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Found 1,259 results

  1. Celiac.com 07/06/2017 - Each New Year you will find a plethora of articles on weight loss. Unfortunately, for those with celiac disease, weight loss is not always an issue, but for some the opposite is true. Though much false information in the medical community remains, such as "you must be underweight to have celiac disease", there are many who are overweight. Whether you want to gain or lose weight, they have one thing in common, the need for nutritious food, and food that does not cause inflammation in the body. If you look at autoimmune diseases, in general, you will notice they have one thing in common, inflammation. Celiac disease – inflammation of the small intestines; multiple sclerosis – inflammation of the central nervous system, Grave's disease – inflammation of the thyroid gland; arthritis – inflammation of the joint tissues and cartilage; Crohn's disease – inflammation of the digestive tract; Alzheimer's disease – inflammation of the brain; transverse myelitis – inflammation of the spinal cord; etc. When we consume foods that we are either allergic to or sensitive to, our white blood cells release toxic chemicals to fight off what it perceives as foreign bodies resulting in inflammation. If our bodies are too busy fighting off inflammation from a non-optimal diet or stress, they do not have enough resources to fight the real bad guys. Some of the foods known to fight or prevent inflammation are spices such as turmeric, curry, cinnamon, ginger, and garlic; tropical fruit such as coconut, pineapple (contains a natural antihistamine), and papaya; green tea; fish oil and fish; and a wide variety of colorful vegetables such as spinach, kale, broccoli, cauliflower, kelp, red peppers, sweet potatoes, and cabbage. Research shows that omega-3's are not only known to reduce inflammation, but it may lower the risk of chronic diseases such as arthritis, cancer and heart disease(1). Because our bodies cannot make omega-3 fatty acids we must obtain them from food or supplements. If your doctor has recommended that you take an omega-3 supplement or increase omega-3 in your diet, it is important that you know the two main types. Omega-3's which are marine-based (fish and fish oil) contain EPA and DHA, where the other contains ALA. ALA omega-3 may be obtained from soybean, canola, and flax seed oils, ground flax seed, and walnuts, as well as kale, spinach, Brussels sprouts, and leafy greens. Though our body does not make omega-3's, it does partially convert ALA to DHA and EPA. Per Harvard School of Public Health, we do not know which, if either, is more beneficial (2,3). Research does show that EPA and DHA do reduce the risk of heart disease in older adults.(4) When ALA is added to our diet it is known to reduce the risk of breast cancer and prostate cancer, as it helps your body metabolize estrogens into a safer form. You may already be aware of the fact that aloe vera contains a gel-like substance that is known to heal. (As a side note, aloe vera products sometimes contain laytex.) Flax seeds contain the same property. It is also high in omega-3, though yellow flax seeds are lower. Brown flax seeds have the most health benefits. Another popular superfood is chia seeds. It does not contain the same properties as flax, however, chia seeds provide similar benefits as flax, and they do not need to be ground in order to reap those benefits. Chia benefits include fiber, calcium, antioxidants, protein, and more. Fiber is known to make one feel full, however, both flax and chia seeds absorb quite a bit of liquid, creating the feeling of fullness for a longer period of time than many other fibers. This is a great and healthy way to lose weight. A misconception about losing weight is to skip meals. When you do this it throws your blood sugar levels out of whack. Some believe this results in weight gain, or at least in no loss. Minimally, it is unhealthy. What does make sense is that if you eat more often such as 4 – 5 times a day, and on a regular schedule, your blood sugar levels maintain balance and your body recognizes that it will receive more food soon, which may prevent it from going into a starvation mode, storing fat. The bottom line is always calorie intake, though. Choose wisely, and avoid the use of refined sugar and artificial sweeteners, as this increases acidity in the body, resulting in inflammation. When chronic inflammation is present in the body it depresses the immune system and creates disease, even tumors.(2) Inflammation really is the precursor to disease. For those with celiac disease needing to gain weight, note that it may take several months to up to a year before your gut is healed enough to absorb nutrients properly. Meanwhile, check the ingredients and foods that you consume to ensure they are truly gluten-free. Due to the lack of labeling laws in the U.S., a food labeled gluten-free may still contain a small amount of gluten. Consume a high calorie diet with healthy fats such as avocado,coconut oil, high calorie nuts such as walnuts and pecans, nut butters, and if dairy-tolerant, cream cheese. Add avocado to your sandwiches, healthy oil to protein shakes and smoothies; consume high carbohydrates such as potatoes; and snack between meals. Individuals who need to avoid dairy may find it difficult at times. There are a number of gluten-free, dairy-free substitutes on the market now. If you are soy and corn intolerant, as well, you may find it difficult to find a dairy-free substitute for butter. A small percentage of dairy intolerant individuals may tolerate goat's milk; and some even tolerate ghee (clarified butter). Because a minute amount of dairy protein may remain in ghee, and because goat's milk is considered dairy, it is best to be tested for food allergies if you suspect a dairy allergy, prior to consuming the above. Previous studies on food allergies focused on antibodies (proteins that attack foreign substances and sometimes even food) found in the blood. In a preliminary study performed by the University of Osio, Norway, it was discovered that food-related antibodies may end up in the gut. When the body mistakes a food for a foreign matter, it creates IgE antibodies (Immunoglobin E), which creates a chain reaction of symptoms. Though the study was performed on those with rheumatoid arthritis (RA), in the participants' intestinal fluid they found antibodies to the following foods: cow's milk, hen, cereal, eggs, codfish, and pork, at higher levels than in non-RA patients.(5) Similar results may be found in those with celiac disease or gluten intolerance, even the general population. We will not know until additional studies are performed. It is definitely food for thought. If you have any type of unexplained symptoms, that medical professionals have not been able to diagnose, consider being tested for other food intolerances or allergies, besides gluten. Consuming foods that cause your immune system to react will only create additional inflammation. There has been much talk that many individuals have had positive results from using Cyrex Labs. You cannot do these tests by mail, as someone must draw your blood. However Cyrex Labs has a list of doctors who will provide this service. If you are not quite sure what you are allergic or sensitive to, another option to consider is an allergy elimination diet. For one month eat only meat, fish, fruit, vegetables, basically a caveman diet, quite a bit stricter than the Paleo Diet. (Definitely check with your doctor first.) Then introduce one food at a time back into your diet. Note that food allergy reactions may be immediate or within a couple of days, where a sensitivity may take longer to show up.(6) This is also a great way to lose weight. If you are new to the gluten-free diet, make sure to introduce new foods, especially gluten free grains, one at the time. Consume the item a few times within a couple of days and wait for 2-4 days and take note whether you have a reaction to it. The reaction may be as complicated as hives, dermatitis herpetiformis, or digestive issues; or as simple as a bad night's sleep or slight bloating. Note that some people may not present any symptoms, even to gluten, and still have celiac disease. The above is referenced for food allergies and sensitivities only. The best advice for anyone who is gluten intolerant is to strictly adhere to the gluten-free diet. One study shows that only 52.1% of those with celiac disease adhere to a gluten-free diet.(7) What will your New Year's resolution be now? References: 1. Omega-3 Fatty Acids University of Maryland Medical System http://www.umm.edu/altmed/articles/omrga-3-000316.htm (Accessed December 6, 2012). 2. Inflammation http://www.arizonaadvancedmedicine.com/articles/inflammation.html (Accessed December 7, 2012). 3. The Nutrition Source, Ask the Expert: Omega-2 Fatty Acids Harvard School of Public Health http://www.hsph.harvard.edu/nutritionsource/questions/omega-3/index.html (Accessed December 6, 2012). 4. Circulating long-chain w-3 fatty acids and incidence of congestive heart failure in older adults: the cardiovascular health study: a cohort study. PubMed http://www.ncbi.nlm.nigh.gov/pubmed/21810709 (Accessed December 6, 2012). 5. Denise Lynn Mann Rheumatoid Arthritis Diet: RA and Food Allergies http://www.arthritistoday.org/conditions/rheumatoid-arthritis/nutrition-and-ra/ra-food-allergies.php (Accessed December 7, 2012). 6. Dr. Jonathan Brostoff, M.D. Food Allergies and Food Intolerance: The Complete Guide to Their Identification and Treatment (2000) 7. Talluri SK, Besur S, Talluri J, Department of Internal Medicine, McLaren-MSU Internal Medicine Residency Program, Flint, MI - A Population-Based Survey of Celiac Disease in the United States http://www.cdc.gov/nchs/events/2012nchs/poster_abstracts.htm#abstract74 (Accessed December 7, 2012).
