• Join our community!

    Do you have questions about celiac disease or the gluten-free diet?

  • Ads by Google:
     




    Get email alerts Subscribe to Celiac.com's FREE weekly eNewsletter

    Ads by Google:



       Get email alertsSubscribe to Celiac.com's FREE weekly eNewsletter

  • Member Statistics

    77,692
    Total Members
    3,093
    Most Online
    ZAK88
    Newest Member
    ZAK88
    Joined
  • 0

    Gluten-degrading Enzymes Could Help Control Adverse Reactions in Celiac Disease


    Jefferson Adams
    Image Caption: Photo: CC--R. Vore

    Celiac.com 02/27/2014 - For many people with celiac disease, one of the numerous downsides of the condition is the constant threat of an adverse reaction triggered by accidental gluten consumption. Because reactions to gluten ingestion can be severe for some celiac patients, many clinicians are looking to see if anything can be done to lessen the effects gluten reactions in celiac patients once they have started.


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    Photo: CC--R. VoreA team of researchers sought to provide at least one possible answer by looking into the safety and efficacy of Aspergillus niger prolyl endoprotease (AN-PEP) to lessen effects gluten reactions in celiac patients. The researchers included G.J. Tack, J.M. van de Water, M.J. Bruins, E.M Kooy-Winkelaar, J. van Bergen, P. Bonnet, A.C. Vreugdenhil, I. Korponay-Szabo, L. Edens, B.M. von Blomberg, M.W. Schreurs, C.J. Mulder, and F. Koning. They are all affiliated with the Department of Gastroenterology and Hepatology, VU University Medical Centre, 1007 MB Amsterdam, The Netherlands.

    For their study, the team enrolled 16 adults with celiac disease as confirmed by positive blood test and biopsy-confirmed subtotal or total villous atrophy. All patients were following a strict gluten-free diet, and showed normalized antibodies and mucosal healing classified as Marsh 0 or I.

    In their randomized double-blind placebo-controlled pilot study, the team had patients consume wheat toast, totaling about 7 grams of gluten per day, with AN-PEP for a two-week safety phase. After a two-week washout period with adherence of the usual gluten-free diet, 14 patients were randomized to receive gluten with either AN-PEP or placebo for there two-week efficacy phase.

    Baseline measurements included complaints, quality-of-life, serum antibodies, immuno-phenotyping of T-cells and duodenal mucosa immuno-histology. The team collected both serum samples and quality of life questionnaires during and after the safety, washout and efficacy phase. They conducted duodenal biopsies after both safety and efficacy phases. The primary endpoint was a change in histological evaluation according to the modified Marsh classification.

    None of the sixteen adults in the study suffered serious adverse events, and no patients withdrew during the trial. Overall scores for the gastrointestinal subcategory of the celiac disease quality (CDQ) remains fairly high throughout the study, indicating that AN-PEP was well tolerated. Through the efficacy phase, CDQ scores for patients consuming gluten with placebo or gluten with AN-PEP remained largely unchanged, and researchers observed no differences between the groups. Moreover, neither the placebo group nor the AN-PEP group developed significant antibody titers, and IgA-EM concentrations remained negative for both groups.

    The team excluded two patients from entering the efficacy phase because their mucosa showed an increase of two Marsh steps after the safety phase, even though their serum antibodies remained undetectable.

    A total of 14 patients were considered histologically stable on gluten with AN-PEP. Also after the efficacy phase, the team saw no significant deterioration in immunohistological and flow cytometric values between the group consuming placebo compared to the group receiving AN-PEP.

    Furthermore, compared to baseline, after two weeks of gluten four out of seven patients on placebo showed increased IgA-tTG deposit staining. In the seven patients receiving AN-PEP, one patient showed increased and one showed decreased IgA-tTG deposits.

    AN-PEP appears to be well tolerated. However, the primary endpoint was not met due to lack of clinical deterioration upon placebo, impeding an effect of AN-PEP.

