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Found 27 results

  1. Addisons Disease Alopecia Anxiety and Depression Ataxia Attention Deficit Disorder / ADHD Autism and Celiac Disease Autoimmune Hepatitis / Chronic Active Hepatitis Bird Fancieris Lung Brain White-Matter Lesions Cerebellar Atrophy Chronic Fatigue Syndrome (myalgic encephalomyelitis or ME, PVS, post viral fatigue syndrome or PVFS) Crohns Disease Congenital Heart Disease Cystic Fibrosis Dental-Enamel Hypoplasia Dyspepsia Epilepsy (with or without cerebral calcification) Farmeris Lung Fibromyalgia and Celiac Disease Fibrosing Alveolitis Follicular Keratosis Gall Bladder Disease Gastroparesis Head Aches (Migraine) IBD - Irritable Bowel Disease Impotency Infertility Inflammatory Bowel Disease Lung Cavities Multiple Sclerosis and Celiac Disease Myasthenia Gravis Pancreatic Disorders / Exocrine Pancreatic Insufficiency Peripheral Neuropathy Polymyositis Polyneuropathy Primary Biliary Cirrhosis Pulmonary Hemosiderosis Recurrent Pericarditis Sarcoidosis Schizophrenia / Mental Problems and Celiac Disease Scleroderma Short Stature, Delayed Puberty Small-Intestinal Adenocarcinomas Spontaneous Abortion and Fetal Growth Retardation Systemic Lupus Erythematosus Thrombocytosis (Hyposplenism) Thrombocytopenic Purpura (ITP) Thyrotoxicosis Vasculitis Vitamin K Deficiency
  2. Abdominal Distention (children) Abdominal Pain, Steatorrhea Anemia - Folate-Deficiency / Iron Deficiency / Pernicious Arthralgia or Arthropathy Arthritis - Rheumatoid Carcinoma of the Oropharynx, Esophagus, and Small Bowel Collagenous Sprue Dermatitis Herpetiformis Diabetes (Type 1) and Celiac Disease Diarrhea Down Syndrome Enteropathy-Associated T-cell Lymphoma Failure to Thrive (children) Hypertransaminasemia IBS - Irritable Bowel Syndrome IgA Deficiency IgA Nephropathy Kidney Disease Liver Disease Low Bone Mass and Celiac Disease Microscopic Colitis / Collagenous Colitis Nerve Disease and Celiac Disease Osteomalacia, Osteoporosis and Celiac Disease Recurrent Aphthous Stomatitis, Recurrent Refractory Sprue / Celiac Disease Sjogrens Syndrome Thyroid Disease (Autoimmune) Ulcerative Jejunoileitis
  3. Celiac.com 03/07/2018 - People with celiac disease can sometimes have hematological issues, including chronic anemia. It might be surprising to hear, but aplastic anemia and celiac disease share a similar underlying autoimmune process, but doctors haven't reported many cases that indicate that the two are connected. In fact, medical literature reveals only three pediatric cases indicating a connection. Recently, clinicians reported the first case in a female pediatric patient. The clinical team included Omar Irfan, Sana Mahmood, Heera Nand, and Gaffar Billoo, with the Medical College and the Department of Pediatrics at Aga Khan University Hospital in Karachi, Pakistan. Their team treated a 6-year-old South Asian girl who had bruises, petechiae, and recent history of loose stools. On evaluation, the team diagnosed the girl to have celiac disease and prescribed a gluten-free diet. Follow-up assessment including bone marrow biopsy showed the girl to have pancytopenia. The team managed the girl's condition with packed red cells, platelets, and diet restrictions, and the girl showed improving platelet counts over yearly follow up visits. Eventually, the girl will need a bone marrow transplant, and the team spoke about that to the girl's parents. This is now the fourth report indicating a connection between celiac disease and aplastic anemia in children, and the clinical team wonders if the connection might be more common than is currently understood. Timely treatment of celiac disease through strict gluten-free diet, or aplastic anemia through immunosuppressive therapy, could help reduce the development of other autoimmune conditions. Because all four pediatric cases reporting potential celiac disease/aplastic anemia association occurred in South East Asia, the authors suggest larger studies to explore this connection. Source: J Med Case Reports. 2018;12(16)
  4. Celiac.com 01/01/2018 - A team of researchers recently set out to conduct a genome-wide association study (GWAS) of general cognitive ability ("g"), further enhanced by combining results with a large-scale GWAS of educational attainment. The research team included Max Lam, Joey W. Trampush, Jin Yu, Emma Knowles, Gail Davies, David C. Liewald, John M. Starr, Srdjan Djurovic, Ingrid Melle, Kjetil Sundet, Andrea Christoforou, Ivar Reinvang, Pamela DeRosse, Astri J. Lundervold, Vidar M. Steen, Thomas Espeseth, Katri Räikkönen, Elisabeth Widen, Aarno Palotie, Johan G. Eriksson, Ina Giegling, Bettina Konte, Panos Roussos, Stella Giakoumaki, Katherine E. Burdick, Antony Payton, William Ollier, Ornit Chiba-Falek, Deborah K. Attix, Anna C. Need, Elizabeth T. Cirulli, Aristotle N. Voineskos, Nikos C. Stefanis, Dimitrios Avramopoulos, Alex Hatzimanolis, Dan E. Arking, Nikolaos Smyrnis, Robert M. Bilder, Nelson A. Freimer, Tyrone D. Cannon, Edythe London, Russell A. Poldrack, Fred W. Sabb, Eliza Congdon, Emily Drabant Conley, Matthew A. Scult, Dwight Dickinson, Richard E. Straub, Gary Donohoe, Derek Morris, Aiden Corvin, Michael Gill, Ahmad R. Hariri, Daniel R. Weinberger, Neil Pendleton, Panos Bitsios, Dan Rujescu, Jari Lahti, Stephanie Le Hellard, Matthew C. Keller, Ole A. Andreassen, Ian J. Deary, David C. Glahn, Anil K. Malhotra, and Todd Lencz. They are variously associated with the dozens of research facilities listed below. Their study provided a large-scale GWAS of cognitive performance, combined with GWAS of educational attainment; 70 independent genomic loci associated with individual differences in cognition. The study found that implicated genes suggest potential treatment targets for cognitive enhancement. The team also observed genetic overlap between cognitive ability and multiple health-related phenotypes. For their genome-wide association study (GWAS) of general cognitive ability ("g"), the team evaluated 107,207 subjects. They further enhanced their data pool by combining results with a large-scale GWAS of educational attainment. They also identified 70 independent genomic loci associated with general cognitive ability. Observing the outcomes, the team saw substantial enrichment for genes triggering Mendelian disorders with an intellectual disability phenotype. Analysis of competitive pathways pointed to neurogenesis and synaptic regulation, as well as the gene targets of two pharmacologic agents: cinnarizine, a T-type calcium channel blocker, and LY97241, a potassium channel inhibitor. According to the researchers: "we observed modest, yet nominally significant, inverse correlations between cognition and autoimmune diseases such as eczema and Crohn's disease, attaining Bonferroni significance for rheumatoid arthritis (rg for MTAG results = −0.2086; p = 1.60E−08). There was also a Bonferroni-significant positive genetic correlation with celiac disease (rg for MTAG results = 0.1922; p = 0.0001)." Full analysis of both the transcriptome and epigenome showed that the