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    Is DGP Serological Test the Wave of the Future for Celiac Disease Testing?


    Destiny Stone

    Celiac.com 03/11/2010 - Many people are confused about which tests provide the most accurate results for a celiac disease diagnosis. In a recent study by a team at the Department of Gastroenternology and Internal Medicine, St. Orsola-Malpigihi Hospital, University of Bologna, Bologna, Italy, researchers evaluated  current testing methods, and made some conclusions about celiac testing that may shed light on the subject for those of us overwhelmed by current conflicting information.


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    Duodenal biopsy is considered to be the universal 'gold standard' for celiac diagnosis. However, in recent years the importance of  serological testing has been been emphasized as a reliable marker for antibodies as well. The tTG antibodies of IgA class are currently recognized to be the most effective test for celiac screening, resulting in up to 95% accuracy.  Although, a new serological test, DGP, is now being investigated as a more reliable alternative to tTG.

    A study was devised to compare the effectiveness of DGP antibodies with that of tTG antibodies, and used a meta-analysis of  eleven studies that were published between 1998 and 2008. The study analyzed the results of 937 patients with untreated celiac, and 1,328 control subjects. The analysis of the eleven studies showed that IgA tTG antibodies revealed a higher likelihood ratio (LR) than IgA DGP antibodies, and IgA tTG antibodies exhibited a lower LR than IgA DGP antibodies. The data between the two antibody tests validates that IgA tTG continues to display the most accurate diagnostic tests for a positive celiac diagnosis, as well as for excluding a negative celiac diagnosis.  However  IgG DGP antibody tests were shown to be more effective at identifying 'false negatives' and had more success in determining celiac in patients that had IgA deficiency, and in children under two years old.

    The results of these tests clearly demonstrate that IgA DGP does not offer any advantages to the IgA tTG antibodies, and is actually less accurate and more expensive. However, IgG  DGP antibodies present an invaluable tool  in screening for celiac disease in cases where IgA tTG tests fail. Eventually, a new antibody screening will hopefully be designed which combines IgA tTG and IgG DGP, and reduces the number of tests currently used in celiac screening. However, intestinal biopsy is always required to confirm the presence of celiac disease no matter what serological tests are involved.

    Source:
    http://www.ncbi.nlm.nih.gov/pubmed/20136587

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    Guest acousticmom

    Posted

    I could use some clarification here:

     

    "The analysis of the eleven studies showed that IgA tTG antibodies revealed a higher likelihood (LR) ratio than IgA DGP antibodies, and IgA tTG antibodies exhibited a lower LR than IgA DGP antibodies."

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    Guest Destiny

    Posted

    I could use some clarification here:

     

    "The analysis of the eleven studies showed that IgA tTG antibodies revealed a higher likelihood (LR) ratio than IgA DGP antibodies, and IgA tTG antibodies exhibited a lower LR than IgA DGP antibodies."

    Likelihood ratio (LR) means that there is a likelihood that a given test result (in this case, tTG & DGP) would be expected in a patient with celiac disease compared with the likelihood that the same result would be expected to be found in a patient without celiac disease. Therefore, what the results are saying is that tTG shows both a higher and lower likelihood ratio than DGP, making it a more effective test for determining the presence of celiac as well as the absence of celiac disease.

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    Scott Adams
    Those patients for whom there is a high suspicion for celiac disease should have a small bowel biopsy which can be obtained by an experienced endoscopist in the distal duodendum. The best noninvasive tests available for screening for asymptomatic celiac disease are the specific serological tests. These are of several varieties: the anti-gliadin, anti-endomysial, or anti-reticulin antibodies. Our experience and the literature support the use as of endomysial antibody test as the single most specific and probably most sensitive for celiac disease. This test has now become available in specialty laboratories as well as in a small number of academic institutions. All of the tests should be done with the subjects on a normal gluten containing diet. A combination of endomysial and gliadin testing would seem to be the most sensitive as a screening method. A positive test is not, however, considered to be diagnostic and would usually require a small bowel biopsy for confirmation. A trial of dietary exclusion of gluten is *not* recommended as a diagnostic test without a prior abnormal biopsy.
    Because the body will recover when one goes gluten-free, the tests will then come up negative. Without a definitive test one may then stray from the diet, as one will feel well and was never sure that they had it in the first place. As for the two tests: The biopsy will look for flattened villi on the intestinal wall. After one goes gluten-free they will grow back. The blood antibodies are formed as a bodys reaction to the presence of the gluten. If no gluten, then no antibodies are present.

    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.

    Jefferson Adams
    Celiac.com 07/21/2009 - Accurate blood tests have revolutionized celiac disease diagnosis. Recently, researchers K.E. Evans, A.R. Malloy, and D.A. Gorard set out to review requests for celiac blood testing at a district general hospital laboratory over a decade, to measure the volume of requests, identify their source of referral, and assess positivity rates, along with subsequent rates of duodenal biopsy and histological confirmation.
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    The data show that, increasingly, most celiac blood tests are now requested by general practitioners, with twice as many women as men being tested.
    Rising requests for blood tests but shrinking rates of positivity suggest that people are getting tested earlier, with fewer or less severe symptoms than in the past. Positive blood tests are often not confirmed histologically.
    Also of note, most patients with celiac disease no longer show classical signs of malabsorption, so diagnosis is often delayed or never made. These days, most adults diagnosed with celiac disease increasingly show few or atypical symptoms.
    Although duodenal or jejunal biopsy remains the gold standard for diagnosing celiac disease, the availability of easy, accurate blood tests has dramatically improved the diagnosis of celiac disease.
    More accurate tests for IgA endomysial antibodies and IgA tissue transglutaminase antibodies have replaced less reliable immunoglobulin (Ig) G and IgA gliadin antibody tests, while sensitivity and specificity of Endomysial antibodies and IgA tissue transglutaminase antibody tests now exceeds 95%.
    Still, doctors recommend biopsy confirmation of positive blood antibody tests, as biopsy of patients with positive blood tests, along with those suspected of having celiac but with negative blood, remains the most comprehensive way of diagnosing celiac disease.
    Aliment Pharmacol Ther 29, 1137-1142


    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.
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    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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    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
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    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
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    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
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    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics

    Jefferson Adams
    Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
    A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.
    For their study, the team collected urine samples from 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIPs and an LFT reader. 
    They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage.
    The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
    Source:
    Gut. 2017 Feb;66(2):250-257.  doi: 10.1136/gutjnl-2015-310148.