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Showing results for tags 'signs'.
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Celiac.com 03/06/2013 - The hallmark of a healthy gluten-free diet is a grocery cart filled with mostly unprocessed, single-ingredient foods such as fresh produce, nuts, and meat. This is the easiest way to avoid gluten, as well as the healthiest way to eat. When you do venture into the central aisles of the grocery store, look for gluten warning signs on packaging to help you identify foods that contain gluten. Looking for those warning signs is more important than ever because companies are catching on to the growing popularity of gluten-free diets and many are labeling their products gluten-free. However, the U.S. Department of Agriculture (USDA) does not regulate how or when the designation of gluten-free can be added to food labels. This clouds the decision-making process for people with gluten intolerance that rely on gluten warning signs on packaging to guide them. Without USDA regulation, even products labeled gluten-free may still be processed on equipment that also processes gluten. While this is not a problem for people eating gluten-free as a dietary choice, it can cause issues for people who are gluten intolerant. Ingredient Keywords Look for warning signs at three places on the ingredient label. The first is underneath the ingredients list, where common allergens such as soy and milk are listed in bold. If wheat is listed there, the product contains gluten. The second place to look is the ingredients list itself. The following words may be signs of gluten due to its nature or to cross-contamination: Wheat Malt Wheat starch Barley Oats Soy sauce (made with wheat) Even seemingly innocuous products may still contain gluten, so it's important to look at all product labels. For example, yogurt and other dairy products sometimes have gluten-containing thickening agents, many sauces and soups contain gluten, and beer is made with barley hops. The third place to look for gluten warning signs on packaging is at the bottom of the ingredients list. In bold, the packaging will declare whether or not the food was processed on equipment that also processes common allergens, including wheat. Cross-contamination can still cause flare-ups, so these foods should be avoided. Safest Foods The best way to avoid gluten is to stick to unprocessed, fresh produce and meat. With grains and processed foods, the best way to stay safe generally is to opt for minimally processed foods with few ingredients, or specialized foods. Strategies for gluten-free shopping include: Foods in the health aisle or in a natural food store are most often accurately marked as gluten-free. Cook what you can at home and take the mystery out of ingredients. Gluten-free bread, for example, can be made at home using the flour of your choice. Do research before shopping - it can save you time and trouble in the long run. While reading food labels may seem intimidating at first, after a few shopping trips, you will be a pro at identifying problem foods and cooking gluten-free, while still eating a healthy range of foods.
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Celiac.com 11/22/2017 - A team of physicians recently reported on the case of a 3-year-old Albanian girl who presented at their clinic with carpal spasms and hand paresthesia. The physicians include Atifete Ramosaj-Morina; A. Keka-Sylaj; V. Hasbahta; A. Baloku-Zejnullahu; M. Azemi; and R. Zunec. A physical exam showed the girl to be in good physical condition, with a body weight of 10.5 kg (10 percentile). She was suffering from carpal spasms and paresthesias of her extremities. Positive Chvostek and Trousseau signs indicated neuromuscular irritability. Blood tests showed severe hypocalcemia with a total serum calcium of 1.2 mmol/L (normal range 2.12 to 2.55 mmol/L), ionized calcium of 0.87 (normal range 1.11 to 1.30 mmol/L), and 24-hour urine calcium excretion of 9.16 mmol (normal range female The team screened the girl for celiac disease with antigliadin immunoglobulin A, anti-tissue transglutaminase, and anti-endomysial immunoglobulin A antibodies. All tests were positive. The girl underwent a duodenal biopsy, which showed lymphocyte infiltration, crypt hyperplasia, and