implicated loci were enriched for genes expressed across all brain regions; mostly in the cerebellum. Interestingly, only genes expressed in neurons were enriched, not those expressed in oligodendrocytes or astrocytes. Lastly, the team observed genetic correlations between cognitive ability and various phenotypes, including psychiatric disorders, autoimmune disorders, longevity, and maternal age at first birth. Source: Cell.com. DOI: http://dx.doi.org/10.1016/j.celrep.2017.11.028 The research team members are variously associated with the following: Campbell Family Mental Health Institute, Centre for Addiction and Mental Health, University of Toronto, Toronto, Canada Institute of Mental Health, Singapore, Singapore BrainWorkup, LLC, Los Angeles, CA, USA Institute for Behavioral Genetics, University of Colorado, Boulder, CO, USA Division of Psychiatry Research, Zucker Hillside Hospital, Glen Oaks, NY, USA Department of Psychiatry, Hofstra Northwell School of Medicine, Hempstead, NY, USA Center for Psychiatric Neuroscience, Feinstein Institute for Medical Research, Manhasset, NY, USA Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA Department of Genetics and Genomic Science and Institute for Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, USA Mental Illness Research, Education, and Clinical Center (VISN 2), James J. Peters VA Medical Center, Bronx, NY, USA Department of Neurology, Bryan Alzheimer's Disease Research Center and Center for Genomic and Computational Biology, Duke University Medical Center, Durham, NC, USA Department of Psychiatry and Behavioral Sciences, Division of Medical Psychology, Duke University Medical Center, Durham, NC, USA Laboratory of NeuroGenetics, Department of Psychology & Neuroscience, Duke University, Durham, NC, USA Human Longevity Inc., Durham, NC, USA Department of Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA Department of Psychology, Yale University, New Haven, CT, USA Department of Psychology, Stanford University, Palo Alto, CA, USA Clinical and Translational Neuroscience Branch, Intramural Research Program, National Institute of Mental Health, National Institute of Health, Bethesda, MD, USA Lieber Institute for Brain Development, Johns Hopkins University Medical Campus, Baltimore, MD, USA Neuroimaging, Cognition & Genomics (NICOG) Centre, School of Psychology and Discipline of Biochemistry, National University of Ireland, Galway, Ireland Neuropsychiatric Genetics Research Group, Department of Psychiatry and Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin, Ireland Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK Department of Psychology, University of Edinburgh, Edinburgh, UK Alzheimer Scotland Dementia Research Centre, University of Edinburgh, Edinburgh, UK Division of Brain Sciences, Department of Medicine, Imperial College, London, UK Centre for Epidemiology, Division of Population Health, Health Services Research & Primary Care, The University of Manchester, Manchester, UK Centre for Integrated Genomic Medical Research, Institute of Population Health, University of Manchester, Manchester, UK Division of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Salford Royal NHS Foundation Trust, Manchester, UK Department of Biological and Medical Psychology, University of Bergen, Bergen, Norway Department of Medical Genetics, Oslo University Hospital, University of Bergen, Oslo, Norway NORMENT, K.G. Jebsen Centre for Psychosis Research, University of Bergen, Bergen, Norway Dr. Einar Martens Research Group for Biological Psychiatry, Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway Department of Psychology, University of Oslo, Oslo, Norway Department of Psychology, University of Edinburgh, Edinburgh, UK Dr. Einar Martens Research Group for Biological Psychiatry, Center for Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge, UK Department of Medical Genetics, University of Helsinki and University Central Hospital, Helsinki, Finland Department of General Practice, University of Helsinki and Helsinki University Hospital, Helsinki, Finland National Institute for Health and Welfare, Helsinki, Finland Folkhälsan Research Center, Helsinki, Finland Helsinki Collegium for Advanced Studies, University of Helsinki, Helsinki, Finland Department of Psychiatry, Martin Luther University of Halle-Wittenberg, Halle, Germany Department of Psychology, University of Crete, Crete, Greece Department of Psychiatry, National and Kapodistrian University of Athens Medical School, Eginition Hospital, Athens, Greece University Mental Health Research Institute, Athens, Greece Neurobiology Research Institute, Theodor-Theohari Cozzika Foundation, Athens, Greece Department of Psychiatry and Behavioral Sciences, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD, USA McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA 23andMe, Inc., Mountain View, CA, USA
  5. Celiac.com 07/21/2017 - In previous studies, a team of scientists led by Professor Anette-Gabriele Ziegler had already shown an association between infections in early childhood and the development of type 1 diabetes. In that study, the researchers saw the highest risk for type 1 diabetes in children who experienced repeated respiratory infections in the first six months of life. Recently, Zeigler and another team of colleagues from the Institute for Diabetes Research at Helmholtz Zentrum München, a partner in the German Center for Diabetes Research (DZD), set out to determine whether infections during infancy are associated with increased risk for celiac disease later on. Their current study shows that the risk of developing celiac disease is particularly high when gastrointestinal tract infections occur during the first year of life. To a lesser extent, an increased disease risk was also seen in connection with early respiratory tract infections. The risk seems to be particularly high for people who experience repeated gastrointestinal infections in the first year of life. Whether the connections with early infections and later celiac risk are causal or are based on changes in the microbiome or specific immune responses is not clear from the data, said first author Dr. Andreas Beyerlein. "However," Beyerlein added, "it seems that the increased risk of celiac disease is associated with a permanent inflammation of the gastrointestinal tract in early childhood and is not caused by a specific viral or bacterial pathogen." The team reached their conclusion after analyzing fully anonymized data provided by the Bavarian Association of Statutory Health Insurance Physicians (Kassenärztliche Vereinigung Bayern) of 295,420 children who were born between 2005 and 2007. Medically attended infections from birth until a median age of 8.5 years were considered in the analysis. A total of 853 children developed gluten intolerance, equivalent to 0.3 percent. Their results appear in the American Journal of Epidemiology. Source: Helmholtz Zentrum München - German Research Center for Environmental Health
  6. 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.