  2. Celiac.com 07/05/2017 - Numerous researchers have documented a connection between celiac disease and type 1 diabetes. One team of researchers recently set out to examine international differences in celiac disease rates and clinical characteristics of youth with coexisting type 1 diabetes and celiac disease compared with type 1 diabetes only. The research team included Maria E. Craig, Nicole Prinz, Claire T. Boyle, Fiona M. Campbell, Timothy W. Jones, Sabine E. Hofer, Jill H.Simmons, Naomi Holman, Elaine Tham, Elke Fröhlich-Reiterer, Stephanie DuBose, Helen Thornton, Bruce King, David M. Maahs, Reinhard W. Holl and Justin T. Warner. To analyze the relationship between outcomes, including HbA1c, height-standard deviation score [sDS], overweight/obesity, and type 1 diabetes with celiac disease versus type 1 diabetes alone, adjusting for sex, age, and diabetes duration, the team created multivariable linear and logistic regression models. The analysis included 52,721 people under 18 years of age with a clinic visit between April 2013 and March 2014. The team used the following data sources: the Prospective Diabetes Follow-up registry (Germany/Austria); the T1D Exchange Clinic Network (T1DX) (U.S.); the National Paediatric Diabetes Audit (U.K. [England/Wales]); and the Australasian Diabetes Data Network (ADDN) (Australia). The researchers found biopsy-confirmed celiac disease in 1,835 young people, or 3.5%. These patients were diagnosed on average at age 8.1 years, with a range of 5.3 to 11.2 years. Most young people (37%) with diabetes upon celiac disease diagnosis had it for less than one year. Eighteen percent with diabetes had it for 1-2 years at celiac diagnosis, 23% had diabetes between 3 and 5 years at celiac diagnosis, while 17% had diabetes for more than 5 years at celiac diagnosis. Celiac disease rates ranged from 1.9% in the T1DX to 7.7% in the ADDN and were higher in girls than boys (4.3% vs. 2.7%, P < 0.001). Children with coexisting celiac disease were diagnosed with diabetes at 5.4 years on average, compared with those with type 1 diabetes only, who were diagnosed at 7.0 years of age, on average. Also, fewer children with both conditions were non-white, 15 vs. 18%. Height-SDS was lower in those with celiac disease (0.36 vs. 0.48) and fewer were overweight/obese (34 vs. 37%, adjusted P < 0.001), whereas average HbA1c values were comparable: 8.3 ± 1.5% (67 ± 17 mmol/mol) versus 8.4 ± 1.6% (68 ± 17 mmol/mol). This study clearly documented that celiac disease is not uncommon in young people with type 1 diabetes. Differences in disease rates may be due to variations in screening and diagnostic practices, and/or risk levels. Although the groups showed similar glycemic control, the research team encourages close monitoring of growth and nutrition in this population, due to the lower height-SDS. Source: Diabetes Care 2017 May; dc162508. The researchers in this study are variously affiliated with the Children’s Hospital at Westmead, Sydney, New South Wales, Australia; University of New South Wales, Sydney, New South Wales, Australia; Charles Perkins Centre Westmead, University of Sydney, Sydney, New South Wales, Australia; Institute of Epidemiology and Medical Biometry, University of Ulm, Ulm, Germany; German Center for Diabetes Research, Munich-Neuherberg, Germany; Jaeb Center for Health Research, Tampa, FL; Leeds Children’s Hospital, Leeds, U.K.; The University of Western Australia, Perth, Western Australia, Australia; Telethon Kids Institute, Perth, Australia; Department of Pediatrics, Medical University of Innsbruck, Innsbruck, Austria; Vanderbilt University Medical Center, Nashville, TN; Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, U.K.; Women’s and Children’s Hospital, Adelaide, South Australia, Australia; Department of Pediatrics, Medical University of Graz, Graz, Austria; St. Helens and Knowsley Teaching Hospitals NHS Trust, St. Helens, U.K.; John Hunter Children’s Hospital, Hunter Medical Research Institute, University of Newcastle, Callaghan, New South Wales, Australia; Lucile Salter Packard Children's Hospital Stanford, Stanford University Medical Center, Palo Alto, CA; and the Children's Hospital for Wales, Cardiff, U.K.
  3. Celiac.com 07/03/2017 - Refractory celiac disease (RCD) is a serious complication of celiac disease. There are two types, RCD I, and RCD II. Unlike RCD type I, RCD type II often leads to enteropathy-associated T-cell lymphoma (EATL), which is associated with clonally expanding T-cells that are also found in the sequentially developing EATL. Using high-throughput sequencing (HTS), a team of researchers recently set out to establish the small-intestinal T-cell repertoire (TCR) in celiac disease and RCD to unravel the role of distinct T-cell clonotypes in RCD pathogenesis. The research team included J Ritter, K Zimmermann, K Jöhrens, S Mende, A Seegebarth, B Siegmund, S Hennig, K Todorova, A Rosenwald, S Daum, M Hummel, and M Schumann. They are variously affiliated with the Institute of Pathology, Charité-University Medicine, Berlin, Germany, the Department of Gastroenterology, Infectious Diseases and Rheumatology, Charité-University Medicine, Berlin, Germany, HS Diagnomics GmbH, Berlin, Germany, the Center for Tumor Medicine, Charité-University Medicine, Berlin, Germany, the Institute of Pathology, University of Würzburg, and Comprehensive Cancer Center Mainfranken (CCCMF), Würzburg, Germany, the Berlin Institute of Health, Berlin, Germany, the Berlin-Brandenburg School for Regenerative Therapies, Berlin, Germany. Their team examined DNA extracted from duodenal mucosa specimens of 9 control subjects, 10 active celiacs, 9 celiacs on a gluten-free diet, 8 RCD type I patients, 8 RCD type II patients, and 3 unclassified Marsh I cases collected from 2002 to 2013. To make their examination, they used TCRβ-complementarity-determining regions 3 (CDR3) multiplex PCR, followed by HTS of the amplicons. They generated an average of 106 sequence reads per sample, consisting of up to 900 individual TCRβ rearrangements. In RCD type II, the most frequent clonotypes (sequence reads with identical CDR3) represent about 43% of all TCRβ rearrangements. This was substantially higher than in control subjects (6.8%; p Repeat endoscopies in individual patients showed that the clonotypes remain stable for up to a few years without clinical symptoms of EATL. Individual patients with RCD type II showed unique dominant clonotypes that were un-related among patients. Celiac-associated, gliadin-dependent CDR3 motifs were only detectable at low frequencies. TCRβ-HTS analysis unravels the TCR in celiac disease, and allows for detailed analysis of individual TCRβ changes. Patients with RCD type II have unique, dominant TCRβ sequences that are critically different from known gliadin-specific TCR sequences, which indicates that these clonal T-cells expand on their own, with no influence from gluten stimulation. Source: Gut. 2017 Feb 10. pii: gutjnl-2016-311816. doi: 10.1136/gutjnl-2016-311816.
  4. Celiac.com 07/01/2017 - Calgary University's Faculty of Arts and Markin Undergraduate Student Research program is designed to give recipients a leg up on research projects that can help advance their academic goals. For one such recipient, Karen Tang, those goals include helping individuals "to effectively self-manage celiac disease and follow a strict gluten-free diet, by teaching people evidence-based strategies." For Tang, the opportunity allows her to combine her interests of psychology and self-compassion with her desire to help chronic disease populations. For those coping with celiac disease, strategies such as self-compassion can be an effective tool for managing their well-being. Tang has been heavily involved in the pilot study for the Promotion of Optimal Well-Being, Education and Regulation for Celiac Disease (POWER-C). The study is the first program specifically designed to teach individuals evidence-based strategies for coping with celiac disease and to help them effectively manage their illness. Tang has spent the fall and winter committed to helping individuals with celiac disease effectively manage their illness, to enhance their health and their quality of life. For many, a strict lifestyle change comes with its own set of problems and challenges. Research indicates that approximately less than 42 per cent of individuals with celiac disease adhere strictly to a gluten-free diet. Tang says, "The purpose of this research is to help individuals to effectively self-manage celiac disease and follow a strict gluten-free diet, by teaching people evidence-based strategies." Ms. Tang presented an update on her research at a mini-symposium on April 7, 2017. Read More at Calgary University's UToday
  5. Celiac.com 06/29/2017 - A team of researchers recently set out to document trends in diagnosis of celiac disease among patients from a single centre from 1958–2014, and and to provide data on rates and numbers of cases in those born in Derby city over 4 decades. The team also sought to explore a possible connection between deprivation and prevalence and characteristics of celiac disease in Asians. The research team included Geoffrey K T Holmes, and A Muirhead. They are affiliated with the Royal Derby Hospital, Derby, UK, and the Department of Public Health, Derby City Council, Derby, UK. The team used National Census information to identify 2,410 adult celiac patients diagnosed in Derby area hospitals. To measure changes in disease rates and individual cases over the study period, the team identified 1,077 patients born within Derby city; 191 of whom were Asian. From 2010–2014, 20 times more patients were diagnosed than during 1975–1979. More than one-quarter of patients (27%) were diagnosed at or above 60 years of age. The team noted a low number of diagnoses in young men. They noted also that most women were diagnosed 35 and 45 years of age, which is 15 years earlier than men. Young women and elderly patients saw the largest increase in diagnosis rates. In 2014, overall prevalence was 1:188. Prevalence in women was 1:138. Nearly 5 percent of the variation was attributed to deprivation. Diagnosis rates in Asians increased markedly, although only 5 percent were diagnosed at 60 years or older, far lower than for whites. The research team calls for more research into the dramatic increase in celiac cases, and the challenges this increase presents for follow-up and new models of care need. They encourage healthcare workers to be alert to the possibility of undiagnosed celiac disease in young men and elderly Asians. They note that a dedicated celiac clinic is helpful for increasing rates of celiac diagnosis. Source: BMJ Open Gastro 2017; 4:e00013. doi:10.1136/bmjgast-2017-000137
