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    Effectiveness of the Sorbitol H2 Breath Test in Detecting Histological Damage Among Relatives of Celiacs


    Scott Adams

    Scand J Gastroenterol. 2003 Jul;38(7):727-31.
    Effectiveness of the sorbitol H2 breath test in detecting histological damage among relatives of coeliacs.
    Tursi A, Brandimarte G, Giorgetti GM, Inchingolo celiac disease.
    Dept. of Emergency, L. Bonomo Hospital, Andria (BA), Italy.


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    Celiac.com 08/07/2003 - An Italian study conducted by Dr. L. Bonomo and colleagues and published in the July 2003 edition of Scandinavian Journal of Gastroenterology concludes that A significant proportion of coeliacs may be missed if relatives are screened by serology only, while the efficacy of sorbitol H2-BT in screening relatives is confirmed. This study confirms that neither a breath test nor serology can replace intestinal biopsy, which remains the gold standard for the diagnosis of celiac disease, thus confirming the continued importance of performing biopsies for diagnosing celiac disease. The studys goal was to determine the diagnostic capabilities of serological tests (antigliadin (AGA), antiendomysium (EMA) and anti-tissue transglutaminase (anti-tTG)) and sorbitol H2 breath test (H2-BT) in the detection of celiac disease in first-degree relatives. The study screened 111 first-degree relatives of 37 celiac families using both test methods to determine candidates for small bowel biopsy. First-degree relatives with abnormal test results underwent a small bowel biopsy, as did those with negative serological and H2 breath test results who had clinical complaints or suspected that they may have celiac disease.

    The biopsy results were expressed using the Marsh classification system, and celiac disease was diagnosed in 49 of the 111 screened relatives of celiacs, or in 44.14%. A breakdown of the results is as follows: 5 showed Marsh IIIc, 8 Marsh IIIb, 16 Marsh IIIa, 13 Marsh II and 7 Marsh I lesions. 19 relatives showed the classical form of celiac disease, 20 showed the sub-clinical form, and 10 showed the silent form. The serological test results indicated an overall positivity of only 36.73%, with strong positive results only in those with severe intestinal damage and Marsh IIIb-c lesions. The sorbitol H2-BT breath test results showed an overall positivity of 83.67%, and showed strong positivity in patients with slight histological damage (Marsh I-IIIa).

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    Guest Donna Hall

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    What I didn't understand from your article was what ratio of people in the study were positive for celiac disease when biopsies were performed when compared to the those who tested positive using the Sorbitol H2 Breath Test.

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  • About Me

    In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease. In 1998 I founded The Gluten-Free Mall, Your Special Diet Superstore!, and I am the co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.

