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  • Jefferson Adams
    Jefferson Adams
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    Predictors for Celiac Disease in Adult Cases of Duodenal Intraepithelial Lymphocytosis

    Caption: Photo: Wikimedia Commons--Eva K.

    Celiac.com 09/15/2014 - Duodenal intraepithelial lymphocytosis (D-IEL) is an early marker for celiac disease, even though a majority of cases are due to non-celiac disease conditions.

    Photo: Wikimedia Commons--Eva K.Researchers I. Aziz, T. Key, J.G. Goodwin, and D.S. Sanders wanted to identify the predictors of celiac disease in patients presenting with D-IEL. For their study, they reviewed 215 adults with D-IEL who had undergone prospective and systematic evaluation for celiac disease and other recognized associations. They confirmed celiac disease based on presence of HLA-DQ2 and/or DQ8, persistence or progression of D-IEL following a gluten challenge, and an improvement in symptoms with a gluten-free diet.

    To compare factors in celiac and non-celiac cases, and to determine their sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV), the team used binary logistic regression models, adjusted for age and sex. They diagnosed celiac disease in 48 cases (22%) and non-celiac in 167 cases (78%). They found no statistical difference between the celiac and non-celiac group in terms of baseline demographics, anemia, hematinics, or clinical symptoms, such as diarrhea, weight loss, abdominal pain.

    Compared with their non-celiac counterparts, celiac patients were significantly more likely to have a positive family history of celiac disease (21% vs. 3.6%, OR 6.73; PPV 62.5%, NPV 81%, specificity 96.4%), positive HLA-DQ status (100% vs. 49.1%; PPV 36.4%, NPV 100%, specificity 50.9%), and presence of endomysial antibody (EMA) (48% vs. 0%; PPV 100%, NPV 87%, specificity 100%); all P≤0.001.

    A total of 29.2% celiac and 83.2% non-celiac cases showed normal tissue transglutaminase antibody (TTG) levels (OR 0.084, P<0.001; PPV 9.2%).

    Between the groups, there was no difference in the prevalence of TTG levels 1 to 2×upper limit of normal (29.2% celiac vs. 14.4% non-celiac; PPV 33% to 38%). However, TTG levels between 3 and 20×ULN were much more common in the celiac group (33.3% vs. 2.4%, PPV 66.6% to 89%), whereas a TTG>20×ULN was exclusive to celiac disease (8.3%, P<0.001, PPV 100%).

    For patients with D-IEL, only a positive EMA or TTG greater than 20×ULN at the outset can yield an immediate celiac diagnosis. On their own, factors such as gastrointestinal symptoms, family history, anemia, or other celiac serology results do not reliably distinguish celiac from non-celiac patients.

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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 "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

  • Related Articles

    Scott Adams
    JAMA 2002;287:1413-1419.
    Celiac.com 04/12/2002 - According to a report published in the March 20th issue of the Journal of the American Medical Association, people with celiac disease are three times more likely to develop non-Hodgkin lymphoma (NHL) than the normal population. Dr. Carlo Catassi and colleagues from the University of Maryland in Baltimore compared the prevalence of celiac disease in 653 NHL patients with more than 5,000 healthy control subjects to determine the NHL-celiac disease occurrence rate. The results indicate that 1% of NHL patients also have celiac disease, in comparison with 0.42% of the healthy controls. Adjustments were made for age and sex, and the final results indicate that the odds ratios for a patient with celiac disease of developing NHL are: 3.1 for all types of NHL, 16.9 for gut NHL, and 19.2 for T-cell NHL. The overall risk, however, for someone with celiac disease developing NHL is only 0.63%.
    The researchers do not feel that their findings support mass screening for celiac disease, but they do feel that selected NHL patients should be screened for celiac disease. We would also like to add that these findings support the screening of people with celiac disease for NHL, which was not directly addressed by the report.

