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  • Jefferson Adams
    Jefferson Adams

    Biopsy Volume Influences Adherence to Celiac Disease Guidelines

    Celiac.com 12/04/2013 - About 1 of of 100 Americans has celiac disease, but most cases remain undiagnosed, partly because of failure on the part of physicians to collect at least four specimens during duodenal biopsy, as per current recommendations.

    Photo: CC--jovikeA team of researchers recently set out to determine whether physician and practice characteristics are associated with these failures.

    The research team included Benjamina Lebwohl, Robert M. Genta, Robert C. Kapel, Daniel Sheehan, Nina S. Lerner, Nina, Peter H. Green, Alfred I. Neugut, and Andrew Rundle.

    For their study, the team used a large national pathology database to identify all adult patients who underwent duodenal biopsy during 2006–2009.

    They used hierarchical modeling to determine whether procedure volume, the number of gastroenterologists per endoscopy suite, and the number of gastroenterologists per capita of the zip code of the practice were associated with adherence to recommendations.

    The team identified 92,580 patients who met their inclusion/exclusion criteria. Patient group was 67% female, averaging 53.5 years of age.

    The team received biopsy specimens from 669 gastroenterologists from 200 endoscopy suites, located in 191 zip codes, with a mean of 3.4 gastroenterologists per suite.

    Multivariate analysis showed that higher procedure volume was associated with decreased adherence to specimen recommendations [odds ratio (OR) for each additional 100 procedures, 0.92; 95% confidence interval (CI), 0.88–0.97; P=0.002].

    Gastroenterologists employed in suites with higher numbers of gastroenterologists reported higher levels of adherence (OR for each additional gastroenterologist, 1.08; 95% CI, 1.04–1.13; P<0.001)

    However, that was not the case for a higher gastroenterologist density in the zip code of the practice (OR for each additional gastroenterologist per capita, 1.01; 95% CI, 0.99–1.03; P=0.21).

    This study suggests that high-volume physicians exhibit lower rates of adherence to biopsy guidelines, possibly because of the additional time required to submit the minimum of four specimens.

    In contrast, doctors working in endoscopy suites with high numbers of colleagues showed higher rates of adherence, possibly because of peer education.

    Basically, doctors who do large numbers of biopsies are more likely to submit too few samples for accurate analysis, whereas doctors working in close contact with large numbers of peers are more likely to follow current recommendations, and to produce better, more accurate results.

    Source:



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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, science, and advanced research, and scientific methods. He previously served as Health News Examiner for Examiner.com, and devised 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 "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

  • Related Articles

    Scott Adams
    The following abstract was submitted to celiac.com directly by William Dickey, Ph.D., a leading celiac disease researcher and gastroenterologist who practices at Altnagelvin Hospital, Londonderry, Northern Ireland.
    Dig Liver Dis. 2005 Sep 29;
    Dickey W, McMillan SA.
    Department of Gastroenterology, Altnagelvin Hospital, Londonderry BT47 6SB, Northern Ireland, UK.
    Celiac.com 10/11/2005 - BACKGROUND.: Serological testing, using IgA class endomysial and tissue transglutaminase antibodies has high sensitivity and specificity for celiac disease and allows case finding by clinicians other than gastroenterologists. We reviewed new celiac patients seen over a 9-year period to determine how the availability of serology, particularly to primary care physicians, has changed rates and sources of diagnosis.
    METHODS.: Files of patients attending a specialist celiac clinic who were diagnosed from 1996 through 2004 were reviewed. Patients with villous atrophy consistent with gluten sensitive enteropathy (Marsh III) on duodenal biopsy were selected. Data analyzed included clinical characteristics, endomysial and tissue transglutaminase antibodies status and source of request for serology.
    RESULTS.: Over the study period 347 new celiac patients, comprising adults and children aged 10 years and over, were identified, of whom 163 (47%) were identified by serological testing in primary care, 152 (44%) at the hospital gastroenterology department and 32 (9%) by other physicians in secondary care. Over three consecutive 3-year periods, the percentage of patients identified in primary care rose from 28% through 47% to 60%, with a rise in total numbers diagnosed from 93 through 118 to 136. There was no change in patient clinical characteristics over the study period. Though tissue transglutaminase antibodies were less sensitive than endomysial antibodies, combined testing obtained a sensitivity of over 90%. Patients identified in primary care were significantly younger and more likely to present with diarrhea as a primary symptom.
    CONCLUSION.: Currently over half of our celiac patients are identified by serological testing in primary care, which has resulted in an overall rise in diagnosis rates. Primary care practitioners have an important role in the diagnosis of celiac disease, particularly of patients who present with non-gastrointestinal symptoms. The contribution of specialists other than gastroenterologists in secondary care is disappointing and may improve with directed education.

