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Celiac.com 10/25/2016 - The 504 Plan stems from Section 504 of the Rehabilitation Act of 1973. This section prevents discrimination against public school students in grades kindergarten through 12 because of disabilities. A 504 plan is meant to "remove barriers" to learning by providing a specific outline on how to make accommodations or modifications on a student-by-student basis. The Rehabilitation Act of 1973 applies to all institutions receiving federal financial assistance, such as public schools. Under this law, public schools must provide a free, appropriate public education and not discriminate against disabled students. This law acknowledges that the disability may not require special education services, but a plan is needed to ensure the student receives an appropriate education accommodating the disability within the classroom. This law must accommodate a special diet, including the gluten-free diet for children with celiac disease. The decision to enroll in the 504 plan is entirely up to you as a parent or guardian. Some parents find that informal discussions and accommodations have been sufficient for having the child's needs met at school. However, having a formal 504 plan in place is valuable, especially as teachers and staffing may change. The 504 plan guarantees by law that your child's needs are met throughout their school career and not just in certain classrooms. You can choose to utilize your 504 plan accommodations any time, and having them in place before you need them can save important time and resources. It can be helpful if your child develops symptoms from gluten exposure, or if you are having trouble with consistent accountability. How to Start Your 504 Plan First you need to contact your child's school. The 504 plan team should include: Primary classroom teacher School counselor or psychologist School nurse Director of food services 504 plan coordinator You will also need a doctor's note to show that your child has been formally diagnosed with celiac disease or non-celiac gluten sensitivity (gluten sensitivity). This note should outline the accommodations required to maintain your child's health, enabling him or her to have equal access to public education. Having a 504 plan in place will also make it much easier to apply for disability accommodation in college. What Information is Included in a 504 Plan? Generally you'll need to provide information about your child's diagnosis and needs including: Year of diagnosis Amount of time on a gluten-free diet Details on why a 504 plan is needed (including how a restricted diet affects a major life activity) Child's developmental level and needs (are they self-reliant in managing the diet? do they need strict supervision? Etc.) A 504 PLAN will specifically outline all of the details of how our child's celiac disease needs to be managed in the classroom. For example you and the 503 plan team can develop an action plan for: Navigating school lunches Snacks Birthday Parties Art Classes Field Trips Holiday Parties I wish that this 504 Plan was available when my son attended school! Do not forget to check your school's ruling on peanut butter. A lot of schools will not allow lunches to contain peanut butter because of severe peanut allergies, and we need to be respectful of other food allergies as we sort through the maze of gluten-free lunch packing. If you have a picky eater or a child who needs to gain weight after their diagnosis, nutritional shakes, power bars and calorie powders can pack a punch. Make sure they are labeled gluten-free. Consult with a registered dietitian to help with your child's meal plan. When you find a winning combo, send enough with your child to share. That will show your child's peers that gluten-free food is not "weird" and your child will have the opportunity to feel part of the group. Recently, the U.S. Department of Agriculture (USDA) mandated that food service workers who manage and handle meals would need to complete education and training requirements in order to maintain their positions. The requirement to maintain professional standards education, which is required by the Healthy, Hunger-Free Kids Act, went into effect on July 1, 2015. Completion of the GREAT Schools program helps school nutrition professionals meet this requirement. You can remind your child's school that completing the GREAT Schools training program does benefit both your child and the cafeteria staff in maintaining the necessary education to work in school food service Additional Resources: BeyondCeliac.org allergicliving.com Understood.org -
