dale Bredesen has argued that "in the past decade alone, hundreds of clinical trials have been conducted for AD, at an aggregate cost of billions of dollars, without success. This has led some to question whether the approach taken to drug development for AD is an optimal one" (2) This is the rationale that underlies his enormously broad therapeutic approach employed in his protocol. Please consider each of the following facets of Bredesen's therapeutic protocol: 1. Serum testing was conducted and subsequent supplement recommendations were made, aimed at improving vitamin, mineral, amino acid, and herb supplements to achieve optimal values. All of the foregoing is aimed at harnessing their putative anti-oxidant function, supporting various facets of metabolism, and making use of their reported anti-inflammatory properties. Chelation therapy was also used to correct heavy metal (mercury, lead, cadmium) toxicity. Non-farmed fish, vegetables, and fruits were emphasized, while meat consumption was either discouraged or patients were encouraged to eat only organic and free range meat. 2. Patients were given their choice of several low glycemic, low inflammatory, low grain diets. By this description, such a diet would exclude or severely limit gluten consumption. 3. Patients were encouraged to engage daily in strategies, including meditation and listening to music, toward reducing their stress levels, which would reduce their cortisol production. Cortisol is a hormone that triggers increased release of glucose into the bloodstream, suppresses the immune system, and inhibits bone formation. In addition to excluding or treating sleep apnea, patients were prescribed melatonin at 0.5 mg daily, toward achieving at least eight hours of sleep each night, thereby reducing production of hunger-inducing ghrelin hormones in the stomach and increasing hunger-suppressing leptin hormones which are produced in the fat cells. Each carries its message to the brain. Reductions in cortisol and ghrelin secretion in combination with increasing leptin production would have a net effect of reducing inflammation while aiding weight loss and reducing blood glucose levels to normal fasting levels and targeting reduction of hemoglobin A1c levels to below 5.5, further reducing inflammation. Optimum levels of thyroid hormones, along with progesterone and pregnenolone were also pursued, along with reductions of free homocysteine to below 7 mg/L by prescription of vitamin B6, B12, and folic acid supplements, to reduce vascular damage and blockage that can be caused by elevated free homocysteine levels. Twice daily dietary supplementation with medium chain triglycerides (MCTs) also provides strategy for altering hormone production aimed at improved cognitive function. In humans, medium chain fatty acids resist storage. They must either be converted to ketone bodies in the liver, or rapidly utilized for energy. Because MCTs can induce the liver to increase ketone production, it provides an alternative energy source for many of the brain's cells, without requiring insulin to usher these ketones into the cells, as glucose does. In essence, adequate ketone production provides an alternative fuel both for many brain and other cells throughout the body. The liver mostly produces the ketone called beta-hydroxybutyrate. This acts not only as a fuel source, but is also a powerful anti-oxidant that does not require insulin to enter the cell, unlike vitamin C, which does require insulin to enter cells. 4. To further promote these values and other facets of wellness arising out of regular activity, patients were asked to exercise for 30 to 60 minutes per day, 4 to 6 days each week. Each and all of the above have been reported somewhere in the literature as valid and valuable as part of reversing dementias, which Bredesen's list of citations supports (2). However, while significant improvements in the dementia symptoms of nine of the ten subjects does argue for the validity of this protocol, wholesale acceptance of all of the concepts here would fail to narrow our focus on those factors that are most likely to contribute to causing the vast majority of the various dementias that are contributing to the emerging epidemic. Bredesen also acknowledges that study participants were encouraged to follow as many instructions as they could. They were not asked or expected to be fully compliant with the instructions they were given. Nonetheless, I would probably err on the side of caution, by implementing as many of these strategies as possible, were I dealing with a loved-one who struggled with dementia. Conversely, I would be most reluctant to accept the interdiction of meats, organic or otherwise. On the other hand, growth promotion using low doses of anti-biotics can result in delivering anti-biotic resistant microbes. Poultry, hogs, and cattle are all high risk meats. Further, grains, especially gluten grains and corn, combine to form the mainstay of feeds used to fatten these animals and birds for market, where weight is the determining factor in the price paid for these meats. Bredesen also pointed, quite rightly, to the small number of subjects as a weakness in his study. However, when 9 of their 10 subjects achieved such remarkable results, especially in the context of the common belief that dementia, at any stage, is irreversible, this study certainly suggests that exploring dementias as a group of metabolic illnesses is a potentially fruitful path. This is a perspective that is enjoying considerable support from a variety of sources. Many researchers have, for the past decade or so, thought of many dementias as type 3 diabetes, with a growing body of support for this perspective amassing in the peer reviewed literature (41). More recently, chronic sleep deprivation has