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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

    Roy Jamron
    Celiac.com 07/01/2006 - With the likelihood that increased intestinal permeability in celiacs caused by gluten damage to the intestinal mucosa leads to a high prevalance of liver damage as well as an increase in food allergy and possible other medical conditions, emphasis on healing the intestinal mucosa should be given an elevated priority. Simply going on a gluten-free diet and waiting months or years for the intestine to heal may not be enough.
    Friendly commensal gut bacteria are an important part of the intestinal barrier, and thus probiotics, such as yogurt, kefir, or supplemental
    probiotic capsules, do help diminish the amount of endotoxins released by pathogenic gut bacteria getting through the barrier. Liver disease studies confirm the benefit of probiotics by reducing inflammation and infection. However, to date, there is no product currently available which can enhance the repair and regeneration process of the mucosal epithelia.
    Undergoing current clinical studies in Crohns patients, Teduglutide may enhance mucosal healing, but requires multiple daily injections:

    Cell Prolif. 2004 Dec;37(6):385-400.
    Teduglutide ([Gly2]GLP-2) protects small intestinal stem cells from
    radiation damage.
    Booth C, Booth D, Williamson S, Demchyshyn LL, Potten CS.
    Abstract:
    http://www.blackwell-synergy.com/doi/abs/10.1111/j.1365-2184.2004.00320.x
    New Crohns Disease Drug Induces Remission Through Mucosal Healing
    By Martha Kerr
    (Free article, free Medscape registration may be required.)
    http://www.medscape.com/viewarticle/533109
    A while back I posted an abstract about a protein called R-spondin1 which is "a specific and potent stimulator of the human epithelial cells that line the gastrointestinal tract and mouth." R-spondin1 is a product being developed by Nuvelo, Inc. of San Carlos, CA designated as NU206. The press release describing NU206 is:
    Nuvelo Announces NU206 Publication in Science (August 18, 2005)
    http://www.corporate-ir.net/ireye/ir_site.zhtml?ticker=NUVO&script=410&item_id=744876
    An article discussing the discovery and potentials of R-spondin1 is available in the New England Journal of Medicine, and free full text of
    that article is available at the address below:
    NEJM.-Volume 353:2297-2299 November 24, 2005 Number 21
    Inducing Intestinal Growth
    Clara Abraham, M.D., and Judy H. Cho, M.D.
    Free Full Text Reprint of NEJM article:
    http://www.e-medicum.com/newsletters/medicinaInterna/verNoticia.php?noticia=51479
    Nuvelo has recently announced plans for the "initiation of a Phase 1 study of NU206, which is being developed for the treatment of cancer therapy-induced mucositis in the second half of 2006." Obviously the benefits of NU206 go beyond that of cancer therapy. Healing the epithelial tissues of celiacs with NU206 may rapidly eliminate increased intestinal permeability and other associated conditions. Nuvelo had a live webcast of its annual shareholder meeting this Wednesday, May 24, at 11:00 am PDT. No new information on NU206 was provided at the meeting other than that plans to initiate the NU206 Phase 1 study are proceding.
    Replay of Nuvelo Webcast:
    http://www.corporate-ir.net/ireye/ir_site.zhtml?ticker=NUVO&script=1010&item_id=1234084


