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    Nuclear Fluorescence Serum Reactivity on Monkey Esophagus - A New Celiac Antibody?


    Destiny Stone
    Image Caption: Monkey Esphagus (photo courtesy of travlinman43)

    Celiac.com 06/24/2010 - Scientists have previously seen a nuclear fluorescence reactivity (NFR) pattern on monkey esophagus in sections which were exposed to celiac disease patients that were sera positive for anti-endomysium antibodies (EMA). Because of this prior knowledge, scientists created a new study to illustrate the NFR, to study  NFR positive results in connection with gluten withdrawal, and also to assess  the possible role of NFR in celiac disease follow-up's.


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    For twelve months, scientists closely evaluated twenty untreated celiac patients, eighty-seven treated celiac patients, and fifteen healthy control subjects. Scientists incubated the sera of all 122 patients on monkey esophagus sections. The goal was to evaluate the existence of NFR by indirect immunofluorescence analysis.

    To asses the rate of NFR in culture supernatants, duodenal mucosa samples from treated celiac patients were challenged with gliadin peptides. Scientists evaluated the reactivity of NFR immunoglobulins (Igs) response to the nuclear extract of human intestinal cells. What they found was that serum NFR was visible in all untreated celiac patients and it persisted for up to 151 +/-37 days from gluten withdrawal. It reappeared in treated celiac patents when they did not stick to their dietary restrictions.

    Serum NFR was also present in two of the healthy control subjects. NFR presented itself before EMA,  in culture supernatants of celiac intestinal mucosa that was challenged with gliadin peptides. The Igs responsible for NFR were labeled as, “IgA2 Subclass”. The NFR had different results than the EMA and anti-nuclear antibodies, although they reacted with two nuclear antigens of 65 and 49 kDa. Thus, a new auto-antibody  named NFR, which is related to celiac disease, was depicted.

    In conclusion, the studies of NFR have demonstrated that NFR detection has potential to be used as a beneficial tool in monitoring compliance of a gluten-free diet, as it has the ability to  diagnose
    slight dietary shifts pertaining to gluten.

    Source:


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  • Related Articles

    Scott Adams
    Nat Med 2000;6:337-342. (March 1, 2000)
    see also: BMJ 2000;320:736 (March 18, 2000)
    (Celiac.com 03/17/2000) Researchers in Britain have identified a dominant epitope of the A-gliadin protein of wheat that is linked to the cause of celiac disease. The findings could eventually influence the diagnosis and treatment of the disease. With the new information Wheat could be genetically engineered to be non-toxic for celiacs, according to Dr. Robert P. Anderson. Also, modified versions of T cell epitopes can have unique antagonistic effects that switch off particular immune responses. The identification of this peptide could be used to develop a blood tests to better diagnose celiac disease, and could also be used to better test food for celiac toxicity.
    Dr. Anderson and his University of Oxford colleagues used a series of 15 amino acid peptides along the A-gliadin sequence (alpha gluten) to stimulate in patients with celiac disease their peripheral blood mononuclear cells, or PBMCs. The peptides were either unmodified or were treated with tissue transglutaminase, which, in the presence or absence of lysine, will convert glutamine to glutamate.
    Researchers successfully stimulated PBMCs in celiac patients who were in remission due to a gluten-free diet with a gluten challenge. Patients were fed wheat bread for either a half day, 3 days, or 10 days, and healthy, non-celiac patients that were fed wheat bread each day for 4 weeks were used as controls. The researchers successfully produced PBMCs from the celiac disease group, who secreted interferon-gamma 6-8 days later, in response to a particular pool of A-gliadin peptides, which had been treated with tissue transglutaminase. A 17-amino-acid peptide, corresponding to the partially deamidated peptide of A-gliadin amino acids 57-73, was optimal for inducing the interferon-gamma secretion, and the responses were restricted to those with HLA-DQ2.
    According to Dr. Anderson: On a more general level, the finding that a host enzyme modifies peptides that are then recognized by the immune system suggests that searching for epitopes important in disease may be more complex than simply reading off protein sequences from sequenced genes. Further, modification of the peptide by tissue transglutaminase that is present in the intestinal lining increases binding of the peptide to HLA-DQ. The researchers also point out that T cells that are responsive to the same A-gliadin peptide are readily induced in celiac disease despite many years of following a gluten-free diet, which indicates a persistence of memory T cells that could be caused by continuing exposure to trace amounts of gluten. The researchers only looked at the A-gliadin peptide, and point out that there is a possibility that other peptides that are structurally unrelated to A-gliadin are also important in celiac disease.

