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Found 16 results

  1. I was diagnosed with Severe Celiacs last November plus 2 forms of glaucoma and recently degenerative arthritis. I'm only 22 and finding all this out is exhausting and stressful, well recently I decided to take a break from the gluten free diet and ordered a stuffed crust pizza from pizza hut, a few things from taco bell and a buffet at golden corral! And I have not gotten sick! Maybe I rash but the rash was there before hand, now I'm concerned my doctor was wrong and misdiagnosed me somehow? Before I started the gluten diet I was severely sick, throwing up and couldn't eat, I thought I had cancer, can someone help idk who else to go to, is this normal? Getting sick and then not getting sick? Oh and the rash has been there for weeks doctor has no idea what it is gonna see specialist, auto immune diseases are in family, I did have pelvic inflammatory disease could that of caused something?
  2. Celiac.com 12/05/2017 - It's not uncommon for people with celiac disease to have other medical conditions, including liver disease, glossitis, pancreatitis, Down syndrome, and autism. By the same token, people with one or more of these associated disorders can be at greater risk for having or developing celiac disease. Until recently, though researchers didn't have much good data on the numbers behind those risk levels. A new database study of more than 35 million people changes that. The study found that, for example, people with autism have celiac disease at rates that are 20 times higher than those without autism. You read that right. People with autism are 20 times more likely to have celiac disease than people from the general population. Reporting on his team's findings at the World Congress of Gastroenterology 2017, lead investigator Daniel Karb, MD, a second-year resident at University Hospitals Case Medical Center in Cleveland, says that doctors who treat autistic patients may want to keep an eye out for celiac-like symptoms. "If you have a patient who is autistic and they have all these unusual symptoms, you might want to screen them for celiac disease," said Karb. Researchers have long known that people with celiac disease can present with unusual symptoms that fall outside the classic celiac symptoms of malabsorption, steatorrhea, malnutrition, abdominal pain, and cramping after eating, "but this is putting numbers to it," said Dr Karb. For their study, Dr. Karb and his colleagues searched the Explorys database, which aggregates electronic health record data from 26 major integrated healthcare systems in the United States. Combing through the records of 35,854,260 people in the database from 2012 to 2017, they found 83,090 celiac disease diagnoses. The investigators uncovered significant connections between celiac disease and 13 other autoimmune disorders, such as type 1 diabetes, Crohn's disease, and ulcerative colitis. In fact, the team found that, except for a condition called primary biliary cholangitis, "[e]very autoimmune disease [they] looked at is associated with celiac disease," Dr. Karb reported. The study indicates that "there is a large undiagnosed burden of celiac disease," he explained. "And a lot of it is probably because of these atypical presentations." As research continues, look for more connections between celiac disease and other inflammatory conditions to be more fully detailed. For more on the World Congress of Gastroenterology 2017. Source: Medscape.com
  3. Celiac.com 12/21/2012 - Over the past several years, researchers have made substantial progress in understanding the causes of autism, which now afflicts about 1 in 88 children. However, very little news of this progress seems to have spread into popular consciousness, much of which continues to focus on the possible role of vaccines. Recent discoveries indicates that one-third or more cases of autism look to be a kind of inflammatory disease, which begins well before birth. In the August 25th issue of the New York Times, Moises Velasquez-Manhoff has very interesting article in which he discusses the widening view among researchers that autism is, in fact, an inflammatory disease. The article is long and comprehensive, and cites numerous studies, findings and experiments. Inflammation is the body's natural response to certain kinds of threats. In a normal body, the immune system uses inflammation in a very precise, targeted way, before returning to a normal state. In autistic individuals, inflammatory signals become the dominant condition, and there is no balancing anti-inflammatory response. A state of chronic inflammation becomes normal. And the more skewed toward inflammation, the more acute the autistic symptoms. This inflammatory deregulation adversely impacts the brains of autistic individuals. Velasquez-Manhoff also cites a number of studies that trace these inflammatory effects back to the inflammatory responses of the mother during pregnancy. Among the studies cited in the article is a population-wide study from Denmark spanning two decades of births, which indicates that infection during pregnancy increases the risk of autism in the child. The study found that hospitalization for a viral infection, like the flu, during the first trimester of pregnancy triples the odds of autism. Bacterial infection, including of the urinary tract, during the second trimester increases chances by 40 percent. Another large Danish study, which included nearly 700,000 births over a decade, found that a mother’s rheumatoid arthritis, a degenerative disease of the joints, elevated a child’s risk of autism by 80 