  7. Pediatrics 2004;113:1672-1676. Celiac.com 07/12/2004 – According to Dr. Nathaniel Zelnik and colleagues from the Technion-Israel Institute of Technology, in Haifa, Israel, the spectrum of neurological disorders among those with celiac disease are greater than previously thought. The researchers studied 111 responses to questionnaires that probed for the presence of neurological disorders and symptoms, and reviewed the respondents medical records. Those who reported neurological symptoms underwent neurological examination and brain imaging or electroencephalogram, and the results were compared with that of 211 matched controls. The researchers found that 57 out of 111 (51.4%) of those with celiac disease also developed neurological disorders, compared with only 42 (19.9%) control patients. The neurological manifestations included hypotonia, developmental delay, learning disorders and ADHD, headache, and cerebellar ataxia. Epileptic disorders were also slightly more common among patients with celiac disease. The prevalence of tic disorders between the two groups did not differ. The effects of a gluten-free diet did differ among the various neurological disorders found by the researchers. Dr. Zelnik concludes that the therapeutic benefit of the gluten-free diet was demonstrated only in patients with transient infantile hypotonia and migraine headache.
  8. Celiac.com 07/20/2015 - Lymphocytic gastritis (LG) is an uncommon gastric disorder with varying symptoms and endoscopic manifestations. LG, along with two forms of H. pylori-negative gastritis [chronic active gastritis (CAG) and chronic inactive gastritis (CIG)], appears to be more common in patients with celiac disease, based on single-center studies. A team of researchers set out to compare the prevalence of LG, CAG and CIG among those with normal duodenal histology or non-specific duodenitis, and those with celiac disease, as defined by villous atrophy, Marsh 3. The research team included B. Lebwohl, P. H. R. Green, and R. M. Genta. The are variously affiliated with The Department of Medicine, Coeliac Disease Center, Columbia University College of Physicians and Surgeons, New York, NY, The Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA, the Miraca Life Sciences, Irving, TX, USA, and the Departments of Pathology and Medicine (Gastroenterology), UT Southwestern Medical Center, Dallas, TX, USA The team analyzed all concurrent gastric and duodenal biopsy specimens submitted to a national pathology laboratory during a 6-year period. They then performed multiple logistic regression to identify independent predictors of each gastritis subtype. They found that a total of 287,503 patients underwent concurrent gastric and duodenal biopsy, with an average age of 52, and most (67%) being female. Compared to patients with normal duodenal histology, LG was more common in partial villous atrophy (OR: 37.66; 95% CI: 30.16–47.03), and subtotal/total villous atrophy (OR: 78.57; 95% CI: 65.37–94.44). Celiac disease was also more common in CAG (OR for partial villous atrophy 1.93; 95% CI: 1.49–2.51, OR for subtotal/total villous atrophy 2.42; 95% CI: 1.90–3.09) and was similarly associated with CIG (OR for partial villous atrophy 2.04; 95% CI: 1.76–2.35, OR for subtotal/total villous atrophy 2.96; 95% CI: 2.60–3.38). From this study, the team concluded that lymphocytic gastritis is strongly associated with celiac disease, with increasing prevalence correlating with more advanced villous atrophy. Chronic active gastritis and chronic inactive gastritis are also significantly associated with celiac disease. Future research should measure the natural history of these conditions after treatment with a gluten-free diet. Source: Alimentary Pharmacology & Therapeutics Volume 42, Issue 2, pages 180–187, July 2015. DOI: 10.1111/apt.13249
  9. Gluten intolerance often presents itself in ways unexpected, including several common skin conditions. Ranging in severity from dermatitis herpetiformis to dry skin, avoiding gluten may have more to do with your plaguing skin concerns than you imagined. Here are some common dermatological concerns associated with celiac disease: Dermatitits Herpetiformis—This painful, blistery condition can be very stressful, especially when misdiagnosed. An inflamed, itchy rash, dermatitis herpetiformis begins as tiny white filled blisters or red spots around hair follicles. Trying to hide or disguise DH, as well as trying to treat it when misdiagnosed can be incredibly stressful for a person. Eczema—Eating a gluten-free diet is becoming an increasingly popular mode of treatment for eczema. Those who are gluten intolerant also tend to have more advanced psoriasis.Psoriasis—Like eczema, psoriasis has in many cases shown improvement when the person is put on a gluten free diet. In Scott Adams’ 2004 article, he also mentioned that psoriasis in those with celiac tends to be more severe. Acne—Links between celiac and malabsorption, as well as hormonal upset can contribute to a greater production of acne. Many birth control pills boast promises of clearer skin, their method is through hormone manipulation. Because many who suffer from gluten intolerance also experience a disruption of normal hormone function, this disharmony can lead to problems with acne. Dry Skin—Also correlated to malabsorption, dry skin is a very common complaint amongst those with celiac. But this condition is one that many people see even after the prescribed treatment of a gluten free diet. Why? Vitamin E rich grains are vital to maintaining skin harmony, but since many who are gluten intolerant begin avoiding grains completely—even those grains that are gluten-free, getting that important Vitamin E in their diets can become a challenge.
