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    Confocal Laser Endomicroscopy and Celiac Disease by Roy Jamron


    Roy Jamron

    Celiac.com 11/07/2006 – We should be hearing more about this in the news soon. A confocal laser endomicroscopy device developed by Optiscan, an Australian company, permits endoscopists to make an accurate real-time diagnosis of celiac disease, bypassing the need to take and prepare and evaluate biopsy specimens in a laboratory. This technique would allow the endoscopist to view and evaluate as many samples as needed to make a correct diagnosis and immediately give the results to the patient. This should reduce diagnostic errors. A paper on Confocal Laser Endomicroscopy in the diagnosis of Celiac disease by R. Leong et al. will be presented in Adelaide, Australia this Saturday, Oct. 14.


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    Australian Gastroenterology Week (AGW) 2006
    Hosted by the Gastroenterological Society of Australia (GESA)
    Adelaide Convention Centre, Adelaide, South Australia
    11-14th October 2006.

    To be presented Oct. 14, 2006:
    Confocal Laser Endomicroscopy in the diagnosis of Celiac disease R Leong

    Optiscans unique and patented technology has miniaturized the microscopes scanning head, so that it is now so small it can fit inside the body. Once the miniaturized scanner is integrated into an endoscope to create an endomicroscope, doctors can for the first time safely and instantly get high quality images of tissue at a cellular level from their patients. This gives doctors new levels of information providing a highly magnified view of living tissue that is entirely consistent with the macroscopic views that they are used to seeing from their endoscopes. This breakthrough technology creates a vast array of new applications, both medical and industrial. Optiscans primary focus is in the medical arena, where it can provide a virtual biopsy, potentially revolutionizing current pathology and histology practices.

    About Optiscan
    http://www.optiscan.com.au/about/about_02.asp

    Sample Images
    http://www.optiscan.com.au/Technology/Images_01.asp

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  • Related Articles

    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
    Celiac.com 05/12/2006 - Dear Colleagues in the Celiac Community: We would like to provide you with a progress report of the Celiac Management Clinic (CMC) at Stanford Medical Center. Realizing that many physicians and gastroenterologists have a limited understanding of the frequency of Celiac Sprue in the population and the subtlety of the clinical manifestations of this disease, we instituted the CMC at Stanford Medical Center in January 2005. This clinic is staffed by Dr. Gail Pyle and myself. A large number of patients who carried the diagnosis of Celiac Sprue have chosen to be seen in consultation--the majority of these did have Celiac Sprue, as estimated from blood antibody tests and the small intestinal (duodenal) biopsy. For many of these patients, comprehensive emphasis on gluten exclusion has been very effective in eliminating symptoms and the malabsorption of nutrients. However, both in this patient group and in those healthy gluten-free Celiac volunteers who participated in the trial supported by the Celiac Sprue Research Foundation in collaboration with the Palo Alto Medical Foundation on pre-treatment of grocery store gluten with a special peptidase(1) there was a surprising discovery. Fully half (~50%) of those presumed to be in remission from the disease had malabsorption of important nutrients. This major finding was a surprise, and it gives us pause concerning Celiac Sprue therapy.
    Is gluten exclusion not optimal or is it insufficient therapy for this large proportion of Celiac Sprue patients?
    The concerns about the effectiveness of long-term dietary therapy in Celiac Sprue have prompted us to reassess our approach to this disease. For those of you who reside within reach of Stanford Medical Center, we invite you to visit us at the Celiac Management Clinic for an up-to-date assessment of the status of your Celiac condition. If you are the one out of every two healthy Celiacs with malabsorption, we will take a comprehensive approach to determine the reasons and to facilitate your return to complete remission.
    If strict gluten exclusion is insufficient to achieve this, we offer other approaches. Indeed, by the end of this year or the beginning of 2007 in collaboration with the Celiac Sprue Research Foundation, we expect to be able to determine the effect of an oral pill therapy for those who continue with malabsorption of nutrients.
    Stanford accepts most PPO insurance and MediCal and MediCare outpatient coverages. Those who suspect they have Celiac Sprue based on symptoms or blood antibody tests will be seen by Dr. Gray, and those with biopsy-verified disease will be seen by Dr. Pyle. For an appointment, call 650-723-6961, and please state that you wish to see us at the Celiac Management Clinic.
    Sincerely,
    Gary M Gray, M.D.
    Professor of Medicine, Emeritus
    (Gastroenterology)
    References:
    Pyle GG, Paaso, B Anderson, BE, Allen D, Marti T, Chaitan Khosla C, Gray, GM. Low-dose Gluten Challenge in Celiac Sprue: Malabsorptive and Antibody Responses. Clinical Gastroenterology and Hepatology, 3: 679-686, 2005. Pyle GG, Paaso, B Anderson, BE, Allen D, Marti T, Li Q, Matthew Siegel, M, Khosla C, Gray, GM. Effect of Pretreatment of Food Gluten With Prolyl Endopeptidase on Gluten-Induced Malabsorption in Celiac Sprue Clinical Gastroenterology and Hepatology, 3: 687-694, 2005.