been similarly implicated in several ways. The first is specific to Alzheimer's disease, where beta amyloid deposits or plaques characterize this ailment. New research has shown that during sleep, brain tissues shrink, while the fluids that surround the brain permeate these tissues and inter-cellular structures, assimilating amyloid, which is a group of protein fragments (peptides) that are waste products of daytime brain cell activities (42). Because there is no lymphatic system in the brain, it has long been believed that the brain did not dispose of its waste products. However, another field of brain research has shown that conduits of these fluids form surrounding the blood vessels, carrying waste products into the bloodstream and, ultimately, out of the brain for disposal (42). Since average nightly sleep duration has shortened from nine hours to seven hours, given the above research findings, this reduction in sleep decreases our nightly capacity to remove waste amyloid and other detritus, leading to the formation and growth of amyloid deposits, which characterize at least one form of dementia. This same culture-wide sleep deprivation also induces memory disturbances and memory losses. It does so by a circuitous route. Throughout the day, each of us encodes memories through our hippocampus, a small region of the brain that is also involved in spatial navigation and contributes, with other parts of the lymbic system, to the regulation of many body functions. During sleep, the day's memories are thought to be processed and integrated with prior knowledge, emotions, and impressions in the neo-cortex. Some researchers are now postulating that this integration process is what results in our dreams (43-45). Regardless of whether it is the author of our dreams, Dr. Robert Stickgold and colleagues have shown that sleep helps us to consolidate the day's learning experiences, thus improving our memory retention. He has also shown that inadequate sleep compromises learning (43). The net result is that we not only need sleep to permit the brain to clean out the day's wastes, we also need it to form and preserve learning. Although Bredesen made no mention of it, there is another complicating factor here. Statin drugs are aimed at reducing cholesterol. However, they have also been shown to induce memory problems. One friend of mine was prescribed a statin drug, and he stopped being able to recognize me. After discontinuing this medication, he told me that I looked familiar, but he couldn't even guess at my name or where he knew me from. He waves hello to me from across the street, but doesn't cross it to visit anymore. And that seems to be where the recovery of his memory is stalled. It is with heart-rending sadness that I occasionally see him in passing. I say hello. But if he doesn't notice me waving or hear me shouting, there isn't even an exchange of greetings. He seems happy enough. So perhaps the loss is mostly mine. 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Celiac.com 06/04/2012 - Non-responsive celiac disease is very much what it sounds like: celiac disease where symptoms seem to resist treatment and continue even in the face of a gluten-free diet. A team of researchers recently set out to look for the most likely causes of persistent symptoms in celiac disease patients on a gluten-free diet. The research team included David H. Dewar, Suzanne C. Donnelly, Simon D. McLaughlin, Matthew W. Johnson, H. Julia Ellis, and Paul J. Ciclitira. They are variously affiliated with King's College London, Division of Diabetes and Nutritional Sciences, Department of Gastroenterology, and The Rayne Institute at St. Thomas' Hospital in London. Their goal for the study was to investigate all patients referred to our center with non-responsive celiac disease (NRCD), to establish a cause for their continued symptoms. For their study, the research team assessed all non-responsive celiac disease who were referred to their gastroenterology center over an 18-mo period. They then established the etiology of ongoing symptoms for these patients. For all patients, the team established a thorough case history and conducted a complete examination with routine blood work including tissue transglutaminase antibody measurement. Additionally, each patient was examined by a specialist gastroenterology dietician to try to spot any gaps in their diets, or any hidden sources of gluten consumption. When possible, the team conducted a follow-up small intestinal biopsy, and compared the results against the biopsies from the referring hospital. Patients with persistent symptoms received colonoscopy, lactulose hydrogen breath testing, pancreolauryl testing and a computed tomography scan of the abdomen. The team monitored patient progress over a minimum of two year period. Overall, the team looked at 112 patients with non-responsive celiac disease. They determined that twelve of those did not actually have celiac disease. Of the remaining 100 patients, nearly half, 45%, were not adequately following a strict gluten-free diet. Of these, 24 (53%) were found to be accidentally consuming gluten, while 21 (47%) admitted to not faithfully following a gluten-free diet. Microscopic colitis was found in 12% and small bowel bacterial overgrowth in 9%. Refractory celiac disease was found in 9%. Three of these were diagnosed with intestinal lymphoma. After 2 years, 78 patients remained well, eight had continuing symptoms, and four had died. In most cases of non-responsive celiac disease, the team found a reversible cause can be found in 90%. In the vast number of those cases, continued consumption of gluten was the main cause. The team is proposing the use of an algorithm for further investigation of the matter. Source: World J Gastroenterol. 2012 Mar 28;18(12):1348-56.

