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    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.

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    Jefferson Adams
    Celiac.com 03/15/2010 - A team of researchers recently set out to investigate mucosal expression of claudins 2, 3 and 4 in the proximal and distal parts of duodenum in children with celiac disease. The team included Dorottya Nagy Szakál, Hajnalka GyÅ‘rffy, András Arató, Áron Cseh, Kriszta Molnár, Mária Papp, Antal DezsÅ‘fi, and Gábor Veres. They are variously associated with the Department of Pediatrics, and the Department of Pathology at Semmelweis University in Budapest, Hungary, and the Department of Medicine at the University of Debrecen in Debrecen, Hungary.
    Duodenal biopsy is an important tool for properly diagnosing celiac disease. However, the issue of finding the best site for taking biopsy samples that will give the best results for diagnosing celiac disease is still not fully resolved.
    Claudins (CLDNs), belong to a large group of related adherent junction proteins, which are known to express characteristic patterns in inflammatory disorders. However, doctors presently know nothing about CLDN expression in people with celiac disease. To address the situation, the team performed a comparative study to examine the CLDN 2, 3 and 4 expressions in both the proximal and distal parts of duodenum in children with celiac disease and in control subjects.
    For the study, they enrolled a total of forty-seven children. Thirty-three had newly diagnosed celiac disease, while fourteen healthy children served as control subjects. The team took biopsies from proximal and distal part of duodenum, and used immunohistochemistry to detect CD3+ intraepithelial lymphocytes and CLDN 2, 3 and 4 protein expressions.
    Whether taken from proximal or distal part of duodenum, biopsies revealed no differences under macroscopic imaging, routine histology and Marsh grading.
    However, in comparison to controls, patients with severe celiac disease showed significantly higher CLDN 2 expression in bulb and in distal duodenum, while non-severe celiac patients showed higher distal CLDN 2 expression. The data showed similar associations regarding CLDN 3 expression. All groups showed similar expression of CLDN 4.
    The data showed that both proximal and distal mucosal duodenal biopsies are suitable for diagnosing villous atrophy in patients with celiac disease.
    Finally, the team noted that increased expressions of CLDN 2 and 3 imply structural changes of tight junction in celiac disease, which may play a role in increased permeability and proliferation observed in celiac disease.
    Source:

    Virchows Archive, Volume 456, Number 3 / March, 2010

    Jefferson Adams
    Celiac.com 06/17/2010 - In a recent letter to the editors of Clinical Chemistry, Carolina Arguelles-Grande, Gary L. Norman, Govind Bhagat, and Peter H. R. Green describe how hemolysis interferes with the detection of anti–tissue transglutaminase antibodies in celiac disease.
    They are variously affiliated with the Departments of Medicine and Pathology at Columbia University's College of Physicians and Surgeons in New York, and with INOVA Diagnostics, Inc., in San Diego, CA.
    Using human recombinant or erythrocyte tTG-IgA–based ELISA assays to measure anti–tissue transglutaminase (tTG) antibodies is one of the favored methods for diagnosing celiac disease.
    However, assessments of various tTG kits have shown variations in sensitivity, which has raised some alarms among clinicians. Many clinicians suspect that hemolysis plays a role in these variations.
    To assess the effect of hemolysis on tTG-IgA titers, the team looked at blood samples from 9 patients with biopsy-confirmed, active celiac disease who chose to participate in the study.
    They split the samples into 3 groups, with three samples in each group. They divided the samples according to tTG-IgA concentration after thawing. They categorized the samples as high titer (>185 U), intermediate titer (100–140 U), and borderline titer (20–50 U).
    The team hemolyzed a whole-blood sample taken from 1 tTG/DGP-seronegative patient. They measured hemoglobin in the sample at 149 g/L of hemoglobin. They repeatedly froze and thawed the sample until 90% of cells hemolyzed. They then serially diluted in ratios of 1:2, 1:5, 1:10, 1:50, 1:100, 1:500 in PBS to obtain hemoglobin concentrations of 67.1, 26.8, 13.4, 2.7, 1.3, and 0.27 g/L, respectively. They then added to each sample at a 1:1 ratio.
    For the tTG sequestration assessment, the team added human recombinant tTG from Diarect AG for final concentrations of 0.04, 0.02, 0.01, and 0.002 g/L. The team used undiluted serum as the baseline titer reference, and serum diluted 1:2 in PBS as a control.
    To measure antibody titers, they used 2 ELISA test kits: QUANTA LiteTM h-tTG IgA (human erythrocyte tTG-IgA based) and Gliadin II (DGP-IgA based) from INOVA Diagnostics, Inc.  The team conducted blinded screens per manufacturer instructions, and compared the results for each group using the Mann–Whitney U-test, with P values <0.05 considered significant.
    They discovered that adding hemolyzed blood (HB) to sera of patients with active celiac disease lowered levels of anti-tTG, with intermediate- and borderline-titer groups seeing the largest reduction. Anti-DGP antibodies remained unchanged.
    Total average titer loss of anti-tTG vs anti-DGP antibodies was 36% vs 13% in the high-titer groups (P 0.026), 45% vs 3% (P = 0.026) in the intermediate titer groups, and 51% vs 2% in the borderline-titer groups (P = 0.0022)
    The team also found that adding ever higher concentrations of hemoglobin lowered the titers of anti-tTG, but not of anti-DGP, causing negative anti-tTG results in samples with low tTG antibody concentrations.
    The anti-tTG titer decreased 2%–65% in the high-titer groups, 1%–81% in the intermediate-titer groups, and 16%–74% in the borderline-titer group at hemoglobin concentrations of 0.3– 67.1 g/L.
    This compares with a decrease in anti-DGP titers of 10%–16% for high-titer groups, 4%–8% for intermediate-titer groups, and 7%–3% for the borderline-titer groups at hemoglobin concentrations of 0.3– 67.1 g/L.
    In all groups, tTG titer reduction was greater at higher concentrations of HB/HGB and gradually recovered as the red tint started to vanish at about 13 g/L of HGB, until complete visual disappearance at about 0.3g/L HGB).
    In the intermediate- and borderline-titer groups, titer reduction induced false-negative results at 20 U, with the anti-tTG, but not anti-DGP assays for HGB concentrations  ≥13 or ≥0.3 g/L, respectively.
    They also found that raising concentrations of exogenous tTG (recombinant human tTG) to intermediate-titer blood samples triggered a significant reduction in anti-tTG assay titers similar to that seen with hemoglobin (range, 32%–82%; mean, 69%), as compared with that of anti-DGP titers (mean, 18%; range, 1%–38%; P = 0.0159).
    Hemolysis is clearly indicated by a red tint in serum plasma, and is one of the most common reasons for labs to reject specimens. Visible hemolysis starts at about 0.5 g/L of hemoglobin and is obvious above 1.3 g/L of hemoglobin.
    The results show that that hemolysis does interfere with the detection of anti-tTG antibodies, and that visibly hemolyzed blood samples generate false-negative anti–tTG-IgA results.
    These findings may explain false-negative tests for celiac disease that arise when clinicians use tTG-IgA assays. They encourage clinicians and laboratories to take measures to avoid hemolysis. If they notice hemolyzed blood samples, they should alert physicians so new blood samples can be taken. If redrawing samples is not possible, hemolyzed samples should be measured for anti-DGP antibodies.
    Clinicians who suspect hemolysis should consider using anti-DGP serological tests, which are not influenced by hemolysis.
    Source:

     Clinical Chemistry. 2010;56:1034-1036. DOI: 10.1373/clinchem.2010.143263

    Jefferson Adams
    Celiac.com 02/23/2011 - In most adults with celiac disease, clinical symptoms disappear with a gluten-free diet. However, the exact effects of a gluten-free diet on rates of mucosal recovery in adults with celiac disease is less certain.
    A group of clinicians recently set out to assess rates of mucosal recovery under a gluten-free diet in adults with celiac disease, and to gauge the clinical prospects of ongoing mucosal damage in celiac patients who follow a gluten-free diet.
    The study group included Alberto Rubio-Tapia, MD; Mussarat W. Rahim, MBBS; Jacalyn A. See, MS, RD, LD; Brian D. Lahr, MS; Tsung-Teh Wu, MD; and Joseph A. Murray, MD.
    Each patient in the study had biopsy-proven celiac disease, and was assessed at the Mayo Clinic. Also, each patient received duodenal biopsies at diagnosis. After beginning a gluten-free diet, each patient had at least one follow-up intestinal biopsy to assess mucosal recovery.
    The study team focused on mucosal recovery and overall mortality. Of 381 adult patients with biopsy-proven celiac disease, a total of 241 (175 women - 73%) had both a diagnostic and follow-up biopsy available for re-review.
    Using the Kaplan–Meier rate of confirmed mucosal recovery to assess these 241 patients, the study group found that 34% of the patients enjoyed mucosal recovery at 2 years after diagnosis (95% with a confidence interval (CI): 27–40 % ), and 66% of patients enjoyed mucosal recovery at 5 years (95% CI: 58–74 % ).
    More than 80% of patients showed some clinical response to the gluten-free diet, but clinical response was not a reliable marker of mucosal recovery ( P = 0.7). Serological response was, by far, the best marker for confirmed mucosal recovery ( P = 0.01).
    Patients who complied poorly with a gluten-free diet ( P < 0.01), those with severe celiac disease defined by diarrhea and weight loss ( P < 0.001), and those with total villous atrophy at diagnosis ( P < 0.001) had high rates of persistent mucosal damage.
    With adjustments for gender and age, patients who experienced confirmed mucosal recovery had lower mortality rates overall (hazard ratio = 0.13, 95 % CI: 0.02 – 1.06, P = 0.06).
    One of the most important findings from this study was that a large number of adults with celiac disease have no mucosal recovery, even after treatment with a gluten free diet.
    Compared to those patients who suffered persistent damage, patients who experienced confirmed mucosal recovery had lower rates of mortality independent of age and gender.
    The group notes that systematic follow-up via intestinal biopsy may be advisable for adults with celiac disease.
    Source:

     Am J Gastroenterol. 9 February 2010; doi: 10.1038/ajg.2010.10

    Jefferson Adams
    Celiac.com 09/03/2014 - What’s potential celiac disease, and what happens to kids who have it and continue to eat a gluten-containing diet?
    Researchers define potential celiac disease as the presence of serum anti-tissue-transglutaminase (anti-TG2) antibodies with normal duodenal mucosa. That is, a positive blood screen, but no intestinal damage. However, not much is known about potential celiac disease because people who have it often show no obvious symptoms. Patients with potential celiac disease present some challenges for doctors trying to determine how likely it is that these patients will develop villous atrophy, the gut damage common in celiac disease patients exposed to gluten.
    A research team conducted a prospective longitudinal cohort study to follow patients with potential celiac disease up to 9 years, and explore the risk factors tied to mucosal damage. The research team included Renata Auricchio MD, PhD, Antonella Tosco MD, Emanuela Piccolo MD, Martina Galatola PhD, Valentina Izzo PhD, Mariantonia Maglio PhD, Francesco Paparo PhD, Riccardo Troncone MD, PhD, and Luigi Greco MD, PhD. They are affiliated with the Department of Medical Translational Science, European Laboratory for the Investigation of Food Induced Disease (ELFID), University Federico II, Naples, Italy.
    For their study, the team found two hundred and ten asymptomatic children with potential celiac disease. They kept 175 of them on a gluten-containing diet. To evaluate histological, immuno-histochemical, and anti-TG2 status, they checked blood antibody levels and clinical symptoms every 6 months, and took a small bowel biopsy every two years. They also genotyped all patients for HLA and non-HLA celiac-associated genes.
    Forty-three percent of patients showed persistently elevated anti-TG2 levels, 20% became negative during follow-up, and 37% showed variations in anti-TG2 course, with many patients testing at zero anti-TG2.
    After three years of follow-up, 86% of study patients continued to have potential celiac disease. After 6 and 9 years, respectively, 73% and 67% of study patients still had normal duodenal structure.
    Individuals prone to develop mucosal damage during the test period were predominantly male, had slight mucosal inflammation at study’s start, and fit a peculiar genetic profile.
    Nine years after follow-up, a large number of patients with asymptomatic potential celiac disease showed reduced antibody production, many even showing zero production, and many of these, with persistently positive anti-TG2, showed no mucosal damage.
    Given the results of this study, and noting that the celiac population is in fact made up of numerous individuals with diverse genetic and phenotypic makeup, the researchers are advising doctors to be cautious in prescribing a strict lifelong gluten-free diet for asymptomatic individuals with potential celiac disease.
    Source:
     The American Journal of Gastroenterology

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    Thank you so much! and yes, I am aware of other allergies. I have leaky gut as well and have a food allergy to potatoes and corn as well and my mother eats those too. So very stressed out. I went downstairs and found a mini fridge and im going to start using that because like you said, handles, faucets, etc are too much. the stress does not help the body either, ive been getting sick three times a week. its very hard.  I am glad there are people who understand! Sounds like you were concerned too
    The cheese and avocado are fine, the gluten was not aerosolized anything like that. NOW if your allergic to wheat there could be some issues being around it like that (some severe cases of peanut allergies can go off if it is in the room) but you would be anaphylactic.  I get the paranoia, it gets to the point of being almost PTSD. You fear to get sick so bad because the weirdest things have bedridden you. I got glutened touching gluten residue on facets, fridge door handles, etc in my old
    Alaskaguy, Here is the research you are looking for they are entitled "Maize prolamins resistant to peptic-tryptic digestion maintain immune-recognition by IgA from some celiac disease patients." and "Maize prolamins could induce a gluten-like cellular immune response in some celiac disease patients." respectively. https://www.ncbi.nlm.nih.gov/pubmed/22298027 https://www.ncbi.nlm.nih.gov/pubmed/24152750 It is like Oats ...Corn can bother a subset of celiac's. ...reintroducing
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