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    Can Better Biopsy Practices Improve Celiac Diagnosis in Children?


    Jefferson Adams

    Celiac.com 03/27/2015 - Researchers don't have any solid idea about how common cases of seronegative celiac disease might be, but many feel strongly that rates of seronegative celiac disease are underestimated in children, and may result in misdiagnosis of celiac cases.

    Photo: CC--Ari BronsteinOne team of researchers wondered if an emphasis on "serology-led" diagnosis might be contributing to a low rate of celiac disease diagnosed in children from the United States. That research team included Deborah L. Preston and Yoram Elitsur, and they recently set out to investigate the rate of celiac disease after upper endoscopy (EGD) with no prior positive celiac serology compared with the rate of celiac disease followed by positive serology.

    The team conducted a retrospective review of that charts of all of the first diagnostic EGDs in children (2009–2013). They split the patients with confirmed celiac disease into 4 groups: group A, positive EGD/positive serology (histology-led diagnosis); group B, positive serology/positive histology (serology-led diagnosis); group C, positive histology followed by negative serology (control 1); and group D, positive serology followed by negative histology (control 2).

    The team reviewed a total of 761 upper endoscopic charts. They confirmed 15 children with celiac disease, for a rate of 1.97%. Group A and group B had similar demographic data or clinical symptoms, and similar rates of celiac disease between histology-led celiac diagnosis (group A) and serology-led celiac diagnosis (group B) (1.18% vs 0.79%, P = 0.273).

    This study showed that endoscopy-led diagnosis and serology-led diagnosis found celiac disease at similar rates.

    This finding suggests that better diagnosis of celiac disease in children requires performing an adequate number of intestinal biopsies in every diagnostic upper endoscopic procedure.

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    Guest Unsworth

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    My son was diagnosed as celiac only after the biopsy, grade IV. The blood test we did before was sero negative. We would have known if it was not for the biopsy.

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  • About Me

    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, and science. He previously served as Health News Examiner for Examiner.com, and provided health and medical content for Sharecare.com.

    Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book Dangerous Grains by James Braly, MD and Ron Hoggan, MA.

  • Related Articles

    Scott Adams
    Castany M, Nguyen H, Pospisil M, Fric P, Tlaskalova-Hogenova H
    Natural killer cell activity in coeliac disease: effect of in vitro treatment on effector lymphocytes and/or target lymphoblastoid, myeloid and epithelial cell lines with gliadin
    Folia Microbiol, 1995 (Praha) 40; 6: 615-620.
    In this study researchers tested the levels of natural killer cell activation in normal people and compared the results with treated celiacs, and found no significant difference. However, after exposing the celiacs blood to gliadin for thirty minutes the researchers found a reduced activation of natural killer cells, which is the bodys first line of defense against malignancy. These results provide further support to the theory that gluten is a carcinogen to celiacs.

    Kathleen La Point
    Celiac.com 04/28/2008 - A life-long gluten-free diet is currently the only treatment for celiac disease. However, many foods thought to be gluten-free actually contain small amounts of gluten, making it difficult to maintain a truly gluten-free diet.
    Gluten is made up of glutenin and gliadin proteins. Gliadin is only partially digested in the small intestine and the resulting peptides are responsible for the inflammation and intestinal tissue damage in people with celiac disease. Because probiotic bacteria have been shown to digest gluten proteins to harmless peptides, supplementation with probiotics may be beneficial for people with celiac disease.
    To begin testing this hypothesis, researchers in Finland added probiotic bacteria to cultures of intestinal epithelial cells (cells that line the intestine) to determine their effect on gliadin-induced cellular damage. Gliadin-induced damage to intestinal epithelial cells includes increased permeability of the epithelial layer, alteration of tight junctions between cells (which controls the passage of materials across the intestinal wall), and structural changes such as “ruffling” of the cell edges. Two probiotic bacterial species were evaluated: Lactobacillus fermentum and Bifidobacterium lactis.
    In this study, B. lactis was able to inhibit permeability caused by gliadin. Additionally, both B. lactis and L. fermentum were able to protect against cell ruffling and alterations in tight junctions. The bacteria alone (without gliadin) did not cause any significant changes to the intestinal epithelial cells.
    Researchers concluded that Bifidobacterium lactis may be a useful addition to a gluten-free diet. Supplementation with this probiotic appears to be able to reduce the damage caused by eating gluten-contaminated foods and may even accelerate healing after initiating a gluten-free diet. It is important to note the researchers do not suggest that supplementation with probiotics could take the place of  a gluten-free diet in the treatment of celiac disease.

    Lindfors et al. Live probiotic Bifidobacterium lactis bacteria inhibit the toxic effects induced by wheat gliadin in epithelial cell culture - Clin Exp Immunol. 2008 Apr 16.