Celiac.com 10/20/2017 - Are doctors even getting close to diagnosing the actual number of cases of celiac disease? Or are they missing the vast majority? Researchers have said for some time that there are far more people with celiac disease than are being diagnosed, and that the vast majority of cases go undiagnosed. So, just how far are we from the actual number? Well, if a new study by Canadian nutrition researchers is any indication, doctors are very far from diagnosing most cases. The team studied the blood work of nearly 3,000 people, and their conclusions are stunning. They say that ninety percent of celiac cases go undiagnosed. How could this be? One reason is that even classic celiac disease symptom, such as abdominal pain, bloating, gas, diarrhea, anemia and weight loss can mimic other conditions. Less classic symptoms such as fatigue, low vitamin C, D and calcium levels can be misleading. Ahmed El-Sohemy, a professor of nutritional science at the University of Toronto, wanted to see whether celiac disease results in subpar nutrition because of poorer absorption of vitamins and minerals. But to find out, he needed Canadian data on the frequency of undiagnosed celiac disease. To that end, El-Sohemy and his colleagues checked blood samples from more than 2,800 individuals in Toronto. One group had an average age of 23, and the other 45. Among their findings is likely ~1%, with 87% of cases being undiagnosed. These findings suggest the need for better screening in high genetic risk groups. Source: BMJOPEN.com

Celiac.com 01/11/2016 - Is celiac disease a disability under the federal Americans with Disabilities Act? The Department of Justice says not necessarily. On the heels of a federal lawsuit that claiming that restaurants are violating federal disability laws by charging more for gluten-free food than for non-gluten-free counter parts, a Department of Justice spokesperson has stated that a 2012 civil rights settlement on behalf of Lesley University students with celiac disease does not make the condition a disability in all cases. DOJ public affairs specialist, Patrick Rodenbush, said settlement at Leslie University did not set a legal precedent, because the "…settlement enforces the rights of students whose food allergies were disabilities, [but] it doesn't necessarily make celiac disease a disability in all cases." This is relevant to a case in California, where federal judge recently denied a motion to dismiss a class action lawsuit alleging P.F. Chang's violates the Americans with Disabilities Act because it charges more for gluten-free items. In the P.F. Chang's case, Judge Ronald Whyte denied P.F. Chang's motion to dismiss because, he wrote, that, although the court had not found specific information proving that celiac disease constituted a disability under the ADA, the "plaintiff has pled sufficient facts to support her claim that she has a disability that impacts a major life activity." Whyte noted "on a more complete factual record, the court might reach a different conclusion." He also stated that it may be difficult, or impossible for Phillips to prove her claims. "The ultimate question is whether P.F. Chang's, in providing gluten-free meals, is providing different products or whether the price differential with regular meals is a pretext for discrimination against those with celiac disease," Whyte wrote. At stake is whether or not food vendors, such as P.F. Chang's can charge higher prices for gluten-free foods than they do for non-gluten-free items. The results of this case are being watched closely by celiacs and by restaurant companies, because a ruling that establishes that people with celiac disease are covered under the federal Americans with Disabilities Act could conceivably have a serious impact on how the restaurant industry approaches gluten-free food. Stay tuned for new developments. Source: legalnewsline.com