percent. Rates of autism in children of mothers with celiac disease were 350 percent higher than normal. Genetic studies had similar findings. Variations in genes associated with regulating the immune system also increase the risk of autism, especially when they occur in the mother. A mother’s diagnosis of asthma or allergies during the second trimester of pregnancy increases her child’s risk of autism. So does metabolic syndrome, a disorder associated with insulin resistance, obesity and, crucially, low-grade inflammation. Yet, viral and bacterials infections themselves do not seem the cause of the autism epidemic. The epidemiology doesn’t support that conclusion. A far more likely culprit is maternal immune dysregulation. Basically, the mother’s attempt to repel invaders, her inflammatory response, seems to be at fault. Research by Paul Patterson, an expert in neuroimmunity at Caltech, supports this idea. In his research, he introduces inflammation in pregnant mice artificially, without a live infection. This causes behavioral problems in the young. In this model, autism results from collateral damage. It’s an unintended consequence of self-defense during pregnancy. Since infantile autism was first described by Leo Kanner in 1943, diagnoses have risen tenfold. During that same period, viral and bacterial infections generally declined. However, overall rates of inflammatory diseases have risen sharply since then. As a group, these diseases include asthma, now estimated to affect 1 in 10 children, rates that have at least doubled since 1980, along with autoimmune disorders, which now afflict 1 in 20. Recently, William Parker at Duke University has chimed in. Some years back, he began comparing wild sewer rats with clean lab rats. The bodies of wild rats tightly controlled inflammation, but those of the lab rats did not. Parker found that the bodies of the wild rats contained high levels of parasites. Parasites are noted for limiting inflammation. One lesson from these rodent experiments is that fixing the maternal dysregulation will most likely prevent autism. That theory is supported by Swiss researchers, who created a lineage of mice with a genetically reinforced anti-inflammatory signal. They then inflamed the pregnant mice. The babies emerged fine, with no behavioral problems. This suggests that if inflammation is controlled during pregnancy, it won’t interfere with fetal brain development. Interestingly, asthma researchers are coming to similar conclusions: preventing inflammation in pregnant women will likely prevent asthma. Dr. Parker has introduced a more aggressive approach. He suggests that by using specially developed worms to restore “domesticated” parasites doctors can correct immune dysregulation. To determine if this is feasible, a trial is under way at the Montefiore Medical Center and the Albert Einstein College of Medicine. The trial is using a medicalized parasite called Trichuris suis, known as a whipworm, to treat autistic adults. The whipworm is native to pigs, and was first used medically to treat inflammatory bowel disease. It has shown anecdotal benefit in autistic children. The article suggests that the future of treating immune dysregulation, and thus preventing diseases like autism and asthma, may lie in reintroducing parasites into the human body. Stay tuned for more updates on this truly fascinating science. Read the full article by Moises Velasquez-Manhoff in the New York Times.
  4. Celiac.com 09/04/2017 - Researchers think they may have discovered an important connection between diet and dementia. For the first time, they have tied a specific dietary pattern to blood markers for inflammation. In addition, they showed that elderly adults who followed a certain dietary pattern had reduced brain gray matter volume, and worse visuospatial cognitive function. The team found that “people who consume less omega 3, less calcium, vitamin E, vitamin D, and vitamin B5 and B2 have more inflammatory biomarkers," study investigator Yian Gu, PhD, Columbia University and the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, New York City, told reporters. Some studies have linked chronic inflammation to an increased risk for AD. But, until now, no research addressed whether diet affects brain and cognitive health by modulating inflammation. "No study has formally tested whether the relationship of diet with cognition, or with the brain, is actually because of inflammation," said Dr Gu. Dr. Gu’s research team conducted a new cross-sectional study on 330 elderly adults from the Washington Heights–Inwood Community Aging Project imaging study. Researchers conducted structural MRI scans on these patients, and measured levels of the inflammatory biomarkers CRP and IL6. Each participant responded to a 61-item questionnaire about food and nutrient intake over the past year. The researchers used the results to craft a statistical model of the inflammation-related nutrient pattern (INP). These new findings suggest that dietary and/or medical treatments that reduce inflammatory markers may be helpful. Results of their study were presented at the Alzheimer's Association International Conference (AAIC) 2017. Source: Alzheimer's Association International Conference (AAIC) 2017