villous atrophy compatible with celiac disease grade IIIb according to the Marsh classification. Following her celiac diagnosis, the team conducted human leukocyte antigen typing, which provided a definite diagnosis of celiac disease. She was started on a gluten-free diet. Apparently, the girl did not follow a gluten-free diet, which caused a recurrence of carpal spasms. At 7 years of age, the girl showed signs of delayed psychophysical development. Although hypocalcemia is not uncommon in people with celiac disease, it is rare for hypocalcemic carpal spasm to be the first manifestation of the disease. Because of this, the doctors urge other physicians to consider the possibility of celiac disease in patients with repeated carpal spasms that seem to resist easy treatment. They indicate that celiac disease should be considered even in the absence of gastrointestinal symptoms, since hypocalcemia and carpal spasm may appear as the first symptoms of celiac disease, even in young children. Source: J Med Case Reports. 2017;11(252)
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Celiac.com 11/04/2016 - Patients in the earliest stages of celiac disease have TG2-autoantibodies present in serum and small-intestinal mucosa. Many suffer abdominal symptoms long before the development of villus atrophy. The classic small-bowel mucosal damage that marks celiac disease develops over time and in stages; from normal villi to inflammation and finally to villus atrophy with crypt hyperplasia. Previously, researchers have shown that intraperitoneal injections of sera from celiac patients or of purified immunoglobulin fraction into mice trigger a condition mimics early-stage celiac disease. Those same researchers recently set out to show whether re-combinantly produced, patient-derived TG2-targeted autoantibodies are alone sufficient to trigger such condition in immune-compromised mice. The research team included Suvi Kalliokoski, Victoria Ortín Piqueras, Rafael Frías, Ana-Marija Sulic, Juha A. E. Määttä, Niklas Kähkönen, Keijo Viiri, Heini Huhtala, Arja Pasternack, Kaija Laurila, Daniele Sblattero, Ilma R. Korponay-Szabó, Markku Mäki, Sergio Caja, Katri Kaukinen, Katri Lindfors. They are various affiliated with the Tampere Center for Child Health Research, the Tampere School of Health Sciences, the Department of Internal Medicine, with BioMediTech at Tampere University Hospital and School of Medicine at the University of Tampere in Tampere, Finland, with the Department of Equine and Small Animal Medicine, Faculty of Veterinary Medicine, and Department of Bacteriology and Immunology at the University of Helsinki in Helsinki, Finland, with the Central Animal Laboratory at the University of Turku in Turku, Finland, with the Comparative Medicine Karolinska Institutet in Stockholm, Sweden, with the Department of Life Sciences at the University of Trieste in Trieste, Italy, and with the Celiac Disease Center, Medical and Health Science Center, Heim Pál Children’s Hospital and Department of Pediatrics at the University of Debrecen in Debrecen, Hungary. Interestingly, mice injected with celiac patient TG2-antibodies showed changes to small-intestinal mucosa, increased lamina propria cellular infiltration and disease-specific autoantibodies in the small bowel, but did not show any clinical signs of celiac disease. Thus, celiac patient-derived TG2-specific autoantibodies seem to be enough to trigger small-bowel mucosal changes in mice, but probably not enough to trigger clinical features on their own. Triggering clinical celiac features likely requires other factors, such as other antibody populations implicated in celiac disease. Source: Amino Acids, pp 1–12. DOI: 10.1007/s00726-016-2306-0