Celiac.com 10/01/2019 - The rate of celiac disease has risen over the last few decades, and some people have questioned whether this could be due to changes in the protein structure of modern wheat strains, compared with their historical counterparts. Two researchers recently set out to test this hypothesis scientifically and devise experiments for understanding the protein composition of historical and modern wheat, determining the presence of antigenic peptides, and quantifying these peptides that trigger an immune reaction in celiac patients. The research team included Maneka Malalgoda, who is a graduate student in the Cereal Science program at NDSU, in collaboration with Dr. Steven Meinhardt, Associate Professor at the Department of Plant Pathology, NDSU. For their study, the looked at 30 varieties of hard red spring wheat released between 1910 and 2013. Gluten forming proteins can be divided into glutenin and gliadin proteins, of which the latter has been implicated in giving rise to the immune reactions associated with celiac disease. When Malalgoda and Meinhardt looked at the gliadin protein profile of hard red spring wheat varieties, they found that specific gliadin protein types called gamma and omega gliadins increased over the years, whereas alpha-gliadin did not. Alpha-gliadin proteins have been linked with celiac antigenicity in previous studies. These results suggest that there's likely little difference in celiac antigenicity between historical and modern wheat varieties, that is, modern wheat is not more likely to trigger celiac disease reactions than historical wheat strains. The team then turned their focus to antigenic peptides causing celiac disease. They learned that both historical and modern varieties of hard red spring wheat contain antigenic peptides. When they analyzed the strains solely on the presence or absence of antigenic peptides, without regard to historic or modern, they found no association between the presence of antigenic peptides and cultivar release year. Lastly, they were able to quantify the two most prominent antigenic peptides, glia alpha-9 and glia alpha-20, and total alpha gliadin. Their data show that the amount of glia alpha-9 and total alpha-gliadin varied randomly across the cultivars, which suggests no connection between celiac antigenicity and the release year of any given strain. Learn more, and to see some figures that show the team's results at acsh.org

Celiac.com 01/16/2017 - Cerebellar ataxias can be caused by a wide range of disease processes, either genetic or acquired. Establishing a clear diagnosis requires a methodical approach with expert clinical evaluation and investigation. A team of researchers recently published a description of the causes of ataxia in 1500 patients with cerebellar ataxia. The research team included M Hadjivassiliou, J Martindale, P Shanmugarajah, R A Grünewald, P G Sarrigiannis, N Beauchamp, K Garrard, R Warburton, D S Sanders, D Friend, S Duty, J Taylor, and N Hoggard. They are variously affiliated with the Academic Department of Neurosciences, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Trust, Sheffield, UK; Sheffield Diagnostic Genetics Service, Sheffield Children's NHS Foundation Trust, Sheffield, UK; the Department of Gastroenterology, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Trust, Sheffield, UK; and the Department of Neuroradiology, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Trust, Sheffield, UK. All patients in the study were referred to the Sheffield Ataxia Centre, UK, and underwent extensive examination, including, where appropriate genetic testing using next-generation sequencing (NGS). The team followed-up patients on a 6-month basis for reassessment