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  • Related Articles

    Scott Adams
    The following report comes to us from The Sprue-Nik Press, which is published by the Tri-County Celiac Sprue Support Group, a chapter of CSA/USA, Inc. serving southeastern Michigan (Volume 7, Number 6, September 1998).
    The degree of mucosal damage varies from one celiac patient to another. Also, the amount of the small intestine that is affected also varies, with the damage usually progressing from the beginning of the small intestine and then moving downward toward the end of the small intestine. This may explain the variable symptoms in different patients. For example, when a significant portion of the small intestine is involved, diarrhea, malabsorption, and weight loss result. When damage is isolated to only the top portion of the small intestine, the only affect may be iron deficiency. (Incidentally, when iron deficiency is not corrected by iron supplements, it is highly likely that celiac disease is the cause of the deficiency.)
    Gluten in a celiacs diet causes the immune system to produce gliadin antibodies in the intestine. Some of these leak into the bloodstream where they can be detected in blood tests. These blood tests are useful for screening for celiac disease, though a small intestinal biopsy remains the gold standard for diagnosing celiac disease (celiac disease).
    There are few diseases for which diet and nutritional issues are more important than for celiac disease. At this time, the only known treatment of celiac disease is the removal of wheat, barley, rye, and oats from the celiacs diet. On the surface this sounds simple, but complete removal of dietary gluten can be very difficult. Gluten-containing grains are ubiquitous in the Western diet. Also, grain-derived food additives such as partially hydrolyzed vegetable protein [and modified food starch] are widely used in processed foods and oral medications. Content labels are often vague or incomplete regarding these additives.
    What further complicates matters is a lack of significant experience on the part of physicians and dietitians in the dietary treatment of celiac disease. This is mainly because there are so few celiac patients for anyone practitioner. Therefore the best sources of dietary information for a new patient are other knowledgeable, more experienced celiacs.
    It is very important that the diet be followed with full and strict compliance. Celiacs, especially if theyve had active celiac disease for a longtime, are at higher than normal risk for GI malignancies.(Fortunately, compliance to a good gluten-free diet returns the risk of malignancy and life expectancy to that of the general population.)Another complication of long-term untreated celiac disease is bone loss, which maybe irreversible in older patients.
    When a large portion of the small intestine is affected by active celiac disease, the result can be a generalized malabsorption problem, resulting in deficiencies of water- and fat-soluble vitamins and minerals. Folic acid deficiency is particularly common in celiac disease because, like iron, it is absorbed in the upper small intestine [where the highest concentration of celiac-related damage generally occurs]. Folic acid is necessary for DNA replication, which occurs in cell turnover. So a deficiency of folic acid can impair the regenerative ability of the small intestine. Vitamin B12, also essential to DNA synthesis, is not malabsorbed as commonly as folic acid.
    Magnesium and calcium deficiency are also common in active celiac disease, because of decreased intestinal absorption AND because these minerals tend to bind with malabsorbed fat which passes through the system. It is particularly important for doctors to assess the magnesium status of celiacs, because without correction of a magnesium deficiency, low levels of calcium and potassium in the blood cannot usually be corrected with supplements. In severe cases, magnesium supplementation should be done intravenously because of the tendency of oral magnesium to cause diarrhea.
    Supplemental calcium generally should be provided to celiacs, possibly with vitamin D, to help restore tissue and bone calcium levels to normal. The exact dose of calcium is not known. Dr. Fine usually recommends 1500-2000 mg of elemental calcium per day, divided into two doses, for several years and sometimes indefinitely. [4], [5], [6]
    Zinc is another mineral that often becomes depleted in patients with chronic malabsorption. Zinc supplementation (usually the RDA via multi-vitamin and mineral supplements) helps avoid skin rashes and restores normal taste.
    Up to 20% of celiacs will continue to experience loose or watery stools even after going on a gluten-free diet. Sometimes this is due to inadvertent gluten in the diet, but a recent study at Dr. Fines medical center showed that in these cases other diseases epidemiologically associated with celiac disease are present.[7] These include microscopic colitis, exocrine pancreatic insufficiency, lactose intolerance, selective IgA deficiency, hypo- or hyperthyroidism, and Type I diabetes mellitus. When diarrhea continues after beginning a gluten-free diet, a search for these associated diseases or others should be undertaken and treated if found.
    The use of cortico steroids has been advocated in celiacs when the response to the gluten-free diet is sluggish or absent. This is necessary more often in older than in younger patients. However, pancreatic enzyme supplements (prescribed by a doctor) may be needed to help digestion and resolve ongoing malabsorption in some patients.
    The endomysial antibody blood test is highly accurate and specific for detecting celiac disease. However, the current method of detecting these antibodies involves an operator looking through a microscope and observing the antibody binding on monkey esophagus or human umbilical cord tissue substrates. The correct interpretation of results is highly dependent on the skill and experience of the technician interpreting the fluorescence pattern through the microscope. Moreover, determination of the amount of antibody present relies upon repeat examinations following dilutions of the blood serum, with the last positive test being reported as a titer.
    A new discovery was reported by a research group in Germany.[8] The antigen substrate of the endomysial antibodies has been identified. This allows the development of a new test that can detect and measure serum endomysial antibodies in one, chemically-based test run [thus greatly reducing the potential for human error and significantly reducing the time needed for each test--ed.] These new tests should be available for clinical use shortly.
    In a recent study, Dr. Fine found that the frequency of positive stool blood tests was greater in patients with total villous atrophy relative to partial villous atrophy, and all tests were negative in treated patients without villous atrophy.[9] This suggests that fecal occult blood may be a non-invasive and inexpensive method of following the response of the damaged intestine to treatment. Also, it should be noted that the high frequency of positive tests due to villous atrophy will decrease the accuracy of the tests when used for cancer screening in this same patient population (which is how these tests are normally used by health care providers).
    There have been two recent reports touting the lack of deleterious effects when 50 grams of oats per day are added to the diet of celiac patients. Although this finding is exciting for celiacs, both studies possess certain limitations. In the first study, published by a Finnish group, the exclusion criteria for symptoms and histopathology were somewhat strict, so that patients with more mild forms of celiac disease seemingly were selected for study. And though no damage to duodenal histology occurred after one year of oats consumption, no physiologic or immunologic parameters of disease activity were measured. Furthermore, several patients in the treatment group dropped out of the study for reasons not mentioned in the article.[10] The second and more recent study involved only 10 patients, studied for twelve weeks. The favorable results of this study must be interpreted with caution because of the small sample size and short study period.[11] Even the one-year treatment period in the Finnish study may be too short to observe a harmful effect, as it is known that small intestinal damage sometimes will not occur for several years following there introduction of gluten to a treated celiac. At the worst, an increase in the incidence of malignancy may result from chronic ingestion of oats, an effect that could take decades to manifest. Therefore, this issue will require further study before oats can be recommended for the celiac diet.

