Jump to content



Celiac.com Sponsor (A1):



Celiac.com Sponsor (A1-m):


  • You've found your Celiac Tribe! Join our like-minded, private community and share your story, get encouragement and connect with others.

    💬

    • Sign In
    • Sign Up
  • Record is Archived

    This article is now archived and is closed to further replies.

    Scott Adams
    Scott Adams

    Follow-Up to the Catassi Study - Scandinavia

    Reviewed and edited by a celiac disease expert.

    Colin, et al, published a follow-up study to the Catassi (Ceeliac Disease in the Year 2000: Exploring the Iceberg - University of Ancona, Italy) in the Scandinavian Journal of Gastroenterology - 28(7):595-8, 1993, which demonstrated that approximately one third of the patients from the Catassi Study who had raised antibodies but no villous atrophy, did have villous atrophy when tested two years later. These results raise the amount of diagnosed celiacs from the Catassi, et al study to over 1 in 200.


    User Feedback

    Recommended Comments

    There are no comments to display.



    Guest
    This is now closed for further comments

  • About Me

    Scott Adams

    Scott Adams was diagnosed with celiac disease in 1994, and, due to the nearly total lack of information available at that time, was forced to become an expert on the disease in order to recover. In 1995 he launched the site that later became Celiac.com to help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives.  He is co-author of the book Cereal Killers, and founder and publisher of the (formerly paper) newsletter Journal of Gluten Sensitivity. In 1998 he founded The Gluten-Free Mall which he sold in 2014. Celiac.com does not sell any products, and is 100% advertiser supported.


  • Celiac.com Sponsor (A17):
    Celiac.com Sponsor (A17):





    Celiac.com Sponsors (A17-m):




  • Related Articles

    Scott Adams
    Am J Clin Nutr 2002;75:914-921.
    Celiac.com 06/06/2002 - Results of a recent study conducted by Anneli Ivarsson and colleagues at Umea University in Sweden suggest that continuing to breast-feed infants while they are being introduced to new foods may reduce their risk of getting celiac disease. Dr. Ivarssons study suggests that the cause of celiac disease may include environmental factors, and not just be limited to genetic factors. Their study evaluated the breast-feeding habits of 627 children with celiac disease and 1,254 healthy children, and specifically looked at their responses to newly introduced foods. The results, published in the May issue of the American Journal of Clinical Nutrition, indicate that dietary patterns of infants may have a strong influence on the bodys immune responses, and certain dietary patterns could lead to lifelong food intolerances. Children under 2 years of age who were still being breast-fed when they were introduced to dietary gluten had a 40% lower incidence of celiac disease.
    Another important factor was the overall amount of gluten in an infants diet, and a direct correlation was found between increased gluten consumption and an increased incidence of celiac disease. According to the researchers, the protective effect of breast feeding was even more pronounced in infants who were breast-fed beyond the introduction of gluten. Ultimately the teams findings indicate that breast feeding infants through the period of gluten introduction can significantly lower their risk of getting celiac disease. More research needs to be done to determine if this protective effect will extend over a lifetime.


    Scott Adams
    Arch Intern Med. 2003;163:1566-1572.
    Ulrike Peters, PhD, MPH; Johan Askling, MD; Gloria Gridley, MS; Anders Ekbom, MD, PhD; Martha Linet, MD
    Celiac.com 07/30/2003 - The following abstract paints a fairly bleak picture for those of us with celiac disease; however, after taking a closer look at it I believe that it has some serious limitations that should not be overlooked, and have likely produced skewed or irrelevant results. For example, the study does not indicate whether or not the patients in it followed a strict gluten-free diet. Other studies have shown that the mortality risk for celiacs decreases to that of the normal population when a gluten-free diet is followed for at least five years, and that it is also affected by how soon the diagnosis is made and how soon treatment begins. It is well known that not following a gluten-free diet will increase a celiacs risk of death by many causes to many times that of the normal population, which is precisely why it is so important to include such information in studies of this type. In my opinion doing a study like this and not including such data is like doing a study on diabetes where perhaps half or more people in the study do not take insulin but ought to, and then publishing the ultra-high mortality rate that would be its outcome: "Conclusion: Diabetics have a 20-fold mortality rate over the normal population." The conclusion would clearly not be true for those who took their insulin.
    Additionally the time period that is covered by this study, 1964-1993, could be considered the dark ages of celiac disease, even in Europe (we actually may be just entering the Renaissance age for celiac disease here in the USA, but this could be argued!). Many doctors during this time did not stress enough to their patients the importance of following a strict gluten-free diet, just as many still do not even do this day. My doctor didnt. He just diagnosed me and said I shouldnt eat gluten (as opposed to telling me that it could kill me if I kept eating it), and he didnt even explain to me HOW to avoid it! Is it possible that some of the folks in this study, diagnosed as far back as 1964, might have had similar experiences with their doctors? I would be willing to bet that at least 50% of the people in this study (if not more) were not following a strict gluten-free diet, or were not following the diet at all. If this is true, it is kind of like studying a group of diabetics whose only treatment was to be told by their doctors that they should avoid sugar, which seems absurd if you think about it.
    Last, the study has considerable bias in that it recruited only hospitalized celiacs, presumably because they were already significantly ill, and those who never made it into a hospital were excluded. It reports findings of auto-immune diseases and small bowel/lymphomaexcesses--these are already well known--but what other researchers may disagree with is the scale of the excess--SMR is always a very crude method ofexpressing this in such studies. - Scott Adams (special thanks to Dr. Geoff Helliwell for his comments on this study)

