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    Scott Adams
    IgA class Reticulin antibodies are found only in Celiac disease and dermatitis herpetiformis. These antibodies are found in approximately 60% of celiac disease patients and 25% of DH patients. This test is falling into disuse because of the limited utility and the availability of better tests. IgA class endomysial antibodies are very specific, occurring only in celiac disease and DH. These antibodies are found in approximately 80% of patient with DH and in essentially 100% of patients with active celiac disease. IgA endomysial antibodies are more sensitive and specific than either reticulin or gliadin antibodies for diagnosis of celiac disease. Antibody titers are found to parallel morphological changes in the jejunum and can also reflect compliance with gluten-free diets. Titers decrease or become negative in patients on gluten free diets and reappear upon gluten challenge.
    The purpose of testing for anti-gliadin antibodies includes, in addition to diagnosis of gluten sensitive enteropathy, monitoring for compliance to a gluten free diet. IgA gliadin antibodies increase rapidly in response to gluten in the diet, and decrease rapidly when gluten is absent from the diet. The IgA anti-gliadin antibodies can totally disappear in 2-6 months on a gluten-free diet, so they are useful as a diet control. By contrast, IgG anti-gliadin antibodies need a long time, sometimes more than a year, to become negative.
    The reverse is also true. That is, a patient with celiac disease who has been on a gluten-free diet and tests negative for IgA anti-gliadin antibodies, will show a rapid increase in antibody production when challenged by gluten in the diet. Approximately 90% of challenged patients will yield a positive IgA anti-gliadin result within 14-35 days after being challenged. The test results you reported are consistent with a patient who is conforming to a gluten-free diet.

    Dr. Ron Hoggan, Ed.D.
    This article originally appeared in the Autumn 2002 edition of Celiac.coms Scott-Free newsletter.
    Copyright © 2002 Scott Adams. All rights reserved worldwide.
    Five years ago I became concerned about weakness in my bones after a couple of surprising fractures. At one point, I broke a rib while shingling a storage-shed roof. I leaned across the peak of the roofs ridge to pick up a shingle. I never expected such light pressure to cause a problem, however, I felt a sudden, sharp pain, and heard an odd sound. This, along with a couple of less dramatic, but similar injuries, caused me enough concern to begin looking into the question of celiac disease and bone strength.
    My explorations taught me that calcium absorption probably is not our main problem. People with celiac disease seem to be able to absorb adequate calcium1, but the primary problem appears to come from excreting too much of it, thus causing us to lose more calcium than we are absorbing. I also learned that research shows little or no benefit from calcium supplementation for celiac patients, while magnesium supplementation alone results in significant improvements2. The explanation for this may be that some of the antibodies caused by active celiac disease attack the parathyroid gland3. This organ is an important player in regulating calcium metabolism. Magnesium is necessary for the body to repair the parathyroid and to maintain its continued good function.
    Being convinced by this research, I began to take magnesium supplements without any calcium. I found that I had to be careful. Too much had me visiting the washroom frequently, and I was afraid that too little would fail to provide me the benefits I was seeking.
    At the same time, I also requested a bone density test. I wanted objective information that would allow me to evaluate the progress I hoped to make. The first test was conducted in March of 1997. The results (called "T scores") are reported based on comparison with the density of bones found in young adults. For instance, a score of 0 indicates that the bone density is about the same as would be found in an average young adult. A score in the minus range indicates a bone that has less mineral and more pores than is found in the same young adult. Thus, a score of –1.0 to –2.5 indicates mild mineral losses, while a score of –2.5 or lower indicates osteoporosis.
    My test results were not as bad as I had feared. The mineral density in my lower back was normal for my age, at –0.23. However, my upper leg, where it fits into my hip, was reported as –2.02, and my forearm was slightly stronger than that of a normal young adult at +0.19.
    As I saw it, there were only two causes for concern. First, at the tender age of 50, my hips were very close to osteoporotic, and certainly at a substantially increased risk of fracture. Such fractures can be very serious. Secondly, since only three skeletal areas had been tested for mineral density—and since there was such a wide range of density reported for each of these areas, it seemed impossible to estimate the density of the rest of the bones in my body.
    About three years after my first bone density test, some Calgary-based research made me suspect that the amount of vitamin D supplements I was taking might be too low4. I increased my intake to 1,000 IU daily.
    By the fall of 2001, I began to wonder if I was being foolish by avoiding calcium supplements based on the reports I had read. I therefore began to supplement 350 mg of calcium each day.
    In July of 2002, I underwent a second bone scan. They did not test my forearm, but the other two areas appear to have improved substantially. The T score for my lower back was now at + 0.06, and the T score for my hip had improved to –0.72.
    I realize that what I am reporting is just one persons experience. It is what the medical professionals call "anecdotal," and does not usually carry much weight. However, my experience does support the only published research of the impact of mineral supplements on bone density in celiac patients that I can find. Based on my own experience, and the relevant research, I am now convinced that magnesium is the most important supplement to consider in the context of celiac disease. I was thrilled to read my latest bone density report. Vitamin D may also be an important factor, but limitations of time and space force me to leave this topic for another day.