  6. Celiac.com 06/28/2017 - Tests to measure serum endomysial antibodies (EMA) and antibodies to tissue transglutaminase (tTG) were developed to screen for celiac disease in patients who are actively eating gluten. However, doctors often use them to monitor patients on a gluten-free diet. Now, making sure celiac patients are successfully following a gluten-free diet is important, as unconscious gluten ingestion can lead to complications over time. But how accurate are these tests for assessing gluten-free compliance in celiac patients? A team of researchers recently set out to assess the sensitivity and specificity of tTG IgA and EMA IgA assays in identifying patients with celiac disease who have persistent villous atrophy despite a gluten-free diet. The research team included Jocelyn A. Silvester, Satya Kurada, Andrea Szwajcer, Ciarán P. Kelly, Daniel A. Leffler, and Donald R. Duerksen. They are variously affiliated with the Farncombe Family Digestive Health Research Institute and Division of Gastroenterology, and the Department of Pathology and Molecular Medicine and Department of Medicine, McMaster University, Hamilton, Ontario. To begin their meta-analysis, the team searched PUBMED, EMBASE, BIOSIS, SCOPUS, clinicaltrials.gov, Science Citation Index, and Cochrane Library databases through November 2016. They included studies of subjects with biopsy-confirmed celiac disease, follow-up biopsies and measurement of serum antibodies on a gluten-free diet, biopsy performed on subjects regardless of symptoms or antibody test results. Their analysis excluded patients with refractory celiac disease, undergoing gluten challenge, or consuming a prescribed oats-containing gluten-free diet. They determined positive or negative findings based on manufacturer cut-off values. They defined villous atrophy a Marsh 3 lesion or villous height:crypt depth ratio below 3.0. They constructed forest plots to determine the sensitivity and specificity of detection for individual studies. For their meta-analysis, they used a bivariate random effects model to determine both sensitivity and specificity. Their search of abstracts revealed 5,408 unique citations, which yielded 442 articles for detailed review. Those reviewed articles yielded just 26 studies that met the team’s inclusion criteria (6 of tTG assays, 15 of EMA assays, and 5 of tTG and EMA assays). Inability to cross-tabulate histologic and serologic findings was the most common reason the team excluded a given study from analysis. They found that serum assays identified patients with persistent villous atrophy with high levels of specificity: 0.83 for the tTG IgA assay (95% CI, 0.79–0.87) and 0.91 for the EMA IgA assay (95% CI, 0.87–0.94). However, the tests showed low sensitivity for detecting villous atrophy: 0.50 for the tTG IgA assay (95% CI, 0.41–0.60) and 0.45 for the EMA IgA assay (95% CI, 0.34-0.57). Results were similar in both pediatric and adult patients. A meta-analysis of biopsy-confirmed celiac patients who received follow-up biopsy while on a gluten-free diet, showed that tests for serum tTG IgA and EMA IgA had low sensitivity, detecting persistent villous atrophy less than 50 percent of the time. The team supports the search for more accurate, non-invasive, markers of mucosal damage in celiac patients who follow a gluten-free diet. Source: Gastroenterology. DOI: http://dx.doi.org/10.1053/j.gastro.2017.05.015
  7. Celiac.com 06/21/2017 - Circulating gluten-specific FOXP3+CD39+ regulatory T cells have impaired suppressive function in patients with celiac disease. What does that mean? Although researchers understand the effector T-cell response in patients with celiac disease pretty well, they really don't know very much about the role played by regulatory T cells (Treg cells) in the loss of tolerance to gluten. To get a better picture, a team of researchers recently set out to define whether patients with celiac disease have a dysfunction or lack of gluten-specific forkhead box protein 3 (FOXP3)+ Treg cells. The research team included L Cook, CML Munier, N3 Seddiki, D van Bockel, N Ontiveros, MY Hardy, JK Gillies, MK Levings, HH Reid, J Petersen, J Rossjohn, RP Anderson, JJ Zaunders, JA Tye-Din, AD Kelleher. For the study, gluten-free patients with celiac disease underwent oral wheat challenge to stimulate recirculation of gluten-specific T cells. The research team collected peripheral blood before and after challenge. To effectively measure the gluten-specific CD4+ T-cell response, they combined traditional IFN-γ ELISpot with a test for antigen-specific CD4+ T cells that does not rely on tetramers, antigen-stimulated cytokine production, or proliferation, but relies instead on antigen-induced co-expression of CD25 and OX40 (CD134). During the gluten challenge, levels of circulating gluten-specific Treg cells and effector T cells both rose sharply, peaking on the sixth day. The team recounts surprise on discovering that about 80% of the ex vivo circulating gluten-specific CD4+ T cells were FOXP3+CD39+Treg cells, which reside within the pool of memory CD4+CD25+CD127lowCD45RO+ Treg cells. Even though they saw normal suppressive function in peripheral polyclonal Treg cells from celiac patients, after a short in vitro expansion, the gluten-specific FOXP3+CD39+ Treg cells showed sharply reduced suppressive function compared with polyclonal Treg cells. The team's study offers the first estimates of FOXP3+CD39+ Treg cell frequency within circulating gluten-specific CD4+ T cells after oral gluten challenge of celiac patients. FOXP3+CD39+ Treg cells made up the majority of all circulating gluten-specific CD4+ T cells, but they showed reduced suppressive function, indicating that Treg cell dysfunction might be a key factor in celiac disease development. This type of research is crucial to help document the genetic physiology of celiac disease, which will help researchers to better understand and treat the disease itself. Source: J Allergy Clin Immunol. 2017 Mar 8. pii: S0091-6749(17)30343-3. doi: 10.1016/j.jaci.2017.02.015. The researchers are variously affiliated with the Immunovirology and Pathogenesis Program, The Kirby Institute, UNSW Sydney, Sydney, Australia, St Vincent's Centre for Applied Medical Research, St Vincent's Hospital, Sydney, Australia; the Infection and Immunity Program, The Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia; Australian Research Council Centre of Excellence in Advanced Molecular Imaging, Monash University, Clayton, Australia; the Immunovirology and Pathogenesis Program, The Kirby Institute, UNSW Sydney, Sydney, Australia; St Vincent's Centre for Applied Medical Research, St Vincent's Hospital, Sydney, Australia, Immunology Division, Walter and Eliza Hall Institute, Parkville, Australia; Department of Medical Biology, University of Melbourne, Parkville, Australia; Department of Surgery, University of British Columbia, Vancouver, British Columbia, Canada; the Institute of Infection and Immunity, Cardiff University School of Medicine, Heath Park, Cardiff, United Kingdom; the Immunology Division, Walter and Eliza Hall Institute, Parkville, Australia; Department of Medical Biology, University of Melbourne, Parkville, Australia; ImmusanT, Cambridge, Massachusetts; and the Department of Gastroenterology, Royal Melbourne Hospital, Parkville, Australia.
  8. Celiac.com 06/12/2017 - Previously, Transcranial Magnetic Stimulation in de novo celiac disease patients has signaled an imbalance in the excitability of cortical facilitatory and inhibitory circuits. Researchers have reported that, after about of 16 months on a gluten-free diet, patients experience a global increase of cortical excitability, which suggests some kind of compensation for disease progression, likely mediated by glutamate. To better assess these finding, a team of researchers recently conducted cross-sectional evaluation of the changes in cortical excitability to TMS after a much longer gluten-free diet. The research team included M. Pennisi, G. Lanza, M. Cantone, R. Ricceri, R. Ferri, C.C. D’Agate, G. Pennisi, V. Di Lazzaro, and R. Bella. They are variously affiliated with the Spinal Unit, Emergency Hospital "Cannizzaro", Catania, Italy, the Department of Neurology IC, I.R.C.C.S. "Oasi Maria SS.", Troina, Enna, Italy, the Department of Medical and Surgical Sciences and Advanced Technologies, Section of Neurosciences, University of Catania, Catania, Italy, the Gastroenterology and Endoscopy Unit, University of Catania, Catania, Italy, the Department "Specialità Medico-Chirurgiche,” University of Catania, Catania, Italy, and the Institute of Neurology, Campus Bio-Medico University, Rome, Italy. For their study, the team enrolled twenty patients who had followed an adequate gluten-free diet for about 8.35 years, on average. They then compared the results with twenty de novo patients, and twenty more healthy controls. The team measured Transcranial Magnetic Stimulation, recorded from the first dorsal interosseous muscle of the dominant hand, as follows: resting motor threshold, cortical silent period, motor evoked potentials, central motor conduction time, mean short-latency intracortical inhibition and intracortical facilitation. De novo patients showed a shorter cortical silent period, while responses for gluten-free diet participants were similar to controls. Regardless of diet, all celiac patients showed a significantly smaller amplitude of motor response than did control subjects, Again, without regard to diet, all celiac patients showed a statistically significant decrease of mean short-latency intracortical inhibition and enhancement of intracortical facilitation with respect to controls. The team also observed that gluten-free celiac patients showed more intracortical facilitation compared to non-gluten-free patients. Neurological examination and celiac disease-related antibodies were both negative. This study showed that a gluten-free diet helps to mitigate the electrocortical changes associated with celiac disease. Even so, in many patients, an intracortical synaptic dysfunction, mostly involving excitatory and inhibitory interneurons within the motor cortex, may persist. The calls for further investigation into the clinical significance of subtle neurophysiological changes in celiac disease. Source: PLoS One. 2017 May 10;12(5):e0177560. doi: 10.1371/journal.pone.0177560. eCollection 2017.
  9. Celiac.com 06/19/2017 - Adults with celiac disease often show atypical symptoms, though it is not uncommon for them to suffer from malabsorption of vitamins and minerals, which can result in disrupt normal bone metabolism. A team of researchers recently set out to evaluate laboratory deficiencies related to bone metabolism, and to assess the relationship between severity of histological damage and the degree of bone mass loss at celiac diagnosis. The research team included L. Posthumus, and A. Al-Toma A of the Department of Gastroenterology and Hepatology, St Antonius Hospital, Nieuwegein, The Netherlands. Their team conducted a retrospective cross-sectional study of 176 adult celiac patients. All patients met the histopathological criteria for clinical celiac disease. The team analyzed biochemical data, including calcium, phosphate, alkaline-phosphatase, vitamin D and parathormone. They classified duodenal histology based on Marsh parameters. They used dual X-ray absorptiometry to determine bone mass density (BMD) at the lumbar and femoral regions. P-values below 0.05 were considered significant. They found no correlation between gastrointestinal symptoms and Marsh histopathological stage (P>0.05). Nearly 50 percent of patients showed vitamin D deficiency (44.5%), while only 5.7% showed hypocalcaemia. Patients with Marsh III did show lower calcium (P<0.05) and parathormone was higher (P=0.01). These patients had lower lumbar T-score (P<0.05). Although low BMD occurred in all age groups, most osteoporotic patients were aged 45-49 years (81.8%). A multiple regression analysis did show that Marsh stage could indicate lower lumbar BMD (r=0.322, B=-1.146, P<0.05). At celiac diagnosis, Marsh histopathological stage can predict low BMD, which can develop into osteoporosis. Based on these data, the team suggests that doctors should consider evaluating bone biomarkers and conducting a dual X-ray absorptiometry exam in celiac patients over 30 years of age. Source: Eur J Gastroenterol Hepatol. 2017 Apr 27. doi: 10.1097/MEG.0000000000000880.
