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Found 8 results

  1. I thought I would make a thread based on this subject, as it is something I am heavily researching right now. I thought I would summarize the research and then talk a bit about my person journey so far. There is research and case studies out there that connect a campylobacter infection to celiac disease. The first is a case study of a woman who had a bad bout of campylobacter. Months after getting it, she continued to have symptoms of GI distress - bloating, nausea, pain. Long rounds of testing for various GI problems, and nothing was positive. One year after her illness, they finally tested her for celiac disease through blood and biopsy, and found it...negative! So they sent her on her way. Five years later, after finding no relief, a follow-up blood test and intestinal biopsy were positive for celiac disease. The authors of the study connect her campylobacter to the onset of the celiac disease, though they make a general connection between all infections and the potential trauma they induce The next study takes it one step farther and directly connects Campylobacter Jejuni to Celiac Disease. It's a bit dense, but the long and short of it is that certain strains of Campylobacter infect the GI cell structure in such a way that it causes an autoimmune response that ultimately leads to the development of Celiac. Here are links to both studies: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2657967/ http://www.ncbi.nlm.nih.gov/pubmed/17729402 On a personal note: Two years ago I got SEVERE food poisoning from milk that was tainted with campylobacter. A multiple day stay in the ICU and weeks of horrible pain left my body a mess - I was told by my doctor I was extremely lucky I didn't come out with bad damage to my liver. I slowly got better for a few months, and then I started to have these "episodes". Vomiting, diarrhea, chills, nausea. They only happened once or twice a month, and my doctor wrote them off as "post infectious IBS". As time went on, the episodes got closer and closer together. We began testing - H Pylori, gastroparesis, blood work, endoscopies - besides finding high inflammation in my stomach, nothing was positive. Eventually they blood-tested for celiac, which was negative. They were stumped. Meanwhile, I was literally wasting away - down to 83 pounds. In desperation, I reached out to a nutritionist, who put me on a very strict elimination diet. I immediately began to feel better. Within a month, I started gaining back weight, and my energy came back. We began introducing foods back. Everything was fine- until we reached gluten. One cracker, and I was back to where I started. The intense abdominal pain, the vomiting, the diarrhea, the chills, and a week of general misery. We took it back out, everything cleared up, and re-tested again 2 months later. Same result. This time, an odd rash down the back of my neck joined the other symptoms. Because the blood test for celiac disease we took back when this thing started was negative, we assumed that the campylobacter must have just damaged my stomach and I simply had a hard time digesting gluten. So out of my diet it went. However, with every accidental glutening the symptoms got worse, as did the rash. Finally I went back to the GI a month ago after a particularly bad "glutening". He took one look at the rash and said it was clearly dermatitis herpetiformis. The problem at this point is that besides the glutening, I had been off gluten for a year and a half. We just adopted four kids, and for me to go on gluten for 2 weeks to do the test properly would be devastating - I would be unable to care for my family in any way for potentially a month due to the severity of the symptoms. So while it is technically undiagnosed, based on the rashes, symptoms, and preceding factors, he was able to say with good confidence that I am developing Celiac.
  2. Celiac.com 07/28/2016 - Celiac disease is an immune-mediated enteropathy triggered by gluten in genetically susceptible individuals. Researchers know that innate immunity plays a role in triggering celiac disease, but they don't understand the connection very well at all. Although previous in vitro work suggests that gliadin peptide p31-43 acts as an innate immune trigger, the underlying pathways are unclear and have not been explored in vivo. The research team included RE Araya, MF Gomez Castro, P Carasi, JL McCarville, J Jury, AM Mowat, EF Verdu, and FG Chirdo. They are variously affiliated with the Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP)(CONICET-UNLP), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina; the Catedra de Microbiología, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina; the Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada; the Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, Scotland, United Kingdom; and with the Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP)(CONICET-UNLP), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina. Their team observed that introduction of p31-43 into the gut of normal mice causes structural changes in the small intestinal mucosa consistent with those seen in celiac disease, including increased cell death and expression of inflammatory mediators. The effects of p31-43 were dependent on MyD88 and type I IFNs, but not Toll-like receptor 4 (TLR4), and were enhanced by co-administration of the TLR3 agonist polyinosinic:polycytidylic acid. Together, these results indicate that gliadin peptide p31-43 activates celiac-related innate immune pathways in vivo, such as IFN-dependent inflammation. These findings also suggest a common mechanism for the potential interaction between dietary gluten and viral infections in the pathogenesis of celiac disease, meaning that certain viral infections may pave the way for celiac disease to develop. Source: Am J Physiol Gastrointest Liver Physiol. 2016 Jul 1;311(1):G40-9. doi: 10.1152/ajpgi.00435.2015. Epub 2016 May 5.