and further investigations, as needed. The team assessed a total of 1500 patients over 20 years. Twenty per cent of those patients had a family history of ataxia, with the remaining having sporadic ataxia. The most common cause of sporadic ataxia was gluten ataxia at 25%. They found a genetic cause in 156, or 13% of sporadic cases, with alcohol excess causing 12% and a cerebellar variant of multiple system atrophy causing 11% of sporadic cases. Using NGS, they obtained positive results in 32% of 146 patients tested. The most common ataxia they found was EA2. A total of 57% of all familial ataxias were supported by genetic diagnosis. The most common genetic ataxias were Friedreich's ataxia (22%), SCA6 (14%), EA2 (13%), SPG7 (10%) and mitochondrial disease (10%). The diagnostic yield following attendance at the Sheffield Ataxia Centre was 63%. Immune-mediated ataxias are common. Advances in genetic testing have significantly improved the diagnostic yield of patients suspected of having a genetic ataxia. Making a diagnosis of the cause of ataxia is essential due to potential therapeutic interventions for immune and some genetic ataxias. Gluten is a culprit is 25% of sporadic ataxia cases, and clinicians should keep this in mind when diagnosing patients, as many of these cases can be reversed with a gluten-free diet. Source: J Neurol Neurosurg Psychiatry. doi:10.1136/jnnp-2016-314863

Celiac.com 09/15/2014 - Duodenal intraepithelial lymphocytosis (D-IEL) is an early marker for celiac disease, even though a majority of cases are due to non-celiac disease conditions. Researchers I. Aziz, T. Key, J.G. Goodwin, and D.S. Sanders wanted to identify the predictors of celiac disease in patients presenting with D-IEL. For their study, they reviewed 215 adults with D-IEL who had undergone prospective and systematic evaluation for celiac disease and other recognized associations. They confirmed celiac disease based on presence of HLA-DQ2 and/or DQ8, persistence or progression of D-IEL following a gluten challenge, and an improvement in symptoms with a gluten-free diet. To compare factors in celiac and non-celiac cases, and to determine their sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV), the team used binary logistic regression models, adjusted for age and sex. They diagnosed celiac disease in 48 cases (22%) and non-celiac in 167 cases (78%). They found no statistical difference between the celiac and non-celiac group in terms of baseline demographics, anemia, hematinics, or clinical symptoms, such as diarrhea, weight loss, abdominal pain. Compared with their non-celiac counterparts, celiac patients were significantly more likely to have a positive family history of celiac disease (21% vs. 3.6%, OR 6.73; PPV 62.5%, NPV 81%, specificity 96.4%), positive HLA-DQ status (100% vs. 49.1%; PPV 36.4%, NPV 100%, specificity 50.9%), and presence of endomysial antibody (EMA) (48% vs. 0%; PPV 100%, NPV 87%, specificity 100%); all P≤0.001. A total of 29.2% celiac and 83.2% non-celiac cases showed normal tissue transglutaminase antibody (TTG) levels (OR 0.084, P<0.001; PPV 9.2%). Between the groups, there was no difference in the prevalence of TTG levels 1 to 2×upper limit of normal (29.2% celiac vs. 14.4% non-celiac; PPV 33% to 38%). However, TTG levels between 3 and 20×ULN were much more common in the celiac group (33.3% vs. 2.4%, PPV 66.6% to 89%), whereas a TTG>20×ULN was exclusive to celiac disease (8.3%, P<0.001, PPV 100%). For patients with D-IEL, only a positive EMA or TTG greater than 20×ULN at the outset can yield an immediate celiac diagnosis. On their own, factors such as gastrointestinal symptoms, family history, anemia, or other celiac serology results do not reliably distinguish celiac from non-celiac patients. Source: J Clin Gastroenterol. 2014 Jul 10.