  5. Celiac.com 12/07/2016 - Refractory celiac disease (RCD) is a form of celiac disease that does not respond to treatment with gluten-free diet, and often involves greater risk of complications. The guts of many RCD patients over-produce effector cytokines, which are supposed to amplify the tissue-destructive immune response. However, it remains unclear if the RCD-associated mucosal inflammation is sustained by defects in counter-regulatory mechanisms. A team of researchers recently set out to determine whether RCD-related inflammation is marked by high Smad7, an intracellular inhibitor of transforming growth factor (TGF)-β1 activity. The research team included S Sedda, V De Simone, I Marafini, G Bevivino, R Izzo, OA Paoluzi, A Colantoni, A Ortenzi, P Giuffrida, GR Corazza, A Vanoli, A Di Sabatino, F Pallone, and G Monteleone. They are variously affiliated with the Department of Systems Medicine at the University of Rome "Tor Vergata," the First Department of Internal Medicine at the Fondazione IRCCS Policlinico San Matteo of the University of Pavia, and with the Department of Molecular Medicine at San Matteo Hospital at the University of Pavia in Pavia, Italy. The team evaluated Smad7 in duodenal biopsy samples of patients with RCD, patients with active celiac, patients with inactive celiac disease and healthy controls by Western blotting, immunohistochemistry and real time-PCR. In the same samples, they used ELISA and immunohistochemistry to assess TGF-β1 and phosphorylated (p)-Smad2/3, respectively. They evaluated pro-inflammatory cytokine expression in RCD samples cultured with Smad7 sense or antisense oligonucleotide. Smad7 protein, but not RNA, expression was increased in RCD, as compared to active and inactive celiac patients and healthy controls. This increased expression was associated with defective TGF-β1 signaling, as marked by diminished p-Smad2/3 expression. TGF-β1 protein content did not differ among groups. Knockdown of Smad7 in RCD biopsy samples reduced IL-6 and TNFα expression. These results show that, in RCD, high Smad7 associates with defective TGF-β1 signaling, and sustains inflammatory cytokine production. These results suggest a novel mechanism by which amplifies mucosal cytokine response in RCD, and suggest that treatments targeting Smad7 might be helpful in RCD. Source: Immunology. 2016 Nov 14. doi: 10.1111/imm.12690.
  6. Celiac.com 08/29/2016 - In 2005 the National Institute of Health indicated more than 23 million Americans suffered from autoimmune disease. Today the projection is 30 million who experience extreme fatigue, muscle and joint pain, muscle weakness, sleeplessness, weight loss or gain, and memory problems as symptoms of autoimmune disorders. Celiac disease has gotten the most attention in antibody research, but the current data on cross-reactivity of antibodies is allowing a better understanding of gluten sensitivity. Antigen reactivity to alpha-gliadin can trigger immune attacks on many individuals beyond those with positive DQ 2, DQ 8 and TTG test results. Gluten ataxia has been identified not only in people with celiac disease, but also in autism, lupus and multiple sclerosis. The lack of muscle control for movement, speech, eye coordination and swallowing can now be assessed in most autoimmune disorders. Gliadin reacts with foods and human tissue antigens causing symptoms beyond the gastro-intestinal tract. A low inflammatory diet customized to each person through testing for cross-reactivity or elimination diet protocols is needed to restore a state of health and well-being (for a copy of Low Inflammatory Diet & Elimination Diets check the author's website at the end of this article). According to Aristo Vojdani, PhD, professor of neuroimmunology at Carrick Institute and Chief Science Advisor for Cyrex Labs, about 50 percent gluten-sensitive individuals are also sensitive to dairy proteins (cow's milk, casein, whey) and sensitivity to oats depends on the variety of the grain and not just contamination from the milling process. In the author's personal experience, a gluten-free diet has many limitations. The reactivity between alpha gliadin and corn, millet, oats, rice and dairy has been denounced as invalid by gastroenterologists and celiac disease researchers. While at a medical school in Missouri, biopsies did not show improvement in villous atropy until all alpha gliadin sources and corn, millet, rice and oats were removed from the diet. Intestinal permeability or leaky gut allows antigens into the blood stream including food proteins, pathogens, and toxic chemicals which can cause inflammation. Continuous antigen exposure to tissues and organs is a factor in developing autoimmune disorders. Symptoms develop silently in the gut, joints and endocrine glands for several years. Tissue destruction with T and B lymphocyte reactions are a warning that autoimmune issues are developing during the next 5 to 10 year period until immunosuppressive drugs like corticosteroids are needed. To reduce the triggers to autoimmune diseases early, nutrition and lifestyle habits need adjusting. A Gluten-free Diet may seem easier today than 10 years ago, but current regulations in many countries allow up to 20 ppm gluten to be labeled "gluten-free". Many gliadin and cross -reactive proteins are most likely still available to create inflammatory symptoms. Assessing Viral Activity is key to managing autoimmune disease symptoms. Viral panels for EBV, Lyme, Bartonella, Mycoplasma, Chlamydia, CMV are available. Nutrition management of viral load is critical for the person with celiac disease and other autoimmune diseases. Reducing Toxic Chemicals is just as important as omitting gluten. Plastics like bisphenol A, heavy metals, pesticide residues, solvents all create inflammation. Water filtration devices that remove fluoride, heavy metals and pathogens plus stainless steel water bottles could reduce the body burden of chemicals that influence digestive function, joint movement, and immune well-being.