  3. Celiac.com 09/18/2017 - Many researchers feel that the rising number of celiac disease cases supports the idea that common infections prior to the onset of autoimmune diseases could play a role in triggering the immune response. Do more respiratory infections in childhood mean a greater likelihood of celiac disease later in life? To answer that question, a team of researchers recently set out to explore the relationship between early clinical events and the development of celiac disease in genetically predisposed infants. The research team included Renata Auricchio, Donatella Cielo, Renato de Falco, Martina Galatola, Valentina Bruno, Basilio Malamisura, Maria Giovanna Limongelli, Riccardo Troncone, Luigi Greco. They are variously affiliated with the Department of Translational Medical Science, and the European Laboratory for the Investigation of Food Induced Diseases, University of Naples Federico II, Naples, Italy; the Department of Pediatrics, University Hospital of Salerno, Salerno, Italy; and Azienda Ospedaliera Gaetano Rummo Via dell'Angelo, Benevento, Italy. The team studied 373 newborns from families with at least 1 relative with celiac disease. They tested participants for human leukocyte antigen DQ2- or DQ8- and followed-up positive infants with clinical and serological assessments. They used cross tabulation and odds ratios to explore the risk associated with single variables, and logistic regression analysis was performed to determine the variables that contributed to the risk of developing celiac disease. They also used stepwise discriminant analysis to determine which variables could distinguish case patients from controls before diagnosis. The overall rate of celiac disease in this group was 6% at 3 years and 13.5% at 5 years of age, while a total of 34 children, developed celiac disease before the sixth year of life, a rate of 14%. According to analysis of adverse events, people with celiac disease shoed a higher frequency of respiratory tract infections in their first 24 months of life. In a stepwise discriminant analysis, which included sex and human leukocyte antigen risk class, only respiratory infections in the second and first years of life significantly contributed to discrimination of case patients versus controls. The team's analysis showed that the frequency of respiratory infections in the first 2 years of life can be used to identify children who later developed celiac disease. Kids with more infections were much more likely to develop celiac disease later on. Clinicians may use this information during diagnosis to help zero in on patients likely to have celiac disease. Source: Pediatrics, September 2017
  4. 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
  5. Celiac.com 11/16/2009 - Could unknown benefits from one of the oldest parasites of the human digestive tract hold the key to cure for celiac disease? Australian scientists think so. Encouraged by successful treatments of Crohn's and ulcerative colitis by American researchers using a pig whipworm (Trichuris sues), a team of Australian researchers is recruiting volunteers with celiac disease for trials using human hookworm (Necator americanus). The researchers have undertaken a similar preliminary study using a human hookworm in Crohn's patients. Researchers hypothesize that the disappearance of intestinal parasites from humans in developed countries may be responsible for the upsurge in many diseases including Celiac Disease, Crohn's, ulcerative colitis, asthma and hay fever. Using a small group of healthy people with celiac disease, the investigators will look to see if human hookworm interferes with the human immune reaction to gluten. Parasites survive partly by interfering with the host's immune response. The mechanisms they use to accomplish this are similar to those required by a person to regulate against the so-called autoimmune disorders, wherein the body begins to fight against itself. The investigators suspect that when parasites are excluded from the environment, some individuals become sufficiently self-reactive to develop an autoimmune disease. Using a small group of healthy people with celiac disease, the investigators will test if a human hookworm, Necator americanus, inhibits immune responsiveness to gluten. Specifically, they will examine whether hookworm infection will change the immune processes and suppress gluten sensitivity in people with celiac disease. Celiac disease is a good model for studying Crohn's disease because both involve similar immune changes. However, celiac patients are usually healthier overall, and, importantly, are not taking powerful immune suppressive drugs, and the provocative antigens (molecules that engage the immune system and provoke the disease) are well known and can be administered or cut out at will. In addition to directly benefitting celiac disease sufferers, this study may provide potential guidance in the use of hookworms to control inflammatory bowel disease. The study is open to people with proven celiac disease who reside in Brisbane, Australia. Those who enroll will be required to avoid gluten for six months. The blinded study will compare disease activity and immunity after a controlled break from the gluten-free diet in celiac patients, before and after hookworm infection. The team will use conventional and experimental methods to examine the disease severity and the immune system of celiac subjects before and after being inoculated with N. americanus. They will then compare immunity levels of the study subjects against those of matched, celiac control subjects (not infected with hookworm), before and after eating four pieces of standard white bread each day for three to five days. The initial study group will be small. The researchers will recruit ten subjects for each arm of the study, for a total of twenty. Initially, ten larvae will be placed on the skin under a light dressing for thirty minutes, followed by five more after twelve weeks. The researchers intend to asses whether the hookworm infection will change the immune processes and suppress gluten sensitivity in people with celiac disease. Outcomes to be measured will be those that reflect the activity of celiac disease. Stay tuned to see if hookworm therapy will be coming to a gastroenterologist near you! Tell us what you think. Would you sign up? Comment below. Source: ClinicalTrials.gov