    Source:

    0


    User Feedback

    Recommended Comments

    Guest Nancy Walton

    Posted

    Thank you for explaining research such as this study. I am most interested in articles that discuss quantitative effects of small amounts of gluten to damage of the small intestines.

    Share this comment


    Link to comment
    Share on other sites

    Seems people with celiac disease react very differently to gluten, especially looking at the info that 2 people had raised Marsh scores but no serum antibodies. This seems to back up the position that not everyone shows a positive antibody even though they have intestinal damage.

    Share this comment


    Link to comment
    Share on other sites
    Guest luke

    Posted

    Ok, it's fine, but how many times do we need to wait for this cure?? One, two, ten years???

    Share this comment


    Link to comment
    Share on other sites


    Your content will need to be approved by a moderator

    Guest
    You are commenting as a guest. If you have an account, please sign in.
    Add a comment...

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoji are allowed.

    ×   Your link has been automatically embedded.   Display as a link instead

    ×   Your previous content has been restored.   Clear editor

    ×   You cannot paste images directly. Upload or insert images from URL.


  • Ads by Google:

  • About Me

    Jefferson Adams is a freelance writer living in San Francisco. He has covered Health News for Examiner.com, and provided health and medical content for Sharecare.com. His work has appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate, among others.

  • Popular Contributors

  • Ads by Google:

  • Who's Online   3 Members, 0 Anonymous, 276 Guests (See full list)

  • Related Articles

    Scott Adams
    Gastrointest Endosc. 2004 Jan;59(1):116-8. Celiac.com 06/28/2004 - This study, although small, indicates that there may be additional damage to the second part of the duodenum caused by celiac disease, and that this can also be used for a marker for diagnosing the disease:

    Dickey W, Hughes D.
    Department of Gastroenterology, Altnagelvin Hospital, Londonderry, Northern Ireland, UK.
    BACKGROUND: There are various, well-documented, duodenal endoscopic markers caused by the villous atrophy of celiac disease. Another abnormality seen in association with villous atrophy, erosions in the second part of the duodenum, is described. To our knowledge, this finding has not been heretofore described in patients with celiac disease.
    METHODS: Five patients with celiac disease and erosions were encountered over a period of 2 years.
    OBSERVATIONS: The erosions were multiple, superficial, and present in the second part of the duodenum but not the duodenal bulb. All 5 patients had findings typical of celiac disease (iron deficiency, osteopenia/osteoporosis), and 4 had at least one other endoscopic marker: scalloped duodenal folds (3), fold loss (2), or mosaic pattern mucosa (2). These patients represented 7% of new cases of celiac disease during the same time period. This pattern of erosion was not observed in over 1200 other patients undergoing upper endoscopy during the study period.
    CONCLUSIONS: In a European population, the finding of erosions confined to the second part of the duodenum is specific for villous atrophy, although sensitivity is low. Erosions in the second part of the duodenum should be added to the list of endoscopic markers of celiac disease.