  10. This article originally appeared in the Autumn 2002 edition of Celiac.coms Scott-Free newsletter. At the University of Chicago Celiac Disease Program, women with celiac disease who have recently become pregnant often contact us. Remarkably, the questions we receive from these women seldom stray from one issue, that is, whether or not to maintain a gluten-free diet while pregnant. Most women mistakenly believe that the gluten-free diet will deprive their developing fetus with the nutrients it needs, and hurt the growing baby. In fact, for a pregnant woman with celiac disease, remaining ON the gluten-free diet is the best and only option for the health of mother and child. The gluten-free diet provides pregnant women and their babies with all of the nutrients they need to grow and be healthy. Fortunately, for all concerned, there have been excellent research studies on fertility, pregnancy and celiac disease conducted by top-notch investigators around the world. While this important research has mainly focused on women, it is important to note that researchers have established (since the 1950s) that men also suffer from infertility due to undiagnosed celiac disease. Celiac Disease and Fertility In research studies to date, the incidence of celiac disease in women with unexplained infertility has been estimated at four to eight percent. While a number of studies have demonstrated that unexplained infertility can be successfully treated with the gluten-free diet, others have shown that there are factors other than malabsorption of nutrients that result in infertility, delayed menarche (the start of the menstrual cycle) and early menopause. In two large case control studies, researchers examined the incidence of delayed menarche, amenorrhea (cessation of the menstrual cycle for short periods of time), and early menopause. Both studies enrolled women with celiac disease who were following the gluten-free diet or eating a gluten-containing diet. They found that women who were not on the gluten-free diet started their menstrual cycle up to a year and a half later than women with celiac disease who were following the diet. In addition, researchers found that up to 39% of women not on the diet experienced periods of amenorrhea, compared to only nine percent of women who were on the gluten-free diet. As you would expect, women with celiac disease who were not on the gluten-free diet were found to enter menopause four to five years earlier than women with celiac disease who were on the diet. Researchers who have studied women with infertility have found that they test positive for celiac disease-related antibodies at a rate that is ten-fold higher than the normal population. They have also demonstrated that women with infertility who are diagnosed with celiac disease do not always exhibit iron, B-12, or folate deficiencies, which points to other celiac disease-related explanations for the development of their infertility. Celiac Disease and Pregnancy Researchers have also studied the effect of the gluten-free diet in pregnant women with celiac disease, in order to determine any impact on the developing fetus and the pregnancy outcome. In a study of 25 patients and 60 pregnancies researchers found that 21% of women who were not on the gluten-free diet experienced pregnancy loss, and 16% of women experienced fetal growth restriction. Researchers also remarked, however, that successful pregnancies occurred before and after diagnoses for many women in the study. In a large Danish study with 211 infants and 127 mothers with celiac disease, researchers found that the mean birth weight of children born to mothers on a gluten-containing diet was significantly lower than babies born to mothers without celiac disease. Interestingly, this same study determined that women on the gluten-free diet gave birth to children weighing more than those born to mothers without celiac disease! In a case-control study that looked at the effect of the gluten-free diet on pregnancy and lactation, investigators learned that women with celiac disease who were not on the gluten-free diet experienced pregnancy loss at a rate of 17.8%, compared to 2.4% of women with celiac disease who were on the gluten-free diet. These researchers found that there was no difference in the occurrence of pregnancy and fertility problems in women with sub-clinical (positive blood test, negative biopsy) or clinical disease (positive blood test, positive biopsy). Finally, in a group of women with celiac disease who had been pregnant more than once, researchers looked at the effect of the gluten-free diet on their future pregnancies. They concluded that the institution of the gluten-free diet upon diagnosis caused a relative 35.6% drop in pregnancy loss, 29.4% drop in low-birth weight babies and an increase of two and a half months of breastfeeding. While the malabsorption of nutrients is not the only cause of fertility and pregnancy-related problems for women with celiac disease, the gluten-free diet is essential to improving the health of women and their babies.
  11. Celiac.com 06/15/2017 - Enteropathy-associated T cell lymphoma (EATL) subtypes are characterized by loss of function of SETD2. Although EATL is rare condition, it is deadly. It is also the most common neoplastic complication of celiac disease. A team of researchers recently conducted whole-exome sequencing of 69 EATL tumors, which helped them to define the genetic landscape of EATL. They found that SETD2 was silenced in 32% of EATL patients, making it the most frequently silenced gene in EATL. The research team included AB Moffitt, SL Ondrejka, M McKinney, RE Rempel, JR Goodlad, CH Teh, S Leppa, S Mannisto, PE Kovanen, E Tse, RKH Au-Yeung, YL Kwong, G Srivastava, J Iqbal, J Yu, K Naresh, D Villa, RD Gascoyne, J Said, MB Czader, A Chadburn, KL Richards, D Rajagopalan, NS Davis, EC Smith, BC Palus, TJ Tzeng, JA Healy, PL Lugar, J Datta, C Love, S Levy, DB Dunson, Y Zhuang, ED Hsi, and SS Dave. The team also noted that the JAK-STAT pathway was the most frequently mutated pathway, with frequent mutations in STAT5B as well as JAK1, JAK3, STAT3, and SOCS1, and that the condition causes highly overlapping genetic alterations among the mutations in KRAS, TP53, and TERT Type I EATL and type II EATL (monomorphic epitheliotropic intestinal T cell lymphoma), which indicates shared mechanisms underlying their causes. To model the effects of SETD2 loss in vivo, the team developed a T cell-specific knockout mouse. These mice manifested an expansion of γδ T cells, indicating novel roles for SETD2 in T cell development and lymphomagenesis. The team's data provides the most comprehensive genetic portrait to date of this rare, but deadly disease, and will likely play a key role in future classifications of EATL. Source: J Exp Med. 2017 May 1;214(5):1371-1386. doi: 10.1084/jem.20160894. Epub 2017 Apr 19. The researchers are variously affiliated with the Duke Center for Genomics and Computational Biology, Duke University, Durham, NC, the Duke Cancer Institute, Duke University School of Medicine, Durham, NC, the Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, OH, the Haematological Malignancy Diagnostic Service, St. James's University Hospital, Leeds LS9 7TF, England, UK, the Haematology Department, Western General Hospital, Edinburgh, Scotland, UK, the Department of Oncology and Research Program Unit, Faculty of Medicine, Helsinki University Hospital Cancer Center and University of Helsinki in Helsinki, Finland, HUSLAB and Medicum, Helsinki University Hospital Cancer Center and University of Helsinki, Helsinki, Finland, the University of Hong Kong, Queen Mary Hospital, Hong Kong, China, the University of Nebraska Medical Center, Omaha, NE, Imperial College London, London, England, UK, the British Columbia Cancer Agency, University of British Columbia, Vancouver, BC, Canada, the University of California, Los Angeles, Los Angeles, CA, Indiana University, Indianapolis, IN, the Presbyterian Hospital, Pathology and Cell Biology, Cornell University, New York, NY, the University of North Carolina at Chapel Hill, Chapel Hill, NC, the Department of Medicine, Duke University School of Medicine, Durham, NC, the Department of Statistical Science, Duke University, Durham, NC, the Hudson Alpha Institute for Biotechnology, Huntsville, AL 35806, and the Department of Immunology, Duke University School of Medicine, Durham, NC.
