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Found 12 results

  1. Celiac.com 04/14/2014 - Exposure to stressful stimuli, such as inflammation, cause cells to up-regulate heat shock proteins (Hsp), which are highly conserved immunomodulatory molecules. Research points to Hsp involvement in numerous autoimmune diseases, including autoimmune bullous diseases and celiac disease. To better understand the role of Hsp in autoimmune bullous diseases, a research team conducted the first investigation of the humoral autoimmune response to Hsp40, Hsp60, Hsp70, and Hsp90 in patients with dermatitis herpetiformis (DH; n = 26), bullous pemphigoid (BP; n = 23), and pemphigus vulgaris (PV; n = 16), the first representing a cutaneous manifestation of celiac disease. The research team included Kasperkiewicz M1, Tukaj S, Gembicki AJ, Silló P, Görög A, Zillikens D, Kárpáti S. They are affiliated with the Department of Dermatology at the University of Lübeck in Lübeck, Germany. In patients with active BP and PV, serum levels of autoantibodies against these Hsp matched the healthy control subjects (n = 9-14), while circulating autoantibodies against Hsp60, Hsp70, and Hsp90 increased at the active disease stage of DH. Further analysis showed that in patients who adopt a gluten-free diet, these anti-Hsp autoantibodies decreased in relation to serum autoantibodies against epidermal and tissue transglutaminase during remission of skin lesions. Larger groups of patients must be studied to confirm these findings, but these results indicate that autoantibodies against Hsp60, Hsp70, and Hsp90 play a key role in the development and maintenance of DH, possibly also in the underlying celiac disease, and may be important in potentially undiscovered disease biomarkers. Source: Cell Stress Chaperones. 2014 Mar 19.
  2. Celiac.com 11/01/2012 - Although most instances of gluten sensitivity manifest as a chronic, autoimmune disorder of the small intestine (celiac disease), around 10% of gluten sensitive patients suffer neurological symptoms. Usually these neurological symptoms accompany the more common intestinal issues, but some patients exhibit neurological symptoms exclusively. For this reason, it is thought that gluten-related symptoms in different parts of the body could be the result of autoimmune reactions to different members of the transglutaminase gene family. A recent lab study suggests that neurological gluten-related symptoms could be the result of an immune reaction to a particular neuronal enzyme known as TG6, and that this reaction occurs separate from other autoimmune reactions to gluten. Sera were collected from 6 groups: 20 newly diagnosed celiac disease patients (pre gluten-free diet) with no neurological symptoms, 34 gluten ataxia patients who tested positive for anti-gliadin antibodies, 17 peripheral idiopathic neuropathy patients, also positive for anti-gliadin antibodies, a control group of 18 genetic (non-gluten related) ataxia patients or individuals with clear family history of ataxia, a second control group of 14 patients with various immune-mediated but gluten-unrelated diseases and a third control group of 19 healthy individuals. Sera were tested through a series of protein analyses and enzyme-linked immunosorbent assays. In the celiac disease group, 18 of 20 patients tested positive for the TG2 autoantibody, with the remaining two testing postive for the TG3 or TG6 autoantibodies. 55% of celiac disease patients had multiple transglutaminase autoantibodies: 45% of all celiac disease patients had antibodies for both TG2 and TG3, 45% had antibodies for both TG2 and TG6, and 35% had antibodies for TG2, TG3 and TG6. Gluten ataxia patients were separated into two groups: those with intestinal symptoms (group GAE), and those without (group GAo). TG2 autoantibodies correlated well with intestinal symptoms: 12 of 15 in the GAE group tested positive for TG2 autoantibodies, while only 1 of 19 in the GAo group tested positive for them. TG3 autoantibody results were similar: group GAE results were comparable to the celiac disease group, while group GAo was no different from the control groups. In contrast, both gluten ataxia groups had similar results for TG6 autoantibodies. Overall prevalence of TG6 autoantibodies in the gluten ataxia group was 62%, compared to 45% in the celiac disease group. Inhibition studies showed that in group GAE (gluten ataxia with intestinal symptoms), autoantibodies reacted separately from one another, with TG2 and TG6 autoantibodies reacting independently of one another to their respective TG isozymes. This, along with the fact that some patients tested positive exclusively for TG6 would suggest that intestinal and neurological gluten-related symptoms are caused by separate immune reactions to different TG isozymes (TG2 and TG6, respectively). This is further supported by postmorten analysis of a gluten ataxia patient without intestinal symptoms, where TG6 deposits were found in the brain (TG6 could not be detected in a normal cerebellum). The findings of this study suggest that with more research, doctors may have another diagnostic tool in the form of TG6 autoantibody tests. This would help determine which patients with gluten sensitivity might be most at risk for developing neurological symptoms. Source: http://www.ncbi.nlm.nih.gov/pubmed/18825674