  7. Celiac.com 04/10/2013 - People with celiac disease or inflammatory bowel disease have higher rates of migraine headaches than their counterparts without those conditions, according to a new study. The research team included Alexandra K. Dimitrova MD, Ryan C. Ungaro MD, Benjamin Lebwohl MD, Suzanne K. Lewis MD, Christina A. Tennyson MD, Mark W. Green MD, Mark W. Babyatsky MD, and Peter H. Green MD. A team of researchers recently set out to assess the rates of migraine headaches in clinic and support group patients with celiac disease and inflammatory bowel disease (IBD) and to compare those with a sample group of healthy control subjects. A number of European studies have shown higher rates of migraine headaches in patients with celiac disease and IBD compared with control subjects. For the study, participants all answered a self-administered survey containing clinical, demographic, and dietary data, as well as questions about headache type and frequency. They also used both the ID-Migraine screening tool and the Headache Impact Test (HIT-6). The research team analyzed five hundred and two subjects who met exclusion criteria. Of these, 188 had celiac disease, 111 had IBD, 25 had gluten sensitivity (GS), and 178 healthy subjects served as controls. Thirty percent of celiac patients, 56% of gluten-sensitive patients, 23% of IBD patients, and 14% of control subjects reported chronic headaches (P < .0001). Using multivariate logistic regression, the team found that all subjects with celiac disease (odds ratio [OR] 3.79, 95% confidence interval [CI] 1.78-8.10), GS (OR 9.53, 95% CI 3.24-28.09), and IBD (OR 2.66, 95%CI 1.08-6.54) had significantly higher rates of migraine headaches than did control subjects. Migraine rates were influenced by female sex (P = .01), depression, and anxiety (P = .0059) were independent predictors of migraine headaches, whereas age >65 was protective (P = .0345). When it came to grading their migraines, seventy-two percent of celiac disease subjects reported having migraine that were severe in impact, compared with 30% of IBD, 60% of GS, and 50% of C subjects (P = .0919). The number of years on gluten-free diet had no influence on the severity of migraines. Migraine headaches were more common in people with celiac disease and IBD patients than in control subjects. The team points out that future studies should screen migraine patients for celiac disease and assess the effects of gluten-free diet on celiac disease patients with migraines. Source: Headache: The Journal of Head and Face Pain. DOI: 10.1111/j.1526-4610.2012.02260.x
  8. Celiac.com 07/17/2012 - To follow up on reported associations between celiac disease and peripheral neuropathy, a research team recently conducted a study of peripheral neuropathic symptoms in celiac disease and inflammatory bowel disease. T.C. Shen, B. Lebwohl, H. Verma, N. Kumta, C. Tennyson, S. Lewis, E. Scherl, A. Swaminath, K.M. Capiak, D. DiGiacomo, B.P. Bosworth, T.H. Brannagan 3rd, and P.H. Green. They are affiliated with the Department of Medicine, Division of Digestive and Liver Diseases at Columbia University Medical Center in New York, NY. For their study, the team recruited patients celiac disease and/or inflammatory bowel disease from the gastroenterology clinics at a medical center and local support groups. The team recruited control subjects without celiac disease or inflammatory bowel disease from the staff of the medical center, and from relatives and attendees at support groups. Researchers had each participant complete a survey that used two validated peripheral neuropathy standards to define and characterize peripheral neuropathy. The team found that 38.9% of participants with celiac disease and 38.7% in the inflammatory bowel disease group (P = 0.97) met criteria for peripheral neuropathy compared with 20.5% in the control group (P < 0.001). Using multiple logistic regression, the researchers found that those with celiac disease had higher odds of peripheral neuropathy (odds ratio, 2.51; 95% confidence interval, 1.82-3.47), adjusted for age, gender, diabetes, vitamin B12 deficiency, and cancer history; as did those with inflammatory bowel disease (odds ratio, 2.78; 95% confidence interval, 1.85-4.18). The results showed that people with celiac disease and/or inflammatory bowel disease had higher rates of peripheral neuropathy than did the general population. Source: J Clin Neuromuscul Dis. 2012 Mar;13(3):137-45.
