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Found 7 results

  1. Past few days I've been working on a diet plan that will hopefully help more than what I've been doing. This morning I woke up feeling like I did a few hundred crunches yesterday though all I did was rest. My constipation problems haven't ever given me this type of discomfort so I'm not sure if it's the intestines actually starting to heal more. Any suggestions or related experiences? Thanks!
  2. Celiac.com 12/22/2016 - The nature of gut intraepithelial lymphocytes (IELs) lacking antigen receptors remains controversial. A team of researchers recently set out to better understand the mechanisms by which innate intraepithelial lymphocytes develop in the intestine and become cancerous in celiac disease patients. The research team included J Ettersperger, N Montcuquet, G Malamut, N Guegan, S Lopez-Lastra, S Gayraud, C Reimann, E Vidal, N Cagnard, P Villarese, I Andre-Schmutz, R Gomes Domingues, C Godinho-Silva, H Veiga-Fernandes, L Lhermitte, V Asnafi, E Macintyre, C Cellier, K Beldjord, JP Di Santo, N Cerf-Bensussan, and B Meresse. They are variously affiliated with the INSERM UMR1163, Laboratory of Intestinal Immunity, Institut Imagine; Laboratory of Human Lymphohematopoiesis; Institut Necker-Enfants-Malades, INSERM UMR1151 and, Biological Hematology, AP-HP Necker-Enfants-Malades; the Université Paris Descartes-Sorbonne Paris Cité and Institut Imagine in Paris, France; AP-HP, Department of Gastroenterology, Hôpital Européen Georges Pompidou, 75015 Paris, France; Institut Universitaire d'Hématologie, Hôpital Saint-Louis, Paris, France; Innate Immunity Unit, Institut Pasteur, 75015 Paris, France; INSERM U 668, Paris, France; Paris-Descartes Bioinformatic Platform, 75015 Paris, France; and with the Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa in Lisbon, Portugal. The team was able to show, in humans and in mice, innate intestinal IELs expressing intracellular CD3 (iCD3(+)) differentiate along an Id2 transcription factor (TF)-independent pathway in response to TF NOTCH1, interleukin-15 (IL-15), and Granzyme B signals. In NOTCH1-activated human hematopoietic precursors, IL-15 induced Granzyme B, which cleaved NOTCH1 into a peptide lacking transcriptional activity. As a result, NOTCH1 target genes necessary for T cell differentiation were silenced, and precursors were reprogrammed into innate cells with T cell marks, including intracellular CD3 and T cell rearrangements. In the intraepithelial lymphoma complicating celiac disease, iCD3(+) innate IELs acquired gain-of-function mutations in Janus kinase 1 or Signal transducer and activator of transcription 3, which enhanced their response to IL-15. The research team observed and described gut T cell-like innate IELs, decoded their pathway of change, and showed their malignant transformation in celiac disease. This study offers an exciting glimpse into the hard work being done in the far corners of celiac disease and cancer research. Source: Immunity. 2016 Sep 20;45(3):610-25. doi: 10.1016/j.immuni.2016.07.018. Epub 2016 Sep 6.
  3. Sorry for handing out too much information here, but I really don't know who else to ask on this one. I'm recovering from my last glutening, which was about 4 weeks ago. One thing I've noticed late in my recovery cycle is that my stools get really crazy. The first week after being glutened I get the usual "Big D." Then the next week or two they're normal. Then about week 4 or 5 they become really strange. They feel solid when they're inside me, but when I go to the bathroom, they totally fall apart in the toilet. It's not watery, like diahrehea (sp?), but comes out solid then separates into thousands of tiny pieces. Sometimes some mucus will come out too. I also noticed that when I have these kind of BMs, I have the sudden urge to go to the bathroom and I can't control it, like with a normal BM. So, if anyone hasn't gotten totally grossed out by my post yet and is still reading, here are my questions: Does anyone else have this issue? Is this a normal part of my intestines recovering from gluten or do I need to look to another food intolerance as a cause? I've been gluten-free for 2 years. I'm only doing gluten-free at the moment, but probably need to get rid of the dairy too as I have really bad sinus problems. Could casein be a cause? Do you think this is something I should go see the doctor for? I had such a bad experience when I went to the gastro doctor that I hesitate to go again. But if I need to visit a gastro dr., I can do some looking around and find a better one, I guess. Thanks for any help and advice you can give me. And sorry if I grossed anyone out
  4. Dig Liver Dis. 2002 Dec;34(12):846-50. Celiac.com 07/12/2004 – In a study designed to determine the causes of continued gastrointestinal problems in celiacs who are on a gluten-free diet, Italian researchers looked at 15 celiac patients who continued to experience symptoms even after 6-8 months on a gluten-free diet. Histology improved in all patients after this time so refractory celiac disease was excluded as the cause. The scientists performed AGA and EMA tests, stool examination, EGD with histological examination of small bowel mucosa, and sorbitol-, lactose-, and lactulose H2-breath tests to determine a possible cause of the patients persistent symptoms. The researchers found that one patient who had Marsh II lesions was fully compliant with his diet but had mistakenly taken an antibiotic that contained gluten. Two of the patients had lactose malabsorption, one had Giardia lamblia, and one had Ascaris lumbricoides infestation. Ten patients were found to have small intestinal bacterial overgrowth (SIBO) by lactulose H2-BT. The doctors prescribed a diet without milk or fresh milk-derived foods to the patients with lactose malabsorption; and treated the patients with parasite infestation with mebendazole 500 mg/day for three days for two consecutive weeks. The SIBO patients were treated with rifaximin 800 mg/day for one week. All of the patients were re-evaluated one month after treatment, and all were symptom-free. The researchers conclude that SIBO affects most celiacs who have persistent gastrointestinal symptoms after going gluten-free.