  12. Celiac.com 06/14/2017 - Some data have suggested a connection between celiac disease and eosinophilic oesophagitis (EoE)/oesophageal eosinophilia (EE). Any potential relationship has implications for treatment. Should the two conditions be treated together, or separately? To better understand any possible connection, and the implications for treatment, a team of researchers recently set out to characterize children with celiac disease+EE in-depth and assess the contribution of each condition to the clinical presentation and treatment response. The research team included Anne Ari, Sara Morgenstern, Gabriel Chodick, Manar Matar, Ari Silbermintz, Amit Assa, Yael Mozer-Glassberg, Firas Rinawi, Vered Nachmias-Friedler, Raanan Shamir, and Noam Zevit. They are variously affiliated with the Institute of Gastroenterology, Nutrition and Liver Diseases, Schneider Children’s Medical Center of Israel, Petach Tikvah, Israel, the Pediatrics Center at Schneider Children’s Medical Center of Israel, Petach Tikvah, Israel, the department of Pathology at Rabin Medical Center in Petach Tikvah, Israel, and the Sackler Faculty of Medicine at Tel Aviv University in Tel Aviv, Israel. The research team conducted a retrospective review of medical records of children with both celiac disease+EE, or isolated EoE diagnosed between 2000 and 2014. They then compared these records with those of patients with isolated celiac disease or epigastric pain. To calculate the frequency of EE, they used endoscopy results of patients with suspected celiac disease or epigastric pain between 2011 and 2014. They used a telephone questionnaire to gather missing data. At a single large, tertiary pediatric center, the team assessed 17 patients with celiac disease+EE, 46 with EoE, 302 with isolated celiac disease, and 247 with epigastric pain. The patients with celiac disease+EE shared characteristics of both individual conditions. While age at diagnosis, family history of autoimmunity/celiac disease and anaemia were similar to most celiac patients, other characteristics such as male gender, personal/family history of atopy, peripheral eosinophilia and oesophageal white papules more closely resembled those of patients with EoE. Most patients with celiac disease+EE tended to present with celiac-associated symptoms, and 63% went on to develop typical EoE symptoms. In celiac disease+EE patients, only 21% saw their EE resolve after a gluten-free diet; another 21% saw their EE normalize after proton pump inhibitor treatment. The rest required EoE-specific treatment. Patients with celiac disease found to have EE share characteristics similar to both isolated celiac disease and EoE. This study indicates that celiac patients with concurrent EE are actually suffering from two separate conditions, rather than celiac-associated eosinophilia. Therefore, in such patients, doctors should consider treating each condition separately. Source: Archives of Disease in Childhood Published Online First: 12 April 2017. doi: 10.1136/archdischild-2016-311944
  13. Celiac.com 06/05/2017 - Doctors diagnose celiac disease by confirming various clinical, genetic, serologic, and duodenal morphology features. Based on retrospective data, recent pediatric guidelines propose eliminating biopsy for patients with IgA-TTG levels more than 10-times the upper limit of normal (ULN), along with a few other criteria. One retrospective study showed that researchers using levels of IgA-TTG and total IgA, or IgA-TTG and IgG against deamidated gliadin (IgG-DGL) could identify patients both with and without celiac disease. A team of researchers recently set out to validate the positive and negative predictive values (PPV and NPV) of these diagnostic procedures. The research team included Johannes Wolf, David Petroff, Thomas Richter, Marcus KH. Auth, Holm H. Uhlig, Martin W. Laass, Peter Lauenstein, Andreas Krahl, Norman Händel, Jan de Laffolie, Almuthe C. Hauer, Thomas Kehler, Gunter Flemming, Frank Schmidt, Astor Rodriques, Dirk Hasenclever, and Thomas Mothes. Their team conducted a prospective study of 898 children undergoing duodenal biopsy analysis to confirm or rule out celiac disease at 13 centers in Europe. They then compared results from antibody tests with results from biopsies, follow-up data, and diagnoses made by the pediatric gastroenterologists. In all cases, diagnosis was made for celiac disease, no celiac disease, or no final diagnosis. Blinded researchers measured levels of IgA-TTG, IgG-DGL, and endomysium antibodies, while tissue sections were analyzed by local and blinded reference pathologists. The team validated two procedures for diagnosis: total-IgA and IgA-TTG, as well as IgG-DGL with IgA-TTG. Patients whose antibody concentrations for all tests were below 1-fold the ULN were assigned to the no celiac disease category. Those whose antibody concentrations for at least one test were above 10-fold the ULN were assigned to the celiac disease category. All other cases were considered to require biopsy analysis. The team calculated the ULN values using the cut-off levels suggested by the test kit manufacturers. They conducted HLA-typing for 449 participants. To extrapolate the PPV and NPV to populations with lower rates of celiac disease, they used models that accounted for how specificity values change with prevalence. In all, the team found 592 patients with celiac disease, 345 who did not have celiac disease, and 24 with no final diagnosis. The TTG-IgA procedure identified celiac disease patients with a PPV of 0.988 and an NPV of 0.934. The TTG-DGL procedure identified celiac disease patients with a PPV of 0.988 and an NPV of 0.958. Their extrapolation model estimated that PPV and NPV would remain above 0.95 even at a disease prevalence as low as 4%. Meanwhile, tests for endomysium antibodies and HLA type did not increase the PPV of samples with levels of IgA-TTG 10-fold or more above the ULN. Interestingly, the pathologists disagreed in their analyses of duodenal morphology about 4.2% of the time, a rate comparable to the error rate for serologic tests. This study validates the use of the TTG-IgA procedure and the TTG-DGL procedure in lieu of biopsy to diagnose pediatric patients with or without celiac disease. Source: Gastroenterology. DOI: http://dx.doi.org/10.1053/j.gastro.2017.04.023 The researchers are variously affiliated with the Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, Medical Faculty of the University and University Hospital, Leipzig, Germany, the Institute for Medical Informatics, Statistics & Epidemiology (IMISE), University of Leipzig, Germany, the Department of Paediatrics, University of Oxford, Oxford, United Kingdom, the Translational Gastroenterology Unit, Nuffield Department of Medicine, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom, the, University Children's Hospital Halle, Germany, the Medical School, Hannover, Germany, Helios Hospital, Department of Paediatrics, Plauen, Germany, the Children's Hospital Prinzessin Margaret, Darmstadt, Germany, the University Children's Hospital Graz, Austria, the Children's Hospital, Justus Liebig University Giessen, Germany, the University Children's Hospital Leipzig, Germany, the Children's Hospital of the Clinical Centre Sankt Georg Leipzig, Germany, the Clinical Trial Centre, University of Leipzig, Germany, the DKD Helios Children's Hospital, German Clinic for Diagnostics, Wiesbaden, Germany, the University Children's Hospital, Technical University Dresden, Germany, and the Alder Hey Children's National Health Service Foundation Trust, Liverpool, United Kingdom.
  14. Celiac.com 04/07/2014 - Histologically non-responsive celiac disease (NRCD) is a potentially serious condition found in celiac disease patients who suffer persistent villous atrophy despite following a gluten-free diet (GFD). Currently, the only way to monitor patient progress rely on invasive and costly serial duodenal biopsies. Looking for better options, a team of researchers recently set out to identify antibody biomarkers for celiac disease patients that do not respond to traditional therapy. The research team included B. N. Spatola, K. Kaukinen, P. Collin, M. Mäki, M. F. Kagnoff, and P. S. Daugherty. They are affiliated with the Department of Chemical Engineering, University of California, Santa Barbara in California, the Department of Gastroenterology and Alimentary Tract Surgery and the Center for Child Health Research at the University of Tampere and Tampere University Hospital in Tampere, Finland, with the Department of Medicine at Seinäjoki Central Hospital in Seinäjoki, Finland, and with the Laboratory of Mucosal Immunology in the Departments of Medicine and Pediatrics at the University of California San Diego in La Jolla, California. Using flow cytometry to screen bacterial display peptide libraries, the team was able to identify the epitopes specifically recognized by antibodies from patients with NRCD, but not by antibodies from responsive celiac disease patients. By comparing ELISA results for sera from 15 NRCD patients and 45 patients with responsive celiac disease, all on a strict GFD for at least 1 year, the team confirmed that deamidated gliadin was the antigen mimicked by library peptides. They identified the dominant consensus epitope sequence by unbiased library screening QPxx(A/P)FP(E/D). The epitope sequence was highly similar to reported deamidated gliadin peptide (dGP) B-cell epitopes. They also found that anti-dGP IgG measurement by ELISA discriminated between NRCD and responsive celiac disease patients with 87% sensitivity and 89% specificity. Most importantly, they found that dGP antibody levels correlated with the severity of mucosal damage, meaning that IgG dGP levels may be useful in monitoring small intestinal mucosal recovery on a GFD in NCRD patients. The team found that celiac patients with NRCD can be spotted by their increased levels of anti-dGP IgG antibodies even when the patients are following strict gluten-free diets Lastly, they feel that anti-dGP IgG assays may be useful for monitoring mucosal damage and histological improvement in celiac disease patients on a strict GFD. Source: Aliment Pharmacol Ther. 2014;39(4):407-417.
  15. Celiac.com 04/25/2017 - A recent issue of JAMA, the US Preventive Services Task Force (USPSTF) critically examines screening for celiac disease in asymptomatic adults, adolescents, and children. Celiac disease exhibits a broad spectrum of symptoms, from subtle or no symptoms to severe malabsorption. Celiac diagnoses have increased significantly over the past few decades, in part because of greater awareness, but possibly because of an actual increase in disease rates. Researchers estimate current rates of celiac disease at 0.71% among US adults, and 0.76% among US children. However, most celiac disease in the population remains undetected, despite wide availability of accurate serologic tests. Screening may be a good way to detect the disease, especially in people who have known risk factors, but have not yet developed symptoms. Noting a profound lack of supporting evidence in the medical literature, the USPSTF states bluntly that "the current evidence is insufficient to assess the balance of benefits and harms of screening for celiac disease in asymptomatic persons." The group recommends more research in this area. USPSTF admits its review of this topic might be criticized as premature, but emphasizes the need for data to provide direction with regards to best practices. The group used rigorous methodology to assess the effectiveness of celiac disease screening in an asymptomatic population, and found the resulting evidence to be thin in inconclusive. Their conclusion and recommendation will likely disappoint numerous clinicians, and more than a few patients. By design, the task force focuses solely on asymptomatic persons, or persons with unrecognized symptoms. They note that screening the general population could potentially detect not only asymptomatic patients, but also patients who lack typical symptoms such as weight loss, diarrhea, or malabsorption. In summary, current evidence on the effectiveness of screening for celiac disease in asymptomatic populations is scarce or absent and certainly insufficient to recommend for or against screening, as indicated in the USPSTF Recommendation Statement. Remember, the USPSTF is not anti-screening, they are pro-screening evidence. Since most celiac disease is undetected, and may present with variable symptoms, the group states that it is "reasonable that clinicians should have a low threshold for testing for celiac disease, especially in high-risk populations such as those with an affected family member or type 1 diabetes mellitus." Clinicians should routinely seek information on the patient’s family history of celiac disease. As celiac testing becomes easier and cheaper, and as gluten-free food becomes more available, it becomes more important for researchers provide the data to determine the best practices for screening and treating celiac disease. They stress the need for more comprehensive studies to assess best celiac screening practices in both high-risk groups, and in the general population, which includes most people with undetected celiac disease. The also note the possibility that the rise in gluten-free dieting by people without an official celiac diagnosis might be an indication of the uncertainty of current screening and diagnostic approaches. Source: Jamanetwork.com
  16. Celiac.com 09/23/2015 - Wheat products are a key component of human diets worldwide. Despite the many beneficial aspects of consuming wheat products, it is also a trigger for several diseases such as celiac disease, wheat allergy, and non-celiac gluten sensitivity (NCGS). A team of researchers recently set out to examine the relationship between celiac disease, non-celiac gluten sensitivity and irritable bowel syndrome. The research team included M El-Salhy, JG Hatlebakk, OH Gilja, and T. Hausken. They are variously affiliated with the Section for Gastroenterology, Department of Medicine, Stord Hospital, Stord, Norway, the Section for Neuroendocrine Gastroenterology, Division of Gastroenterology, Department of Clinical Medicine, University of Bergen, Bergen, Norway, the National Centre for Functional Gastrointestinal Disorders, Department of Medicine, and the National Centre for Ultrasound in Gastroenterology, Department of Medicine, Haukeland University Hospital, Bergen, Norway. Celiac disease and irritable bowel syndrome (IBS) patients have similar gastrointestinal symptoms, which can result in celiac disease patients being misdiagnosed as having IBS. Therefore, celiac disease should be excluded in IBS patients. A considerable proportion of celiac disease patients suffer from IBS symptoms despite adherence to a gluten-free diet (GFD). The inflammation caused by gluten intake may not completely subside in some celiac disease patients. It is not clear that gluten triggers symptoms in NCGS, but there is compelling evidence that carbohydrates in wheat such as fructans and galactans do. Based on their results, the team feels that it is likely that NCGS patients are a group of self-diagnosed IBS patients who self-treat using a gluten-free diet. Source: Nutr J. 2015 Sep 7;14(1):92. doi: 10.1186/s12937-015-0080-6.