    Jefferson Adams
    Celiac.com 03/05/2010 - A team of researchers recently studied therelationship between increased levels of antigliadin antibodies andintestinal barrier gene variants.
    The research team included V.M. Wolters, B. Z. Alizadeh, M. E. Weijerman, A. Zhernakova, I. M. vanHoogstraten, M. L. Mearin, M. C. Wapenaar, C.Wijmenga, M. W. Schreurs.They are affiliated with the Department of Pediatric Gastroenterology,UMC Utrecht, Utrecht, The Netherlands.
    Numerous genes may affectintestinal barrier function, including MAGI2, MYO9B, and PARD3, whichhave a close association with celiac disease. Gauging intestinalpermeability is tough to do, so researchers can test indirectly byusing antibodies against gliadin and Baker's yeast (anti-Saccharomycescerevisiae antibodies).
    The goal of the study was to determinewhether intestinal permeability, represented by antibodies againstgliadin, was connected to MAGI2, MYO9B, and PARD3.
    The teamanalyzed patients with Down syndrome, a population with suspectedincreased intestinal permeability. The team examined connectionsbetween AGA and ASCA.
    The team genotyped 126 Down syndromepatients for six single-nucleotide polymorphisms in MAGI2 (rs1496770,rs6962966, rs9640699), MYO9B (rs1457092, rs2305764), and PARD3(rs10763976).
    They then performed an allele dosage associationof these risk genes and AGA levels. They also found a strongcorrelation between AGA and ASCA (p < 0.01).
    Subjects withone or more risk genotypes showed lower average AGA levels (trend testp = 0.007) and made up a larger number of patients with normal AGAlevels (p = 9.3 x 10(-5)).
    Celiac-associated risk genotypesare associated with lower AGA values rather than higher AGA values.This all means that, regarding the increased prevalence of elevated AGAin patients with Down syndrome, there are other immunologic factors atplay. These may involve altered induction and/or maintenance oftolerance.
    Source:
    Hum Immunol. 2010 Feb 3.


    Jefferson Adams
    Celiac.com 02/22/2012 - A research team recently conducted a dense genotyping non-HLA risk loci previously associated with immune-mediated diseases in individuals with celiac disease. The study was conducted under the auspices of the Genetics Department, University Medical Center and University of Groningen, The Netherlands.
    The team used variants from the 1000 Genomes Project pilot European CEU dataset, along with data from additional re-sequencing studies, to densely genotype a total of 183 non-HLA risk loci previously associated with immune-mediated diseases in 12,041 individuals with celiac disease and in 12,228 control subjects.
    They were able to discover thirteen new celiac disease risk loci reaching genome-wide significance. This discovery brings the number of loci known to be associated with celiac disease, including the HLA locus, to forty.
    The team found multiple independent association signals in more than one in three of the loci. This is likely due to a combination of common, low-frequency and rare genetic variants.
    Compared to earlier data, such as those from HapMap3, the large study group and the dense gene mapping made for a much higher resolution of the pattern of linkage disequilibrium and suggested localization of many signals to finer scale regions.
    In all, the team found that 29 of the 54 fine-mapped signals seemed to be localized to single genes and, in some instances, to gene regulatory elements.
    Finally, they defined the complex genetic architecture of the risk regions of celiac disease. They also refined the risk signals for celiac disease, which provide support for the next steps in understanding its causes.
    The research team included G. Trynka, K. A. Hunt, N. A. Bockett, J. Romanos, V. Mistry, A. Szperl, S. F. Bakker, M. T. Bardella, L. Bhaw-Rosun, G. Castillejo, E. G. de la Concha, R. C. de Almeida, K. R. Dias, C. C. van Diemen, P.C. Dubois, R. H. Duerr, S. Edkins, L. Franke, K. Fransen, J. Gutierrez, G. A. Heap, B. Hrdlickova, S. Hunt, L. P. Izurieta, V. Izzo, L. A. Joosten, C. Langford, M. C. Mazzilli, C. A. Mein, V. Midah, M. Mitrovic, B. Mora, M. Morelli, S. Nutland, C. Núñez, S. Onengut-Gumuscu, K. Pearce, M. Platteel, I. Polanco, S. Potter, C. Ribes-Koninckx, I. Ricaño-Ponce, S. S. Rich, A. Rybak, J. L. Santiago, S. Senapati, A. Sood, H. Szajewska, R. Troncone, J. Varadé, C. Wallace, V. M. Wolters, and A. Zhernakova. The study team also included B. K. Thelma, B. Cukrowska, E. Urcelay, J. R. Bilbao, M. L. Mearin, D. Barisani, J. C. Barrett, V. Plagnol, P. Deloukas, C. Wijmenga, and D. A. van Heel, who are variously affiliated with the Spanish Consortium on the Genetics of Coeliac Disease (CEGEC), the PreventCD Study Group, and the Wellcome Trust Case Control Consortium (WTCCC).
    Source:

    Nat Genet. 2011 Nov 6;43(12):1193-201. doi: 10.1038/ng.998.