Celiac.com 10/24/2012 - Doctors can face challenges when attempting to diagnose celiac disease in patients who have already begun a gluten-free diet, and/or when the results of tests are inconsistent. To better understand this problem, a group of researchers set out to assess the benefits of an in vitro gliadin challenge. The research team included Raffaella Tortora, MD, Ilaria Russo, PhD, Giovanni D. De Palma, MD, Alessandro Luciani, PhD, Antonio Rispo, MD, Fabiana Zingone, MD, Paola Iovino, MD, Pietro Capone, MD and Carolina Ciacci, MD. The study cohort included 57 patients without celiac disease, 166 patients with untreated celiac disease, 55 patients with celiac disease on a gluten-free diet, and 59 patients with challenging diagnosis. The team provided all patients with endoscopy for collection of duodenal samples, which served for the diagnosis of celiac disease and for the in vitro evaluation of the gliadin-induced mucosal expression of seven inflammatory markers: PY99, ICAM-1 (intercellular cell adhesion molecule), HLA-DR, CD3, CD25, CD69, and transglutaminase 2 IgA. Diagnostic work-up for celiac disease included the search of specific serum antibodies. Researchers asked patients in the challenging diagnosis group to stop gluten-free diet to facilitate the search for these antibodies under untreated conditions. They used the area under the receptor-operated curve (ROC) for statistical analyses on accuracy. For patients with and without celiac disease (not including those on a gluten-free diet) HLA-DR offered the best accuracy for diagnosing celiac disease (area under ROC = 0.99). Combining the data from the HLA-DR with data of other markers did not increase test accuracy. The team found similar results in the 39 patients of the difficult diagnosis group undergoing the search celiac disease-speciï¬c antibodies under untreated conditions. In vitro testing of mucosal HLA-DR to gliadin is an accurate tool for the diagnosing celiac disease, and also works in patients who are hard to diagnose. Source: Am J Gastroenterol 2012; 107:111–117; doi:10.1038/ajg.2011.311; published online 27 September 2011

Celiac.com 04/01/2013 - There haven't been many studies that evaluate the usefulness of capsule endoscopy in equivocal celiac disease. A team of researchers recently set out to conduct an evaluation of capsule endoscopy in adult celiac disease, and to assess its potential role in equivocal cases of celiac disease compared with patients with biopsy-proven and serology-proven celiac disease who have persisting symptoms. The research team included M. Kurien, K.E. Evans, I. Aziz, R. Sidhu, K. Drew, T.L. Rogers, M.E. McAlindon, and D.S.Sanders. They are affiliated with the Department of Gastroenterology at Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Foundation Trust in Sheffield, South Yorkshire, United Kingdom. To determine the use of capsule endoscopy in patients with equivocal celiac disease, compared to patients with biopsy-proven and serology-proven celiac disease who have ongoing symptoms. To do this, the team conduced a prospective cohort study of 62 patients with equivocal celiac disease and 69 patients with non-responsive celiac disease. They measured outcome according to the diagnostic yield of capsule endoscopy in equivocal cases and accuracy of mucosal abnormality detection in patients with non-responsive celiac disease. They found that the 62 cases of equivocal celiac disease could be divided into two subgroups: group A, with 32 cases of antibody-negative villous atrophy, and group B with 30 cases of Marsh 1-2 changes. In group A, using capsule endoscopy, the team was able to diagnose celiac disease or Crohn's disease in 9 of 32 patients (28%), compared with just 2 of the 30 patients in group B (7%; P = .044). In patients with persistent celiac disease symptoms, the team made significant capsule endoscopy findings in 8 of 69 patients (12%), including 2 cases of enteropathy-associated lymphoma, 4 cases of type 1 refractory celiac disease, 1 polypoidal mass histologically confirmed to be a fibroepithelial polyp, and 1 case of ulcerative jejunitis. This outcome was significantly lower than the diagnostic yield of capsule endoscopy in antibody-negative villous atrophy (P = .048). It is important to remember that this study was restricted to a single clinic. That said, this is the first time that researchers have used capsule endoscopy to systematically evaluate equivocal celiac disease. Because the diagnostic rates for capsule endoscopy in patients with antibody-negative villous atrophy are better than that of capsule endoscopy in patients with celiac disease with persisting symptoms, the researchers are encouraging the use of capsule endoscopy in equivocal cases, especially in cases where patients antibody-negative villous atrophy. Source: Gastrointest Endosc. 2013 Feb;77(2):227-32. doi: 10.1016/j.gie.2012.09.031.

