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Showing results for tags 'celiac-associated'.
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Celiac.com 06/03/2013 - Thrombophilias are defined as a group of inherited or acquired disorders that increase a person’s risk of developing thrombosis (abnormal “blood clotting”) in the veins or arteries. People with celiac disease may present with thromboembolic features that have multiple contributing factors, such as hyperhomocysteinemia, B12 andor folate deficiency, methylenetetrahydrofolate reductase mutations, and protein C and S deficiency due to vitamin K deficiency. However, there has been no research into how the well known thrombogenic factors, antiphosphatidylserine/prothrombin and antiprothrombin relate to celiac disease. A team of researchers recently studied the thrombophilic network of autoantibodies in celiac disease. The research team included Aaron Lerner1, Nancy Agmon-Levin, Yinon Shapira, Boris Gilburd, Sandra Reuter, Idit Lavi and Yehuda Shoenfeld. They are variously affiliated with Epidemiology and Community Medicine, and the Pediatric Gastroenterology and Nutrition Unit in the Carmel Medical Center of the B. Rappaport School of Medicine at the Technion-Israel institute of Technology in Haifa, Israel, with the Zabludowicz Center for Autoimmune Diseases at Sheba Medical Center in Tel-Ashomer, Israel, and with Aira e.v./Aesku.Kipp Institute in Wendelsheim, Germany. For their study, the team assessed blood autoantibody levels in 248 people, and then classified them into one of three groups. Group 1 included 70 children with confirmed celiac disease. They averaged 7.04 years of age (±4.3 years), with a male to female ratio of 1.06 to 1. Group 2 was a healthy control group that included 88 children, averaging 6.7 years of age (±4.17 years), with a male to female ratio 0.87 to 1. The team then compared the pediatric population to group 3, which included 90 adults who were family members (parents) of group 1 (age: 34.6 ±11.35 years, male to female ratio 1.2). The check antibodies using enzyme-linked immunosorbent assay. Results showed average optical density levels of serum antiphosphatidylserine/prothrombin immunoglobulin G antibodies of 32.4 ±19.4, 3.6 ±2.5 and 16.1 ±15.8 absorbance units in groups 1, 2 and 3 respectively (P less than 0.0001), with 45.7%, 0% and 7.8% of groups 1, 2 and 3 respectively positive for the antibody (P less than 0.01). Average optical density levels of serum antiphosphatidylserine/prothrombin immunoglobulin M antibodies were 14.2 ±8.7, 6.7 ±6.4 and 12.4 ±15.5 absorbance units in groups 1, 2 and 3 respectively (P less than 0.0001), with 7.1%, 3.4% and 9.9% of groups 1, 2 and 3 positive for the antibody. Average optical density levels of serum antiprothrombin and antiphospholipid immunoglobulin G antibodies were higher in groups 1 and 3 compared with 2 (P less than 0.005) and in groups 1 and 2 compared with 3 (P less than 0.01), respectively. Groups 1, 2 and 3 tested positive for antiphospholipid immunoglobulin G antibodies (groups 1 and 2 compared with 3) . Celiac disease blood samples contain a higher antiprothrombin immunoglobulin G level compared with controls. These results suggest that increased exposure of phospholipids or new epitopes representing autoantigens have their origins in the intestinal injury, endothelial dysfunction, platelet abnormality and enhanced apoptosis recently described in celiac disease. Those autoantibodies might play a pathogenic role in celiac-associated thrombophilia, and may also make good targets for possible preventive anticoagulant therapy. Source: BMC Medicine 2013, 11:89. doi:10.1186/1741-7015-11-89 -
Celiac.com 01/05/2017 - Patients who have both pancreatic disease and celiac disease can experience adverse endocrine and exocrine changes. When this happens, severe clinical changes with marked nutritional alteration may result. For some patients, a gluten-free diet can help improve endocrine and exocrine pancreatic function. Also, numerous studies show that people with celiac disease have higher rates of type 1 diabetes mellitus. In part, this relationship was possibly due to shared human leukocyte antigen alleles, DR3, and by linkage disequilibrium, DQ2. Besides this hypothesized common "immune-mediated" etiopathogenesis, some celiacs with pancreatic disease likely have developed secondary diabetic changes from severe exocrine pancreatic failure, driven in part by celiac-induced protein malnutrition. Some researchers estimate that more than one in five celiac patients have defective pancreatic function, possibly due to impaired release of peptides, because of mucosal endocrine cell loss. Researcher Hugh J. Freeman recently set out to evaluate the prevalence of type 1 diabetes in celiac disease. He is a gastroenterologist affiliated with the Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Prospective studies using an initial screening