    Jefferson Adams
    Celiac.com 06/29/2012 - A group of researchers recently set out to study cases of positive tissue transglutaminase antibodies with negative endomysial antibodies to determine whether or not such cases amount to celiac disease.
    The team included Thomas Hornung; Pavel Gordins; Clare Parker; and Nicholas Thompson. They are variously affiliated with the departments of Gastroenterology, and Immunology at the Northern Deanery of Newcastle upon Tyne, and with the department of Gastroenterology at Freeman Hospital in Newcastle upon Tyne in the UK.
    The most sensitive and specific blood tests for diagnosing celiac disease are those that detect immunoglobulin A (IgA) antibodies against human tissue transglutaminase (tTGA) enzyme, and those that measure aspects of connective tissue covering individual smooth muscle fibers, endomysial antibodies (EMA).
    Because of the high sensitivity (up to 98%) and high specificity (around 96%) reported for the tTGA assay, detection of tTGA is currently the primary blood test used in screening for celiac disease.
    The tTGA test also has a high negative predictive value approaching 100%, which makes it an excellent test for excluding celiac disease in both high and low risk groups. In contrast, positive predictive value of the tTGA test is rather poor with values between 28.6% and 60.2% being reported in several studies.
    EMA, on the other hand, has extremely high specificity values close to 100% and positive predictive value values approaching 80%.[5 10] However, compared with tTGA, EMA has lower sensitivity, usually under 90%.
    This being the case, the present standard celiac disease screening strategy is to first use tTGA, and then confirm positive results using EMA. However, doing it this way, doctors often end up with a group of patients who show divergent test results.
    For their study, the researchers wanted to gauge the percentage of patients with positive tTGA and negative EMA, but who were confirmed with celiac disease upon biopsy, and to identify factors in these patients that may help to increase diagnostic accuracy in such patients.
    The research team identified 125 consecutive patients with positive tTGA and negative EMA, who subsequently underwent endoscopy with at least two biopsies from the second part of the duodenum.
    The team charted any tTGA result over 15 U/ml as positive. They excluded any patients with known celiac disease at the time of testing.
    They then reviewed patient notes to assess indications for celiac disease serological screening, including the presence of iron deficiency anaemia, and symptoms such as diarrhea or weight loss, and family history of celiac disease. They defined diarrhea as a bowel frequency of more than three times a day.
    They then assessed histological evidence of celiac disease based on subsequent duodenal biopsies, plus Marsh grading. In cases where patient histology was unclear, they relied on the clinical assessment of a consulting gastroenterologist. Unclear histology included minimal/mild increase in intraepithelial lymphocytes of not more than 30 per 100 enterocytes and without villous atrophy, plus mild villous blunting with no increase in intraepithelial lymphocytes.
    They then categorized patients as either celiac disease negative, or celiac disease positive. Patients with no histological evidence of celiac disease on duodenal biopsies or equivocal histology plus overall clinical impression of celiac disease absence were categorized as celiac disease negative. Patients with histological evidence of celiac disease on duodenal biopsies or equivocal histology plus overall clinical impression of celiac disease presence were categorized as celiac disease positive.
    To measure IgA anti-tTGA antibody the team used a commercially available enzyme linked immunosorbent assay called Aeskulisa, manufactured by Aesku Diagnostics GmbH in Wendelsheim, Germany.
    To detect IgA anti-EMA with the standard immunofluorescent method, they used commercial slides of monkey oesophagus sections (Euroimmun, Euroimmun AG, Lübeck, Germany). They used conjugated sheep antihuman IgA as a secondary antibody, relying on a test manufactured by Instrumentation Laboratory UK Ltd., in Warrington, UK.
    Overall, the team categorized 113 patients (90.4%) as celiac disease negative. Of these, 102 patients had no histological features of celiac disease, while 11 patients had unclear histology plus an overall clinical impression of not having celiac disease.
    They categorized twelve patients (9.6%) as celiac disease positive. Of these, 10 patients had positive histology, and two patients had unclear histology plus an overall clinical impression of having celiac disease.
    Of those with positive histology, 17% were Marsh grade I, 8% were Marsh grade II, 33% were Marsh grade IIIa, 17% were Marsh grade IIIb and 25% were Marsh grade IIIc. Those with celiac disease were more likely to be older and to have a higher tTGA level. The groups showed no difference in any clinical parameter.
    Source:
    Frontline Gastroenterol. 2012;3(2):81-83.

