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    A New Simple Stool Test For the Detection of Small Intestinal Damage Due to Gluten Sensitivity


    Scott Adams


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    American Journal of Clinical Pathology, April 2000 - A New Method of Quantitative Fecal Fat Microscopy and its Correlation with Chemically Measured Fecal Fat Output, by Kenneth Fine, M.D. and Frederick Ogunji Ph.D

    (Celiac.com 07/09/2000) Patients with gluten sensitivity should be evaluated for nutrient malabsorption because if present, this means there is small intestinal damage and institution of a gluten-free diet is imperative to prevent osteoporosis and other nutrient deficiency syndromes. Furthermore, a test at the time of diagnosis serves as a baseline to be compared to later if needed. For more than 50 years, the primary method used to assess for the presence of small intestinal damage and nutrient malabsorption in patients with celiac disease has been a 72-hour quantitative stool collection. However, because this method requires that patients accurately collect all the stools they pass for 3 days (missed stools lead to falsely low results), the test is logistically difficult for medical centers unaccustomed to the procedure, and the voluminous specimens usually are abhorred by patients and laboratory technicians. It poses obvious problems for children who cannot or will not collect all their stools, as well as for patients with chronic diarrhea, who may have bowel movement frequencies reaching 15 or more per day and/or fecal volumes as high as 2 or 3 liters per day. For these reasons, physicians evaluating patients with suspected or proven gluten sensitivity often avoid tests for intestinal malabsorption altogether.

    Recently, researchers at the Intestinal Health Institute in Dallas, Texas have developed a new method for quantitating fecal fat excretion that requires collection of only a single stool specimen. Development of this method was based on the fact that as more fat is malabsorbed, the fat globules in stool become more numerous and larger. In a study published in the April 2000 issue of the American Journal of Clinical Pathology entitled A New Method of Quantitative Fecal Fat Microscopy and its Correlation with Chemically Measured Fecal Fat Output, Kenneth Fine, M.D. and Frederick Ogunji Ph.D. tested 180 patients and found a highly statistically significant linear correlation between quantitative fecal fat microscopy (the new method) and chemically measured fecal fat output (the old method). They also showed that their microscopic analysis of just one stool gives comparable results to analysis of an entire 3-day collection. These researchers have, thus, shown that a dedicated quantitative analysis of one stool under a microscope can detect the rise in fecal fat due to intestinal malabsorption (or pancreatic maldigestion) as accurately as 3-day stool collections, making this latter test a thing of the past for most patients.

    This new stool test for intestinal malabsorption and other celiac-testing is available for order online from a laboratory set up by Drs. Fine and Ogunji to serve the needs of celiac patients. It is called EnteroLab and can be accessed at http://www.enterolab.com/.

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    Guest Bradley

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    Good article more people suffer from gluten intolerance than is appreciated. This little test will make a difference!

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  • Related Articles

    Scott Adams
    The following excerpt was taken from the November 24, 1996 edition of the The Sprue-nik Press, which is published by the Tri-County Celiac Sprue Support Group (TCCSSG), a local chapter of CSA/USA located in southeast Michigan.
    Dr. Joseph Murray, of the Mayo Clinic Rochester, MN, is a gastroenterologist who specializes in treating Celiac disease. Dr. Murray gave us the standard definition of celiac disease: celiac disease is a permanent intolerance to gluten that results in damage to the intestine and is reversible with avoidance of dietary gluten. There are some important parts in this definition:
    Permanent: The effects of celiac disease may change from time to time. You may be sicker at one phase of your life than at another. For example, you may be sicker at age two, may seem to get better during the teenage years, may be sick again in your 20s (but with different symptoms), and then present with bone problems when you are in your 50s. So there may be different phases, but it is a PERMANENT intolerance. You do NOT outgrow it; you do not go through phases where you dont have it anymore. (That used to be what was thought and TAUGHT in medical schools.).
    Damage to the intestine: There is definitely intestinal damage; without it you cannot define . For some people the damage is severe, for others it is not so severe. It is the cases which are not so severe that can be difficult to diagnose. If the damage is mild then the person interpreting the biopsy might not even think of celiac disease as being a possible cause of the damage.
    Reversible: The damage should be reversible. Dr. Murray says there are about 5% of people with what he believes is celiac disease in whom at one point in their lives the damage becomes irreversible. In these cases there is intestinal damage that does not completely recover. It may partially heal, but not completely. One can infer that they have the same condition as celiacs that do recover, based on their history. There may be something different about that group of patients in their immune systems that makes them different, but that is an area that is still being actively researched.