IgA tissue transglutaminase antibody assay (tTG) were done at the university center, while a total of 125 male and 108 female children and adolescents with type 1 diabetes mellitus were evaluated from an established pediatric diabetes clinic. Of these, 15 male and 11 female patients had elevated tTG titers, of whom 19 were also positive for endomysial antibodies. Among these cases, 1 was already known to have celiac disease. Small intestinal biopsies were done in the other 18 children positive for both antibodies. In all, histopathological changes consistent with celiac disease were detected, ranging from increased numbers of intraepithelial lymphocytes to severe crypt hyperplastic villous atrophy (i.e., so-called Marsh 3 lesion). Studies also suggested that serial tTG titers in insulin-dependent diabetic children might play a useful clinical role in monitoring compliance to a gluten-free diet, possibly of value since close monitoring of compliance of children to a gluten-free diet may be exceedingly difficult. In this study, over 40% of diabetic children were asymptomatic, and yet, prospective serological screening facilitated selection for small intestinal biopsy evaluation. Overall, 7.7% of this entire pediatric patient population had biopsy features common in celiac disease. A subsequent European study found 8.6% of diabetic children and adolescents to have tTG positivity; many had no symptoms, or only non-specific or mild gastrointestinal symptoms. Prior studies have shown increased serum amylase levels in about 25% of patients, indicating possible low-grade pancreatic inflammation. Later studies examined exocrine pancreatic function in celiac disease by measuring fecal elastase-1 concentrations along with magnetic resonance imaging (MRI) showed pancreatic insufficiency in 4 of 90 celiacs, or 4.4% (1 mild, 3 severe), while MRI was normal in all 4 of these celiac patients. In contrast, a study from India shows exocrine pancreatic insufficiency in 10 of 36 young adults under 30 years of age, based on fecal elastase determinations. Of these, over 80% showed reversal of elevated fecal elastase values on a gluten-free diet. Most had moderate to severely abnormal small bowel biopsies (i.e., Marsh 2-3C) and only 1 had recurrent bouts of acute pancreatitis. Structural changes based on imaging studies were rarely encountered. Although his own study, like a number of others, has documented the relationship between pancreatic exocrine function and celiac disease, Dr. Freeman calls for further longer-term study to determine if these observations can be verified by other centers. Source: Ann Gastroenterol. 2016 Jul-Sep; 29(3): 241–242. Published online 2016 May 20. doi: 10.20524/aog.2016.0048 PMCID: PMC4923808 -
Celiac.com 02/18/2015 - It's well documented that HLA-DQ molecules play a role in the pathogenesis of celiac disease through the presentation of gluten peptides to CD4(+) T cells. The α- or β-chain sharing HLA molecules DQ2.5, DQ2.2, and DQ7.5 display different risks for the disease. Researchers have recently showed that T cells of DQ2.5 and DQ2.2 patients recognize distinct sets of gluten epitopes, which indicates that these two DQ2 variants select different peptides for display. To figure out if this is the case, the research team performed a comprehensive comparison of the endogenous self-peptides bound to HLA-DQ molecules of B-lymphoblastoid cell lines. The research team included E. Bergseng, S. Dørum, M. Arntzen, M. Nielsen, S. Nygård, S. Buus, G.A. de Souza, and L.M. Sollid. They are variously affiliated with the Centre for Immune Regulation, Department of Immunology, University of Oslo and Oslo University Hospital-Rikshospitalet, Oslo, Norway. The team began by isolating peptides from affinity-purified HLA molecules of nine cell lines. They then subjected the isolated peptides to quadrupole orbitrap mass spectrometry and MaxQuant software analysis. They identified 12,712 endogenous peptides at very different relative abundances. Hierarchical clustering of normalized quantitative data revealed significant differences in repertoires of peptides between the three DQ variant molecules. They identified peptide-binding motifs using the neural network-based method, NNAlign. The binding motifs of DQ2.5 and DQ7.5 concurred with previously established binding motifs, but the binding motif of DQ2.2 was remarkably different from that of DQ2.5, with position, P3 being a major anchor having a preference for threonine and serine. This is interesting for the reason that three recently identified epitopes of gluten recognized by T cells of DQ2.2 celiac patients harbor serine at position P3. This study shows that relative quantitative comparison of endogenous peptides sampled from our protein metabolism by HLA molecules can provide clues to understand HLA association with disease. Source: Immunogenetics. 2015 Feb;67(2):73-84. doi: 10.1007/s00251-014-0819-9. Epub 2014 Dec 12.