    3. From the September 1998 newsletter of the Houston Celiac-Sprue Support Group, a chapter of CSA/USA, Inc. 4. Ciacci C, Maurelli L, et el, Effects of dietary treatment on bone mineral density in adults with celiac disease; factors predicting response, Am J Gastroenterol, 1997; 92 (6): 992-996.

    5. Mautalen C, Gonzalez D, et al, Effect of treatment on bone mass, mineral metabolism, and body composition in untreated celiac patients, Am J Gastroenterol, 1997; 2 (2):313-318.

    6. Corazza gluten-free, Di Sario A, et al, Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult coeliac disease, Bone, 1996; 18 (6):525-530.

    7. Fine, KD, Meyer RL, Lee EL, The prevalence and causes of chronic diarrhea in patients with celiac sprue treated with a gluten-free diet, Gastroenterol, 1997; 112 (6):1830-1838.

    8. Dieterich W, Ehnis T, et al, Identification of tissue transglutaminase as the autoantigen of celiac disease, Nat Med, 1997; 3 (7):797-801.

    9. Fine KD, The prevalence of occult gastrointestinal bleeding in celiac sprue, N Engl J Med, 1996; 334 (18):1163-1167.

    10. Janatuinen EK, Pikkarainen PH, et al, A comparison of diets with and without oats in adults with celiac disease, N Engl J Med, 1995; 333 (16):1033-1037.

    11. Srinivasan U, Leonard N, et al, Absence of oats toxicity in adult coeliac disease, BMJ, 1996; 313 (7068):1300-1301.

    Scott Adams
    Pediatrics 2005;115:1341-1346.
    Celiac.com 05/31/2005 – According to Canadian researchers, the use of Tissue Transglutaminase Antibody (tTG) Screening may soon replace the use of the small bowel biopsy to diagnose celiac disease in children. The researchers reviewed the charts of 103 children who were screened for celiac disease using both small bowel biopsy and tTG. Fifty-eight of the children were found to have positive biopsy results, and out of these, 48 had very high tTG levels (over 100 U), 7 had middle tTG levels (20-100 U), and 3 had low levels (less than 20 U). Out of the 49 children with the highest tTG levels, all but one of them had a positive biopsy result. There were 3 biopsy-positive children who had low tTG levels, two who were found to be IgA negative, and one who had a duodenal ulcer.
    According to the researchers, using tTG values of greater than 100 U and less than 20 U, and knowing the patients IgA status, tTG testing was "98% sensitive and 97% specific in detecting celiac disease." The researchers also point out that the cost of diagnosis could be cut by 30% by utilizing tTG screening. The researchers conclude that children with high tTG titers can proceed straight to a gluten-free diet--if they respond well then their diagnosis is confirmed—if not they can proceed to a biopsy.
    Although the authors dont address this issue specifically, this method would likely lead to an increase in the diagnosis rate of celiac disease, as many people are unwilling to undergo a biopsy--or have their children undergo one.