  5. Research indicates that rod-shaped bacteria, of the species Clostridium, Prevotella, and Actinomyces, in the proximal small intestine may contribute to some cases of celiac disease in children. Recent data builds on previous research by the team from 1985 to 1996, which proved that rod-shaped bacteria were present in the proximal small intestine of Swedish children with celiac disease, but not in those without celiac disease. For the current study, Sten Hammarström and colleagues from Umeå University in Sweden used an electron microscope to scan proximal small intestine biopsies from 45 children with celiac disease taken between 2004 and 2007, and 18 without the condition. To identify the bacteria, they used 16S ribosomal DNA sequencing in DNA extracted from biopsies washed with solution containing an agent that enriches bacteria attached to the epithelial lining. In healthy children with no celiac disease, Streptococcus and Neisseria bacteria are most common of the normal, mucosa-associated microbial flora of the proximal small intestine, along with a limited number of other genera, including Veillonella, Gemella, Actinomyces, Rothia, and Hemophilus. Surprisingly, the researchers found that microbial flora of the proximal small intestine in biopsies from celiac disease patients differed only slightly from that of the control subjects. Only a single biopsy tested positive for rod-shaped bacteria. This finding made the team to look more closely at the microbial flora of nine frozen celiac disease samples that showed the presence of rod-shaped bacteria. In these samples, microbial flora were substantially richer in Clostridium, Prevotella, and Actinomyces compared with biopsies lacking rod-shaped bacteria. The researchers also note that all three types of bacteria could be found in two current celiac disease biopsies taken from children born during the celiac disease epidemic in Sweden in 1985–1996, when the earlier study was carried out. During this time, rates of celiac disease in children younger than 2 years of age increased four-fold. “We hypothesize that the increased frequency of rod-shaped bacteria in the jejuna mucosa of celiac disease children at least partly was due to the changes in infant-feeding practice during that time,” write the researchers. The changes resulted from new national feeding recommendations for infants to delay the introduction of gluten-containing foods from 4 to 6 months. This meant that many more children consumed their first gluten without the protective benefits of breastfeeding, the researchers write. The recommendation was later reversed. The study by Hammarström and co-workers supports their conclusion that these rod-shaped bacteria may contribute to celiac disease in genetically susceptible individuals by uptaking and transforming gluten into large immunogenic peptides, which can then cross with the bacterium through the epithelium, or interfere with the barrier action of the epithelium to permit the passage of gluten into the under-laying tissue. “Such bacteria could be seen as an adjuvant promoting T-cell activation,” they say. “Whether the identified bacteria have any of these properties remain to be elucidated.” Am J Gastroenterol 2009; 104: 3058–3067
  6. TI- Disaccharidasen-Aktivitaten als Beurteilungskriterium der Dunndarmschleimhaut. AU- Stern M; Plettner C JN- Monatsschr Kinderheilkd; 131 (5) p264-8 PY- May 1983 AB- Activities of lactase, sucrase, and maltase were determined in small intestinal biopsies of 125 children with Coeliac disease, cows milk protein intolerance, transient gluten intolerance, nonspecific enteropathies, and controls. Four cases of primary disaccharidase deficiencies could be identified. In the enteropathies, morphometric data were more closely correlated to the degree of the mucosal lesion (r = -0.92 for crypt depth) than were disaccharidase activities (r = 0.61 for lactase). In a stepwise discriminate analysis of the patient groups, based upon immunological, morphometric, and biochemical variables, lactase activity was a valuable secondary criterion, ranking third among the variables used.
  7. TI- Proba prowokacyjna u dzieci z nietolerancja biaLek mleka krowiego i glutenu: ocena reakcji klinicznych i zmian w bLonie sluzowej jelita cienkiego. AU- Kaczmarski M CS- Kliniki Chorob Zakaznych Dzieci AM w BiaLymstoku. JN- Pol Tyg Lek; 45 (8-9) p161-5 PY- Feb 19-26 1990 AB- Provocation test (re-introduction of the noxious protein) was carried out in two groups of patients: (a) with intolerance to the cow-milk proteins (41 children) treated with milk-free diet for 6-24 months, and ( with gluten intolerance (26 children) treated with gluten-free diet for 6-36 months. The following parameters were compared: type and frequency of the clinical symptoms seen in these patients prior to the introduction of allergen-free diet. Moreover, the type of observed morphological changes in the small intestine mucosa following provocation test were analyzed in the groups of 7 patients. A two-year elimination of milk from the diet produces milk tolerance in about 61% patients; clinical symptoms in the remaining children are diversified. Re-introduction of gluten with the diet (provocation test) produces recurrence of gluten intolerance in 96% of children treated with gluten-free diet for 2-3 years. Recurrence of the disease was accompanied by the atrophy of the intestinal villi.
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