    Jefferson Adams
    Celiac.com 02/04/2015 - For kids with a predisposition to celiac disease, does the age at which they first eat gluten have any connection with their risk for celiac disease? A team of researchers wanted to figure out whether the age at which a child first eats gluten carried any associated with risk for celiac disease, for genetically predisposed children. The Environmental Determinants of Diabetes in the Young (TEDDY) is a prospective birth cohort study.
    The research team included Carin Andrén Aronsson, MSca, Hye-Seung Lee, PhD, Edwin Liu, MD, PhD, Ulla Uusitalo, PhD, Sandra Hummel, PhD, Jimin Yang, PhD, RD, Michael Hummel, MD, PhD, Marian Rewers, MD, PhD, Jin-Xiong She, PhD, Olli Simell, MD, PhD, Jorma Toppari, MD, PhD, Anette-G. Ziegler, MD, PhD, Jeffrey Krischer, PhD, Suvi M. Virtanen, MD, PhD, Jill M. Norris, MPH, PhD, and Daniel Agardh, MD, PhD, for the The Environmental Determinants of Diabetes in the Young (TEDDY) Study Group.
    They are variously affiliated with the Department of Clinical Sciences, Lund University, Malmö, Sweden; the Pediatrics Epidemiology Center at the Department of Pediatrics of the Morsani College of Medicine at University of South Florida in Tampa, Florida; the Digestive Health Institute at the University of Colorado, Children’s Hospital Colorado in Denver; the Barbara Davis Center for Childhood Diabetes at the University of Colorado in Aurora, Colorado; the Department of Epidemiology, Colorado School of Public Health, University of Colorado at Denver in Aurora, Colorado; the Institute of Diabetes Research, Helmholtz Zentrum München, and Klinikum rechts der Isar, Technische Universität München, and Forschergruppe Diabetes e.V., Neuherberg, Germany; The Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Georgia Regents University, Augusta, Georgia; Department of Pediatrics, Turku University Hospital, Turku, Finland; the Department of Physiology and Pediatrics, University of Turku, Turku, Finland; the National Institutes for Health and Welfare, Nutrition Unit, Helsinki, Finland; the School of Health Sciences, University of Tampere, Tampere, Finland; and the Research Center for Child Health at Tampere University and University Hospital and the Science Center of Pirkanmaa Hospital District, Tampere, Finland.
    For their study, the team followed up on 6,436 newborn infants who had been screened for high-risk HLA-genotypes for celiac disease in Finland, Germany, Sweden, and the United States.
    At clinical visits every third month, the team collected information about infant feeding.
    The first outcome was persistent positive for tissue transglutaminase autoantibodies (tTGA), the marker for celiac disease.
    The second outcome was celiac disease, defined as either a diagnosis based on intestinal biopsy results, or as persistently high levels of tTGA.
    The team found that Swedish children consumed their first gluten at an earlier age, 21.7 weeks on average, compared with 26.1 weeks for children from Finland, and just over 30 weeks for kids from Germany, and the United States (P < .0001).
    Over about a follow-up period ranging from 1.7–8.8 years, but averaging about five years, the team found that 773 (12%) children developed tTGA and 307 (5%) developed celiac disease.
    Compared with US children, Swedish children saw an increased risk for tTGA, with a hazard ratio of 1.74 [95% CI: 1.47–2.06]) and celiac disease, with a hazard ratio of 1.76 [95% CI: 1.34–2.24]), respectively (P < .0001).
    Gluten introduction before kids turn 17 weeks or after 26 weeks was not associated with increased risk for tTGA or celiac disease, adjusted for country, HLA, gender, and family history of celiac disease, neither in the overall analysis nor on a country-level comparison.
    TEDDY, is one of several recent studies that confirm that the age at first gluten introduction was not an independent risk factor for developing celiac disease.
    Source:
    Pediatrics; January 19, 2015. doi: 10.1542/peds.2014-1787

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    Thanks Posterboy, that was interesting information.  I believe that I had read something elsewhere about tetracycline, at least, being used instead of, or along with, Dapsone for severe or refractory cases of DH. Unfortunately, even if I had medical insurance (which I do not), and had a regular doctor who was even willing to recognize and accept my condition for what it is, I don't know what kind of luck I would have in persuading that hypothetical doctor to give me a particular and non-sta
    Healthysquirrel,  Please have your doctor check your Vitamin D level!   Vitamin D deficiency is related to vertigo https://www.ncbi.nlm.nih.gov/pubmed/27386060 Vitamin D can help with high IgE https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5263170/ Low vitamin D and low ferritin are tied https://www.ncbi.nlm.nih.gov/pubmed/29385099 Dry eye problems including blepharitis can be helped with vitamin d and vitamin a https://www.ncbi.nlm.nih.gov/pmc/articles
    He's still going to have to eat gluten even for an endoscopic biopsy. 2 weeks minimum. Plus guidelines say no dx on an endoscopic biopsy alone - you have to have the positive blood to go with it. Even that 2 weeks will deposit more antibodies under his skin if he's got dh.  Let me put it this way. The gut damage is the gut damage & if he's celiac & it sounds like he is but we don't have labs to prove it, then there is a treatment for it. Only 1 treatment for it. A very strict gluten
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