  3. 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
  4. Celiac.com 10/29/2012 - Celiac disease with epilepsy and cerebral calcifications, also known as CEC, is a rare form of celiac disease that is accompanied by occipital epilepsy. Past studies have suggested that the neurological symptoms could be the result of a folate deficiency, as folate levels are typically low in patients suffering from CEC. However, a recent case report indicates that as with other neurological gluten-related diseases (such as gluten ataxia), there may be some correlation between CEC and TG6 autoantibodies, indicating that the disease is autoimmune in nature. The case study focuses on a four year old boy who suffered from 30+ minute long complex partial seizures every two to three days. He was given antiepileptic drugs (carbamazepine, sodium valproate, levetiracetam), but these only slightly helped reduce seizure frequency. After one year, MRI and CT scans revealed bilateral occipital calcifications over parieto-occipital regions of the brain. The patient also suffered from chronic diarrhea: endoscopy and biopsy confirmed villous atrophy and patient tested positive for antibodies associated with celiac disease. His folate levels were also markedly low. After being placed on a gluten-free diet, the patient's symptoms, including seizures, cleared within two weeks. After the seizures had ceased, the patient was given folate supplements, and taken off antiepileptic drugs. Gluten challenge caused a relapse of all symptoms. At the time of the report, the patient had been gluten-free and seizure-free for 18 months, and showed improved behavior and reading and writing abilities. Because the patient responded so well to gluten-free diet treatment before being given folate supplements and all symptoms resumed during gluten challenge, it would seem that the neurological symptoms of CEC are the result of immune mechanisms rather than vitamin deficiencies or malabsorption. Most CEC patients have low folate levels; folate deficiency was previously thought to play a causative role in the disease, but this case study brings that conclusion into question. Furthermore, the patient tested positive for TG6 autoantibodies, which are associated with gluten ataxia (another gluten-related disease with neurological symptoms, which are an autoimmune response). More studies are required, but this case study suggests that gluten ataxia is not the only gluten-related disease with autoimmune neurological manifestations. Source: http://www.ncbi.nlm.nih.gov/pubmed/22845673
  5. Celiac.com 05/28/2012 - Two researchers recently conducted an assessment of the contribution of celiac disease autoantibodies to the disease process. The researchers were Katri Lindfors, of the Pediatric Research Center, University of Tampere & Tampere University Hospital and Katri Kaukinen, affiliated with both the School of Medicine, at the University of Tampere, and the Department of Gastroenterology & Alimentary Tract Surgery at Tampere University Hospital, both in Tampere, Finland. The protein transglutaminase 2 is a multifunctional protein that plays a role in cellular adhesion. Moreover, transglutaminase 2 has been identified as the auto-antigen in celiac disease, and in untreated celiac disease. In addition to being present in the serum, the transglutaminase 2-targeted autoantibodies are bound to their antigen in the basement membrane underlining the small-bowel mucosal epithelium. Furthermore, studies have shown that disease-specific transglutaminase 2-targeted autoantibodies have a range of biological effects on different cell types. By using Caco-2 intestinal epithelial cells, Lindfors and Kaukinen show that serum transglutaminase 2-targeted autoantibodies from untreated celiac patients inhibit the adhesion of these cells. These results offer an important direction for future research to improve the basic understanding of celiac disease pathogenesis, and especially how disease-specific autoantibodies function as the disease progresses. Source: Clin Immunol. 2012;8(2):151-154.