  10. Celiac.com 03/13/2015 - People who suffer from celiac disease with persistent villous atrophy do not face any higher risk of ischemic heart disease or atrial fibrillation, according to a recent study by a research team in Sweden. This is important, because patients with celiac disease do face an increased risk of death from cardiovascular causes, so it is mildly encouraging that persistent villous atrophy resulting from gluten exposure does not appear to affect overall or cardiovascular mortality. The research team, led by Dr. Jonas F. Ludvigsson from Karolinska University Hospital in Stockholm, studied 7,440 celiac disease patients, 43% with persistent villous atrophy, who had follow-up biopsies, along with up to five controls each, matched for age, gender, county, and calendar year. Overall risk of ischemic heart disease was not significantly higher in the patients with celiac disease. After adjusting for age at follow-up biopsy, gender, duration of celiac disease, and other factors, they found no significant difference in the risk of ischemic heart disease risk between patients with villous atrophy and those with mucosal healing. Similarly, patients with villous atrophy had no higher risk of atrial fibrillation than those with mucosal healing. Factors associated with ischemic heart disease risk included being male, older, and having lower educational levels. Factors associated with atrial fibrillation risk included being male and being older. Source: Medscape
  11. Celiac.com 05/20/2011 - Over the years, researchers have been discovering more and more about celiac disease, an autoimmune disease which is caused by gluten, a protein found in wheat, barley, and rye. Studies have linked the disease to a variety of other medical conditions, such as irritable bowel syndrome, rheumatoid arthritis, and osteoporosis. Researchers have now found a connection between celiac disease and asthma. Asthma is chronic lung disease that causes the passages of the lungs to become inflamed and narrowed, resulting in wheezing, shortness of breath, tightness in the chest area, and coughing. It often begins in childhood, and according to the U.S. Department of Health and Human services, more than 22 million people suffer from the condition. Many studies have linked asthma to airborne allergens, but doctors have begun to look into food culprits as well. One such study shows a connection to celiac disease, which isn’t an allergy but rather an autoimmune response to gluten. In a study published in the Journal of Allergy and Clinical Immunology, European researchers found that celiac individuals were 60 percent more likely to develop asthma than those without the condition. Celiac disease affects approximately one percent of the population and without treatment, which is a gluten-free diet, can cause a variety of physical and mental symptoms including chronic fatigue, headaches, malnutrition, chronic headaches, and stomach problems. Dr. Jonas Ludvigsson of Orebro University Hospital and the Karolinska Institutet in Sweden and his colleagues compared more than 28,000 Swedish celiac patients to more than 140,000 similar people without the disease. The study concluded that only a link between the two could be demonstrated, not that one condition causes the other; the researchers weren’t able to identify the reason for the association. One possible factor may be Vitamin D. According to Reuters Health, Dr. Ludvigsson said in an email, "Personally, I think the role of vitamin D deficiency should be stressed." Vitamin D has been demonstrated to be a factor in the development of tuberculosis and osteoporosis, both of which celiacs are more likely to develop. In celiac disease, gluten causes an autoimmune reaction that causes the immune system to attack the small intestine, specifically the villi, the finger-like structures that absorb the nutrients from food; thus celiac patients usually exhibit deficiencies in vitamins and minerals. If a celiac patient isn’t getting enough vitamin D into their system, according to Dr. Ludvigsson, the risk for asthma disease may be increased. According to Dr. Ludviggson, Swedish celiac patients adhere well to the gluten-free diet. The study didn’t determine how closely the 28,000 subjects were sticking to their diets, but Ludviggson told Reuters health, "Generally dietary compliance is high in Sweden, so I actually believe that also patients with good adherence are at increased risk of asthma.” It is recommended that people who suspect they may have celiac disease or asthma should consult with a qualified medical practitioner for testing, diagnosis, and treatment. Resources: U.S. Department of Health & Human Services: http://www.nhlbi.nih.gov/health/dci/Diseases/Asthma/Asthma_WhatIs.html Gluten Free Society: Gluten Sensitivity Increases the Risk for Asthma: http://www.glutenfreesociety.org/gluten-free-society-blog/gluten-sensitivity-increases-the-risk-for-asthma/ Reuters: Asthma linked to celiac disease: http://www.reuters.com/article/2011/02/24/us-asthma-linked-celiac-disease-idUSTRE71N4WF20110224
  12. Celiac.com 04/15/2013 - Enteropathy-associated T cell lymphoma (EATL) is a gut cancer that often ends in death. Currently, doctors have very little idea what factors might help patients survive. The manner in which clinical presentation, pathological features and therapies influence EATL outcome was the subject of a recent study by a team of researchers. The research team included: G. Malamut; O. Chandesris; V. Verkarre; B.Meresse, C. Callens, E. Macintyre, Y. Bouhnik, J.M. Gornet; M. Allez; R. Jian; A. Berger; G. Châtellier; N. Brousse, O. Hermine, N. Cerf-Bensussan, and C. Cellier. They are variously affiliated with the Université Paris Descartes, the Gastroenterology Department of Hôpital Européen Georges Pompidou, APHP, and Inserm U989 in Paris, France. For their study, the team evaluated the medical files of 37 well-documented patients with celiac disease and T-cell lymphoma. They then analyzed lymphoma and intestinal mucosa by histopathology, multiplex PCR and intestinal intraepithelial lymphocytes phenotyping. Using Kaplan-Meier curves with Logrank test and Cox Model they then analyzed patient survival and prognostic factors. They found 15 patients with lymphoma-complicated non-clonal enteropathy, celiac disease, two patients with type I refractory celiac disease, and 20 patients with clonal type II refractory celiac disease. Twenty-five patients underwent surgery with resection of the main tumor mass in 22 cases. Univariate analysis showed that non-clonal celiac disease, serum albumin levels under 21.6g/L at diagnosis, chemotherapy and surgical resection predicted good survival (p=0.0007, p Multivariate analysis showed that serum albumin level>21.6g/L, chemotherapy and reductive surgery were all significantly associated with increased survival rates (p The results reinforce the value of assessing celiac disease type in patients with T-cell lymphoma, and suggest that a combination of nutritional, chemotherapy and reductive surgery may improve survival rates in cases of EATL. Source: Dig Liver Dis. 2013 Jan 9. pii: S1590-8658(12)00438-0. doi: 10.1016/j.dld.2012.12.001.