    Jefferson Adams
    Celiac.com 10/12/2012 - What is the relationship between breastfeeding, the age of gluten introduction and rates of celiac disease?
    A number of studies have shown that increased breastfeeding may provide some protection against celiac disease. However, one study found no change in the overall prevalence of celiac disease in breastfed infants compared to controls, suggesting that breastfeeding may only delay the presentation of the disease but, does not prevent it. Other studies show no significant difference in the prevalence of celiac disease between breastfed and non-breastfed patients.
    Data from the Swedish celiac disease epidemic suggest a 3% prevalence of celiac disease in the children born during the epidemic. An analysis by Ivarsson et al. of children born during the epidemic, found that children under 2 years of age had a lower risk of celiac disease if they were still being breastfed when dietary gluten was introduced (odds ratio 0.59, 95, with a confidence interval 0.42–0.83). Children who continued breastfeeding after gluten was introduced to their diet showed a further decrease in the risk for celiac disease (OR 0.36, 95% CI 0.26–0.51).
    A meta-analysis that included the Ivarsson data, showed celiac disease risk was significantly lower in infants who were breastfed at the time of gluten introduction (pooled OR 0.48, 95% CI 0.40–0.59), compared to infants who were not breastfed at the time of first gluten exposure.
    A later study, by Akobeng and others, estimated that breastfeeding all babies in the UK at the time of gluten introduction, would prevent 2500 cases of celiac disease every year.
    The best data currently available on celiac disease and the age of gluten introduction comes from a prospective study by Norris et al. The study followed 1560 children in Denver between 1994 and 2004. This study showed that children exposed to gluten in the first 3 months of life had a fivefold increased risk of having celiac disease than children exposed to gluten between 4 and 6 months of age, while children exposed to gluten at 7 months old or later had an almost twofold increased risk compared with those exposed at 4 to 6 months (hazard ratio 1.87, 95% CI 0.97–3.60).
    When the analysis was limited to biopsy-diagnosed celiac disease, the hazard ratio was 23.97 (95% CI 4.55–115.9) for children exposed to gluten during the first 3 months of life compared to the 4–6 months exposure group, and 3.98 (95% CI 1.18–13.46) in the group exposed at 7 months or later
    What remains unclear, is whether breastfeeding and the age of introduction of gliadin prevent celiac disease or merely delay its onset.
    To clarify the relationship between breastfeeding, the age at which gluten is introduced into the diet, and celiac disease, the EU has funded a prospective study, called PREVENTCD, FP6, in 10 European centers. The PREVENTCD study recruited pregnant women with a family history of celiac disease, and determined HLA4 of the newborn at birth.
    By the end of December 2010, researchers had recruited a total of 1345 children at birth and enrolled 986 with positive HLA DQ status.
    Researchers instructed mothers to breastfeed for 6 months, if possible. Beginning at the age of 4 months, the researchers placed the infants into randomized study groups, and fed them 100 mg of gliadin or a non-gliadin placebo every day.
    The full data won't be available until all children reach the age of 3 years of age, but the researchers hope that the study will offer definitive answers on the relationship between breastfeeding and the age of gluten introduction and rates of celiac disease.
    Until new information become available, the ESPGHAN Committee on Nutrition recommendations remain in effect. This recommendations state that gluten should be introduced to infants no earlier than 4 months of age, and no later than 7 months, and that the introduction should be gluten be made while the infant is still being breastfed.
    This information was compiled by researcher R. Shamir of the Institute for Pediatric Gastroenterology, Nutrition and Liver Diseases, at the Schneider Children's Medical Center of Israel, Petah Tikva, affiliated with Sackler Faculty of Medicine, Tel Aviv University in Ramat Aviv, Israel.
    Source:
    Isr Med Assoc J. 2012 Jan;14(1):50-2.

    Jefferson Adams
    Celiac.com 03/31/2014 - Celiac disease is an autoimmune disorder that occurs in genetically susceptible individuals who carry the genetic markers HLA DQ2 or DQ8. About one in three people carry these genetic markers, while researchers estimate that the global prevalence of celiac disease is somewhere between one- and two-percent.
    A gluten-free diet remains the only treatment for celiac disease, but researchers are looking into new therapies aimed at gluten modification.
    A team of researchers have reviewed a number of promising new celiac disease therapies aimed at gluten modification.
    The researchers include S. Stoven, J.A. Murray, and E. Marietta, of the Division of Gastroenterology and Hepatology, Department of Internal Medicine at the Mayo Clinic in Rochester, Minnesota.
    Their review in Clinical Gastroenterology & Hepatology discusses gluten-based therapies including wheat alternatives and wheat selection, enzymatic alteration of wheat, oral enzyme supplements, and polymeric binders as exciting new therapies for treatment of celiac disease.
    Unfortunately, the full study is only available to subscribers, but anyone with the inclination to subscribe can read it online.
    Source:
     Clin Gastroenterol Hepatol. 2012 Aug;10(8):859-62. doi: 10.1016/j.cgh.2012.06.005.