  17. Celiac.com 05/30/2017 - Huff Post recently featured a good article on empowering kids with food allergies, including celiac disease. The article, by Miriam Pearl, suggests that parents seek to promote awareness and self-reliance in such children, rather than simply providing for them quietly and looking to protect them from allergens. The basic message is to help kids gain all the skills needed to manage their condition, rather than seeking to rescue them. Pearl writes that "The more practice [children] have managing themselves in the outside world the better they will get at it." She offers a number of useful tips to help parents along. First, she says, start early. It's never too early to let kids know what's going on, and what you're doing to help them maintain their health. Second, work to make the children aware of the things that impact their health. Show them what it's like to shop, cook, and advocate for themselves. Third, strive to show, teach and model everything they must know about safe foods and danger foods. Fourth, take them to the store with you and let them find gluten-free items. Among other benefits, this will help them learn to read labels. Fifth, enlist their help in packing their lunches. Sixth, ask them to listen to whenever and wherever you ask for food that is safe. Seventh, make sure they learn to carry their own snacks, just in case they can't control what food is around them. If they learn to do it early, they might avoid learning the hard way, which happens when you forget to provide snack for them, and they go hungry while everyone else eats. Lastly, when dining out, engage them in your effort to get answers from waiters every time you order food. Helping children to clearly see and understand the challenges of being gluten-free and having food allergies, and what it means to deal with those challenges on a daily level, help prepare them to make the right choices when confronted with unfamiliar or uncomfortable situations involving gluten-free food. This, in turn, helps them lead happier, healthier gluten-free lives. Source: HuffPost.com
  18. Celiac.com 10/01/2010 - Scleroderma is a chronic, systemic autoimmune disease characterized by tissue fibrosis, or hardening, vascular changes, and autoantibodies. There are two forms of scleroderma. The first is called limited systemic sclerosis/scleroderma cutaneous, and manifests mainly affect the hands, arms and face. This form of scleroderma was earlier known as CREST syndrome, because symptoms included Calcinosis, Raynaud's phenomenon, Esophageal dysfunction, Sclerodactyly, and Telangiectasias. This form of scleroderma triggers pulmonary arterial hypertension in up to one third of patients, which is the most serious problem. The second, less common form of scleroderma is called diffuse systemic sclerosis/scleroderma. This form progresses quickly and affects large areas of skin and one or more internal organs, generally the kidneys, esophagus, heart and lungs. A recent letter by doctors R. Thonhofer M. Trummer, and C. Siegel noted that capillaroscopy shows an active pattern of scleroderma in celiac disease. They are affiliated with the Department of Internal Medicine at the State Hospital Muerzzuschlag, and with the Department of Rheumatology at the Medical University of Graz in Austria. Their letter notes that previous studies have shown celiac disease to be associated with higher rates of Raynaud’s phenomenon, sclerodactyly, arthritis, polymyositis, pericarditis, vasculitis, and scleroderma. The doctors describe the case of a 41-year-old, non-smoking woman, who presented with Raynaud's phenomenon and progressive weight loss. For nearly twenty years, the woman had suffered symptoms of Raynaud's phenomenon, with classical tricolore phenomenon and symmetrical bilateral involvement of hands, with lesser effect on her feet. The woman's weight loss had persisted for two years, accompanied by unspecific abdominal symptoms including meteorism and episodic diarrhea. The attacks of Raynaud's phenomenon seemed to be triggered by exposure to cold or by emotional stress. The doctors ruled out digital ulcers, vibration injury, and ingestion of toxic agents as possible causes. A color Doppler ultrasound examination of the arteries of the upper and lower extremities showed nothing remarkable. Radiographs of the hands, feet, clavicles, cervical, and lumbar spine were also not remarkable. Nailfold capillaroscopy of digits two to five bilaterally showed capillary loss in some areas, mild, focally moderate to severe disorganization of the vascular architecture, frequent giant capillaries, and hemorrhages adjacent to enlarged, nearly normal, and giant capillaries. The patient showed negative test results for anti-nuclear antibodies, complement factors, anti-DNA antibodies, anti-neutrophil cytoplasmic antibodies, anti-cardiolipin antibodies, cryoglobulinaemia, and rheumatoid factor. Erythrocyte sedimentation rate and C-reactive protein were in the normal range. The patient showed positive screens for anti-endomysial antibodies and anti-tissue transglutaminase antibodies. Endoscopy and several biopsies of the large bowel and terminal ileum showed nothing remarkable. Gastroduodenoscopy showed normal mucosa in the upper gastrointestinal tract. Looking at biopsy results from different parts of the duodenum, the team found an increase in intraepithelial lymphocytes, with about 60 to 70 per 100 enterocytes, along with shortening of the epithelial cells, and a reduction of globlet cells. As a result of antibody testing, anamnesis, and histology, the team was able to make a diagnosis of celiac disease. After the patient began treatment with a gluten-free diet, the abdominal symptoms and weight loss subsided, and the Raynaud's phenomenon attacks became less frequent. Clinical and laboratory evaluation over the last four years have not shown any connective tissue disease in the patient. The team used capillaroscopy every 6 months to show that the pattern of damage remained unchanged, and was not improved by the gluten-free diet within the first year. After 18 months, the vascular architecture showed some improvement, with no further bleeding or enlarged capillaries. Repeated examinations after that point showed similar, near-normal findings. There have been previous reports of several rheumatological disorders, including Raynaud's phenomenon in people with celiac disease, but this seems to be the first report of extensive microvascular damage, similar to capillary changes in scelroderma, documented by nailfold capillaroscopy in a patient with celiac disease. Because they excluded any underlying connective tissue disease or other secondary causes of Raynaud's phenomenon, the team's findings support a causal relationship between celiac disease and Raynaud's phenomenon, especially in regards to the described capillary pattern. Normalization of the patient's vascular architecture after a year and a half on a gluten-free diet further bolster their findings. The team admits the possibility of evolving scelroderma in the patient, but points out that the negative laboratory testing, organ screening, and inconspicuous clinical examination would seem to make that scenario highly unlikely. It will be interesting to see what doctors can learn through additional nailfold capillaroscopy investigations into the special capillary pattern in celiac disease patients. Source: Scand J Rheumatol.Vol. 1, No. 1, Jul 2010. DOI: 10.3109/03009742.2010.489230
  19. Celiac.com 05/24/2017 - Refractory celiac disease (RCD) is a rare manifestation of celiac disease that is difficult to treat, and often results in death from enteropathy-associated T-cell lymphoma. Doctors looking to treat RCD have found very limited success with a number of immunosuppressive medications (IMs), including azathioprine, systemic corticosteroids, or regular budesonide. A team of researchers at the Mayo Clinic recently set out to assess open-capsule budesonide (OB) treatment on RCD patients, including those who saw no improvement with previous IM treatments. The research team included Saurabh S Mukewar, Ayush Sharma, Alberto Rubio-Tapia, Tsung-Teh Wu, Bana Jabri and Joseph A Murray. The team first looked for RCD patients treated with OB at Mayo Clinic, Rochester, Minnesota from 2003 to 2015. They then reviewed demographic, serologic, and clinical variables in these patients. The team found a total of 57 patients who received OB as treatment for suspected RCD. Based on clonal T-cell receptor gamma gene rearrangement or aberrant phenotype of intraepithelial lymphocytes (IELs), the team classified 13 patients (23%) as having RCD-2 and 43 (75%) as RCD-1. The team was unable to determine TCR gene rearrangement status for one patient (2%). Most patients were women (69%), with an average age of 60.5 (+/- 3.5) years, while average body mass index was 28.4 kg/m2. Nearly 75% of patients suffered from diarrhea, with an average of 6 bowel movements per day (range, 4–25). Nearly half of these patients failed to improve with IM treatment. Twenty-four patients (42%) were anemic, while 12 patients (21%) had hypoalbuminemia. Biopsies showed Marsh 3 lesions in all patients, broken down as follows: 19% were Marsh 3a, 46% were Marsh 3b, and 35% were Marsh 3c. After OB therapy, 92% showed clinical improvement, while 89% showed histologic improvement. Subsequent biopsies showed that 7 out of 13 patients with RCD-2 (53%) displayed an absence of the previously observed clonal TCR gamma gene rearrangement/aberrant IEL phenotype. During the follow-up period, two patients died of enteropathy-associated T-cell lymphoma. Most RCD patients show clinical and histopathologic improvement with OB treatment, including those who previously failed to respond to other IMs. These results show that treatment with open-capsule budesonide is a promising option for patients looking to manage RCD. Source: The American Journal of Gastroenterology, (21 March 2017). doi:10.1038/ajg.2017.71
  20. Celiac.com 05/08/2017 - Do non-celiacs who eat a gluten-free diet face a greater risk of developing coronary heart disease? To shed some light on this question, a team of researchers recently set out to assess levels of long-term term gluten consumption in connection with the development of coronary heart disease. The research team included Benjamin Lebwohl, Yin Cao, instructor, Geng Zong, Frank B Hu, Peter H R Green, Alfred I Neugut, Eric B Rimm, Laura Sampson, Lauren W Dougherty, Edward Giovannucci, Walter C Willett, Qi Sun, and Andrew T Chan. They are variously affiliated with the Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA; the Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA; the Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; the Department of Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA, USA; the Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA; and the Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA. For their prospective cohort study, the team looked at 64,714 women in the Nurses’ Health Study and 45,303 men in the Health Professionals Follow-up Study. None of the subjects had any history of coronary heart disease, and all completed a 131 item semiquantitative food frequency questionnaire in 1986 that was updated every four years through 2010. The researchers estimated gluten consumption based on the results of the food frequency questionnaires. Their study looked for patients who developed coronary heart disease, specifically fatal or non-fatal myocardial infarction. The team’s study data covered 26 years of follow-up, totaling 2,273,931 person years, 2431 women and 4098 men developed coronary heart disease. Participants in the lowest fifth of gluten intake had 352 incidences of coronary heart disease per 100,000 person years, while those in the highest fifth had a rate of 277 events per 100,000 person years. This equates to 75 fewer cases of coronary heart disease per 100,000 person years. After adjusting for known risk factors, the researchers noted that patients in the highest fifth of estimated gluten intake had a multivariable hazard ratio for coronary heart disease of 0.95 (95% confidence interval 0.88 to 1.02; P for trend=0.29). After further adjusting for intake of whole grains, and leaving the remaining variance of gluten corresponding to refined grains, the multivariate hazard ratio was 1.00 (0.92 to 1.09; P for trend=0.77). In contrast, after additional adjustment for intake of refined grains (leaving the variance of gluten intake correlating with whole grain intake), estimated gluten consumption was associated with a lower risk of coronary heart disease (multivariate hazard ratio 0.85, 0.77 to 0.93; P for trend=0.002). Long term dietary intake of gluten was not associated with risk of coronary heart disease. However, the researchers do stress the importance of dietary whole grains, and that their absence may increase the risk of cardiovascular disease. Because of this, the team discourages people without celiac disease, or some other medical reason, from adopting a gluten-free diet. Source: BMJ 2017;357:j1892 (Published 02 May 2017)