  13. Pediatric Allergy and Immunology Volume 16 Issue 5 Page 428 - August 2005 Celiac.com 09/27/2005 – Italian researchers have discovered a link between celiac disease and chronic urticaria (hives). The researchers conducted a case control study that screened 79 children with chronic urticaria for celiac disease, then compared the results to that of 2,545 healthy controls in order to determine the clinical relevance of any association. Children and adolescents who had chronic hives for at least 6 weeks that did not respond to oral antihistamines were used as subjects in the chronic urticaria group, and each group was screened for celiac disease via anti-transglutaminase and anti-edomysial antibodies, with confirmation done via endoscopic intestinal biopsy. The researchers found celiac disease in 4 of the 79 chronic urticaria group—a full 5%, and in 17 of the 2,545 controls (0.67%). The four children found to have celiac disease in the chronic urticaria group were put on a gluten-free diet and after 5-10 weeks their chronic urticaria symptoms completely disappeared (while it took 5-9 months for their serological tests for celiac disease to return to normal). The researchers conclude that the presence of celiac disease in children with chronic urticaria is significantly more frequent than in controls, and children with chronic urticaria should be screened for celiac disease, and, if it is found, they should be treated with a gluten-free diet.
  14. Celiac.com 10/10/2012 - Celiac disease is associated with type 1 diabetes (T1D), but little is known about the connection between celiac disease and diabetic retinopathy (DRP) in patients with T1D. A research team recently set out to determine whether celiac disease is associated with a higher risk of diabetic retinopathy (DRP) in patients with T1D. The researchers included Kaziwe Mollazadegan, MD; Maria Kugelberg, MD, PHD; Scott M. Montgomery, PHD; David S. Sanders, MB, CHB, FRCP, MD, FACG; Johnny Ludvigsson; MD, PHD; and Jonas F. Ludvigsson, MD, PHD. They are affiliated with the Pediatric Clinic, and the Department of Clinical and Experimental Medicine in the Division of Pediatrics at Linköping University in Linköping, Sweden, with St. Erik Eye Hospital, and the Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; the Department of Pediatrics, and the Clinical Research Centre at Örebro University Hospital in Örebro, Sweden, Gastroenterology and Liver Unit, Royal Hallamshire Hospital and University of Sheffield, Sheffield, U.K. Their study shows that longstanding celiac disease is associated with an increased risk of diabetic retinopathy in patients with type 1 diabetes. The team conducted a population-based cohort study, in which they used the Swedish National Patient Register to identify 41,566 patients diagnosed with diabetes from 1964 to 2009, and who were 30 years of age or younger at the time of diagnosis. The team defined celiac disease as the presence of villous atrophy (Marsh stage 3) according to small intestinal biopsies performed between 1969 and 2008, with biopsy reports obtained from Sweden’s 28 pathology departments. During follow-up, the team found 947 T1D patients with celiac disease. They used Cox regression analysis with celiac disease as a time-dependent covariate to estimate adjusted hazard ratios (aHRs) for DRP in patients with T1D and celiac disease, and to compare them with patients with T1D but no celiac disease. The results showed that the longer the patients had celiac disease, the higher their risk of DRP. Once the team adjusted the results by time from celiac disease diagnosis, people with T1D and celiac disease showed a lower risk of DRP in the first 5 years after celiac disease diagnosis (aHR 0.57 [95% CI 0.36–0.91]), followed by a neutral risk in years 5 to Between 10 and 15 years after diagnosis, patients with coexisting celiac disease showed a risk of 2.83 for DRP [95% CI 1.95–4.11. More than 15 years after follow-up, that higher risk rate went up to 3.01 [1.43–6.32]). So, having celiac disease for more than 10 years is a risk factor for the development of DRP in patients with T1D. Therefore, the researchers note, physicians should conduct intense DRP monitoring in patients with long-standing celiac disease and T1D. Source: Diabetes Care
  15. Celiac.com 04/22/2011 - A research team recently set out to examine multiple independent variants in 6q21-22 associated with susceptibility to celiac disease in the Dutch, Finnish and Hungarian populations. The study team included Elisabet Einarsdottir, Marianna R Bevova, Alexandra Zhernakova, Alienke Monsuur, Lotta LE Koskinen, Ruben van't Slot, Chris Mulder, M Luisa Mearin, Ilma R Korponay-Szabo, Katri Kaukinen, Kalle Kurppa, Juha Kere, Markku Mäki, Cisca Wijmenga and Päivi Saavalainen. Studies in Dutch, Finnish and Hungarian populations have shown that a locus on chromosome 6q21-22 carries higher susceptibility to celiac disease. This same locus has previously been associated with susceptibility to other autoimmune diseases such as Crohn's disease and type 1 diabetes. The study team conducted fine mapping on 446 independent individuals with celiac disease and 641 control subjects of Dutch origin. The team tested 872 tagging single-nucleotide polymorphisms (SNPs) in a 22 Mb region of chromosome 6. To identify risk variants in this region, the team followed up on the 12 most promising SNPs in 2071 individuals from 284 Finnish and 357 Hungarian celiac disease families. Numerous markers in the region showed strong associations with celiac disease in the Dutch material. Two SNPs, rs9391227 and rs4946111, showed strong association with celiac disease in the Finnish population. The rs9391227 connection is the strongest such connection yet found in the Finnish (P=0.003, OR 0.66), as well as the combined Dutch, Finnish and Hungarian populations (P=3.6 × 10−5, OR 0.76). The rs9391227 site is located downstream from the HECT domain and ankyrin repeat containing, E3 ubiquitin protein ligase 1 (HACE1) gene and is contained within a region of strong linkage disequilibrium enclosing HACE1. A meta-analysis of the three populations showed two additional independent, susceptibility variants in the 6q21-22 region. The team confirmed the 6q21-22 region as a celiac disease susceptibility locus; one that is independently associated with a number of other conditions, and which may implicate ubiquitin-pathways in celiac disease susceptibility. Source: European Journal of Human Genetics , (16 February 2011) | doi:10.1038/ejhg.2011.2
