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Showing results for tags 'pathology'.
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Celiac.com 01/18/2016 - How come only 2% to 5% of genetically susceptible individuals develop celiac disease? Researchers attempting to answer that question have turned their focus to environmental factors, including gut microorganisms, that may contribute to the development of celiac disease. In a recent study, published in The American Journal of Pathology, researchers using a humanized mouse model of gluten sensitivity found that the gut microbiome can play an important role in the body's response to gluten. Their data show that the rise in overall celiac disease rates over the last 50 years may be driven, at least partly, by variations in gut microbiota. If this proves to be true, then doctors may be able to craft "specific microbiota-based therapies" that "aid in the prevention or treatment of celiac disease in subjects with moderate genetic risk," says lead investigator Elena F. Verdu, MD, PhD, Associate Professor, Division of Gastroenterology, Department of Medicine, Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON (Canada). For their study, the team used mice that express the human DQ8 gene, which makes them genetically susceptible to inflammatory responses to gluten, researchers compared immune responses and pathology in the guts of mice that differed in their gut microorganisms. The three groups included germ-free mice, clean–specific-pathogen-free (SPF) mice with microbiota free of opportunistic pathogens and Proteobacteria, and conventional SPF mice that were colonized with a mixture of microorganisms including opportunistic pathogens and Proteobacteria. For example, the microbial profile of conventional SPF mice included Staphylococcus, Streptococcus, and Helicobacter, while the clean SPF had none. Researchers already know that growth and activation of intraepithelial lymphocytes (IELs) is an early sign of celiac disease. This research team saw that gluten treatment led to increased IEL counts in germ-free mice, but not in clean SPF mice. The gluten-induced IEL response in germ-free mice was accompanied by increased cell death in the cells lining the gastrointestinal tract (enterocytes), as well as anatomical changes in the villi lining the small intestine. The germ-free mice also developed antibodies to a component of gluten, known as gliadin, and displayed pro-inflammatory gliadin-specific T-cell responses. A non-gluten protein, zein, did not affect IEL counts, indicating that the response was gluten specific. Meanwhile, the mice colonized with limited opportunistic bacteria (clean SPF), did not develop gluten-induced pathology, compared to germ-free mice or conventional SPF mice with a more diverse microbiota. Interestingly, this protection was suppressed when clean SPF mice were supplemented with an enteroadherent E. coli isolated from a patient with celiac disease. These results are preliminary, and other researchers stress that the specific role of Proteobacteria in celiac disease should not be over interpreted. In an accompanying Commentary, Robin G. Lorenz, MD, PhD, of the Department of Pathology at the University of Alabama at Birmingham, writes that these findings "implicate opportunistic pathogens belonging to the Proteobacteria phylum in celiac disease; however, this does not indicate that Proteobacteria cause celiac disease." Instead, Dr. Lorenz suggests, there may be numerous possible avenues by which Proteobacteria enhance the exposure and immune response to gluten or gliadin. So, the takeaway here is that, while these early results are highly interesting and certainly merit follow-up, it's way too early to say that certain types of gut bacteria may be driving celiac disease, and any types of bacterial treatments that might prevent celiac disease from developing are just the stuff of imagination. Still, this is an important discovery that might pave the way for exactly such types of therapy in the future, so stay tuned. Source: The American Journal of Pathology
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Celiac.com 01/02/2012 - To properly diagnose celiac disease doctors must observe classic histological changes to small bowel mucosa. Success rates can vary among clinics and practitioners. A clinical team recently compared biopsy interpretation between different pathology practice types. A research team recently assessed variability in small bowel histopathology reporting between different pathology practice settings, and its impact celiac disease diagnosis. The researchers included Carolina Arguelles-Grande, Christina A. Tennyson, Suzanne K. Lewis, Peter H. R. Green, and Govind Bhagat. The team used a pathologist to blindly assessed biopsies from community hospitals (n=46), university hospitals (n=18) and commercial laboratories (n=38) for differences in histopathology reporting and agreement in