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Celiac.com 06/20/2016 - Are there genetic correlations between PTSD and mental disorders or immune-related disorders? What role does genetics play in PTSD, if any? A team of researchers recently set out to discover genetic loci associated with the lifetime risk for PTSD in 2 groups from the Army Study to Assess Risk and Resilience in Service members (Army STARRS). The research team included Murray B. Stein, MD, MPH, Chia-Yen Chen, ScD; Robert J. Ursano, MD; Tianxi Cai, ScD; Joel Gelernter, MD; Steven G. Heeringa, PhD; Sonia Jain, PhD; Kevin P. Jensen, PhD; Adam X. Maihofer, MS; Colter Mitchell, PhD; Caroline M. Nievergelt, PhD; Matthew K. Nock, PhD; Benjamin M. Neale, PhD; Renato Polimanti, PhD; Stephan Ripke, MD5; Xiaoying Sun, MS; Michael L. Thomas, PhD; Qian Wang, PhD; Erin B. Ware, PhD; Susan Borja, PhD; Ronald C. Kessler, PhD; Jordan W. Smoller, MD, ScD; for the Army Study to Assess Risk and Resilience in Service-members (STARRS). They are variously affiliated with the Department of Psychiatry, and the Department of Family Medicine and Public Health, UCSD, La Jolla, the Psychiatry Service of the Veterans Affairs San Diego Healthcare System, San Diego, California, the Department of Psychiatry at Massachusetts General Hospital and Harvard Medical School, Boston, the Stanley Center for Psychiatric Research, Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, the Department of Psychiatry, Uniformed Services University of the Health Sciences in Bethesda, Maryland, the Harvard T. H. Chan School of Public Health, Boston, Massachusetts, the Department of Psychiatry, Genetics, and Neurobiology at Yale University in New Haven, Connecticut, the Institute for Social Research, University of Michigan, Ann Arbor, the Department of Psychology, Harvard University, Cambridge, Massachusetts, the Department of Computational Biology and Bioinformatics, Graduate School of Arts and Sciences at Yale University, New Haven, Connecticut, the National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, and with the Department of Health Care Policy, Harvard Medical School, Boston, Massachusetts The study looked at subjects from two coordinated genome-wide association studies of mental health in the US military. The first study, the New Soldier Study (NSS), included 3,167 unique patients with PTSD and 4,607 trauma-exposed control subjects. The NSS data were collected from February 1, 2011, to November 30, 2012. The second study, the Pre/Post Deployment Study (PPDS), included 947 unique patients with PTSD and 4,969 trauma-exposed control subjects. The PDDS data were collected from January 9 to April 30, 2012. The primary analysis compared lifetime DSM-IV PTSD cases with trauma-exposed controls without lifetime PTSD. Data were analyzed from March 18 to December 27, 2015. The team used logistic regression models to conduct association analyses for PTSD among European, African, and Latino Americans by study, followed by meta-analysis. They also estimated heritability, genetic correlation and pleiotropy with other psychiatric and immune-related disorders. The NSS population of 7,774 patients was just over 80% male, and about 21 years old, while the PPDS population of 5,916 patients was 94.4% male, and about 26.5 years old. A genome-wide significant locus was found in ANKRD55 on chromosome 5 (rs159572; odds ratio [OR], 1.62; 95% CI, 1.37-1.92; P = 2.34 × 10−8) and persisted after adjustment for cumulative trauma exposure (adjusted OR, 1.64; 95% CI, 1.39-1.95; P = 1.18 × 10−8) in the African American samples from the NSS. They also found a genome-wide significant locus in or near ZNF626 on chromosome 19 (rs11085374; OR, 0.77; 95% CI, 0.70-0.85; P = 4.59 × 10−8) in the European American samples from the NSS. They did not find any similar results for either single-nucleotide polymorphism in the corresponding ancestry group from the PPDS sample, in other ancestral groups, or in transancestral meta-analyses. Overall, they saw no significant evidence for single-nucleotide polymorphism–based heritability, and they found no significant genetic correlations between PTSD and 6 mental disorders or 9 immune-related disorders. They did find significant evidence of a single-gene linking PTSD and rheumatoid arthritis and, to a lesser extent, psoriasis. Beyond that, they didn't find not much to support any connection to specific gene locations. The researchers are calling for additional studies "to replicate the genome-wide significant association with ANKRD55—associated in prior research with several autoimmune and inflammatory disorders—and to clarify the nature of the genetic overlap observed between PTSD and rheumatoid arthritis and psoriasis." Source: JAMA Psychiatry. Published online May 11, 2016. doi:10.1001/jamapsychiatry.2016.0350
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