  16. Celiac.com 03/07/2011 - Although the HLA-DQ locus is clearly the strongest genetic factor influencing the development of celiac disease, it is certainly possible that other genes play supporting roles. Identifying these genes could help shed light on why certain genetically susceptible individuals develop celiac while others can happily (and healthily) eat gluten. NALP1 and NALP3 are genes that encode proteins involved in assembling the inflammasome, which is exactly what it sounds like – a complex of proteins that promotes inflammation. Gain-of function mutations – those that render the protein perpetually active, rather than responsive to activating signals – in NALP3 are known to cause autoinflammatory diseases, and NALP1 polymorphisms have been associated with the autoimmune diseases vitiligo, type I diabetes, and Crohn’s disease. NALP1 is found at high levels in T cells and Langerhans cells, but is also expressed in glandular epithelial structures including the stomach and gut. So a team of researchers in Trieste, Italy led by Dr. Sergio Crovella decided to check if polymorphisms in these genes might be associated with celiac disease as well. Their work is reported in the January 18, 2011 issue of The American Journal of Gastroenterology. They sequenced the DNA of 504 unrelated Italian children and adolescents with celiac disease and 256 healthy controls. They were looking for two particular polymorphisms in each gene, as these were already known to be associated with immune disorders. They did find differences in the frequency of the different individual alleles between celiac patients and controls, but these differences did not reach the levels of statistical significance. The combination of both NALP1 variants together, however, was significantly more common in study participants with celiac. NALP1 and NALP3 assemble the inflammasome by inciting the expression of the proinflammatory cytokine interleukin-1β , which in turn promotes autoreactive T cell function. The authors suggest that perhaps people with altered levels of responsiveness to interleukin-1β might be predisposed to autoimmunity. More work is needed to elucidate the role these NALP proteins might play in the intestinal damage that occurs in celiac disease. Source: Am J Gastroenterol advance online publication, 18 January 2011; doi: 10.1038/ajg.2010.474
  17. Celiac.com 07/09/2010 - The enteropathy associated with common variable immunodeficiency (CVID) is the most common symptomatic primary antibody deficient syndrome, with an estimated prevalence of one in one-hundred thousand to one in fifty thousand. However, the relationship between CVID and Enteropathy is still unclear. CVID is characterized by decreased levels of of two or more serum immunoglobulin (Ig) isotypes and the presentation of reoccurring infections specifically in the respiratory tract. Gastrointestinal symptoms are widespread with CVID patients as exhibited in as many as 50% of patients presenting with chronic diarrhea. A team of doctors evaluated the medical files of 50 CVID patients who exhibited gastrointestinal symptoms to determine the “clinical and hitopathological features of the enteropathy associated with CVID”. Fifteen patients were excluded from the study because they did not meet the recognized criteria for CVID. Data was collected from all patients and included, gender, age, symptoms, body mass index (BMI), as well as parasitological stool testing. Blood samples were taken from each test patient including hemogram, serum protein electrophoresis and measurements of serum folic acid, vitamin B12, iron, and calcium. The doctors found the mean age for initial CVID diagnosis to be 36.8 years. Four of the patients were discovered to have a family history of immunodeficiency. 40% of the patients that were tested were determined to have immunodeficiency as revealed by their digestive symptoms. Chronic diarrhea was observed as the most common gastrointestinal symptom with a rate of 92% of the patients studied. Gluten-free diet was initiated by 12 patients with villous atrophy, but clinical improvements and partial villous healing only occurred in two patients. Interestingly, the two patients presenting with celiac antibodies, did not show an improvement of symptoms. All patients showed positive improvements from steroid therapy. Furthermore, as a result of this study, the observing doctors concluded, that of the CVID patients exhibiting gastrointestinal symptoms, histological lesions were found in around 80% of the biopsies taken from the colon, stomach, or small bowel. The enteropathy corresponding with CVID was found to have has many features that differentiate it from other etiopathological conditions including celiac disease. While replacement Ig therapy was demonstrated to be inadequate for improving gastrointestinal symptoms, steroids, specifically budesonide,were proven successful in reducing inflammation and restoring mucosal architecture. Source: The American Journal of Gastroenterology , (15June2010) | doi:10.1038/ajg.2010.214
  18. Celiac.com 03/19/2010 - Celiac disease is a chronic inflammatory disorder of the gut triggered by an adverse immune response to dietary gluten proteins in genetically susceptible individuals. One of the first ways the body responds to offending proteins in an adverse celiac disease response is by producing mucous via IgA secretion in an effort to neutralize offending antigens and pathogens. A team of researchers recently sought to better document the relationships between immunoglobulin-coated bacteria and bacterial composition in feces of celiac disease patients, untreated and treated with a gluten-free diet (GFD) and healthy controls. The research team included Giada De Palma, Inmaculada Nadal, Marcela Medina, Ester Donat, Carmen Ribes-Koninckx, Miguel Calabuig, and Yolanda Sanz. They observed that intestinal dysbiosis and reduced immunoglobulin-coated bacteria are associated with celiac disease in children. Both untreated and treated celiac disease patients showed markedly lower levels of IgA, IgG and IgM-coated fecal bacteria compared to healthy controls. Celiac disease patients showed substantially reduced ratio of Gram-positive to Gram-negative bacteria compared to control subjects. Untreated celiac disease patients showed less abundant group proportions (P<0.050) of Bifidobacterium, Clostridium histolyticum, C. lituseburense and Faecalibacterium prausnitzii than did healthy controls. Untreated celiac disease patients showed more abundant group proportions (P<0.050) of Bacteroides-Prevotella than in control subjects. Both untreated and treated celiac disease patients showed significantly impoverished (P<0.050) levels of IgA coating the Bacteroides-Prevotella compared with healthy controls. From these results, the research team concluded that intestinal dysbiosis plays a role in reduced IgA-coating bacteria in celiac disease patients. This offers a fresh perspective into the possible relationships between the gut microbiota and the host defenses in celiac disease patients. Source: BMC Microbiology 2010, 24 February