  9. Celiac.com 11/28/2012 - A team of researchers recently set out to determine whether childhood antianaerobic antibiotic exposure is associated with the development of inflammatory bowel disease (IBD). Their findings show that children who are treated with antianaerobic antibiotics face a significantly higher risk of developing IBD. The team included Matthew P. Kronman, MD, MSCE, Theoklis E. Zaoutis, MD, MSCE, Kevin Haynes, PharmD, MSCE, Rui Feng, PhD, and Susan E. Coffin, MD, MPH.They are affiliated variously with the Division of Infectious Diseases, Seattle Children’s Hospital at the University of Washington in Seattle, Washington, the Division of Infectious Diseases at The Children’s Hospital of Philadelphia, and the Department of Biostatistics and Epidemiology, the Center for Clinical Epidemiology and Biostatistics at the Perelman School of Medicine at the University of Pennsylvania in Philadelphia, Pennsylvania. The team's findings appear in the 24 September issue of Pediatrics. To get a better picture regarding use of antibiotics on children and a possible connection to IBD, the team conducted a retrospective cohort study using data from 464 UK ambulatory practices in The Health Improvement Network. The study looked at all children in the network with 2 or more years of follow-up from 1994 to 2009. The team screened and excluded anyone with previous IBD. They then cataloged all antibiotic prescriptions used by all children in the study. Finally, they tracked the children's data from practice enrollment and IBD development, practice de-registration, 19 years of age, or death. Their defined study parameters included the following antianaerobic antibiotics: penicillin, amoxicillin, ampicillin, penicillin/β-lactamase inhibitor combinations, tetracyclines, clindamycin, metronidazole, cefoxitin, carbapenems, and oral vancomycin. Their study looked at 1,072,426 children for a total of 6.6 million person-years of follow-up. Of those children, 748 developed IBD. Children treated with antianaerobic antibiotics had nearly 1.52 cases of IBD per ten-thousand person years, while those who were not given antibiotics saw just 0.83 cases per ten-thousand person-years; for an 84% relative risk differential. Antibiotic exposure throughout childhood was associated with the development of IBD, but this relationship decreased with increasing age at exposure. That is, the longer doctors waited to give children antibiotics, the more the risk of iBD went down. Children treated with antibiotics before 1 year of age showed an adjusted hazard ratio of 5.51 (95% confidence interval [CI]: 1.66–18.28), while that decreased to 2.62 (95% CI: 1.61–4.25) for children first treated at 5 years old, and to 1.57 (95% CI: 1.35–1.84) for those first treated at 15 years of age. Overall, each course of antibiotics increased the IBD hazard by 6% (4%–8%). The study showed that children who received two or more antibiotic courses were more highly likely to develop IBD than those who received 1 to 2 courses, with adjusted hazard ratios of 4.77 (95% CI: 2.13–10.68) versus 3.33 (95% CI: 1.69–6.58). So, based on this study, treating children with antianaerobic antibiotics puts them at risk for developing IBD. It will be interesting to see how the medical community responds to this study, and whether there is greater effort made to avoid giving these powerful antibiotics to children. What do you think? Do you have IBD? Did you receive these antibiotics as a kid? Let us know your thoughts by commenting below. Source: Pediatrics; 24 September 2012