    Scott Adams
    Celiac.com 02/27/2006 - Kappler M, Krauss-Etschmann S, Diehl V, Zeilhofer H, Koletzko S. Detection of secretory IgA antibodies against gliadin and human tissue transglutaminase in stool to screen for celiac disease in children: validation study. BMJ. 2006 January 28; 332(7535): 213-14.
    Study Abstract:

    Objective:
    To evaluate two commercial stool tests for detection of secretory IgA antibodies against gliadin and human tissue transglutaminase for diagnosis of celiac disease in children with symptoms.
    Setting: Tertiary care childrens hospital.
    Participants: Coded stool samples from 20 children with newly diagnosed celiac disease and 64 controls. Six children with celiac disease had stool tests every two weeks for three months after starting a gluten-free diet.
    Main Outcome Measures: Secretory IgA antibodies against gliadin and human tissue transglutaminase in stool samples, determined in duplicate by using recommended cut-off limits.
    Results: Sensitivity of fecal antibodies against human tissue transglutaminase was 10% (95% confidence interval 1% to 32%), and specificity was 98% (91% to 100%). For antibodies against gliadin, sensitivity was 6% (0% to 29%) and specificity was 97% (89% to 100%). Optimisation of cut-off limits by receiver operating characteristic analysis and use of results of both tests increased sensitivity to 82%, but specificity decreased to 58%. All follow-up stool tests remained negative, except for two positive anti-gliadin results in one patient, six and 10 weeks after the gluten-free diet was started.
    Conclusions: Neither stool test was suitable for screening for celiac disease in children with symptoms.
    Dr. Kenneth Fine Comments on this Study:
    Dont Throw the Baby Out With the Bath Water!
    Letter to the Editor BMJ
    Kamran Rostami, M.D., Ph.D. Department of Medicine, Gloucestershire Royal Hospital Gloucester, UK
    Kenneth Fine, M.D. The Intestinal Health Institute, Dallas, Texas, USA
    We have read with interest the article by Kappler et al recently published in your journal (1) and feel several issues deserve mention. This article is very timely in light of the growing worldwide awareness of immunologic sensitivity to dietary gluten and celiac disease, as well as appreciation of its high prevalence; these facts are driving the need for more widely available, low cost, non-invasive screening tests. Stool testing for these disorders holds great promise for screening because it does not require any invasion of body tissues, is of relatively low cost, and could be widely available combining medical care delivery of such tests with home testing.
    While our first criticism of this study is its small cohort size (20 patients), the results are intriguing, but in our opinion have been misinterpreted by the authors. First, there is a potential methodological flaw in this study whereby a serologic method was apparently transferred intact to analyze stool. The aspects of a serologic ELISA method possibly requiring modification for use in stool include but are not limited to: degree to which the sample is diluted prior to analysis; technique and amount of washing of plates during ELISA analysis (because of greater solid contaminant of fecal fluid vs. serum); mathematical conversion of detected optical density to a Unit; and how that calculated Unit is interpreted relative to a normal vs. abnormal cutoff. Utilizing fecal antigliadin and antitissuetransglutaminase IgA antibody testing in this way were reported to be very insensitive (6-10%) but highly specific (97-98%) for celiac disease. Such results should be interpreted as possibly possessing either a misassigned cutoff value (i.e., one that was too high), or possibly introduction of an artificial element that drove fecal antibody concentrations down (such as over-diluting the stool, improper handling or storage of specimens allowing ex vivo destruction of antibody, or centrifuging the stool at the wrong speed driving antibody into the pellet; the authors mentioned destruction of antibody during transit within the GI tract, but antibody is very stable within the GI tract, and has been detected in stool by many authors). Nevertheless, as performed in this study, such a highly specific stool test for celiac disease could be used as a pre-screening test of sorts, able to specifically and non-invasively detect celiac disease, perhaps with a home collected stool specimen. At the worst, 6-10% of celiac patients could be identified even before presenting to a medical institution.
    The authors went on to correct a potential cutoff error, using optimization of cut-off limits by receiver operating characteristic analysis, and found that resetting the cut-off value and combining the tests could possess an 82% sensitivity and 58% specificity. Again the authors discounted these findings, in our opinion failing to grasp their importance. Although they did not report the corrected accuracy results of antigliadin test alone, their stool test may have outperformed serum antigliadin antibody, the serologic test in longest use in screening for celiac disease. Many investigators have lost confidence in the presumed lack of specificity of antigliadin antibody alone as a screening test for celiac disease because of the paradigm within which it has been applied, that is, villous atrophic celiac disease. It is also known that its sensitivity is highly dependent on the degree of small intestinal villous atrophy present (2). Most importantly today however, in our opinion, with the wealth of expanding knowledge on the broadening clinical spectrum of gluten-sensitive disorders (3), it should at least have been considered and/or discussed by Kappler et al that in their optimized cut-off analysis, a positive fecal antigliadin antibody may have been a true sign of immunologic sensitivity to gluten either in an evolutionary phase before the onset of villous atrophic celiac disease (4), or in gluten sensitive individuals who may never develop classic celiac disease but who suffer symptoms and associated autoimmune disorders nevertheless. When interpreted in this context, the authors results may have been clinically important. We feel further study of this method with improved attention to methodological issues pertaining to stool, and broader clinical application beyond classic celiac disease is warranted.
    References:
    1. Kappler M, Krauss-Etschmann S, Diehl V, Zeilhofer H, Koletzko S. Detection of secretory IgA antibodies against gliadin and human tissue transglutaminase in stool to screen for celiac disease in children: validation study. BMJ. 2006 January 28; 332(7535): 213-14.
    2. Rostami K, Kerckhaert J, Tiemessen R, von Blomberg BM, Meijer JW, Mulder CJ. Sensitivity of antiendomysium and antigliadin antibodies in untreated celiac disease: disappointing in clinical practice. Am J Gastroenterol. 1999 Apr;94(4):888-94.
    3. Ferguson A, Arranz E, OMahony S. Clinical and pathological spectrum of celiac disease--active, silent, latent, potential. Gut. 1993 Feb;34(2):150-1.
    4. Arranz E, Ferguson A. Jejunal fluid antibodies and mucosal gamma/delta IEL in latent and potential celiac disease. Adv Exp Med Biol. 1995;371B:1345-8.