  21. Celiac.com 05/18/2017 - Researchers understand pretty well that celiac disease is driven in part by an accumulation of immune cells in the duodenal mucosa as a consequence of both adaptive and innate immune responses to undigested gliadin peptides. Mast cells are innate immune cells that produce a majority of co-stimulatory signals and inflammatory mediators in the intestinal mucosa. A team of researchers recently set out to evaluate the role of mast cells in the development of celiac disease. The research team included Barbara Frossi, PhD, Claudio Tripodo, MD, Carla Guarnotta, PhD, Antonio Carroccio, MD, Marco De Carli, MD, Stefano De Carli, MD, Marco Marino, MD, Antonino Calabrò, MD, and Carlo E. Pucillo, MD. They are variously affiliated with the Department of Gastroenterology and Digestive Endoscopy at the University Hospital of Udine in Udine, Italy; the Department of Medical and Biological Sciences, University of Udine, Udine, Italy; the Second Unit of Internal Medicine, University of Udine, Udine, Italy; the Department of Experimental and Clinical Biomedical Sciences “Mario Serio,” University Hospital of Florence, Florence, Italy; the Tuscany Referral Center for Adult Coeliac Disease, AOU Careggi, Florence, Italy; the Department of Health Science, University Hospital of Palermo in Palermo, Italy; and the Department of Internal Medicine and Specialist at the University Hospital of Palermo in Palermo, Italy. For their study, the research team scored intestinal biopsy results from celiac patients according to Marsh classification, and characterized those results for leukocyte infiltration and MC distribution. They also characterized mast cell reactivity to gliadin and its peptides via in vitro assays. The team found that infiltrating mast cells reflected the severity of mucosal damage, and their numbers were increased in patients with higher Marsh scores. They noted that mast cells responded directly to non-immunodominant gliadin fragments by releasing pro-inflammatory mediators. Their immunohistochemical analysis of infiltrating mast cells, along with the effects of gliadin peptides on intestinal mast cells, indicates that patients in with advanced celiac disease face an increase in pro-inflammatory mast cell function. This result was also tied to increased neutrophil accumulation, the prevalence of M1 macrophages, and the severity of tissue damage. This study clearly describes the progressive stages of celiac disease, and shows that mast cells are a prominent feature of the inflammatory process. These results show that mast cells are associated with the onset and progression of celiac disease, and that the view of celiac disease should be revised to account for the contribution of mast cells in the onset and progression of the disease; and in the development any new celiac treatments. Source: Journal of Allergy, & Clinical Immunology. DOI: http://dx.doi.org/10.1016/j.jaci.2016.08.011
  22. Celiac.com 05/19/2017 - Did you know that now, according to Beyond Celiac 83% of those with celiac disease are misdiagnosed or undiagnosed? Did you know that the average time a person waits to be correctly diagnosed, according to Daniel Lefler, M.D., M.S, of the Celiac Center at Beth Israel Deaconness Medical Center is still six to 10 years? This has changed little in the past 10 years, even though celiac disease can lead to a number of other disorders including infertility, reduced bone density, neurological disorders, some cancers, and other autoimmune diseases. Over a four year period, people with undiagnosed celiac disease cost an average of $3,964 more than the healthy individuals (Source: Long et al, 2010. Did you know that 5 - 22% of people with celiac disease have an immediate family member (first degree relative who also has celiac disease, and that there isn't yet a pharmaceutical treatment or cure for it? In 2009 WebMD reported that, in the USA, celiac disease has quadrupled over the last 50 years, yet many people who have the disease remain undiagnosed. Still Dr. Stefano Guandalini, N.D. Director of the Celiac Disease Center at the University of Chicago told WebMD, "Many of these people have no symptoms, but many do have symptoms that are not recognized for what they are. We believe that only five percent of people with celiac disease know they have it". Is there any wonder that a woman at the dietician's office at our local hospital where I sometimes volunteer did not know she had celiac disease? This is because she was only experiencing symptoms of joint and muscle pains, abdominal pain and laboratory tests only showed anemia. She was first referred to an orthopedic specialist, then an internist, and neither checked for celiac disease or questioned her further. "Hello!!" Are there still general practitioners out there who are not aware that there is a blood test for celiac disease? Some people experience symptoms found in celiac disease such as a "brain fog," depression, ADHD like behavior, abdominal pain, bloating, diarrhea, constipation, headaches, bone or joint pain, and chronic fatigue when they have gluten in their diet, yet do not test positive for celiac disease. The terms non-celiac gluten sensitivity (NCGS) and non-celiac wheat sensitivity (NCWS) are generally used to refer to this condition. When removing gluten from their diet it removes symptoms. At my first biopsy of the bowel the gastroenterologist failed to biopsy the jejunum. My blood test was positive, the biopsy of the dermatitis herpetiformis proved positive too, and it wasn't until I insisted on a second biopsy of my jejunum that I was diagnosed. If I had not been persistent, I would have given up after the first biopsy and continued itching and ingesting gluten. Persistence, or stubborn determination (i.e. knowing my own body) paid off, but it took a year for the dermatitis herpetiformis to totally rescind, most particularly the sores on my scalp. You know your own body better than anyone; you know when something is wrong. If your grocery store fails to give you good service you go elsewhere. The Celiac Disease Foundation, both in Canada and the United States, can help you find the right doctor to discuss your symptoms so you can get diagnosed and treated. Shop and find your own healthcare practitioner. Do not allow a doctor tell you that you are neurotic, perimenopausal, or their favorite: "stressed." Since there are more than 200 known celiac disease symptoms which may occur in the digestive system or other parts of the body, and some people develop celiac disease as a child, others as an adult, you owe it to yourself to keep checking and researching and reading magazines like Celiac.com's Journal of Gluten Sensitivity, because, according to the Mayo Clinic, there is no cure for celiac disease. The American Journal of Gastroenterology, at ScienceDirect.com, offers a nationwide view of celiac disease, and conducted two randomized trials that tested strategies of early or delayed gluten introduction in infants, and neither strategy appeared to influence the risk for celiac disease. They also indicated that breastfeeding did not protect against celiac disease. "While disappointing, these results should spur the study of wider environmental risk factors beyond infant feeding, such as intrauterine and perinatal exposure as well as environmental influences later in life, including drug exposure, microbial infections, and the mictobionme. Given that celiac disease can develop at any age, it is imperative to study these proposed triggers so as to elucidate the loss of tolerance to gluten and to develop future intervention strategies." At the start of the Gastroenterology study, between 2000 and 2001 - 11.1 out of every 100,000 people had celiac disease. Toward the end of the study - between 2008 and 2010 it was up to 17.3 out of every 100,000 people. However, researchers noted that the incidence of celiac disease plateaued after 2004. It is no big surprise that they believe, according to Dr. Stefano Guandalini, M.D. "that only about 5 percent of people with celiac disease know they have it." Web MD reported that "Celiac Disease had quadrupled." Many physicians I approached whilst completing this survey indicated it was physician knowledge of the signs and symptoms of celiac disease that has caused a greater increase in celiac testing and the use of a simple blood test (tTG-IgA). The Tissue Transglutaminase Antibodies test will be positive in about 98% of patients with celiac disease who are on a gluten-containing diet. The same test will come back negative in about 98% of healthy people without celiac disease. Although rare, patients with celiac disease could have a negative antibody test result. There is also a slight risk of a false positive test result, especially for people with associated autoimmune disorders like Type 1 Diabetes, autoimmune liver disease, Hashimoto's thyroiditis, psoriatic or rheumatoid arthritis, and heart failure. This test is not good for someone who has been following a gluten-fre diet on their own. A biopsy of the small intestine is still considered the only way to diagnose celiac disease by many doctors. Many parents are reluctant to submit their young child to a biopsy of the Jejeunum and have used only blood tests, including the IgA Endomysial antibody (EMA). This test has a specificity of almost 100% but it is not as sensitive as the tTG-IGA test, because about 10% of people with celiac disease do not have a positive EMA test. Also, it is VERY expensive in comparison to the tTG-IgA and it requires the use of primate esophagus or human umbilical cord, so it is usually reserved for difficult to diagnose patients. The Total Serum IgA is used to test for IgA deficiency, a condition associated with celiac disease that can cause a false negative tTC-IgA or EMA result. If you are IgA deficient, our doctor can order a DGP or tTg-IgC. The decimated gliadin peptide (DGP-IgA and IgG) is a test that can be used to further screen for celiac disease in individuals with IgA deficiency or people who test negative for tTg or EMA antibodies. Even though it is very rare, it is possible for someone with celiac disease to have negative antibody test results. So please do not become discouraged even with negative results, if you are still experiencing symptoms talk with your physician and undergo further medical evaluation. Keep in mind that some of these tests are not medically covered by insurance. Did you know that you can get genetic testing for celiac disease? People with celiac disease carry one or both of the HLA DQ2 and DQ8 genes. So do up to 25 - 30% of all people. Carrying HLA DQ2 and/or DQ8 is not a diagnosis of celiac disease, nor does it mean you will ever develop celiac disease. However, if you carry HLA DQ2 and/or DQ8 your risk of developing celiac disease is 3% instead of the general population risk of 1%. Since celiac disease is genetic this means it runs in families. First degree family members (parents, siblings, children) who have the same genotype as the family member with celiac disease, have up to a 40% risk of developing celiac disease. The overall risk of developing celiac diseases when the genotype is unknown is 7% to 20%, which is a big difference! We cannot blame ALL physicians for the lack of a correct diagnosis. It is one of the most puzzling, multi-faceted diseases, and a patient going into their family physician's office may have very vague symptoms. Thousands of dollars may be spent on blood tests, referrals to specialists, x-rays, and scans before a diagnosis is found. There is nothing more deflating or frustrating to someone who has a myriad of legitimate symptoms than to be told that they are either depressed, stressed or suffering from an overactive imagination. Sources: The American Journal of Gastroenterology https://celiac.org http://www.beyondceliac.org