    Kathleen La Point
    Celiac.com 12/23/2008 - Metabolites are small–molecule products of biochemical processes in the body’s cells. Analysis of these metabolites can detect changes in the body caused by chemical toxicity, disease, gene mutations, or diet. Bacteria in the gut also contribute to this “metabolic signature”, so it is also a way to understand changes in gut microbe populations.
    Because metabolites are excreted from the cells into blood and urine, collecting these samples can be easy, noninvasive, and inexpensive. Chemical techniques like nuclear magnetic resonance (NMR) spectroscopy are used to analyze the samples. The results of NMR spectroscopy are chemical patterns, showing the simultaneous alterations of many compounds. The measurement and analysis of multiple metabolite changes in response to genetic changes or environmental stimuli is known as metabonomics.
    Metabonomics has a number of potential applications. Ease of sample collection may enable researchers to develop a rapid screening tool for diseases like celiac disease. Using metabonomics, it is not necessary to know the specific metabolites that differ in people with a given disease (the disease biomarkers). Rather than looking for the presence or absence of a particular biomarker, the overall pattern of metabolite concentrations is compared to patterns of people known to have the disease (the metabolic signature of the disease) and patterns of people who do not have the disease. Large numbers of metabolites are analyzed simultaneously, instead of one by one, providing a snapshot into what is happening in the cells at a given time.
    In this first study to investigate the metabonomic signature of celiac disease, blood and urine samples of 34 people with celiac disease were analyzed at the time of diagnosis, which was based on antibody tests and confirmed with biopsies of the small intestine. These patterns were compared to the metabolite patterns of 34 people without celiac disease. Using blood samples, researchers were able to predict celiac disease up to 83% of the time. Analysis of urine samples gave accuracy of about 70%.
    These accuracy rates are lower than those achieved with antibody tests, but this is only the first small study and refining the techniques may significantly improve accuracy rates.In addition, analyzing the metabolic signature may lead to a greater understanding of celiac disease and the cause of its various symptoms. For example, results from this study included lower levels of some metabolites such as pyruvate (a product of glucose breakdown) coupled with elevated levels of other metabolites such as glucose and 3-hydroxybutyric acid (a by-product of fat breakdown) in people with celiac disease.
    These results suggest a possible explanation for chronic fatigue experienced by up to 87% of patients with celiac disease—a possible impairment in the body’s ability to use glucose for energy. As expected, evidence of altered gut bacteria was also found, as were an increase in metabolites that indicate an increased intestinal permeability (“leaky gut”). After 12 months of a strict gluten-free diet, these altered metabolite patterns reverted to normal.
    Metabonomics is an emerging field of study, which like genomics, holds great promise in the understanding, diagnosis, and treatment of diseases like celiac disease.
    Reference:
    Bertini I, et al. The metabonomic signature of celiac disease. Journal of Proteome Research. 2008 Dec 11 [Epub ahead of print]