     
     

    Jefferson Adams
    Celiac.com 04/10/2009 - According to the latest findings by a Norwegian research team, the inner workings of a particular enzymatic reaction is helping scientists figure out how celiac disease develops.
    In the latest issue of the Journal of Proteome Research, doctors Siri Dørum, Burkhard Fleckenstein, and associates at Norway’s University of Oslo and Rikshospitalet University Hospital describe how they used a quantitative MS method to chart a significant association between the amount of deamidation and the rate at which various epitopes are recognized by T cells of people with celiac disease.
    The team set out to determine whether the rate of TG2 deamidation correlates with T cell recognition of gluten peptide epitopes.
    Celiac disease is a common digestive disorder, in which people suffer from an adverse reaction to gliadin proteins in the gluten of wheat, barley, and rye. When people with celiac disease eat gluten, an adverse immune reaction occurs, in which the intestinal villi, the finger-like projections that line the small intestine and serve to absorb nutrients, suffer damage and eventually flatten and disappear.
    Currently, the only treatment is the adoption of a gluten-free diet that eliminates exposure to the proteins that trigger the immune response. In most cases, the gluten-free diet heals the intestinal damage.
    So, how does gluten exposure cause this adverse immune system reaction? Much of this process remains a mystery, but there appears to be a strong genetic component. It is known that most people with celiac disease display the human leukocyte antigen (HLA) molecules DQ2 or DQ8, which function as receptors on antigen-presenting cells.
    The standard method of measuring deamidation is to tie the transglutaminase activity to a secondary enzymatic reaction, which gives off ammonium. But this method is not direct, and if there are multiple peptides in a mixture, which may be highly complex, one can only assess the total production of ammonium.
    By contrast, the MS method allows the detection of changes on each peptide, and allows the locations of those modifications to be pinpointed within each peptide.
    The team achieved their results by measuring the centroid masses of the peptides’ isotopic envelopes before TG2 treatment, and comparing the results to the values obtained after TG2 treatment.
    Depending on the sequence context, the glutamine residues were shown to influence the extent of residual deamidation by TG2. Additionally, they team revealed that peptide length also plays a key role in the process—the longer the given gliadin peptide, the more likely it is to have deamidated glutamines.
    The team examined an array of gluten peptides with known epitopes, both individually and in mixture, to assess the degree of deamidation. A 33-mer, shorter α-gliadin peptides, and one peptide from γ-gliadin all showed rapid deamidation. The rest of the peptides showed only partial deamidation, even after a long period of incubation.
    They observed that the frequency of the T cell response in celiac disease patients seems to be tied to the rate of peptide deamidation. T cells from nearly every patient recognized the 33-mer and the α-gliadin peptide, which also served as good TG2 substrates. In comparison, the glutamines of most γ-gliadin peptides were deamidated less often and were recognized less frequently by patient T cells.
    However, one γ-gliadin peptide showed itself to be an exception. The γ-II epitope functions as an excellent substrate for TG2, but is poorly recognized by T cells. Another factor may be proteolytic stability, as it is understood that the γ-II epitope is part of a gluten fragment that is less stable than the 33-mer.
    By analyzing gluten peptides using MS, researchers were able to figure out whether the rate of glutamine deamidation by TG2 impacts the recognition of these peptides by the immune systems of those with celiac disease.

    J. Proteome Res., 2009, 8 (4), pp 1748–1755
     

    Jefferson Adams
    Celiac.com 02/06/2013 - Villous atrophy (VA) in the small intestine is one of the prime features of celiac disease, and has been associated with increased mortality, but it is unknown if mortality is influenced by mucosal recovery.
    To better understand the relationship between mucosal healing and mortality in celiac disease, a research team set out to determine whether persistent villous atrophy is associated with mortality in celiac disease patients.
    The research team included B. Lebwohl, F. Granath, A. Ekbom, S.M. Montgomery, J.A. Murray, A. Rubio-Tapia, P.H. Green, and J.F. Ludvigsson. They are variously affiliated with the Celiac Disease Center at the Department of Medicine of Columbia University College of Physicians and Surgeons in New York, NY, the Clinical Epidemiology Unit at the Department of Medicine of Karolinska University Hospital and Karolinska Institutet in Stockholm, Sweden.
    The team used biopsy reports from every pathology department (n = 28) in Sweden to identified 7,648 individuals with celiac disease, which they defined as the presence of villous atrophy, and who had undergone a follow-up biopsy within 5 years of diagnosis. They used Cox regression to assess mortality according to follow-up biopsy.
    Celiac patients were 28.4 years of age, on average, and 63% were female. The average follow-up after diagnosis was 11.5 years. Overall, patients who underwent follow-up biopsy had lower mortality rates than those who did not undergo follow-up biopsy (Hazard Ratio 0.88, 95% CI: 0.80-0.96).
    Of the 7648 patients who underwent follow-up biopsy, 3317 (43%) showed persistent villous atrophy. In all, 606 (8%) patients died. However, patients with persistent villous atrophy died at about the same rates as those with mucosal healing (HR: 1.01; 95% CI: 0.86-1.19).
    Also, children with persistent villous atrophy showed no increase in mortality (HR: 1.09 95% CI: 0.37-3.16) or adults (HR 1.00 95% CI: 0.85-1.18), including adults older than age 50 years (HR: 0.96 95% CI: 0.80-1.14).
    Mortality rates for celiac patients with persistent villous atrophy are about the same as for celiac patients with healthy guts. So, persistent villous atrophy is not tied to higher mortality for celiac disease patients. That means that even though a follow-up biopsy will help doctors to spot refractory disease in symptomatic patients, persistent villous atrophy is not useful in predicting future mortality.
    Source:
    Aliment Pharmacol Ther. 2013 Feb;37(3):332-9. doi: 10.1111/apt.12164.

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