    Jefferson Adams
    Celiac.com 02/04/2013 - Ever wonder what happens to all those celiac disease patients who volunteer to do a gluten-challenge in the name of science? Well, the short answer is that they likely suffer, and may incur gut damage, at least in the short term.
    A team of researchers looking for ways to reduce or eliminate that problem recently conducted a study using larazotide acetate, a first-in-class oral peptide that prevents tight junction opening, and may reduce gluten uptake and associated problems.
    The research team included C. P. Kelly, P. H. R. Green, J. A. Murray, A. DiMarino, A. Colatrella, D. A. Leffler, T. Alexander, R. Arsenescu, F. Leon, J. G. Jiang, L. A. Arterburner, B. M. Paterson, R. N. and Fedorak. They are affiliated with the Celiac Center of Beth Israel Deaconess Medical Center at Harvard Medical School in Boston, the Celiac Disease Center at Columbia University in New York, NY, the Division of Gastroenterology and Hepatology at the Mayo Clinic in Rochester, MN, Thomas Jefferson University Hospital in Philadelphia, PA, the Pittsburgh Gastroenterology Associates in Pittsburgh, PA, with Gastrointestinal Specialists of Troy, MI, the Department of Internal Medicine at the University of Kentucky, in Lexington, KY, with Alba Therapeutics Corporation in Baltimore, MD, and with the Division of Gastroenterology at the University of Alberta in Edmonton, AB.
    The team wanted to find out how well larazotide acetate worked and how well it was tolerated by celiac disease patients undergoing a gluten challenge.
    To do this, the team conducted an exploratory, double-blind, randomized, placebo-controlled study that included 184 patients who maintained a gluten-free diet before and during the study.
    After a gluten-free diet run-in, the team randomly divided patients into groups and gave them either larazotide acetate in doses of 1, 4, or 8 mg three times daily, or a placebo. Both groups also received 2.7 grams of gluten daily for six weeks.
    The team then assessed ratios of lactulose-to-mannitol (LAMA), an experimental biomarker of intestinal permeability, and measured clinical symptoms by Gastrointestinal Symptom Rating Scale (GSRS) and anti-transglutaminase antibody levels.
    They found no significant differences in LAMA ratios between larazotide acetate and placebo groups. Larazotide acetate 1-mg limited gluten-induced symptoms measured by GSRS (P = 0.002 vs. placebo).
    They did find that the average ratio of anti-tissue transglutaminase IgA levels was 19.0 over baseline in the placebo group compared with 5.78 (P = 0.010) in the 1mg larazotide acetate group, 3.88 (P = 0.005) in the 4mg larazotide acetate group, and 7.72 (P = 0.025) in the 8mg larazotide acetate group.
    Both the larazotide acetate and placebo groups showed similar rates of "adverse events."
    Overall, the team found that larazotide acetate reduced gluten-induced immune reactivity and symptoms in celiac disease patients undergoing gluten challenge and was generally well tolerated.
    However, the team found no significant difference in LAMA ratios between the larazotide acetate and placebo groups.
    Even though they did not find anything revolutionary, the results and design of their study will likely be helpful in shaping future gluten-challenge studies in patients with celiac disease.
    Source: 
    Aliment Pharmacol Ther. 2013;37(2):252-262.

    Jefferson Adams
    Higher Risk of Non-alcoholic Fatty Liver Disease After Celiac Diagnosis
    Celiac.com 06/29/2015 - Non-alcoholic fatty liver disease is a common cause of chronic liver disease. There's good data showing that celiac disease changes intestinal permeability, and that treatment with a gluten-free diet often causes weight gain, but so far there is scant documentation of non-alcoholic fatty liver disease in patients with celiac disease.
    A team of researchers recently set out to assess increased risk of non-alcoholic fatty liver disease following diagnosis of celiac disease. The research team include Norelle R. Reilly, Benjamin Lebwohl, Rolf Hultcrantz, Peter H.R. Green, and Jonas F. Ludvigsson. They are affiliated with the Department Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden, and the Department of Pediatrics at Örebro University Hospital, Örebro University in Örebro, Sweden.
    The team assessed the for risk of non-alcoholic fatty liver disease diagnosed from 1997 to 2009 in 26,816 individuals with celiac disease to 130,051 matched reference individuals.
    The team excluded patients with any liver disease prior to celiac disease. They also excluded individuals with a lifetime diagnosis of alcohol-related disorder to minimize misclassification of non-alcoholic fatty liver disease. They used Cox regression estimated hazard ratios for non-alcoholic fatty liver disease.
    Their results showed that over 246,559 person-years of follow-up, 53 individuals with celiac disease had a diagnosis of non-alcoholic fatty liver disease (21/100,000 person-years).
    In comparison, in the reference group showed 85 individuals diagnosed with non-alcoholic fatty liver disease during 1,488,413 person-years (6/100,000 person-years).
    This corresponded to a hazard ratio of 2.8 in the celiac group (95% CI), with the highest risk estimates of 4.6 seen in children (95% CI).
    The risk increase in the first year after celiac disease diagnosis was 13.3 (95% CI), but remained significantly elevated at 2.5 even beyond 15 years after celiac diagnosis of celiac disease (95% CI).
    Individuals with celiac disease do have an increased risk of non-alcoholic fatty liver disease compared to the general population.
    Excess risks were highest in the first year after celiac disease diagnosis, but continued at least 15 years after celiac diagnosis. This much more comprehensive study provides much clearer and convincing data than any of the previous studies, and will likely serve as a baseline that clinicians have been lacking to this point.
    Source:
    Journal of Hepatology, June 2015Volume 62, Issue 6, Pages 1405–1411. DOI: http://dx.doi.org/10.1016/j.jhep.2015.01.013