diagnosis of celiac disease and degree of villous atrophy (VA) by k analysis. Data showed very good agreement for primary diagnosis between the authors and university hospitals (k=0.888), but only moderate agreement compared with community hospitals (k=0.465) or commercial labs (k=0.419). The review showed that diagnosis varied in 26 (25%) cases, leading to a 20% increase in celiac disease diagnosis after review. The 49 patients diagnosed with celiac disease by both institutions showed fair agreement in degree of VA (k=0.292), with moderate agreement between the authors and commercial laboratories (k=0.500) and fair agreement with university hospitals (k=0.290) or community hospitals (k=0.211). In 27% of cases, the degree of VA was upgraded, while VA was downgraded in just 2% of cases. Data also showed poor agreement for Marsh score categories 1 and 2 (k<0.0316), with both missed at other centers, and just fair or moderate agreement for Marsh scores 3a and 3b. They found that data on the degree of VA and intraepithelial lymphocytosis were lacking in 26% and 86% of reports, while non-quantifiable descriptors, such as ‘blunting’ or ‘marked atrophy’ were common. The data show that community-based hospitals and commercial pathology labs are under-diagnosing celiac disease-related histological changes. To combat variations in biopsy interpretation and reduce under-diagnosis of celiac disease, the team calls for greater celiac disease awareness and uniformity in small bowel biopsy reporting among pathologists. Source: Journal of Clinical Pathology (2011). doi:10.1136/jclinpath-2011-200372
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Celiac.com 08/29/2007 - A study that appeared in the August issue of Journal of Clinical Gastroenterology, found that celiac disease and small intestinal bacterial growth both show increased levels of intraepithelial lymphocytes (IELs), especially gammadelta+ IELs. A sharp increase in gammadelta+ IELs has been noted in people with celiac disease, but little is known about the role of this particular class of IELs in other intestinal pathologies. A team of researchers led by J.M. Remes-Troche set out to assess the levels of IEls, especially of gammadelta+, in the duodenal mucosa biopsies from individuals w/ celiac disease and to compare them with those of patients with small intestinal bacterial overgrowth (SIBO), and irritable bowel syndrome (IBS). The study team looked at 12 individuals with untreated celiac disease, 8 patients with SIBO, and 10 patients with diarrhea-predominant IBS. All patients were given an upper-endoscopy for mucosal biopsy and jejunal aspirate. Intraepithelial cells were isolated from 2 small bowel biopsies, and labeled with monoclonal antibodies CD103-PE (phycoerythrin), CD3-FITC (fluoresecein isothio-cynate), celiac disease-7R-PE, CD45RO-APC (allophycocyanin), and TcR gammadelta-FITC. Researchers conducted flow cytometry analysis using a standard FACScan. Total IEL levels and subsequent levels were catalogued as percentages as follows: 16.7 +/- 6% for IBS patients; 25.7 +/- 17% for SIBO patients; and 26 +/- +/- 13% in celiac patients (P=0.2). Patients with SIBO & celiac disease showed significantly higher percentages of gammadelta+ IELs (14.6 +/- 8% and 15.7 +/- 13%) compared to IBS patients (4.1 +/- 2.5%, P<0.05). The results of the study indicate that gammadelta+ IELs might play a crucial role against intestinal bacterial infections. Journal of Clinical Gastroenterology. 2007 Aug;41(7):671-676 health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
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The following was taken from THE SPRUE-NIK PRESS, September 1995. The University of Maryland School of Medicine sponsored a conference on July 14-15, 1995 entitled Celiac Disease: The Dark Side of the Gastrointestinal Planet, by Salvatore Auricchio, MD, summarized by Jim Lyles. Dr. Auricchio is Professor and Chairman of Pediatrics at the University Frederico II in Naples, Italy. celiac disease manifests itself in the small intestine. A distinct pattern of abnormalities has been observed [comments in braces have been added by Jim Lyles]: Villous atrophy [partial or complete flattening of the finger-like projections in the small intestine] Hyperplasia of the crypts of Lieberkuhn [the crypts under the villi become highly elongated when compared with normal crypts] Increased plasma cell and lymphocyte infiltration of the lamina propria [more lymphocytes under the epithelial or outer layer of the villi. Lymphocytes are the cells that fight off viruses, etc.] Increased intraepithelial lymphocytes [more lymphocytes within the epithelial cells. The epithelial cells form the outer layer of the intestine and allow nutrients to pass through from the intestine into the bloodstream] Abnormalities in the epithelial cells which become flattened, cuboidal, and pseudo- stratified [layered].
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