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/21/2018 - Would you buy a house advertised as ‘gluten-free’? Yes, there really is such a house for sale. 
    It seems a Phoenix realtor Mike D’Elena is hoping that his trendy claim will catch the eye of a buyer hungry to avoid gluten, or, at least one with a sense of humor. D’Elena said he crafted the ads as a way to “be funny and to draw attention.” The idea, D’Elena said, is to “make it memorable.” 
    Though D’Elena’s marketing seeks to capitalizes on the gluten-free trend, he knows Celiac disease is a serious health issue for some people. “[W]e’re not here to offend anybody….this is just something we're just trying to do to draw attention and do what's best for our clients," he said. 
    Still, the signs seem to be working. D'elena had fielded six offers within a few days of listing the west Phoenix home.
    "Buying can sometimes be the most stressful thing you do in your entire life so why not have some fun with it," he said. 
    What do you think? Clever? Funny?
    Read more at Arizonafamily.com.

    Advertising Banner-Ads
    Bakery On Main started in the small bakery of a natural foods market on Main Street in Glastonbury, Connecticut. Founder Michael Smulders listened when his customers with Celiac Disease would mention the lack of good tasting, gluten-free options available to them. Upon learning this, he believed that nobody should have to suffer due to any kind of food allergy or dietary need. From then on, his mission became creating delicious and fearlessly unique gluten-free products that were clean and great tasting, while still being safe for his Celiac customers!
    Premium ingredients, bakeshop delicious recipes, and happy customers were our inspiration from the beginning— and are still the cornerstones of Bakery On Main today. We are a fiercely ethical company that believes in integrity and feels that happiness and wholesome, great tasting food should be harmonious. We strive for that in everything we bake in our dedicated gluten-free facility that is GFCO Certified and SQF Level 3 Certified. We use only natural, NON-GMO Project Verified ingredients and all of our products are certified Kosher Parve, dairy and casein free, and we have recently introduced certified Organic items as well! 
    Our passion is to bake the very best products while bringing happiness to our customers, each other, and all those we meet!
    We are available during normal business hours at: 1-888-533-8118 EST.
    To learn more about us at: visit our site.

    Jefferson Adams
    Celiac.com 06/20/2018 - Currently, the only way to manage celiac disease is to eliminate gluten from the diet. That could be set to change as clinical trials begin in Australia for a new vaccine that aims to switch off the immune response to gluten. 
    The trials are set to begin at Australia’s University of the Sunshine Coast Clinical Trials Centre. The vaccine is designed to allow people with celiac disease to consume gluten with no adverse effects. A successful vaccine could be the beginning of the end for the gluten-free diet as the only currently viable treatment for celiac disease. That could be a massive breakthrough for people with celiac disease.
    USC’s Clinical Trials Centre Director Lucas Litewka said trial participants would receive an injection of the vaccine twice a week for seven weeks. The trials will be conducted alongside gastroenterologist Dr. James Daveson, who called the vaccine “a very exciting potential new therapy that has been undergoing clinical trials for several years now.”
    Dr. Daveson said the investigational vaccine might potentially restore gluten tolerance to people with celiac disease.The trial is open to adults between the ages of 18 and 70 who have clinically diagnosed celiac disease, and have followed a strict gluten-free diet for at least 12 months. Anyone interested in participating can go to www.joinourtrials.com.
    Read more at the website for Australia’s University of the Sunshine Coast Clinical Trials Centre.

    Source:
    FoodProcessing.com.au

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.