    References:
    Marsh MN. Bone disease and gluten sensitivity: time to act, to treat, and to prevent. Am J Gastroenterol. 1994 Dec;89(12):2105-7. Rude RK, Olerich M. Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. Osteoporos Int. 1996;6(6):453-61. Kumar V, Valeski JE, Wortsman J. Celiac disease and hypoparathyroidism: cross-reaction of endomysial antibodies with parathyroid tissue. Clin Diagn Lab Immunol. 1996 Mar;3(2):143-6. Embry AF, Snowdon LR, Vieth R. Vitamin D and seasonal fluctuations of gadolinium-enhancing magnetic resonance imaging lesions in multiple sclerosis. Ann Neurol. 2000 Aug;48(2):271-2. Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His new book "Dangerous Grains" is available at Celiac.com.

    Scott Adams
    Celiac.com 11/08/2005 - Today a team of scientists at Alba Therapeutics Corporation (Alba) and the University of Maryland School of Medicine reported a direct link between gluten-induced intestinal permeability and zonulin in tissues from patients with celiac disease. The investigators were able to successfully prevent gluten-induced intestinal tissue leak with the administration of the zonulin antagonist FZI/0 (AT-1001). AT-1001 is an orally administered peptide currently under development for the treatment of celiac disease. Published in the November issue of the Scandinavian Journal of Gastroenterology, these results describe the role that leaky gut plays in celiac disease and the role that zonulin plays in establishing the leak. These results are another milestone towards understanding the role of zonulin in celiac disease, says Alessio Fasano, M.D., lead author of the paper, professor of pediatrics, medicine and physiology at the University of Maryland School of Medicine and director of its Center for Celiac Research.
    These results reinforce our conviction that AT-1001 has great therapeutic potential and we look forward to confirming these observations in celiac patients soon, stated Alba CEO Dr. Blake M. Paterson.
    About Zonulin
    Zonulin is a signaling protein that transiently and reversibly opens the tight junctions (tj) between the cells of epithelial and endothelial tissues such as the intestinal mucosa, blood brain barrier and pulmonary epithelia. Zonulin appears to be involved in many diseases in which leakage occurs via paracellular transport across epithelial and endothelial tight junctions (tj),
    and thus may play an important potential role in the treatment of autoimmune diseases.
    About Celiac Disease
    Celiac disease is a T-cell mediated auto-immune disease that occurs in genetically susceptible individuals and is characterized by small intestinal inflammation, injury and intolerance to gluten. According to the National Institutes of Health, celiac disease affects approximately 3 million Americans, although the diagnosis is rarely made. The only treatment for celiac disease is complete elimination of gluten from the diet, which results in remission for some patients.
    About Alba
    Alba Therapeutics Corporation is a privately held biopharmaceutical company based in Baltimore, Maryland. Alba is dedicated to commercializing disease-modifying therapeutics and drug delivery adjuvants based on the zonulin pathway. Albas lead molecule, AT-1001, is targeted towards the treatment of celiac disease and other auto-immune illnesses.
    Contact: Dr. Blake Paterson
    Alba Therapeutics Corporation
    (410) 522-8708

    Jefferson Adams
    Celiac.com 06/15/2012 - Diagnosing celiac disease can be challenging for doctors if a patient has already started a gluten-free diet, and/or when test results are inconsistent.
    A research team set out to evaluate the in vitro gliadin challenge in such patients. Researchers included Raffaella Tortora MD; Ilaria Russo PhD; Giovanni D De Palma MD; Alessandro Luciani PhD; Antonio Rispo MD; Fabiana Zingone MD; Paola Iovino MD; Pietro Capone MD; and Carolina Ciacci MD
    They are variously affiliated with the Department of Clinical and Experimental Medicine at Federico II University of Naples in Naples, Italy; the Department of Surgery, Endoscopy Unit at Federico II University of Naples in Naples, Italy; the Institute of Pediatrics at the University of Foggia in Foggia, Italy; and the University of Salerno, School of Medicine, Gastroenterology at Campus di Baronissi in Salerno, Italy.
    For their study, the team included 57 patients without celiac disease (negative controls), 166 patients with untreated celiac disease and 55 patients with celiac disease following a gluten-free diet (positive controls), and 59 patients with difficult diagnosis.
    The team conducted duodenal biopsies on all patients which provided the data for diagnosing the celiac disease and for the in vitro evaluation of the gliadin-induced mucosal expression of seven inflammatory markers: PY99, ICAM-1 (intercellular cell adhesion molecule), HLA-DR, CD3, CD25, CD69, and transglutaminase 2 IgA.
    As part of their diagnostic work-up for celiac disease, the team included a test for specific serum antibodies. The team asked patients in the difficult diagnosis group to discontinue their gluten-free diets to that they could test for antibodies under untreated conditions.
    To maintain statistical accuracy, the team used the area under the receptor-operated curve (ROC) to analyze the results.
    They found that HLA-DR was most accurate in diagnosing celiac disease on negative controls and positive controls, excluding patients on a gluten-free diet (area under ROC=0.99). Test accuracy did not increase by combining HLA-DR data with data of other markers.
    The results were similar in the 39 patients of the difficult diagnosis group who underwent the test for celiac disease-specific antibodies under untreated conditions.
    Finally, the results showed that in vitro response of mucosal HLA-DR to gliadin is an accurate tool for diagnosing celiac disease, including in patients with difficult diagnosis.
    Source:
    The American Journal of Gastroenterology. 2012;107(1):111-117.

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