    Jefferson Adams
    Celiac Patients on a Gluten-free Diet Face Increased Risk of Nonalcoholic Fatty Liver Disease
    Celiac.com 10/24/2018 - Although some research has shown a connection between a gluten-free diet, altered macronutrient intake and metabolic syndrome, not much good data exists on the risk of nonalcoholic fatty liver disease in patients with celiac disease who follow a gluten-free diet. A team of researchers recently set out to assess the prevalence and relative risk of nonalcoholic fatty liver disease in celiac patients treated with a gluten-free diet.
    The research team included F. Tovoli; G. Negrini; R. Farì; E. Guidetti; C. Faggiano; L. Napoli; L. Bolondi; and A. Granito of the Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy.
    For many patients with metabolic syndrome, nonalcoholic fatty liver disease is common. To try to get some better information, the researchers devised a case-control study, with prospective enrollment of celiac disease outpatients following a gluten-free diet and control subjects. 
    For the study, the team matched patients by age, gender and metabolic risk factors, such as overweight, diabetes mellitus, total cholesterol, and triglycerides, using a 1:1 ratio.  The team diagnosed nonalcoholic fatty liver disease according to the criteria set by the European Association for the Study of the Liver.
    In all, they compared 202 celiac disease patients and 202 control subjects. The raw rate of nonalcoholic fatty liver disease was 34.7% and 21.8% in the celiac disease and control group, respectively. Using binary logistic regression, the team demonstrated that those with celiac disease faced an increased risk for nonalcoholic fatty liver disease. 
    Meanwhile, the relative risk for nonalcoholic fatty liver disease was substantially higher in non-overweight celiac disease patients. Nearly 35% of celiac disease patients on a gluten-free diet also had nonalcoholic fatty liver disease, that’s a risk three times greater than the general population. 
    The team recommends that doctors tailor their celiac treatment approaches to better help celiac disease patients with nonalcoholic fatty liver disease to get proper nutritional intake, which will help to reduce the risk of long-term liver-related events.
    Source: Aliment Pharmacol Ther. 2018;48(5):538-546.

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    Thank you so much, cyclinglady. Yes, very helpful! I want to tell her the exact tests I want.  I am thinking I should request: tTG-IgA Total serum IgA Do you agree? I am on a super high-deductible health plan, so I end up paying for all of these, so I don't want to go overboard while still being as sure as I can be. Not related to celiac (as far as I know) but I was also reminded that my sister has the MTHFR gene mutation (homozygous C variant), so I need to ask her to be tested for that as well... She is going to think I am nuts, and that is fine. ;)
    Oh no!  One celiac test?  Only one was given?  The TTG IgA, I assume or you just got the Immunoglobulin A (IGA) test?  You should insist on the complete celiac panel.  You should also know that  some people with DH do not test positive on any of the celiac blood tests.  If your skin biopsies are negative, make sure they biopsy was taken correctly — not on the rash, but adjacent.  This mistake is make ALL THE TIME by dermatologists.   Because of what you disclosed in another post, you should consider asking a Gastroenterologist and not your GP (who seems to know little about celiac disease and testing) why you had small intestinal damage (per initial biopsies) went gluten free and later a second biopsy revealed a healed small intestine, yet you were not given a celiac diagnosis.   Later, it seems you started consuming gluten again or were getting traces of gluten into your diet, and now may have developed or worsened your DH. Quote: “Hi, I have been trying to get a celiac diagnosis for awhile now. I had an endoscopy years ago that showed flatted villi but the biopsy said "possible sprue or possible duodonitis." I went g.f. and had another test a few years later. The villi were normal but I had what I thought was a d.h. rash. The dermatologist said it did not look like d.h. and said it was just eczema.  To test myself, I started eating gluten again. I have occasional bowel issues but not like I had years ago.” Now my legs look like I have d.h. again.” You can go gluten free and safely prepare gluten in your house.  I did this for 12 years when my hubby was gluten free and before I was shockingly diagnosed.  You just can not ingest gluten.  The only thing you need to avoid is flour because flour has been documented to stay in the air or fall on surfaces for up to 24 hours (one reason not to have a coffee in a bakery or donut shop — sit outside!)  You can cook pasta, make sandwiches, open a box of cookies....whatever!  Just do not use loose flour.   If he needs a birthday cake, have a friend bake it at their house.  Or he may love a gluten-free cake.  Soon I will be baking my kid a gluten-free Chocolate Mayonnaise Cake for her birthday and she is not celiac!  She actually prefers it to a gluten-containing bakery cake!   There are plenty of alternate grains besides wheat, barley and rye for your son.  Think outside the box.   I have said this before you should get your son tested for celiac disease.  I have allergies and I never had a positive for wheat.  Wheat allergies and celiac disease are separate issues.  He may very well have celiac disease.  Why?  Because his mom had a positive intestinal biopsy and went gluten free and then had a repeat intestinal biopsy and healed.  I am not a doctor, but that is pretty damning evidence.  Maybe you need to consult with an attorney who specializes in malpractice.  You appear to have been put through a diagnostic nightmare.   I hope this helps.  Mothers need to take care of themselves first, so that they can help their children.  It is like the oxygen masks on an airplane.  Adults are instructed to put their mask on first before assisting others (e.g. children).        
    Some people with DH do lousy on the blood antibody tests.  They hoard all their gliaden antibodies in their skin instead of their bloodstream.  So they may test negative on blood antibodies but still have plenty of antibodies in the skin.  Sometimes they even flunk the endoscopy tests for the same reason.
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