Celiac.com 05/13/2013 - Intestinal absorption capacity is currently regarded as the best way to assess overall digestive intestinal function. Earlier reference values for intestinal function in healthy Dutch adults were based on a study that was conducted in an inpatient metabolic unit setting in a relatively small series. A team of researchers recently used bomb calorimetry to measure normative values of intestinal absorption in healthy ambulant adults. The research team included N. J. Wierdsma, J. H. C. Peters, M. A. E. van Bokhorst-de van der Schueren, C. J. J. Mulder, I. Metgod & A. A. van Bodegraven They are variously affiliated with the Department of Nutrition and Dietetics, the Department of Gastroenterology, Small Bowel Unit, and the Department of Clinical Chemical Laboratory at VU University Medical Centre in Amsterdam, and the Department of Gastroenterology and Hepatology of Red Cross Hospital in Beverwijk, The Netherlands. The present study aimed to readdress and describe the intestinal absorption capacity of healthy adults, who were consuming their usual (Western European) food and beverage diet, in a standard ambulatory setting. The researchers evaluated twenty-three healthy subjects, ranging form 22–60 years old, using a 4-day nutritional diary to determine levels of nutritional intake (energy and macronutrients). They then collected fecal samples over three days to measure mean fecal losses of energy (by bomb calorimetry), fat, protein and carbohydrate. Finally, they calculated intestinal absorption capacity by determining the differences between intake and losses. They found that average (SD) daily feces production was 141 grams, of which, 49 grams (29%) was dry weight, Overall, the samples contained 891 (276) kJ [10.7 (1.3) kJ g1 wet feces; 22.6 (2.5) kJ g1 dry feces], 5.2 (2.2) g fat, 10.0 (3.8) g protein and 29.7 (11.7) g carbohydrates. Mean (SD) intestinal absorption capacity of healthy subjects was 89.4% (3.8%) for energy, 92.5% (3.7%) for fat, 86.9% (6.4%) for protein and 87.3% (6.6%) for carbohydrates. They found that average intestinal energy absorption was approximately 90%. These data serve as normative values for both stool nutrient composition and intestinal energy and macronutrient absorption in healthy adults on a regular Dutch diet in an ambulatory setting. Source: J Hum Nutr Diet. doi:10.1111/jhn.12113 -
Celiac.com 04/18/2011 - In an effort to improve diagnosis of celiac disease in patients already on a gluten-free diet, a team of researchers recently evaluated HLA-DQ2-gliadin tetramers for detection of gluten-specific T cells in peripheral blood and histological changes in the duodenum after a short gluten challenge as a diagnostic tool. The study team included Margit Brottveit MD, Melinda Ráki MD, PhD, Elin Bergseng MScPharm, PhD, Lars-Egil Fallang MSc, PhD, Bjørg Simonsen BLS, Astrid Løvik MSc, Stig Larsen MSc, PhD, Else Marit Løberg MD, PhD, Frode L Jahnsen MD, PhD, Ludvig M Sollid MD, PhD, and Knut EA Lundin MD, PhD. They are associated variously with the Department of Gastroenterology, the Department of Medicine, and the Department of Pathology at Oslo University Hospital in Ullevål, Norway, the Centre for Immune Regulation at the Institute of Immunology at the University of Oslo and Oslo University Hospital, the Department of Pathology at Oslo University Hospital in Rikshospitalet, Norway, and the Norwegian School of Veterinary Medicine, Oslo, Norway. For their study, the team evaluated HLA-DQ2+ individuals on a gluten-free diet for at least 4 weeks. 35 patients had uncertain diagnosis, 13 patients had celiac disease, and 2 healthy subjects served as disease controls. The team challenged each participant with four slices of gluten-containing white bread per day for 3 days (d1–d3). The team took biopsy samples via esophagogastroduodenoscopy on d0 and d4, and scored the biopsies using Marsh criteria. On d0 and d4, team isolated peripheral blood celiac disease 4+ T cells, stained them with HLA-DQ2-gliadin peptide tetramers, and analyzed the results using flow cytometry. After the gluten challenge, 11 of the 13 celiac disease patients showed a positive tetramer test, while four of them also showed typical histological changes on biopsy. Of the 35 patients with uncertain celiac diagnosis, 3 were found to have celiac disease. Two of these three patients showed both positive tetramer stains and histological changes in biopsies after gluten challenge. Overall, the team found celiac disease in about ten percent of the group with self-prescribed gluten-free diet. From these results, the team concluded that tetramer staining for gluten-specific T cells is a sensitive method in detecting an immune response in celiac disease patients after a short gluten challenge. SOURCE: Am J Gastroenterol advance online publication 1 March 2011; doi: 10.1038/ajg.2011.23 -
Celiac.com 06/23/2010 - A team of researchers evaluated the possibility of diagnosing celiac disease using quantitative analysis of videocapsule endoscopy images. The team included Edward J. Ciaccioa, Christina A. Tennysonb, Suzanne K. Lewisb, Suneet, Krishnareddy, Govind Bhagat, and Peter H.R. Green. They are variously associated with the Department of Pharmacology, Department of Medicine, Department of Pathology, Columbia University College of Physicians and Surgeons in New York. Images taken with videocapsule endoscopy can be useful for diagnosing celiac disease, but their interpretation is highly subjective. Quantitative disease markers might help to determine the degree of villous atrophy and efficacy of treatment. The team gathered capsule endoscopy images from a group of 11 celiac patients with small bowel pathology, and from a group of 10 control patients. Images had a resolution of 576×576 pixels, with 256 grayscale tones, and a frame-rate of 2 s−1. The team measured over 10×10 pixel sub-images for pixel brightness and image texture. They then averaged the results for for 56×56 sub-images per frame. For each patient, the team took measurements at from five locations in the proximal to distal small intestine. At each location, they figured measurements using 200 consecutive image