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Celiac.com 10/30/2007 - Many studies over the years have supported the idea that celiac disease is a permanent condition, and that those who strayed from the strict gluten-free diet that forms the core of celiac treatment risked relapsing and suffering the telltale intestinal damage associated with celiac disease. However, it was generally assumed that symptoms of celiac disease and associated intestinal degradation occurred within two years of reintroducing gluten back into the diet. The medical journal GUT recently published a paper by Matysiak-Budnik et al. concerning the natural history of celiac disease, which indicates that classic celiac damage to the intestinal lining may take years or decades to develop in some cases. A team of researchers looked at 61 adults who had been diagnosed with celiac disease as children, and who felt themselves to be asymptomatic for anywhere from 3 to 21 years, with a group average of 11 years. An exam revealed that 48 of the 61 test subjects indeed showed villous atrophy with crypt hypoplasia. The 13 other patients showed no celiac-associated intestinal damage. Strangely, 2 of the 13 patients with no signs of damage had showed such damage a short time after gluten was reintroduced into their diets, only to return to normal as they continued to consume gluten. From this, the researchers concluded that some people might actually become truly latent and tolerate gluten with no adverse effects. It’s also possible that such people actually still have celiac disease and that the intestinal damage has yet to recur, as villous atrophy occurs only at the tail end of celiac disease. In fact, delayed relapse of celiac disease after gluten reintroduction supports the notion that people with normal mucosa may in fact have celiac disease. Still, it is highly uncommon for patients with celiac disease to show no clinical symptoms on a long-term gluten-inclusive diet. The level of celiac disease+ intraepithelial lymphocytes has proven to be more useful than mucosal Marsh Type 1 lymphocytes in revealing early developing celiac disease in such cases and in general. Reliable diagnosis of celiac disease is important, as untreated celiac disease carries a broad range of associated risks including markedly higher rates of certain cancers. A recent study also suggests celiac disease may also adversely impact both the peripheral the central nervous systems. However, regarding the 13 asymptomatic patients, the original diagnosis of celiac would seem to be accurate in each case, as each had celiac-type HLA, either HLA DQ2 or DQ8, and their follow-up exam results showed that 5 of those patients had positive serum antibody results and higher densities of small bowel mucosa celiac disease+ and CD3+ intraepithelial lymphocytes than did the non-celiac control groups. Two of the 13 patients developed symptoms of a relapse during the follow-up. The study team concluded that the “2 year rule” for reintroducing gluten is invalid and supports the view that celiac disease exists beyond villous atrophy. As villous atrophy of the small intestine is only one manifestation of genetic gluten intolerance, and that the present diagnostic guidelines based on mucosal damage and ignoring early developing celiac disease and dermatitis herpetiformis is only one incarnation of celiac disease. GUT 2007; 56:1339-1340 Katri Kaukinen, Pekka Collin, Medical School, University of Tampere and Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, Tampere, Finland Markku Ma¨ki, Medical School, University of Tampere and Department of Paediatrics, Tampere University Hospital, Tampere, Finland
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