  19. Celiac.com 02/26/2010 - Data increasingly supports an association between rs6822844 at the IL2-IL21 region and multiple autoimmune diseases in individuals of European descent. A number of autoimmune diseases share susceptibility genes, pointing to similar molecular mechanisms. A team of researchers recently set out to assess evidence for a general susceptibility locus by looking for association between rs6822844 at the Il2-Il21 region and numerous autoimmune diseases. The research team included Amit K. Maiti, Xana Kim-Howard, Parvathi Viswanathan, Laura Guillén, Adriana Rojas-Villarraga, Harshal Deshmukh, Haner Direskeneli, Güher Saruhan-Direskeneli, Carlos Cañas, Gabriel J. Tobön, Amr H. Sawalha, Alejandra C. Cherñavsky, Juan-Manuel Anaya, and Swapan K. Nath Their joint effort was underwritten by grants from the National Institutes of Health (NIH - Grant Number: 5R01-AI-063622, P20-RR-020143), Colciencias (Grant Number: 2213-04-16484), Rosario University School of Medicine, and the Colombian Association of Rheumatology. The goal of the study was to replicate the association between rs6822844 and 6 different immune-mediated diseases in non-European populations, and to conduct disease-specific and overall meta-analyses using data from previously published studies. The team evaluated case-control associations between rs6822844 and celiac disease in subjects from Argentina; rheumatoid arthritis, type 1 diabetes mellitus, primary Sjögren's syndrome, and systemic lupus erythematosus in subjects from Colombia; and Behçet's disease in subjects from Turkey. They compared allele and gene distribution between cases and controls. They conducted meta-analyses using data from the present study and previous studies. The team found significant associations of rs6822844 with systemic lupus erythematosus (P = 0.008), type 1 diabetes mellitus (P = 0.014), rheumatoid arthritis (P = 0.019), and primary Sjögren's syndrome (P = 0.033) but not with Behçet's disease (P = 0.34) or celiac disease (P = 0.98). Cases and controls from Argentina and Colombia showed little evidence of population differentiation (FST = 0.01), which suggests that association was not influenced by population substructure. Disease-specific meta-analysis shows strong association for rheumatoid arthritis (Pmeta = 3.61 × 10-6), inflammatory bowel disease (IBD; Crohn's disease and ulcerative colitis) (Pmeta = 3.48 × 10-12), type 1 diabetes mellitus (Pmeta = 5.33 × 10-5), and celiac disease (Pmeta = 5.30 × 10-3). Total meta-analysis across all autoimmune diseases supports association with rs6822844 (23 data sets; Pmeta = 2.61 × 10-25, odds ratio 0.73, with 95% confidence interval 0.69-0.78). The team concludes that an association exists between rs6822844 and multiple autoimmune diseases in non-European populations. Meta-analysis provides strong confirmation for strong association across multiple autoimmune diseases in populations of both European and non-European ancestry. Arthritis & Rheumatism; Volume 62 Issue 2, Pages 323 - 329 http://www3.interscience.wiley.com/journal/123266977/abstract?CRETRY=1&SRETRY=0
  20. 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.
  21. Celiac.com 04/10/2007 - According to a recent Swedish research report, the adverse immune response to gluten may be tied to a specific set of dendrite cells in the small intestine. A team led by Dr. J.F. Ludvigsson of Orebro University Hospital set out to compare rates of bone fracture in patients with celiac disease versus those from normal individuals. The goal of the study was to assess the connection between celiac disease and fractures. The study used Cox regression to examine over 13,000 patients with celiac disease, along with 65,000 people among the general population who were sex and age-matched. The Study tallied 1365 first hip fractures 4867 non-hip fractures. The results showed celiac disease to be a contributing factor in fractures at a rate of 4 fractures per 100,000 people per year, compared to a rate of 2 fractures per 100,000 people per year for non-celiacs. The study calculated the following hazard ratios for celiac-associated hip fracture: Adults: ¼ 2.1; 95% CI ¼ 1.8–2.4 Children: ¼ 2.6; 95% CI ¼ 1.1–6.2 For celiac-associated non-hip fractures, the hazard ratios were: Adults: ¼ 1.4; 95% CI ¼ 1.3–1.5 Children: ¼ 1.1; 95% CI ¼ 1.0–1.2 The study concludes that both adults and children with celiac disease run a significant risk of increased hip fractures and fractures of any type. These increased risks continue for at least 20 years following diagnosis. The study did not measure risk for undiagnosed celiacs, but common sense would indicate that the risks would be the same, or perhaps even greater. Clearly, more research is needed to determine the reasons for these increased fracture risks among celiac patients, and also to determine the associated risks for non-celiacs. Aliment Pharmacol Ther 25, 273–285 health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
  22. Celiac.com 09/13/2008 - Men who are diagnosed with celiac disease in adulthood tend to be shorter than those diagnosed and treated in childhood. A team of Israeli researchers led by Dr. Batia Weiss and colleagues recently set out to compare the adult height of people with celiac disease who were diagnosed and treated as children, against the height of those diagnosed as adults. The researchers analyzed the height of 290 patients—83 men and 207 women. Patients were grouped according to age at diagnosis. The 113 patients of group 1 were diagnosed before age 18 years, while the 177 patients of group 2 were diagnosed after age 18 years. The average adult height was 178.4 cm for men of group 1, and 176.3 cm for men of group 2, (p = 0.22). The height Z scores for men were 0.22 for group 1 and -0.08 for group 2 (p = 0.022). Researchers noted a significant inverse relationship between the age of the men at celiac disease diagnosis and their final adult height. For women, average adult height was 163.0 cm for group 1 and 162.6 cm for group 2, (p = 0.68). Height Z scores were -0.05 for the women of group 1 and -0.11 for the women of group 2 (p = 0.68). Researchers noted no significant relationship between age at diagnosis and final height in women. The exact reasons for these gender-related height differences remain unknown. They may have to do with variations in timing and duration of growth in puberty, the increased nutritional demands of adolescent men, or gender-related hormonal differences. Regardless of the exact reasons for these results, this study is just the latest of many to drive home the importance of early detection and treatment of celiac disease for everyone. American Journal of Gastroenterology 2008; 103:1770-1774.