  6. Celiac.com 01/29/2010 - A team of researchers recently set out to compare levels of glutamic acid decarboxylase antibody (anti-GAD), islet cell antibody (ICA), thyroperoxidase antibody (anti-TPO), thyroglobulin antibody (anti-TG), antinuclear antibodies (FANA), antibodies to double-stranded DNA (anti-ds DNA), antibody to Sjögren syndrome A antigen (anti-SSA), antibody to Sjögren syndrome B antigen (anti-SSB), Smith antibody (anti-Sm), smooth muscle antibodies (ASMA), and antimitochondrial antibody liver-kidney microsome (AMA-LKM) in patients with celiac disease against healthy control subjects, and autoimmune hypothyroid patients. The research team included Erkan Caglar, Serdal Ugurlu, Aliye Ozenoglu, Gunay Can, Pinar Kadioglu, and Ahmet Dobrucali. They are affiliated variously with Fatih Sultan Mehmet Education and Research Hospital, the Cerrahpasa Medical Faculty at the University of Istanbul, and Ondokuz Mayis University in Samsun, Turkey. They studied a total of 31 patients with celiac disease, 34 patients with autoimmune hypothyroidism and 29 healthy subjects. The team used immunofluorescence to assess anti-SSA, anti-SSB, anti-Sm, anti-ds DNA, anti-GAD, anti-TPO and anti-TG were studied by Enzyme-Linked Immunosorbent Assay (ELISA), and AMA-LKM, ASMA, ANA and ICA. Researchers used retrospective analysis to assess clinical data and the results of free thyroxine-thyroid stimulating hormone (FT4-TSH). The team used SPSS ver 13.0 for data analysis, and the χ2 method for comparisons within groups. They found that the frequency of anti-SSA, anti-SSB, anti-GAD, anti-Sm, anti-ds DNA, AMA-LKM, ASMA, ANA and ICA did not differ significantly between the groups. They found levels of anti-TPO and anti-TG antibodies to be markedly higher (<0.001) in autoimmune hypothyroid patients as compared with other groups. Previous studies have shown an increased frequency of autoimmune diseases of other systems in people with celiac disease. Autoimmune antibodies specific for other autoimmune diseases appeared no more frequent in people with celiac disease. Source: U.S. National Library of Medicine, National Institutes of Health
  7. Celiac.com 12/03/2009 - Clinicians recently described a case of severe osteoporosis with high bone turnover, in which they found neutralizing autoantibodies against osteoprotegerin to be present. They also report finding autoantibodies against osteoprotegerin in three additional patients with celiac disease. The clinical team reporting the findings was made up of Philip L. Riches, M.R.C.P., Euan McRorie, F.R.C.P., William D. Fraser, Ph.D., F.R.C.Path., Catherine Determann, B.Med.Sci., Rob van’t Hof, Ph.D., and Stuart H. Ralston, M.D. They are associated with the Rheumatic Diseases Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh (P.L.R., E.M., C.D., R.H., S.H.R.); and the Unit of Clinical Chemistry, School of Clinical Sciences, University of Liverpool, Liverpool (W.D.F.) — both in the United Kingdom. The adult patient presented severe, high-turnover osteoporosis associated with subclinical celiac disease and autoimmune hypothyroidism. The clinicians found circulating autoantibodies against osteoprotegerin. Autoantibodies against osteoprotegerin block the inhibitory effect of osteoprotegerin on signaling by the receptor activator of nuclear factor (NF)-κB (RANK). The patient's osteoporosis did not respond to celiac disease treatment of a gluten-free diet, but completely reversed with bisphosphonate therapy. Immunoglobulins purified from specimens of the patient’s serum abolished the inhibitory effect of osteoprotegerin on RANKL-induced NF-κB signaling in vitro, while those from the control serum did not, which indicates the presence of neutralizing autoantibodies against osteoprotegerin. The clinicians used immunoprecipitation assay for osteoprotegerin on non-fasting patient serum samples at several points during the course of his illness, as well as from 10 age-matched healthy male controls, 15 patients with celiac disease, and 14 patients with autoimmune hypothyroidism. They used bicinchoninic acid assay to measure protein content. Serum samples from the 10 healthy controls and the 14 patients with autoimmune hypothyroidism showed no evidence of circulating autoantibodies against osteoprotegerin, while the serum samples from 3 of the 15 patients (20%) with celiac disease did show antibodies. Autoantibodies against osteoprotegerin may be connected to the development of high-turnover osteoporosis, but whether autoantibodies against osteoprotegerin contribute to the pathogenesis of osteoporosis in celiac disease patients remains unknown. Source: N Engl J Med 2009;361:1459-65.