    Abstract
    :
    "Background: Patients with celiac disease have an increased risk of death from gastrointestinal malignancies and lymphomas, but little is known about mortality from other causes and few studies have assessed long-term outcomes."
    "Methods: Nationwide data on 10,032 Swedish patients hospitalized from January 1, 1964, through December 31, 1993, with celiac disease and surviving at least 12 months were linked with the national mortality register. Mortality risks were computed as standardized mortality ratios (SMRs), comparing mortality rates of patients with celiac disease with rates in the general Swedish population."
    "Results: A total of 828 patients with celiac disease died during the follow-up period (1965-1994). For all causes of death combined, mortality risks were significantly elevated: 2.0-fold (95% confidence interval [CI], 1.8-2.1) among all patients with celiac disease and 1.4-fold (95% CI, 1.2-1.6) among patients with celiac disease with no other discharge diagnoses at initial hospitalization. The overall SMR did not differ by sex or calendar year of initial hospitalization, whereas mortality risk in patients hospitalized with celiac disease before the age of 2 years was significantly lower by 60% (95% CI, 0.2-0.8) compared with the same age group of the general population. Mortality risks were elevated for a wide array of diseases, including non-Hodgkin lymphoma (SMR, 11.4), cancer of the small intestine (SMR, 17.3), autoimmune diseases (including rheumatoid arthritis [sMR, 7.3] and diffuse diseases of connective tissue [sMR, 17.0]), allergic disorders (such as asthma [sMR, 2.8]), inflammatory bowel diseases (including ulcerative colitis and Crohns disease [sMR, 70.9]), diabetes mellitus (SMR, 3.0), disorders of immune deficiency (SMR, 20.9), tuberculosis (SMR, 5.9), pneumonia (SMR, 2.9), and nephritis (SMR, 5.4)."
    "Conclusion: The elevated mortality risk for all causes of death combined reflected, for the most part, disorders characterized by immune dysfunction."