  10. Celiac.com 03/24/2010 - Celiac disease is a permanent intolerance to gluten ingestion, which is predisposed in individuals with human leukocyte antigen (HLA ) and DQ2 or DQ8 haplotype. Celiac is an autoimmune disease and there has been mounting evidence indicating a substantial connection between celiac and other autoimmune disorders such as, autoimmune thyroiditis and diabetes mellitus type 1. Additionally, recent evidence has surfaced correlating a relationship between celiac and inflammatory bowel disease (IBD). An Italian study was designed to research a gene commonly associated with celiac disease known as MYO IXB, which was recently found to be mutated in IBD patients as well. Additionally, the chromosome 4q27 region is also associated with celiac disease and other autoimmune diseases, and predisposes patients to ulcerative colitis, indicating a common genetic code for these diseases. Although, other IBD risk factors were not found to be candidate genes for celiac disease. Italian patients with IBD were tested for celiac disease and their results were lower than expected, and lower than compared with the general population. celiac disease was found to be more prevalent in patients with ulcerative colitis than in those with Crohn's disease. Ulcerative colitis is typically isolated to the colon and is not present in the small intestine. However, there have been reports of diffuse duodenitis in ulcerative colitis patients which is sometimes mistaken for celiac disease. The gastroduodenal association with Crohn's disease varies from 30% to 80% of patients. Celiac disease and inflammatory bowel are not related, they are merely two diseases that sometimes cross the same path. While the prevalence of celiac disease in Italian IBD patients was typically low indicating no close relationship between celiac disease and inflammatory bowl disease, the mutual relationship of these diseases lies in the fact that patients with both conditions frequently share a history of iron-deficient anemia. It is thus important for patients that are unresponsive to treatments for IBD and are prone to incessant anemia, to also test for celiac disease. Source: Science Direct
  11. Celiac.com 05/11/2012 - Horses are susceptible to inflammatory small bowel disease, and the condition effects horses in much the same way as it effects humans. As with its human counterpart, equine inflammatory small bowel disease (ISBD) is an idiopathic pathologic condition that seems to be growing more and more common. A research team recently conducted a study to examine the possibility that gluten may play a role in equine ISBD. The researchers were J.H. van der Kolk, L.A. van Putten, C.J. Mulder, G.C. Grinwis, M. Reijm, C.M. Butler, B.M. von Blomberg of the Department of Equine Sciences, Medicine Section, Faculty of Veterinary Medicine at the University of Utrecht, in Utrecht, in the Netherlands. For their study, the team assessed antibodies that are known to be important in the diagnosis of human celiac disease: IgA antibodies to human recombinant and guinea pig tissue-transglutaminase (TGA), native gliadin (AGA), deamidated-gliadin-peptides (DGPA), and primate and equine endomysium (EMA). The team measured these antibodies using blood samples from three different groups of horses: Twelve ISBD affected horses on a gluten-rich diet, along with two control groups. The first control group included 22 horses on a gluten-rich diet, and the second included 25 horses on a gluten-poor diet. The researchers measured differences (p < 0.05) in the groups using the Wilcoxon test. They found that both ISBD-affected horses and gluten-rich control group had significantly (p < 0.0004) higher hrTGA titers than gluten-poor control group. However, ISBD horses did not show significantly higher levels of any of the celiac disease related antibodies when compared to gluten-rich controls. Still, They found significantly higher antibody levels (TGA, EMA and DGPA) in one of the ISBD horses. They put that horse, 14-year-old stallion, on a gluten-free ration for 6 months. They then reassessed his antibodies and found a significant reduction of antibody levels, along with clinical recovery associated with improved duodenal histopathology. The researchers write that this is the first such study assessing gluten-related antibodies in horses and that the results suggest a potential pathogenic role of gluten in at least some cases of equine ISBD. These clinical results suggest that further study into the immunologic basis of possible gluten-sensitive enteropathy in horses might have important implications for the human manifestation of the disease. Source: Vet Q. 2012 Apr 10.