  8. Celiac.com 09/24/2009 - Could a reduced level of antibodies against infectious agents indicate a protective role for such infections in T1DM development in susceptible individuals? Recent research points in that direction. Type 1 diabetes mellitus (T1DM) is an autoimmune disease with intricate and poorly understood associations between genetic and environmental factors. A joint Israeli-Colombian research team recently set out to examine the connections between anti-infectious antibodies and autoimmune-associated autoantibodies in patients with Type I diabetes mellitus and their close family members. Among other things, their findings confirmed a strong association between celiac disease and Type 1 diabetes mellitus. The research team was made up of Ilan Krause, Juan Manuel Anaya, Abigail Fraser, Ori Barzilai, Maya Ram, Verónica Abad, Alvaro Arango, Jorge García, and Yehuda Shoenfeld. The team compared levels of antibodies to numerous infectious agents and of autoimmune-associated antibodies between Colombian T1DM patients, their close family members and healthy control subjects. T1DM patients showed substantially reduced levels of antibodies against several infectious agents, including: cytomegalovirus (P= 0.001); Epstein-Barr virus (P= 0.02); Helicobacter pylori (P= 0.01); and Toxoplasma (P= 0.001). T1DM patients showed markedly elevated levels of IgG-anti-gliadin antibodies (P= 0.001) and IgG-antitissue transglutaminase antibodies (P= 0.03), and a marginal connection with anti-centromere antibodies (P= 0.06). T1DM patients also showed a reduced level of antibodies against infectious agents that may be associated with their younger ages, but could also indicate a protective role for such infections in T1DM development in susceptible individuals. The results reinforce the connection between T1DM and celiac disease, though the possible connection with the anti-centromere antibody requires a deeper examination. Studies like this are important to help build a record of all of the points of contact between these associated conditions so we can begin to understand the intricate web that ties these conditions together, and inch toward the deeper causes that lie at the heart of the mystery of celiac disease, diabetes, and so many other auto-immune/inflammatory disorders. Source: Annals of the New York Academy of Sciences - Volume 1173 Issue Contemporary Challenges in Autoimmunity, Pages 633 - 639
  9. Am J Gastroenterol 2000;95:1742-1748. Celiac.com 09/20/2000 - A new study published in the July issue of the American Journal of Gastroenterology by Dr. Vincenzo Toscano and colleagues at the Universita La Sapienza in Rome indicates that adolescent patients with celiac disease have elevated levels of anti-thyroid and anti-pancreatic autoantibodies. The results indicate that gluten plays a key role in the observed autoimmunity, and may in some cases result in organ dysfunction. Previous studies have shown that antibodies directed against endocrine glands develop in a high proportion of patients who have celiac disease. In many cases a gluten-free diet is abandoned by many patients in adolescence, and the researchers studied such a group to determine whether anti-endocrine antibodies and endocrine function were affected by the presence or absence of gluten. Their study indicates that 9 of 44 celiac disease patients tested positive for at least one anti-thyroid autoantibody. The same numbers of patients tested positive for anti-pancreatic autoantibodies. Additionally, one patient was diabetic, two others exhibited preclinical hypothyroidism, and one had clinical hypothyroidism. Further, 10 of 19 patients on a diet containing gluten were positive for at least one antibody, in comparison with five of 25 patients on the gluten-free diet, and the distribution of autoantibodies was significantly different between the two groups. Dr. Toscanos team concludes that gluten consumption is associated with a high prevalence of anti-endocrine autoantibodies.
  10. 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.
  11. Dig Dis Sci 2000;45:403-406. (Celiac.com 04/10/2000) Italian researcher Dr. Tarcisio Not, of Clinica Pediatrica, I.R.C.C.S., Trieste, and colleagues, have concluded that a relatively high percentage of patients with autoimmune thyroiditis also have celiac disease. They studied 172 patients who had autoimmune thyroid disorders, and two control groups. Their control groups were comprised of 498 patients with other diseases, and 4,000 healthy patients. The method used by the researchers was a blood test that looks for IgA-class endomysium antibodies using immunofluorescence. Their results, which were published in the February issue of Digestive Diseases and Sciences, show that the prevalence of celiac disease is 3.4% in patients with autoimmune thyroiditis, compared with 0.6% and 0.25% among the two control groups. They also found a connection between untreated celiac disease, gluten consumption, and autoimmune disorders. The researchers believe that undiagnosed celiac disease can cause other disorders by switching on some as yet unknown immunological mechanism. Untreated celiac patients produce organ-specific autoantibodies. Further, By following these subjects longitudinally, it has been seen that not only do the anti-gliadin antibodies and anti-endomysium antibodies disappear after 3 to 6 months of a gluten-free diet, but so do the organ-specific autoantibodies. In conclusion the Italian researchers suggest that patients with autoimmune thyroiditis could benefit from a screening for celiac disease, which could eliminate the symptoms and limit the risk of developing other autoimmune disorders.
  12. Mdki M, Hupponen T; Holm K, Hallstrom O, _Gut_ 1995; Feb 3692) pgs. 239-42 In a study of 238 children and adolescents with insulin dependent diabetes mellitus (IDDM), serum IgA reticulin antibody tests were performed once a year. During the initial testing, within one year of the onset of IDDM, 5 children (2%) were positive. During follow up, 11 of the antibody-negative children (5%) became positive; of these 9 were shown to have silent celiac disease by jejunal biopsies. This study suggests that repeated serological screening and biopsies should be considered to detect late developing, clinically silent celiac disease among patients with IDDM.
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