    Jefferson Adams
    Celiac.com 10/28/2009 - Celiac disease is a T cell-mediated autoimmune disease, and a number of clinicians have described up-regulation of T-bet and phosphorylated signal transducers and activators of transcription (pSTAT)1, both of which are key transcription factors for the development of T helper type 1 (Th1) cells, in the mucosa of patients with untreated celiac disease.
    A team of researchers recently used transcription factor analysis to examine whether celiac patients up-regulate T-bet and pSTAT1 expressions in peripheral blood
    and whether such up-regulation may be associated with celiac disease activity.
    The research team was made up of G. Frisullo, V. Nociti, R. Iorio, A. K. Patanella, D. Plantone, A. Bianco, A. Marti, G. Cammarota, P. A.  Tonali, and A. P. Batocchi of the Department of Neurosciences at the Catholic University in Rome, Italy.
    The team used flow cytometry to analyze T-bet, pSTAT1 and pSTAT3 expression in CD4(+), CD8(+) T cells, CD19(+) B cells and monocytes from peripheral blood of 15 untreated and 15 treated celiac disease patients and 30 controls, and longitudinally in five celiac patients before and after dietary treatment.
    The team measured the results using enzyme-linked immunosorbent assay (ELISA), interferon (FN)-gamma, interleukin (IL)-17 and IL-10 production by peripheral blood mononuclear cell (PBMC) cultures.
    Patients with untreated celiac disease showed higher T-bet expression in CD4(+), CD8(+) T cells, CD19(+) B cells and monocytes and IFN-gamma production by PBMC, than either treated celiac patients or control subjects.
    CD4(+)T cells, B cells and monocytes from untreated celiac patients showed higher pSTAT1 expression than either treated celiac patients or controls. Only in monocytes from untreated patients showed increased pSTAT3 compared with treated celiac patients and controls. Data from longitudinal evaluation of transcription factors corroborated these findings.
    Flow cytometric analysis of pSTAT1 and T-bet protein expression in peripheral blood mononuclear cells could be useful and sensible markers in the follow-up of celiac disease patients to evaluate disease activity and response to dietary treatment.
    Being able to spot celiac disease early is key to achieving optimal outcomes for celiac patients. The development of simple, reliable, low-cost tests is key to that effort. Stay tuned for more developments regarding celiac disease testing, screening and diagnosis.
    Source:
    Clinical & Experimental Immunology, Volume 158 Issue 1, Pages 106 - 114


    Jefferson Adams
    Celiac.com 12/27/2011 - Non-controlled studies suggest that Rifaximin may improve celiacdisease symptoms in such cases. However, up to now, no controlledtrials have been conducted.
    A team of researchers used a double-blind clinical trial to assess the effectiveness of rifaximin in relieving gastrointestinal symptoms in patients with poorly responsive celiac disease. They also assessed the effects of rifaximin on lactulose-hydrogen breath tests in those patients.
    The research team included Matthew S. Chang, Maria T. Minaya, Jianfeng Cheng, Bradley A. Connor, Suzanne K. Lewis, and Peter H. R. Green.
    Small intestinal bacterial overgrowth (SIBO) is one of the main reasons that certain people with celiac disease fail to respond well to a gluten-free diet, and why they often suffer persistent symptoms.
    To make their assessment, the team designed a single-center, double-blind, randomized, controlled trial of patients with biopsy-proven celiac disease and persistent gastrointestinal symptoms despite following a gluten-free diet.
    For the trial, the team 25 randomly assigned patients received a placebo, while the other 25 received rifaximin (n = 25) 1,200 mg daily for 10 days.
    For each patient, the team then used the Gastrointestinal Symptom Rating Scale (GSRS) and administered lactulose-hydrogen breath tests at weeks 0, 2, and 12.
    The team defined an abnormal breath test as showing either: (1) a rise in hydrogen of C20 parts per million (ppm) within 100 min, or (2) two peaks C20 ppm over baseline.
    They found that rifaximin had no effect on GSRS scores, regardless of baseline breath tests.
    Using a multivariable regression model, they found that the length of a patient's gastrointestinal symptoms significantly predicted overall GSRS scores (estimate 0.029, p.006).
    According to criteria 1 and 2, respectively, SIBO was present in 55 and 8% of patients at baseline, intermittently present in 28 and 20% given placebo, and 28 and 12% given rifaximin.
    Results showed no difference SIBO rates between placebo and treatment groups at weeks 2 and 12.
    From their study, the team concludes that rifaximin does not improve gastrointestinal symptoms, and that hydrogen breath tests do not reliably show which patients will respond favorably to antibiotic therapy.
    Source:

    Dig Dis Sci (2011) 56:2939–2946

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    Dr. Ron Hoggan, Ed.D.
    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.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    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
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    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.