Celiac.com 06/14/2010 - Enteropathy associated T-cell lymphoma (EATL) is a rare type of for which there are currently no standardized diagnostic or treatment protocols. A team of researchers recently evaluated enteropathy-associated T-cell lymphoma and compared standard therapies with a novel regimen including autologous stem cell transplantation The research team included Michal Sieniawski, Nithia Angamuthu, Kathryn Boyd, Richard Chasty, John Davies, Peter Forsyth, Fergus Jack, Simon Lyons, Philip Mounter, Paul Revell, Stephen J. Proctor, and Anne L. Lennard. The team describe EATL in a population-based setting and evaluates a new treatment with aggressive chemotherapy and autologous stem cell transplantation (ASCT). In 1979, the Scotland and Newcastle Lymphoma Group began to collect data on all patients newly diagnosed with lymphoma in the Northern Region of England and Scotland. The research team reviewed the records of patients diagnosed with EATL from 1994 and 1998. 54 patients had features of EATL. The overall annual rate was 0.14/100,000. Doctors treated 35 patients with systemic chemotherapy (mainly anthracycline-based chemotherapy) and with surgery. They treated 19 patients with surgery alone. Patients showed a median progression-free survival (PFS) of 3.4 months and overall survival (OS) of 7.1 months. Starting in 1998 patients eligible for intensive treatment received the novel regimen IVE/MTX (ifosfamide, vincristine, etoposide/methotrexate)–ASCT, with a total 26 patients included. PFS and OS at the five year mark were 52% and 60%, respectively, a substantial improvement over the historical group treated with anthracycline-based chemotherapy (P .01 and P .003, respectively). In contrast to the poor outcomes when treated with conventional therapies, the IVE/MTX-ASCT regimen offers acceptable toxicity and significantly improved outcome for cases of EATL. Researchers are affiliated variously with the Department of Haematological Sciences, Newcastle University, Newcastle upon Tyne; the Department of Haematology, Craigavon Area Hospital, Portadown; the Department of Haematology, University Hospital of North Staffordshire, Stoke on Trent; the Department of Haematology, Western General Hospital, Edinburgh; the Department of Haematology, Raigmore Hospital, Inverness; the Department of Haematology, Harbour Hospital, Poole; the Department of Haematology, Sunderland Royal Hospital, Sunderland; the Department of Haematology, University Hospital of North Tees, Stockton on Tees; and the Department of Haematology, Staffordshire General Hospital, Stafford, United Kingdom Source: Blood, 6 May 2010, Vol. 115, No. 18, pp. 3664-3670. DOI 10.1182/blood-2009-07-231324.

Celiac.com 05/04/2010 - A team of clinicians recently set out to assess the effectiveness of treating collagenous sprue with a combination of gluten-free diet and steroids. The team was made up of Alberto Rubio-Tapia, Nicholas J. Talley, Suryakanth R. Gurudu, Tsung-Teh Wu, and Joseph A. Murray. They are affiliated variously with the Division of Gastroenterology and Hepatology of the Mayo Clinics in Scottsdale, Arizona, Jacksonville, Florida, and Rochester, Minnesota, and the Division of Anatomic Pathology in Rochester Mayo Clinic. Deposits of subepithelial collagen that form a distinctive band in the small bowel are one of the clinical hallmarks of collagenous sprue. For the study, the team evaluated clinical characteristics, treatments, and outcomes of patients with collagenous sprue. The team looked at medical records for thirty patients with collagenous sprue from the Mayo Clinics from Scottsdale, Jacksonville, and Rochester, for the periods covering 1993 and 2009. 21 of the patients were female (70%), ranging in age from 53–91 years. The majority of patients suffered from severe diarrhea and weight loss. However, collagenous spore is commonly associated with collagen deposits or chronic inflammation in other parts of the gastrointestinal tract, as well as other immune-mediated disorders. 16 patients (53%) were hospitalized to treat dehydration, while 21 patients (70%) suffered from associated immune-mediated diseases, the most common of which was celiac disease. Other common associated diseases included microscopic colitis, hypothyroidism, and autoimmune enteropathy. Subjects showed subepithelial layers of collagen deposits in the small bowel ranging from 20 –56.5μm, and averaging 29 μm thickness. Eight patients showed subepithelial collagen deposits in the colon or stomach. 24 patients (80%) showed a positive clinical response to treatment with a combination of a gluten-free diet and immunosuppressive drugs. Nine patients showed confirmed histologic improvement, while five patients experienced complete remission. Of two patients who died, one succumbed to complications from collagenous sprue, while one died of another illness. Most patients with collagenous sprue show a positive clinical response to a combination of gluten-free diet and steroids. Source: Clinical Gastroenterology and Hepatology 2010;8:344–349. doi:10.1016/j.cgh.2009.12.023