    Scott Adams
    Celiac.com 2/13/2003 - This new study emphasizes the importance of following a strict gluten-free diet, and getting regular follow-up biopsies after your diagnosis. It also speaks to the need to discover whether or not you may have additional food intolerance, such as to cows milk (casein), soy, corn, etc., as some of these can also cause intestinal damage similar to that of celiac disease. -Scott Adams

    Lee SK, Lo W, Memeo L, Rotterdam H, Green PH.
    Gastrointest Endosc 2003 Feb;57(2):187-91
    Current affiliations: Department of Surgical Pathology and Medicine, Columbia University College of Physicians and Surgeons, New York, New York.
    BACKGROUND: The diagnosis of celiac disease requires characteristic histopathological changes in an intestinal biopsy with clinical improvement in response to a gluten-free diet. Endoscopy with procurement of biopsy specimens is often performed to document response to the diet, but there are little data on the appearance of treated celiac disease. This study examined the endoscopic and histopathological appearance of the duodenum of patients with celiac disease whose diet was gluten-free.
    METHODS: A cohort of 39 adult patients (mean age 52 years, range 20-74 years) with biopsy-proven celiac disease was retrospectively reviewed. All had responded clinically to a gluten-free diet that they had maintained for a mean of 8.5 years (range 1-45 years). The endoscopic and histopathological appearances of the duodenal mucosa were reviewed. Blinded review of the diagnostic (initial) and post-treatment biopsy specimens was also performed to assess response of individual patients to the diet.
    RESULTS: The endoscopic appearance was normal in 23%, reduced duodenal folds were present in 46%, scalloping of folds in 33%, mucosal fissures in 44%, and nodularity in 33%. There was more than 1 abnormality present in 46%. Histology was normal in only 21%. The remainder had villous atrophy (69% partial, 10% total). Paired (diagnostic and follow-up) biopsy specimens were reviewed blindly for 12 patients. The mean (SD) intraepithelial lymphocyte count fell from 61 (22) to 38 (17) (normal
    CONCLUSIONS: Despite a good clinical response, abnormal endoscopic and histopathological appearances persist in the majority of patients with celiac disease treated with a gluten-free diet.
    PMID: 12556782

    Scott Adams
    Gastroenterology, Oct 2003, Vol 125, No 4, p1264-67
    Celiac.com 10/08/2003 - An article by Vader et al. published in the October 2003 edition of the journal Gastroenterology discusses recent insights into celiac disease pathogenesis, and the possibility of detoxifying gluten for celiacs. After describing the toxic process of gluten peptides in celiacs in some detail, Vader et al. examined the possibility of detoxifying gluten in the wheat kernel: "The effect of comparable substitutions in the immunodominant 9-gliadin epitope. One mutation, consisting in the substitution of a glutamine (residue) by a proline residue, decreased T cell recognition. Further: "Interestingly, given the similarities between the respective codons for glutamine and proline, this substitution was achieved by changing a single nucleotide at the DNA level. This mutation, resulting in an exchange between the 2 most frequent amino acids in prolamins, suggests that detoxification of gluten might be achievable by site-directed mutagenesis of wheat without affecting the unique baking properties of gluten." They go on by emphasizing that due to the complexity of the amino acid sequences found in wheat, achieving a detoxified wheat using this method would be difficult.
    Later in the article Shan et al. propose detoxifying gluten in the intestine of a celiac with "a peptidase therapy based on the use of a bacterial endoprolyl protease." Although this therapy has been tested as effective in rats, it has not yet been tested in humans. Further: "Using intestinal biopsies mounted in Using chambers, we have observed that several gliadin-derived peptides, including the 33 mer, can be efficiently degraded into amino acids during their epithelial transport and processing in control patients and in patients on a gluten-free diet, arguing against a major intrinsic intestinal defect of proteolysis of proline-rich peptides. The situation was different in patients with active disease in which a significant amount of peptide entered undigested into the mucosa. In the latter cases, however, it remains unclear whether entrance of the intact peptides was related only to altered epithelial processing or favored by a more active mechanism that remains to be elucidated." So this also may not be an effective way to detoxify gluten.
    Finally the article explores the possibility of treating the disease using vaccinotherapy which would be based on the central role of the adaptive antigluten T-cell response: "Senger et al. observed that intranasal administration of whole gliadin or of one of its isoforms could partially inhibit the systemic T-cell response to the parenteral challenge by whole gliadins in HLA-DQ8-transgenic mice." Further: "Using unmodified gluten, however, entails an important risk of enhancing immunization. An alternative strategy might be to develop peptide analogues able to interfere with HLA-class II binding and T-cell activation and to redirect the immune response toward tolerance. This approach has been successful in several experimental models of autoimmune diseases and has provided encouraging results in patients with multiple sclerosis." These type of therapies, however, run the risk of enhancing immunization instead of promoting tolerance.
    The article concludes in a hopeful tone: "Although the ultimate goal of producing wheat deprived of toxicity remains remote and perhaps inaccessible, our broadening knowledge of celiac disease pathogenesis offers a growing number of alternative strategies to the gluten-free diet. Much work, hopefully soon supported by the development of an accurate animal model, is needed to evaluate the feasibility, efficiency, and risks of these approaches. In the vast majority of cases, celiac disease is a benign disease. Its current treatment, although constraining, is safe and efficient, and the cost and benefits of any other treatment will require a thorough appraisal. Furthermore, one unresolved key issue is to simply define who deserves treatment. The wide clinical spectrum of the disease might reflect a wide level of individual sensitivity, some of which could be compatible with a normal diet. Epidemiologic studies providing a precise appraisal of the risk of complications are therefore needed to substantiate the need of a treatment in individuals with silent or pauci-symptomatic disease determined by serologic studies."