  6. Celiac.com 10/05/2015 - Studies on early life infections and risk of later celiac disease (celiac disease) are inconsistent but have mostly been limited to retrospective designs, inpatient data, or insufficient statistical power. A team of researchers recently set out to determine whether early life infections are associated with increased risk of later celiac disease using prospective population-based data. The research team included K. Mårild, C.R. Kahrs, G. Tapia, L.C. Stene, and K. Størdal. T Division of Epidemiology at the Norwegian Institute of Public Health in Oslo, Norway, the Department of Medical Epidemiology & Biostatistics at the Karolinska Institutet in Stockholm, Sweden, and with the Department of Pediatrics at Østfold Hospital Trust in Fredrikstad, Norway. This study is based on the Norwegian Mother and Child Cohort Study, and includes prospective, repeated assessments of parent-reported infectious disease data up to 18 months of age for 72,921 children born between 2000 and 2009. The team identified celiac disease patients through parental questionnaires and the Norwegian Patient Registry. Logistic regression was used to estimate odds ratios adjusted for child's age and sex (aOR). Their data showed that, over an average follow-up period (ranging from 4.5-14.5 years, and averaging 8.5 years, 581 children (0.8%) were diagnosed with celiac disease. Children with ten or more infections up to age 18 months had a significantly higher risk of later celiac disease, as compared with children with four or less infections (aOR=1.32; 95% confidence interval (CI)=1.06-1.65; per increase in infectious episodes, aOR=1.03; 95% CI=1.02-1.05). The aORs per increase in specific types of infections were as follows: upper respiratory tract infections: 1.03 (95% CI=1.02-1.05); lower respiratory tract infections: 1.12 (95% CI=1.01-1.23); and gastroenteritis: 1.05 (95% CI=0.99-1.11). The results were largely unchanged even after making additional adjustments for maternal celiac disease, education level, smoking, birth weight, prematurity, infant feeding practices, birth season, and antibiotic treatment. This is the first large-scale population-based cohort study of this association. These results are in line with earlier studies that suggest that early life infections may have a role in celiac disease development. However, further study is needed to fully eliminate surveillance bias and reverse causation as non-causal explanations for this association. Source: Am J Gastroenterol. 2015 Sep 8. doi: 10.1038/ajg.2015.287.
  7. I used to be under the impression that celiac disease was a condition that arose when one was born. According to Dr. Fasano's more recent research, we now know that this is not the case. People can go 70 years tolerating gluten just fine before it causes problems. One of the things that has intrigued me is the recommendation to keep infants away from gluten until 4-6 months have lapsed. I believe this has to do with intestinal permeability allowing greater quantities of gluten to travel through thus making the immune system not cope well and thus resulting in it malfunctioning and destroying the gut and developing defective memory cells that will be there for the rest of their lives. I also often hear of people being diagnosed with celiac disease after a cold, flu or gastrointestinal infection. If this is the case, is it possible that avoiding gluten during a time of emotional stress or infection (and then re-introducing after fully recovering from the event) may prevent the onset of celiac disease? Let me know your thoughts.
  8. Celiac.com 01/14/2013 - Sweden has seen a sharp rise in cases of celiac disease in children under two years of age. A research team recently studied the possible connection between early infections and celiac disease, along with their possible role in the explosion of celiac cases in Swedish children. The research team included Anna Myléus, Olle Hernell, Leif Gothefors, Marie-Louise Hammarström, Lars-Åke Persson, Hans Stenlund and Anneli Ivarsson. They are affiliated with the Epidemiology and Global Health, Department of Public Health and Clinical Medicine at Umeå University, Pediatrics unit of the Department of Clinical Sciences at Umeå University, the Immunology unit of the Department of Clinical Microbiology at Umeå University in Umeå, Sweden, and with the International Maternal and Child Health, Department of Women's and Children's Health in Uppsala University in Uppsala, Sweden. The team used a questionnaire to carry out a population-based incident case-referent study. The questionnaire went out to 475 cases and 950 referents, and included questions on family characteristics, infant feeding, and the child's general health. All cases of celiac disease cases were diagnosed before two years of age, and fulfilled the diagnostic criteria of the European Society for Pediatric Gastroenterology, Hepatology and Nutrition. The team randomly selected referents, matched by criteria, from the national population register. The final analysis included 373 (79%) cases of confirmed celiac disease and 581 (61%) referents, for a total of 954 children. For each case of celiac disease, the team matched complete information on main variables of interest with one or two referents. The results showed that children who suffered three or more parental-reported infectious episodes, regardless of type of infection, during the first six months of life faced a significantly higher risk for later celiac disease.. This risk remained after the team adjusted for infant feeding and socioeconomic status (odds ratio [OR] 1.5; 95% confidence interval [CI], 1.1-2.0; P=0.014). Infants who had several infectious episodes, and whose parents introduced dietary gluten in large amounts, compared to small or medium amounts, after breastfeeding was discontinued faced an even greater risk (OR 5.6; 95% CI, 3.1-10; P<0.001). This study suggests that children who suffer repeated infections before age two face an increased risk for developing celiac disease later on. The risk was even greater in children who suffered repeated infections and whose parents introduced gluten in large quantities after weening. The team concludes that early infections probably made a minor contribution to the rise in celiac disease cases in Swedish children relative to the amounts of gluten introduced into the children's diets after weening. Source: BMC Pediatrics 2012, 12:194 doi:10.1186/1471-2431-12-194
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