  12. Celiac.com 03/28/2012 - A clinical research team wanted to determine if adding ascorbate (vitamin C) to gliadin-stimulated biopsy culture could reduce the mucosal immune response to gliadin in people with celiac disease. The research team included D. Bernardo, B. Martínez-Abad, S. Vallejo-Diez, E. Montalvillo, V. Benito, B. Anta, L. Fernández-Salazar, A. Blanco-Quirós, J. A. Garrote, and E. Arranz. They are affiliated with the Mucosal Immunology Lab of the Department of Paediatrics & Immunology at Spain's Universidad de Valladolid-CSIC. Their quest was fueled by the understanding that the IL-15/NF-κB axis plays a key role in celiac disease. Because ascorbate is known to inhibit effects on NF-κB, the IL-15/NFκB axis looks like a good possible molecular target for reducing gliadin-induced inflammation in celiac disease. For their study, the team conducted in vitro gliadin challenges (100 μg/ml) on duodenal biopsy explants from treated patients with celiac disease. Challenges were conducted with and without 20mM ascorbate. As an internal control, the team used an extra tissue explant in basal culture. The team then measured secretion levels of nitrites (3h), and IFNγ, TNFα, IFNα, IL-17, IL-13, and IL-6 (24h) on the supernatants. They measured IL-15 using western-blot on whole protein duodenal explants. When the team added ascorbate to in vitro culture gliadin-challenged biopsies, they found that the ascorbate blocked secretion of nitrites (p=0.013), IFNγ (p=0.0207), TNFα (p=0.0099), IFNα (p=0.0375), and IL-6 (p=0.0036), as compared with samples from culture that received no ascorbate. They also found that the addition of ascorbate reduced cytokine secretion to levels even lower than those observed in basal cultures (IFNγ: p=0.0312; TNFα: p=0.0312; IFNα: p=0.0312; and IL-6: p=0.0078). Moreover, the gliadin-challenge triggered IL-15 production in biopsies from treated celiac disease patients, while IL-15 was completely blocked in the cultures that received ascorbate. Interestingly, ascorbate completely blocked IL-15 production even in the only treated celiac disease-patient who showed basal IL-15 production. From these results, the team concludes that ascorbate reduces the mucosal inflammatory response to gluten in an in vitro biopsy culture. As such, ascorbate might offer supplementary benefits in future celiac disease therapy. Source: Allergol Immunopathol (Madr). 2012 Jan-Feb;40(1):3-8.
  13. Celiac.com 02/27/2012 - The relationship between celiac disease and inflammatory bowel disease has not been well documented. One study that hasn't gotten too much attention was published in 2008. To get a better idea regarding any connection, a team of researchers studied rates of celiac disease in patients with inflammatory bowel disease, along with the rates of inflammatory bowel disease in patients with celiac disease. The research team included J.S. Leeds, B.S. Höroldt, R. Sidhu, A.D. Hopper, K. Robinson, B. Toulson, L. Dixon, A.J. Lobo, M.E. McAlindon, D.P. Hurlstone, and D.S. Sanders. They are affiliated with the Gastroenterology and Liver Unit of Royal Hallamshire Hospital in Sheffield, UK. The team recruited patients from clinics specializing in inflammatory bowel disease and celiac disease, along with control subjects from the local population. They then tested subjects for Antigliadins, endomysial, tissue transglutaminase antibodies and total IgA levels. They offered duodenal biopsy to patients with positive antibodies. The team reviewed colonoscopy and biopsy data for celiac patients. In all, the team assessed 305 patients with celiac disease, 354 patients with IBD, and 601 healthy control subjects. The IBD group included 154 patients with ulcerative colitis (UC), 173 with Crohn's disease, 18 with indeterminate colitis, and nine cases of microscopic colitis. Forty-seven patients showed positive antibodies, while three patients showed villous atrophy upon biopsy. All three patients with villous atrophy showed positive anti-tissue transglutaminase antibodies, but only two tested positive for endomysial antibody (EMA). Ten celiac patients had IBD (5 UC and 5 lymphocytic colitis). Five control subjects had celiac disease, while two had IBD (1 Crohn's disease and 1 UC). Stepwise multiple logistic regression showed that only antibody positivity was a factor (p<0.0001). The results showed that people with celiac disease had IBD at rates ten times higher than the control group (odds ratio 9.98, 95% CI 2.8-45.9, p=0.0006), while patients with IBD had celiac disease at about the same rates control subjects (odds ratio 1.02, 95% CI, 0.24-4.29, p=1.0). Source: Scand J Gastroenterol. 2008;43(10):1279-80