    Destiny Stone
    Celiac.com 03/26/2010 - Mass screening studies among the general population for celiac disease show a prevalence of approximately 0.5-1.0% in adults and in children. Yet, despite the growing numbers of newly diagnosed celiac disease patients, most cases still remain undiagnosed and therefore, untreated. In part, the masses of misdiagnosed or undiagnosed  celiac disease  patients are a result of the variety of disguises  celiac disease can have. Celiac disease can manifest into a multitude of symptoms including, but by no means exclusive to, malabsorption syndrome, diarrhea, anemia, infertility and osteoporosis.
    It has been demonstrated that there is a clear advantage to early testing for celiac disease. Early testing can aide in  avoiding the irreversible damages that come from diagnosis later in life, such as stunted growth and organ damage. It is also faster for children to heal from intestinal lesions caused from undiagnosed celiac disease, when diagnosed early on. New evidence shows that 10 years after being diagnosed with celiac disease, 66% of the children diagnosed exhibited improvement in their health and overall quality of life; indicating that mass screening at an early age is critical.
    This study was based on a previous study performed by  mass screening for celiac disease by a group of scientists in the Netherlands between 1997 and 1998, who studied 6,127 asymptomatic children between the ages of two and four. Using endomysial antibodies (IgA EmA) testing, the children were screened for celiac disease. 57 seropositive children were then given biopsies. The scientists compared different testing methods for celiac disease, evaluated their serological persistence over time, and determined optimum cut-off points for the testing. Using serological samples obtained at biopsy, EmA and tTGA was assessed for each subject studied. Human leukocyte antigen  (HLA)-typing was obtained from 55 children; 26 of those had normal biopsies and were genetically predisposed for celiac disease and 29 of the children had small-bowel alterations known to be  distinctive traits for celiac disease. Of the 26 children with normal biopsies, 4% of them tested positively for HLA-DQ8, and the other 96% tested positive for HLS-DQ2. Of the 29 children diagnosed with celiac disease, all of them tested positive for HLA-DQ2. However, a proportionately  large number of children who tested EmA-positive and were diagnosed with celiac disease, had normal biopsies and were thus regarded as  false positives.
    The results of this test confirmed that celiac disease antibody levels may fluctuate in children who are genetically predisposed for  celiac disease. While the reason for the transient antibodies is still not known, it has been suggested that children who are seropositive but have normal small-intestine biopsies, potentially have celiac disease, and are susceptible to developing gluten sensitive enteropathy as they get older. Future testing is needed to establish results for this hypothesis.
    However, children with histological alterations in their small-intestine biopsy indicative of celiac disease, had considerably higher antibodies for EmA than those without celiac disease.  The tTGA levels were significantly higher and occurred with more frequency in children with celiac disease than in children without celiac disease. EmA persisted in all celiac disease children, but only in 50% of the non-celiac disease children. tTGA was evident in 83% of celiac disease children, and 15% in non-celiac disease children. Additionally, increasing the cut-off points  provided a reduction of false positives, but resulted in lowering test sensitivity. While optimization of standard cut-off points reduced unnecessary biopsies by 50%-96%, it also reduced test sensitivity.
     In conclusion, celiac disease antibodies are proven to be transient in children genetically predisposed to celiac. It is therefore crucial for medical providers to reduce the number of unnecessary biopsies. As this study has demonstrated,  to reduce the number of unnecessary biopsies by 85%, serological mass screening methods may be improved by repeating EmA and/or tTGA in children who test seropositive after 6 months, and before continuing to biopsy.
    Source:

    http://www.ncbi.nlm.nih.gov/pubmed/20047580

    Jefferson Adams
    Celiac.com 03/18/2015 - Getting high-quality biopsy specimens is key to making accurate celiac disease diagnoses. Endoscopists may take either a single- or double-biopsy specimen with each pass of the forceps.
    Does it matter whether they take one or two? Is two better than one?
    A team of researchers recently set out to answer those questions, by comparing the quality of biopsy specimens obtained with the single-biopsy and double-biopsy techniques.
    The research team includes M. Latorre, S.M. Lagana, D.E. Freedberg, S.K. Lewis, B. Lebwohl, G. Bhagat, and P. H. Green of the Celiac Disease Center, Department of Medicine, Columbia University, New York, New York, USA.
    Their prospective cohort study looked at patients undergoing upper endoscopy with confirmed, suspected, or unknown celiac disease status. A total of 86 patients enrolled in the study, 47% with known celiac disease, 36% with suspected celiac disease, and 17% with an unknown celiac disease status.
    In each case, patients received four biopsy specimens from the second portion of the duodenum. Two were made using the single-biopsy technique of 1 bite per pass of the forceps, and two more using the double-biopsy technique, which takes 2 bites per pass of the forceps.
    Specimens were blindly reviewed to determine orientation, consecutive crypt-to-villous units, and Marsh score. Well-oriented biopsy specimens were noted in 66% of patients with the single-biopsy technique and 42% of patients with the double-biopsy technique (P < .01).
    Analysis of matched pairs showed improved orientation with the single-biopsy technique (odds ratio 3.1; 95% confidence interval, 1.5-7.1; P < .01). This persisted in subgroup analysis of patients with known celiac disease (P = .02), villous atrophy (P = .02), and a final diagnosis of celiac disease (P < .01).
    Now, this is just a single-center trial, so results need to be compared with results from additional cities.
    Interestingly, these results suggest that one bite is actually better than two, because the single-biopsy technique improves the yield of well-oriented duodenal biopsy specimens.
    For best results, the endoscopists should consider taking only one biopsy specimen per pass of the forceps in patients undergoing biopsies of the duodenal mucosa.
    Source:
    Gastrointest Endosc. 2015 Jan 29. pii: S0016-5107(14)02380-3. doi: 10.1016/j.gie.2014.10.024.

  • 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. &nbsp;doi: 10.1136/gutjnl-2015-310148.