    Jefferson Adams
    Celiac.com 06/03/2008 - Among the main things doctors look for when they’re trying to make a classic diagnosis of celiac disease are small intestinal mucosal membrane villous atrophy and inflammation. However, the latest research indicates that these criteria are possibly too narrow, leading to a lack of diagnosis and treatment of people with celiac disease. If this turn out to be the case, then far more people than previously imagined may suffer from celiac disease and not even know it.
    In an effort to find out if present current diagnostic criteria are in fact too narrow, Finnish researchers led by Markku Maki, MD, professor of pediatrics at the University of Tampere, Celiac Disease Study Group, Tampere, Finland, evaluated 145 patients who were presumed to have celiac disease. Just under half (71) of the patients showed positive endomysial antibodies, and out of these only 48 patients met the textbook definition for celiac disease.
    The research team then split the 23 patients left into two groups. They put the first group on a gluten-free diet for one year, and the second group on a on a standard gluten-inclusive diet for one year. At the end of the year, the doctors conducted follow-up biopsies on all 23 patients. The doctors discovered that the patients who had been on the gluten-free diet did in fact have celiac disease (even though they didn't have any obvious symptoms), and any symptoms that they did have disappeared—they lost their endomysial antibodies and any inflammation that was detected in their intestinal mucosa.
    On the other hand, the patients in the second group whose diets included gluten showed no such positive changes, and their symptoms continued. The still showed positive endomysial antibodies, along with inflammation of intestinal mucous membrane, and gluten-induced lesions in the small intestine.
    The study director said that each of the patients on the gluten-free diet had chosen to remain gluten-free thereafter, and that the patients on the gluten-inclusive diet had chosen to eliminate gluten from their diets and over time also became symptom-free—endomysial antibody-free and showed signs of healing of the mucous membrane.
    Other studies have shown that over time untreated patients who show positive endomysial antibodies may develop the gut injury that is currently required as part of the criteria for diagnosing celiac disease. A greater understanding of the negative effects of untreated or undiagnosed celiac disease, coupled with better testing methods have led to a new strategy that allow doctors to detect celiac disease as early as possible—before any serious damage can occur—this new strategy is likely to be resoundingly welcome among celiac disease sufferers.
     Hopefully the results of this study and others like it will lead to a new awareness among doctors, and will ultimately lead to better methods for diagnosing celiac disease at an earlier stage. This could ultimately mean less suffering and long term physical damage for many people.
    Presented at 2009 Digestive Disease Week in San Diego, CA by Dr. Kurppa, a member of Dr. Maki’s research team, on Tuesday, May 20 at 10:30 a.m. Pacific Time in room 10 (San Diego Convention Center).

  • 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:
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    Cover and refrigerate for at least 1 hour. 
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    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.
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    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). 
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    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.
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    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.