  14. Celiac.com 06/19/2009 - Specialty pharmaceutical and diagnostic company, Prometheus Laboratories Inc., announced results from two recent studies concerning the use of serologic testing to predict inflammatory bowel disease (IBD). The first study assessed the consistency of biomarkers in patients who received multiple Prometheus IBD Serology 7 tests within a two-year period. Overall levels for repeat testing orders were just 2.2%. Original and repeat tests showed a high degree of agreement. Average variation in biomarker serum concentrations ran between 2.2 EU/mL and 4.3 EU/mL. Results agreed with prior studies suggesting biomarker stability over similar time periods. Further studies are needed to gauge the impact of therapy on biomarker stability over the long term. A second, multi-center clinical study of 1,574 subject samples brought the total development cohort of the test to a more heterogeneous 3,626 patient samples. Results with this large patient cohort further showed that combining multiple markers with Prometheus' Smart Diagnostic Algorithm permits clinicians to better distinguish IBD vs. non-IBD and Crohn's disease vs. ulcerative colitis, compared to standard cutoff value analysis of the individual markers alone. Prometheus IBD Serology 7 combines multiple serologic markers with a proprietary Smart Diagnostic Algorithm, increasing test sensitivity by more than 25% over single marker sensitivity values. Source: Medical News Today
  15. Clin Chem Lab Med. 2004;42(10):1092-7 Celiac.com 01/22/2005 - A study by Italian researchers has found that anti-tissue transglutaminase (tTG) antibodies, once considered to be identical to anti-endomysial antibodies (EMA) in celiac disease, can also be found in patients with inflammatory bowel disease. The researchers looked at serum and intestinal tTG levels in 49 patients with Crohns disease, 29 patients with ulcerative colitis, 45 patients with celiac disease, 85 autoimmune patients as disease controls, and 58 volunteers as healthy controls. Additionally, Immunoglobulin A (IgA) anti-recombinant human tissue transglutaminase and anti-endomysial antibody detection in sera and fecal supernatants, along with adsorption of positive sera with recombinant human tissue transglutaminase, were performed on all patients. The researchers detected an increase in tTG concentration in all patients with celiac disease, and also low positive values in those with Crohns disease and ulcerative colitis, however the EMA were only detected in those with celiac disease. According to the researchers, the "Data highlight that both circulating and intestinal anti-tissue transglutaminases are detectable in inflammatory bowel disease, and that they are related to disease activity. These features underline that, in addition to anti-tissue transglutaminase, an anti-endomysial antibody test is necessary in the diagnostic work-up of celiac sprue, especially in patients with known inflammatory bowel disease." This study supports others that have found that the sole use of tTG to diagnose celiac disease may lead to misdiagnoses, and EMA testing must be performed to make an accurate celiac disease diagnosis.
  16. Am J Gastroenterol 2000;95:2154-2156,2285-2295. Celiac.com 10/14/2000 - According to new research done by Dr. Andrew J. Wakefield, of the Royal Free and University College Medical School, in London (published in the September issue of the American Journal of Gastroenterology) children with developmental disorders seem to be at risk of developing a unique type of inflammatory bowel disease (IBD). This newly discovered type lacks the typical features seen in Crohns disease and ulcerative colitis. The researchers studied 60 children with developmental disorders (50 had autism, five had Aspergers syndrome, two had disintegrative disorder, one had attention deficit hyperactivity disorder, one had schizophrenia and one had dyslexia.) whose ages ranged from 3 to 16 years old to compare the clinical and histologic features against 37 developmentally normal controls who underwent evaluation for possible IBD. According to Dr. Wakefield and colleagues The combination of ileocolonic lymphoid nodular hyperplasia and colitis in children with developmental disorders distinguished them from developmentally normal children with similar symptoms (including abdominal pain and constipation) in whom lymphoid nodular hyperplasia and histopathological change were uncommon. They emphasize that their finding are consistent with those of other recent case studies, and that in their study inflammatory changes were detected in the upper gastrointestinal tract that were unique in children with autism and IBD, compared with developmentally normal children with IBD. Further, there is accumulating evidence of a specific type of enterocolitis in autism that makes it tempting to suggest that a gut-brain interaction is involved in the pathogenesis of what many researchers are now calling autistic enterocolitis. The detection of opioid peptides of dietary origin in the urine of some of the affected children further supports this theory. The team emphasizes that further studies and more evidence is needed to establish a direct link between an inflamed gut and the brain in those with autism.
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