frames (100 s). For classification with a nonlinear discriminant function, they computed mean frame-to-frame pixel brightness, image texture, periodicity in brightness, and estimated wall motion or intestinal motility. By pooling the data, the team found that images from the celiac group showed greater texture than did images from control group (p < 0.001). Images from the celiac disease group exhibited more frame-to-frame brightness variation as well (p = 0.032). Celiac patients showed longer dominant period of brightness in celiacs (p = 0.001), which may indicate reduced motility. Markers for three-dimensional nonlinear classification of celiacs versus controls showed sensitivity of 92.7% and specificity of 93.5%. Both celiac patients and control subjects showed an approximately linear association between dominant period and small intestinal transit time (r2 = 0.42 and r2 =0 .55, respectively). The results show that videocapsule images can be used to reveal villous atrophy throughout the small intestine, and to distinguish individuals with celiac disease from individuals without mucosal atrophy. Source: Science Direct. doi:10.1016/j.cmpb.2010.02.005
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Celiac.com 02/24/2010 - Proper clinical diagnosis of celiac diseasestill relies on confirmation of histological evidence of villousatrophy via biopsy. Getting a good sample can sometimes be tricky. Ifhistological sections are not optimally oriented, then diagnosis may bemore difficult. As a result, doctors can sometimes fail to confirm theproper diagnosis. A team of researchers recently set out tostudy the viability of confirming histological evidence of villousatrophy in real time, during upper gastrointestinal endoscopy, in liveduodenal mucosa of patients with celiac disease, using endocytoscopy, anovel diagnostic technique allowing in vivo real-time visualization ofmucosa under 450x magnification. The research team included T. Matysiak-Budnik, E. Coron1, J.-F. Mosnier, M. Le Rhun1, H. Inoue,and J.-P. Galmiche. They are associated variously with the Institutdes Maladies de l'Appareil Digestif - INSERM U913, CIC 04 et Serviced'Hépato-Gastroentérologie, Hôtel Dieu, CHU de Nantes, France, theService d'Anatomie Pathologique, E.A. Biometadys, CHU de Nantes,France, and the Digestive Disease Center, Showa University NorthernYokohama Hospital, Japan The team studied sixteen subjects withclinically proven celiac disease, together with seven controls subjectswith no celiac disease. They took endocytoscopic images from multipleareas and then made a blind comparison against standard histology. Endocytoscopy revealed three distinct patterns of in vivo histology. First,in all controls and eight celiac disease patients (n = 15),endocytoscopy revealed the presence of normal-appearing, long, thinvilli, lined with clearly distinguishable surface epithelial cells,considered to be normal duodenal mucosa. Second, in four celiacdisease patients, endocytoscopy revealed the presence of thick,shortened villi, reflecting partial villous atrophy. Finally,in four celiac disease patients, endocytoscopy revealed the totalabsence of villi, along with the presence of enlarged crypt orifices,reflecting total villous atrophy. The team found solid agreement between endocytoscopy and standard histology in all 16 patients with celiac disease. Fromtheir results, they conclude that endocytoscopy permits live,real-time, noninvasive imaging and assessment of villous architecture,and looks to be a promising method for in vivo evaluation of duodenalmucosa in celiac disease. Source: Endoscopy: DOI: 10.1055/s-0029-12438
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A team of researchers recently to examine the design of new high affinity peptide ligands for HLA-DQ2 using a positional scanning peptide library. The research team included U. Jüse, Y. van de Wal, F. Koning, L. M. Sollid, B. Fleckenstein with the Centre for Immune Regulation, Institute of Immunology, Oslo University Hospital-Rikshospitalet, Oslo, Norway. HLA-DQ2 (DQA1*0501/DQB1*0201) is associated with several immune disorders including celiac disease, which results from an inappropriate T-cell response to gluten. Researchers hope that interference with peptide presentation by HLA-DQ2, perhaps through the use of of peptide blockers, might lead to new treatment strategy for such HLA associated disorders. For such strategies to work, it will be necessary to identify ligands that bind much better to HLA-DQ2 than the disease related epitopes. The team used a positional scanning nonapeptide library to determine the optimal amino acids for each position of the HLA-DQ2 binding frame. By combining the optimal residues in each position, the team was able to design high affinity binders to HLA-DQ2. Interestingly, the decapeptide with highest affinity was composed of the most favorable residues in each position. This sequence bound 50-fold better than the immunodominant gluten epitope DQ2-alpha-I-gliadin what makes it an interesting lead compound for the development of blockers. The correlation between measured and predicted affinities was poorer for some natural HLA-DQ2 ligands, but notably these peptides did not have optimal amino acids at all positions. The team's method offers a straightforward approach for developing high affinity binders to HLA class II molecules. Source: Hum Immunol. 2010 Jan 24.