  23. Celiac.com 05/16/2017 - A number of studies have indicated that kids with celiac disease face an increased risk for mood disorders, anxiety and behavioral disorders, ADHD, ASD, and intellectual disability. A new study by a team of researchers in Sweden puts it more precisely. They put the increased risk for psychiatric disorders in children with celiac disease at 1.4-fold over kids without celiac disease. The research team assessed the risk of any type of childhood psychiatric disorders, including psychosis, mood, anxiety, and eating disorders, psychoactive substance misuse, behavioral disorder, ADHD, ASD, and intellectual disability, in children aged 18 and younger, along with their siblings. The researchers included Agnieszka Butwicka, MD, PhD, of the department of medical epidemiology and biostatistics, Karolinska Institute, Stockholm, Sweden, and colleagues. For each of the 10,903 children with celiac disease, the research team randomly selected 100 non-celiacs from the general population. These control subjects were then matched by gender and year and country of birth. For each of the 12,710 siblings of celiac disease subjects, the research team randomly assigned 100 healthy control siblings from the general population. These were also matched by gender, year and country of birth of both siblings. Both sets of siblings were required to be free of celiac disease to age 19. The researchers reviewed histological data on patients who showed villous atrophy in small intestine biopsy specimens between 1969 and 2008, and equated villous atrophy with celiac disease. In the main cohort study, the researchers estimated the risk for any psychiatric disease, as well as specific psychiatric disorders (ie, mood, anxiety, eating, and behavioral disorders, as well as neuropsychiatric disorders such as attention deficit hyperactivity disorder (ADHD), autistic spectrum disorders (ASD), and intellectual disability) in children with celiac disease, compared with general population controls. They used sibling analyses to assess whether underlying familiar factors could account for the associations. As a comparing factor, they compared the risk for psychiatric disorders in the siblings against the risk in siblings of the general population. The team conducted both univariate and multivariate analyses, adjusting for maternal/paternal age at the child's birth, maternal/paternal country of birth, level of education of highest-educated parent, and the child's gestational age, birthweight, Apgar score, and history of psychiatric disorders prior to recruitment. During follow-up, 7.7% of children were diagnosed with a psychiatric disorder. A positive association was found in the first univariate analysis between celiac disease and any psychiatric disorder, which remained even after the researchers adjusted for maternal/paternal age at childbirth and country of birth, parental education level, and child's gestational age, birthweight, Apgar score, and previous history of psychiatric disorders. The overall prevalence of psychiatric disease in the entire sample celiac disease patients was about 7% (95% CI, 6.4%-7.4%). That number remained steady in the 10 years after biopsy. However, once the researchers analyzed the findings by cohort, they found that rates of psychiatric disorders had actually increased 8-fold over that 10-year period. The siblings of celiac disease patients showed no increased risk for any psychiatric disorder. The study showed that psychiatric disorders "may precede a diagnosis of celiac disease in children." The research team called this finding "important." They write that their study also offers "insight into psychiatric comorbidities in childhood celiac disease over time." The study showed that children with celiac disease definitely faced an elevated risk for specific psychiatric disorders, including mood disorders (HR, 1.2; 95% CI, 1.0-1.4), anxiety disorders (HR, 1.2; 95% CI, 1.0-1.4), eating disorders (HR, 1.4; 95% CI, 1.1- 1.8), behavioral disorders (HR, 1.4; 95% CI, 1.2-1.6), ADHD (HR, 1.2; 95% CI, 1.0-1.4), ASD (HR, 1.3; 95% CI, 1.1-1.7), and intellectual disability (HR, 1.7; 95% CI, 1.4-2.1). Although the study showed that patients with celiac disease are more likely to have prior psychiatric disorders (OR, 1.8; 95% CI, 1.5-2.1; P The team notes that they have yet to determine "the mechanisms underlying the association between celiac disease and psychiatric orders." The fact that the siblings of celiac disease patients showed no increased risk of psychiatric disorders indicates that these may be an "effect of celiac disease per se rather than common genetic or within-family environmental factors," the researchers add. The researchers conclude that their study "underscores the importance of both mental health surveillance in children with celiac disease and a medical workup in children with psychiatric symptoms." This study offers yet another piece in the complex puzzle that is celiac disease. It emphasizes the need for doctors and parents to remain on the lookout for potential psychiatric issues when dealing with children who have celiac disease. Source: Psychiatry Advisor
  24. Celiac.com 05/01/2017 - To avoid symptoms, and promote full gut healing, people with celiac disease should follow a strict gluten-free diet. Oats might increase the nutritional value of a gluten-free diet, but their inclusion for people with celiac disease remains controversial, and data have been conflicting. A team of researchers recently set out to determine the safety of adding oats to a gluten-free diet for patients with celiac disease. The research team included María Inés Pinto-Sánchez, Natalia Causada-Calo, Premysl Bercik, Alexander C. Ford, Joseph A. Murray, David Armstrong, Carol Semrad, Sonia S. Kupfer, Armin Alaedini, Paul Moayyedi, Daniel A. Leffler, and Elena F. Verdú. They are variously affiliated with the Department of Medicine, Farncombe Family Digestive Research Institute, McMaster University in Hamilton, Ontario, Canada, the Leeds Gastroenterology Institute, St. James's University Hospital in Leeds, UK, the Leeds Institute of Biomedical and Clinical Sciences at the University of Leeds in Leeds, UK, the Department of Gastroenterology and Hepatology, Mayo Clinic, Rochester in Minnesota, US, the Celiac Disease Center at University of Chicago Medicine in Chicago, Illinois, US, the Celiac Disease Center at Columbia University, New York City, New York, US, and the Division of Gastroenterology, Beth Israel Deaconess Medical Center, Boston, MA, US. For their systematic review and meta-analysis of clinical and observational studies, the team searched the Cochrane Central Register of Controlled Trials, MEDLINE, and EMBASE databases for clinical trials and observational studies on the effects of including oats in gluten-free diet of celiac patients. The studies reported patient symptoms, serology test results, and histologic assessments. The team used the GRADE approach to assess the evidence. Out of 433 total studies, the team found 28 that met their criteria for analysis. Of these, 6 were randomized and 2 were not-randomized controlled trials comprising a total of 661 patients. The remaining studies were observational. All randomized controlled trials used pure, uncontaminated oats. Their results showed that celiac patients who consumed oats for 12 months experienced no change in symptoms, histologic scores, intraepithelial lymphocyte counts, or serologic test results. To provide a more authoritative conclusion, they call for clinical double-blind, placebo-controlled, randomized trials, using commonly available oats sourced from different regions. Source: Gastroenterology
  25. Celiac.com 08/19/2015 - For the first time since it was described and named by 1st century Greek physician Aretaeus of Cappadocia, first linked to wheat in the 1940's, and specifically linked to gluten in 1952, scientists have discovered the cause of celiac disease. Professor Ludvig Sollid, and his team at the Centre for Immune Regulation at University of Oslo, have discovered that people with celiac disease suffer from one of two defective human leukocyte antigens (HLAs), which cause the immune system to see gluten molecules as dangerous, triggering the immune response that causes classic celiac-associated inflammation and other symptoms. To be true, the team was not working in the dark. They were armed with a complete map of the genes, an understanding that two types of HLA (HLA-DQ2 and HLA-DQ8) predispose a person for celiac disease, and the very crucial recent discovery by a team of German colleagues that celiac patients have antibodies for a very precise enzyme: transglutaminase 2. "We also found that the bits of gluten that were presented to the T-cells have some changes caused by an enzyme in the body – transglutaminase 2", says Sollid. HLAs are proteins which act as markers, binding to fragments of other proteins, and telling T-cells how to treat them. So it wasn't much of a stretch for Professor Sollid's team to determine that the defective HLAs bind to fragments of gluten, causing the T-cells to treat them as bacteria or viruses. Basically, two HLA types present gluten remnants to the T-cells, causing the T-cells to regard the gluten as dangerous, and to trigger immune reactions that cause inflammation in the intestines, and this is what causes celiac disease. "We think that this is huge," Sollid said. "We understand the immune cells that are activated and why they are activated." At present, Professor Sollid and his group are investigating how antibodies against transglutaminase are formed. This is a simple, but huge moment in the annals of medicine and in the annals of celiac disease. It's a discovery that will help researchers develop new approaches to treatment, and/or a cure for celiac disease in the future. Source: Med.uio.no
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