    Jefferson Adams
    Celiac.com 06/04/2010 - A team of researchers recently set out to assess the positive predictive value of blood test screening for possible cases of celiac disease.
    The team included Peter Toftedal, Christian Nielsen, Jonas Trolle Madsen, Kjell Titlestad, Steffen Husby, and Søren Thue Lillevang. They are affiliated with the Hans Christian Andersen Children's Hospital, and the Department of Clinical Immunology of Odense University Hospital in Denmark. P. Toftedal and Ch. Nielsen made contributions to the final published article.
    In deciding which possible celiac disease cases might require duodenal biopsy, doctors rely mainly on tests for celiac disease antibodies, such as immunoglobulin A (IgA) anti-tissue transglutaminase (anti-tTG), IgA endomysium antibody (EMA), IgA and IgG anti-gliadin antibodies (IgA and IgG AGA).
    For their study, the research team wanted to assess the diagnostic quality of blood testing for possible cases of celiac disease. They did this by performing celiac disease blood tests (IgA and IgG AGA, anti-tTG and EMA) on 11,915 subjects.
    They then combined the serological data with clinical data and duodenal biopsy results using a unique Danish personal identification number.
    They found that positive predictive value (PPV) fluctuated in accordance with various combinations of positive celiac disease antibodies. They found the highest predictive value (97.6%) when results for IgA and IgG AGA, anti-tTG and EMA antibodies were all positive.
    The team used a logistic regression model at initial blood screening to predict the probability of later biopsy-proven celiac disease in relation to concentrations of IgA AGA and anti-tTG.
    They found that anti-tTG concentrations correlated strongly with EMA positivity, number of additional positive antibodies, and higher PPV.
    The anti-tTG concentration upon first blood screening for celiac disease was highly informative in relation to EMA positivity, number of additional celiac disease specific antibodies and PPV.
    Lastly, results for the high-risk patient group showed that
    anti-tTG and IgA AGA concentrations at initial serological screening accurately predicted probability of future biopsy-proven celiac disease.
    Source:

    Clin Chem Lab Med 2010;48:685–91. DOI: 10.1515/CCLM.2010.136

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    Jefferson Adams
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    Source:
    FoodProcessing.com.au