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Celiac.com 10/02/2009 - A team of researchers led by Michelle M. Pietzak, M.D., of the University of Southern California Keck School of Medicine in Los Angeles, recently conducted a large-scale study to identify HLA-DQ haplotypes most connected with increased risk of celiac disease. Their results show that for people with elevated risk factors for celiac disease, it is in fact possible to stratify risk based on HLA-DQ genotype, according to results of the study published in the September issue of Clinical Gastroenterology and Hepatology. The research team analyzed blood samples from 10,191 subjects with elevated risk for celiac disease due to clear clinical symptoms, an affected family member, or the presence of other conditions associated with celiac disease. They found that eight major genotype groups commonly tested positive for anti-endomysial immunoglobulin A. They also noted a steady progression of elevated risk rising from 2.11 percent for DQ8 heterozygotes up to 28.28 percent for DQ2.2+DQ7.5 homozygotes. Additionally, they discovered that the relative risk for anti-endomysial immunoglobulin A positivity of DQ8 homozygous:heterozygous was about the same as DQ2 homozygous:DQ2.5 heterozygous samples, with an odds ratio of about 4.0 for each. Based on the results, the team concludes that the information might "further quantify the relationship between the expression of celiac disease-associated heterodimers and the occurrence of celiac disease, aid in characterizing previously indeterminate cases, and potentially avoid intestinal biopsies when used in combination with highly sensitive and specific serology." The add that "targeting these high-risk alleles might aid the design of peptide immuno-therapeutic strategies to augment the gluten-free diet." Prometheus Laboratories underwrote the study, and all study authors work or consult for the company. Source: Clinical Gastroenterology and Hepatology - September, 2009.
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Celiac.com 09/30/2009 - Are non-inflammatory gluten peptide analogs effective as biomarkers for celiac disease? Recent research indicates that they just might represent an effective new tool in the management of celiac disease. In the August 28th issue of Chemical Biology, a team of researchers from Stanford University's Department of Biochemistry issues a call for new tools to manage celiac disease, a lifelong immune disease of the small intestine. Non-inflammatory gluten peptide analogs may be one of the important new tools in that effort. The research team is made up of M. T. Bethune, M. Crespo-Bosque, E. Bergseng, K. Mazumdar, L. Doyle, K. Sestak, L. M. Sollid, and C. Khosla. They note that current drug trials are sparking a researchers to seek non-invasive biomarkers of gluten-induced intestinal change. They note also that they have synthesized and characterized non-inflammatory gluten peptide analogs in which Asn or His replace key Gln residues. As with their pro-inflammatory associates, these genetic markers resist gastrointestinal proteases, are susceptible to glutenases, and permeable across enterocyte barriers. In contrast with gluten peptides, however, the markers are not commonly acknowledged by transglutaminase, HLA-DQ2, or disease-specific T cells. In vitro and animal tests prove that the biomarkers can reveal shifts in intestinal permeability as well as glutenase-catalyzed gastric detoxification of gluten. As a result, they call for controlled clinical studies to assess the use of these peptides as markers for abnormal intestinal permeability in celiac patients and for the effectiveness of glutenase in clinical trial and treatment of celiac disease. Chem Biol. 2009 Aug 28;16(8):868-81.