    Jefferson Adams
    Celiac.com 05/15/2009 - Certain proteins found in the gluten of wheat, rye and barley trigger adverse responses in people with gluten intolerance and celiac disease. This happens when the offending gluten proteins encounter the immune systems of susceptible individuals, triggering a CD4+ T-cell mediated immune response, together with inflammation of the small intestine. However, a number of gluten proteins contain no T-cell stimulatory epitopes, and so trigger no such adverse immune response. So, not all gluten is equally offensive to celiacs, and some may be both well tolerated and useful for making better bread.
    Gluten proteins are found in multiple gene sites on chromosomes 1 and 6 of the three different genomes of hexaploid bread wheat (Triticum aestivum) (AABBDD).
    Gluten is the stuff that makes bread delightfully chewy, among other desirable properties, so being able to successfully incorporate non-offending gluten into bread recipes might yield better breads that are safe for consumption by folks with celiac disease. Obviously, being able to produce high-quality, celiac-safe bread on a commercial scale would be of tremendous benefit for both producers and consumers. Currently, most gluten-free bread contains no gluten, as it has been difficult or impractical to separate the offending proteins from the non-offending proteins.
    Recently, a team of researchers based in the Netherlands attempted to  remove celiac disease-related protein from Chinese Spring wheat while maintaining the beneficial bread-baking properties.
    The team was made up of Hetty C. van den Broeck, Teun W. J. M. van Herpen, Cees Schuit, Elma M. J. Salentijn, Liesbeth Dekking, Dirk Bosch, Rob J. Hamer, Marinus J. M. Smulders, Ludovicus J. W. J. Gilissen and Ingrid M. van der Meer.
    The team used a set of deletion lines of Triticum aestivum cv. Chinese Spring to assess the results of removing individual gluten sites on both the level of the T-cell stimulatory epitope in the gluten proteome and the favorable qualities of the flour.
    To measure the reduction of T-cell stimulatory epitopes, the team used monoclonal antibodies that recognize T-cell epitopes contained in gluten proteins. They then clinically tested the deletion lines for their dough mixing properties and dough composition.
    The team's attempts to remove the alpha-gliadin site from the short arm of chromosome 6 of the D-genome (6DS) yielded in a favorable decrease in the presence of T-cell stimulatory epitopes, but also yielded a significantly loss of favorable baking properties.
    However, by deleting the omega-gliadin, gamma-gliadin, and LMW-GS locations from the short arm of chromosome 1 of the D-genome (1DS), researchers were able to strip offending T-cell stimulatory epitopes from the proteome while maintaining technological properties.
    The team concludes that their data hold important implications for lowering the quantity of T-cell stimulatory epitopes in wheat, and promoting the creation of celiac-safe wheat varieties that will potentially yield breads of higher quality than currently available.

    BMC Plant Biology 2009, 9:41
     


    Jefferson Adams
    Celiac.com 03/22/2013 - Enterocyte damage is one of the common features of celiac disease, and often results in malabsorption. Presently, doctors don't know very much about the recovery of enterocyte damage and its clinical consequences. Serum intestinal fatty acid binding protein (I-FABP) is a marker that allows researchers to study enterocyte damage.
    A research team set out to determine the severity of enterocyte damage in adult-onset celiac disease, how it responds to a gluten-free diet, and the correlation among enterocyte damage, celiac disease autoantibodies and histological abnormalities during the course of disease.
    The research team included M. P. M. Adriaanse, G. J. Tack, V. Lima Passos, J. G. M. C. Damoiseaux, M. W. J. Schreurs, K. van Wijck, R. G. Riedl, A. A. M. Masclee, W. A. Buurman, C. J. J. Mulder, and A. C. E. Vreugdenhil. They are affiliated with the Department of Paediatrics & Nutrition and Toxicology Research Institute Maastricht (NUTRIM) at Maastricht University Medical Centre in Maastricht, the Netherlands.
    For their study, the team first determined I-FABP blood levels in 96 biopsy-proven adults with celiac disease, and in 69 patients following a gluten-free diet. They used 141 individuals with normal antitissue transglutaminase antibody (IgA-tTG) levels as a control group.
    They found that levels of I-FABP were related to the degree of villous atrophy (Marsh grade) and IgA-tTG. Patients with untreated celiac disease showed higher I-FABP levels (median 691 pg/mL) compared with control subjects (median 178 pg/mL, P < 0.001) and correlated with Marsh grade (r = 0.265, P < 0.05) and IgA-tTG (r = 0.403, P < 0.01).
    I-FABP blood levels in patients following a gluten-free diet dropped substantially, but not within the range found in control subjects, even though they showed normalization of IgA-tTG levels and Marsh grade. Celiac patients with elevated I-FABP levels who did not respond to gluten-free diet showed persistent histological abnormalities.
    The team's main finding was that enterocyte damage, as assessed by serum I-FABP, correlates with the severity of villous atrophy in celiac disease at the time of diagnosis.
    Even though enterocyte damage improves upon treatment with a gluten-free diet, the majority of patients still show substantial enterocyte damage despite the absence of villous atrophy and low IgA-tTG levels.
    Thus, they conclude that elevated I-FABP levels that do not respond to a gluten-free diet likely point to histological abnormalities and warrant further evaluation.
    Source:
    Aliment Pharmacol Ther. 2013 Feb;37(4):482-90. doi: 10.1111/apt.12194.


  • Popular Now

×
×
  • Create New...