    Scott Adams
    Gut 2005;54:54-59. Celiac.com 01/20/2005 - A link between untreated celiac disease and a rare enteropathy-type T-cell lymphoma (ETTL) has been well established by several studies. According to Dr. Karin Ekstrom Smedby of the Karolinska Institute in Stockholm and colleagues, there is also an increase in the prevalence of other types of lymphomas in those with celiac disease, such as B cell and non-intestinal lymphomas. In their study the researchers reviewed and reclassified 56 cases of malignant lymphomas that occurred in 11,650 hospitalized celiac disease patients in Sweden. The observed numbers of lymphoma subtypes were compared with those expected in the Swedish population. The researchers discovered that a majority of the lymphomas were not intestinal T-cell lymphomas, but were B-cell non-Hodgkin lymphoma (NHL). In addition, 44% of the patients with B cell NHL had a history of other autoimmune/inflammatory diseases. As expected, the relative risks for T-cell NHL and primary gastrointestinal lymphomas were markedly increased. According to the researchers: "Most lymphomas complicating coeliac disease are indeed related to the disease and are not of the ETTL-type. There was a remarkable aggregation of autoimmune/inflammatory disorders, female sex, coeliac disease, and B cell lymphoma."

    Jefferson Adams
    Celiac.com 05/19/2010 - Enteropathy-associated T cell lymphoma is a serious complication of celiac disease, and a major cause of mortality in untreated celiac disease.
    One possible trigger for Enteropathy-associated T cell lymphoma development is chronic exposure of intraepithelial lymphocytes (IELs) to strong anti-apoptotic signals, that is, signals that interfere in the normal mortality of the IEL cells. These signals are triggered by IL-15, a cytokine that is over-expressed in the enterocytes of people with celiac disease.
    However, researchers have not yet fully mapped the signaling pathway by which IL-15 transmits these anti-apoptotic signals. Researchers consider type II refractory celiac disease (RCDII) to be a middle step between celiac disease and enteropathy-associated T cell lymphoma.
    Eliminating abnormal IELs at the RCDII stage would likely block EATL development. So far, though, scientists have not found successful immunosuppressive and/or chemotherapeutic approaches able to accomplish this, and RCDII outcomes remain very poor.
    A team of researchers recently set out to map the IL-15–driven survival pathway in human IELs, and to determine whether IL-15 triggered pathway in human intraepithelial lymphocytes represents a possible new target in type II refractory celiac disease and enteropathy-associated T cell lymphoma.
    The research team was made up of Georgia Malamut, Raja El Machhour, Nicolas Montcuquet, Séverine Martin-Lannerée, Isabelle Dusanter-Fourt, Virginie Verkarre, Jean-Jacques Mention, Gabriel Rahmi, Hiroshi Kiyono, Eric A. Butz, Nicole Brousse, Christophe Cellier, Nadine Cerf-Bensussan, and Bertrand Meresse.
    The are variously affiliated with INSERM U989, the Université Paris Descartes, Faculté de Médecine René Descartes, the Department of Gastroenterology, AP-HP, Hôpital Européen Georges Pompidou, the Institut Cochin, Université Paris Descartes, CNRS (UMR 8104), INSERM U1016, the Department of Pathology, AP-HP, of the Hôpital Necker-Enfants Malades in Paris, with the Division of Mucosal Immunology, Department of Microbiology and Immunology at the Institute of Medical Science at the University of Tokyo in Japan, and the Inflammation Department of AMGEN Inc., in Seattle, Washington, USA.
    Their current findings reveal that the survival signals IL-15 directs to freshly isolated human IELs, and to human IEL cell lines derived from celiac disease patients with type II refractory celiac disease, depend on anti-apoptotic factors Bcl-2 and/or Bcl-xL.
    The signals require IL-15Rβ, Jak3, and STAT5 for proper function, but functioned independently of PI3K, ERK, and STAT3. In support of these findings, the team recorded elevated levels of Bcl-xL, phospho-Jak3, and phospho-STAT5 in IELs from patients with active celiac disease and RCDII.
    Moreover, by incubating patient duodenal biopsies with a fully humanized human IL-15–specific Ab, the team effectively blocked Jak3 and STAT5 phosphorylation.
    Also, treatment with IL-15–specific Ab caused IEL cell mortality, and wiped out the massive IEL build-up in mice over-expressing human IL-15 in their gut epithelium.
    The study marks the first successful mapping of the IL-15–driven survival pathway in human IELs, and demonstrates that IL-15 and its downstream effectors are meaningful therapeutic targets in RCDII.
    These findings will likely help to pave the way for the development of successful immunosuppressive and/or chemotherapeutic treatments that destroy abnormal IELs at the RCDII stage and help to block EATL development, improving outcomes for RCDII patients.
    Source:

    Journal of Clinical Investigation doi:10.1172/JCI41344

    Jefferson Adams
    Celiac.com 01/18/2012 - A number of small studies have shown a connection between celiac disease and various gastrointestinal (GI) cancers, but the results haven't been corroborated by larger studies, or by blood and biopsy analysis of large populations. That means that researchers just haven't been able to say with certainty what the results of those smaller studies might mean about cancer risks for the larger population.
    Recently, a clinical team set out to assess GI cancer risks for a larger population. The study team included Peter Elfström, Fredrik Granath, Weimin Ye, and Jonas F. Ludvigsson. They assessed risk GI cancers by using data from large groups of patients with either celiac disease, inflammation, or latent celiac disease.
    They assessed data from 28,882 patients with celiac disease, all with villous atrophy, and Marsh scores of 3. They also assessed data for 12,680 patients with inflammation, all with Marsh scores of 1–2. They evaluated biopsy samples at 28 different pathology centers.
    They assessed a third group of 3705 patients with latent celiac disease, that is, with normal mucosa, but positive blood tests. The team then compared the results against data from an age- and sex-matched population.
    They found that 372 of the patients with celiac disease developed incident GI cancers, while 347 patients with inflammation, and 38 with latent celiac disease developed GI cancers.
    That means that the first year after diagnosis and initial biopsy, celiac disease carried a 5.95-times greater risk of incident GI cancer, with a 95% confidence interval [CI], 4.64–7.64). The hazard ratio
    for inflammation was 9.13 (95% CI, 7.19–11.6) and for latent celiac disease was 8.10 (95% CI, 4.69–14.0). After the first year, patients showed no significant increase in GI cancer risk.
    The HR for celiac disease was 1.07 (95% CI, 0.93–1.23), for inflammation it was 1.16 (95% CI, 0.98–1.37). HR for latent celiac disease it was 0.96 (95% CI, 0.56–1.66).
    The absolute risk for any GI cancer in people with celiac disease was 101/100,000 person-years, with an excess risk of 2/100,000 person-years.
    The results carried some relatively good news. That is, even though celiac disease, inflammation, and latent disease all increase a person's risk for GI cancers in the first year after diagnosis, there is no increase in risk beyond the first year.
    Source:

    Clinical Gastroenterology and Hepatology. Volume 10, Issue 1 , Pages 30-36, January 2012

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    Got the result today, and it is indeed the IgG only, and it is "negative" with a result of: <10.0 Units I have sent a message to my doctor requesting that she at least also order the TTG IGA test. However, I'm assuming that this result does at least significantly lower the likelihood that I have celiac? This is all just a shot in the dark anyhow... but after 8 years of unsatisfactorily diagnosed mystery joint pain, I don't want to only half-explore an option and then abandon it without a reasonably definitive result.
    It sounds like you were not given the full celiac panel. The full celiac panel includes: TTG IGA
    TTG IGG
    DGP IGA
    DGP IGG
    EMA
    IGA You have to be eating gluten daily for 12 weeks before the blood test. A positive on any one blood test should lead to a gastroenterologist doing an endoscopy /biopsies to confirm a celiac diagnosis.    
    Yep, dang just realized I had a $10 off code in my email for the coffee you could have used. Yeah I love the coffees, some are odd. Most dessert ones require you to sweeten to bring it out, some you only taste cold. They are fun to play with and I love how they give me enjoyment when it comes to food.
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