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Celiac.com 01/11/2007 – Researchers in Finland have determined that many patients with untreated celiac disease show the presence of intestinal endomysial autoantibodies (EmA), even in the 10-20% of cases where their serum EmA is negative. The researchers also believe that the negative serum EmA test in these cases is an indication of more advanced and long-standing celiac disease. Normally positive serum EmA is close to 100% accurate, however there is a subset of around 10-20% of patients where the test is negative even though they do have the disease. Dr. Katri Kaukinen and colleagues at the University of Tampere looked at 177 celiac disease patients and found that 22 were serum EmA-negative. A common theme among the 22 serum EmA-negative patients was that they were older and had more abdominal symptoms and other complications that indicated a more advanced stage of celiac disease than their serum EmA-positive counterparts. The research team found that even though the EmA antibodies could not be detected in the blood of these 22 patients, they could be detected in the small bowel mucosa in all of them, and none were detected in 20 control patients. Dr. Kaukinen and colleagues believe that the use of intestinal EmA antibody detection should be used in seronegative individuals who are suspected to have celiac disease. This study further supports Dr. Kenneth Fines use of IgA antigliadin antibodies in the stool to detect gluten sensitivity, and one has to wonder if the EmA antibodies, if detectable in the small bowel mucosa, would not also be detectable in the patient’s stool, and if so would that not be a much better and more cost-effective way to perform such a screening? Gut 2006;55:1746-1753. -
Celiac.com 02/25/2005 - Today a team of scientists at Alba Therapeutics Corporation and the University of Maryland School of Medicine report a direct link between zonulin-mediated increased intestinal permeability and Type 1 Diabetes (T1D) in the BB/wor Rat Model of Diabetes. Even more remarkable, the investigators were able to successfully prevent the onset of the autoimmune destruction of pancreatic beta cells and the onset of T1D in these animals by using the specific zonulin blocker AT-1001. Daily, oral administration of the drug beginning before the onset of auto-immunity in the diabetic prone rats cut the incidence of the disease by 2/3, and completely blocked the development of autoimmune antibodies in the treatment responders. Published in the latest issue of the Proceedings of the National Academy of Science (PNAS), these results constitute the first successful result in preventing the autoimmune process characteristic of T1D by blocking the zonulin-mediated abnormal intestinal permeability. These results go well beyond the development of a prevention strategy for T1D, says Dr. Alessio Fasano, lead author of the paper and Professor of Pediatrics, Medicine and Physiology and The University of Maryland School of Medicine. They open a new field of investigation in which the interplay between host and environment at the mucosal level may help us understanding the molecular basis of many diseases. These results reinforce our conviction that the zonulin pathway provides a roadmap for the discovery and development of innovative products to treat many important diseases, including diabetes, in ways previously thought to be inconceivable stated Dr. Blake M. Paterson. These preclinical proof-of-concept results with AT-1001 support the salvaging of beta cell function in pre-diabetics or in new-onset diabetes, giving us the impetus to rapidly move through the development process, bringing this dream to a reality for treatment in the diabetes community. T1D is an autoimmune disease that results in the destruction of the insulin producing cells of the pancreas, the islet beta cells. Current treatment of T1D is limited to the administration of insulin and other medications to treat the consequence of diabetes, elevated blood sugar and the complications thereof. The inability to treat the cause of T1D - a process known as autoimmunity, in which the bodys immune system attacks the beta cells of the pancreas - has been the key obstacle to the freeing patients from the yoke of this disease. Autoimmune diseases are thought to occur in individuals with the genetic pre-disposition to attack and destroy various organ tissues by the bodys own immune system. This immune misrecognition is thought to be triggered by the presence of an environmental stimulus; in the case of T1D, the trigger is unknown. While the majority of research efforts have focused on identifying the trigger of T1D and modifying immune pathways, little is known about how such a trigger might enter the body and about how such an entry-way might serve as a target for the treatment of the disease. The discovery of zonulin - a gatekeeper of intestinal barrier function, and its involvement in celiac disease, led to the hypothesis that its malfunction could be involved in a series of other autoimmune diseases characterized by a leaky gut, including T1D. Previous work by Dr. Alessio Fasano has shown a close association of celiac disease in children at risk of developing T1D and led to the novel discovery research in support of AT-1001. About Alba: Alba Therapeutics is a Baltimore based biopharmaceutical company dedicated to commercializing disease-modifying therapeutics and drug delivery adjuvants based on the zonulin pathway. Albas lead molecule, AT-1001, is targeted towards the treatment of Celiac Disease and Type 1 Diabetes and is in the final stages of pre-human testing. Contact Alba Therapeutics Corporation, Baltimore Dr. Blake Paterson, 410-522-8708
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