  23. Celiac.com 08/14/2007 - It has long been documented that there is a connection between celiac disease and neoplasm. In fact, in the 1960s, a population-based study reported a 100-fold increase in risk of non-Hodgkins lymphoma in patients with celiac disease. It has also been shown that people with celiac disease are at greater risk for developing small bowel adenocarcinoma. Also, studies have shown an increased mortality rate from cancer among celiac patients, and there is mounting, but not conclusive evidence that a gluten-free diet provides a measure of protection against the development of malignancies. Strangely, several studies have documented a lower risk of breast cancer among celiac patients. However, to date, very little is known about the associated factors, particularly with regard to the development of gastrointestinal malignancies and their corresponding risk levels. A study recently published in BMC Gastroenterology documents the efforts of a team of Italian doctors to evaluate the risks of developing various types of gastrointestinal neoplasms associated with delayed diagnosis of celiac disease and the resulting consumption of gluten over time. The team was made up of doctors Marco Silano; Umberto Volta; Anna Maria Mecchia; Mariarita Dessì; Rita Di Benedetto; and Massimo De Vincenzi. The team studied a group of 1,968 celiac patients from 20 GE referral centers between 01 January 1982 & 31 March 2005. Study Shows Higher Rates of Gastrointestinal Malignancy that Increase with Age in Patients with Delayed Diagnosis of Celiac Disease According to the results of the study celiac patients have an increased risk of developing cancer which corresponds directly with the age of diagnosis of celiac disease. This increased risk applies to gastro-intestinal malignancies. An accurate screening for tumors should be performed in patients diagnosed with celiac disease in adulthood. On average, the mean age of celiac patients who developed a neoplasm, either sooner or later, was 47.6 +/- 10.2 years, compared with 28.6 =/- 18.2 years in those did not develop neoplasm. BMC Gastroenterology 2007, 7:8 (9 March 2007) health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
  24. Gut. 2004 Jan;53(1):149-51 Celiac.com 12/31/2003 – Italian researchers report in the journal Gut that their previous hypothesis which was based on their hospital study that reported a 1 in 80 incidence of celiac disease in pregnant women and an unfavorable pregnancy outcome for them needs to be revised. With the goal of proving their initial research the group conducted a "large population based study on a stratified sample from the whole Campania region" in Italy. The study looked at 5,055 pregnant women and tested them for IgA class anti-tissue transglutaminase (TGASE) antibodies using the ELISA method. In addition "Endomysial antibodies (EMA) were investigated on thin sections of human cord blood by an immunofluorescence test. The HLA class II DQA1*0501/DQB1*02 and DQA1*0301/DQB1*0302 haplotypes were assessed using the Eurospital Eu-DQ kit." The researchers found that 51 of the 5,055 patients tested positive for celiac disease, and 12 women with known celiac disease were added to the results which yielded a ratio of 1 in 80 pregnant women with celiac disease, results that matched the groups first study. When the celiac-positive groups birth outcomes were compared with the normal group the researchers did "not observe an excess risk of abortion, premature delivery, small birth weight, or intrauterine growth retardation," although anemia was more frequent in the celiac disease group. The researchers conclude that "undiagnosed coeliac disease is frequent among pregnant women (>1%) but is not associated with an unfavorable outcome of pregnancy."
  25. Eur J Gastroenterol Hepatol 2000;12:645-648. Celiac.com 08/13/2000 - According to Drs. Simon D. Johnston and R.G. Peter Watson from Royal Victoria Hospital in Belfast, Northern Ireland, UK, the incidence of undiagnosed celiac disease is higher among those with small bowel lymphoma, as reported in the June issue of the European Journal of Gastroenterology and Hepatology. According to the researchers: It is not clear whether the increased risk of small bowel lymphoma seen in typical celiac disease also applies to unrecognized or screening-detected celiac patients. To find an answer, they retrospectively identified 69 cases of small-bowel adenocarcinoma and 69 cases of small-bowel lymphoma from five pathology laboratories in Northern Ireland. From a group composed of one patient with known celiac disease, and 12 with previously unrecognized celiac disease, the clinical presentation of adenocarcinoma and lymphoma patients was similar, but perforation was much more common among lymphoma patients. Further, 13 of the lymphoma patients, but none of the adenocarcinoma patients, had villous atrophy at a distant site, all of which were enteropathy-associated T-cell lymphomas. According to the researchers: Comparing the small-bowel lymphoma group to our random sample of the general Northern Ireland population as controls, the odds ratio of 15.72 for unrecognized celiac disease in the small-bowel lymphoma group, clearly indicates that there is an increased risk of unrecognized celiac disease among small-bowel lymphoma patients. Additionally, (s)ince a protective role for a strict gluten-free diet has been demonstrated, it follows that every effort should be made to diagnose celiac disease at every opportunity and raises the issue of whether population screening for celiac disease should be carried out.