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    Gluten Sensitivity Without Celiac Disease


    Jefferson Adams

    Celiac.com 09/28/2012 - Two researchers recently set out to study gluten sensitivity in people without celiac disease. The study was conducted by A. Di Sabatino A, and G.R. Corazza of the Centro per lo Studio e la Curia della Mallatia Celiaca at the Fondazione IRCCS Policlinico San Matteo at the University of Pavia in Italy.


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    Photo: CC--teuobkA number of studies support the existence non-celiac gluten sensitivity, which can be marked by both internal and external symptoms in individuals with normal small-bowel mucosa and negative results on serum anti-transglutaminase and anti-endomysial antibody testing. These symptoms are very similar to traditional celiac disease symptoms, and seem to improve or disappear with the adoption of a gluten-free diet.

    Although researchers are currently debating the clinical aspects of this condition, studies indicate that the prevalence of non-celiac gluten sensitivity in the general population may be many times higher than that of celiac disease.

    Further study and diagnosis of non-celiac gluten sensitivity is being hindered by the lack of a clear definition of the condition. The lack of a clear definition is due at least in part to the fact that there is no single known cause, and the symptoms are likely influenced by a variety of factors.

    More work needs to be done to establish a clear definition for non-celiac gluten intolerance, and to delineate diagnostic protocols. The research team notes that if it turns out that non-celiac gluten sensitivity does in fact have multiple triggers, then treatment options should vary accordingly.

    However, any treatment would likely include a gluten-free diet.

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    Non celiac gluten sensitivity is ME, with the addition of dairy, egg and bean sensitivity.|The allergist I consulted said I'm not allergic to ANYTHING but as long as I follow my diet I am symptom free, but get into trouble whenever I cheat.

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    Guest Jackie Hobbs

    Posted

    My gluten sensitivity is different from any others that I have heard about. It causes what I think is heart pains. My heart beats harder and faster and then I have whole chest pains that go into my arms and jaw. Just a tiny bit of gluten causes me not to be able to sleep at night.

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    I had my first IBS/coeliac type symptoms in February 2012. (I have Hashimoto's and Grave's disease diagnosed in 2009.) After researching a bit, I went gluten-free in April and within two days most of these symptoms disappeared, like magic, along with others that I had had for longer, such as muscle pains in the upper arms. The rest of the symptoms gradually faded over the following weeks. I had suffered from really bad migraines since puberty and these are now greatly reduced in severity and frequency as to hardly need medication. Blood tests were not conclusive as to gluten sensitivity, or allergy as I was already following a gluten-free diet before the tests, and no way would I go back to eating gluten just to demonstrate to others what I already know! No more gluten for me, ever.

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    My gluten sensitivity is different from any others that I have heard about. It causes what I think is heart pains. My heart beats harder and faster and then I have whole chest pains that go into my arms and jaw. Just a tiny bit of gluten causes me not to be able to sleep at night.

    Hi Jackie, just wanted you to know that my heart beats faster and harder after eating also! I do not have the arm and jaw pain. Not yet, anyway. I also have a few other symptoms that don't seem to be mainstream either. Wish there was an easy way to live with this!

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    Guest Beverly Kendrick

    Posted

    I have been eating gluten-free totally for a year now. Most of my eating has been gluten-free for over 10 years. I had the gluten test September 19. 2012. The results came back I didn't have celiac disease. I ate a little gluten for two days. I got very sick. I got told I was seeing the wrong doctor. I will see a different doctor November 6 and take the test again. That is why I tried to eat gluten again. I will probably get told to eat gluten for 4-6 weeks. I will get very sick. I have had allergy tests that let me know I have the allergy. I have allergies to at least 5 gluten-free flours. I do my own cooking. I had a severe reaction to the band they used on my arm. I had told them not to use that material. It is still bothering me 3 weeks later.

     

    I take the Stem tech Nutritional Supplements daily. They really help me out.

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    My gluten sensitivity is different from any others that I have heard about. It causes what I think is heart pains. My heart beats harder and faster and then I have whole chest pains that go into my arms and jaw. Just a tiny bit of gluten causes me not to be able to sleep at night.

    Me too! My heart races and feels like it's pounding out of my chest.

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  • Related Articles

    Jefferson Adams
    Celiac.com 02/14/2011 - In what may seem for some like an obvious finding, a team of Australian researchers has shown that people can suffer gluten intolerance without having celiac disease. Their study is published in The American Journal of Gastroenterology.
    I say obvious, because many in the celiac and surrounding community have long understood and accepted the concept of gluten-intolerance as distinct from celiac disease. Surprisingly, there has been very little scientific research to establish the existence of gluten-intolerance as distinct from celiac disease. That is changing, and the recent Australian study offers some support for gluten-intolerance as distinct from celiac disease.
    For their study, a team of researchers led by Peter Gibson, professor of medicine at Eastern Health Clinical School at Monash University in Australia, recruited 34 people with irritable bowel syndrome, but who were clinically proven to be free of celiac disease. All participants had previously benefited from a gluten-free diet.
    The 34 volunteers were all fed bread and muffins, half of which contained gluten, half of which were gluten-free. Nearly 70 per cent of the volunteers who ate the gluten reported pain, bloating, toilet problems and extreme tiredness.
    ''Gluten is indeed a trigger of gut symptoms and tiredness,'' the researchers concluded. Professor Gibson said: ''These symptoms have a big impact on quality of life. But conservative medicine has not been so good at dealing with this because we haven't had any evidence.''
    A number of the volunteers had sought help from alternative health practitioners, a fact that impaired recruitment of volunteers, as many of these folks had adopted a gluten-free diet without proving or disproving celiac disease via colonoscopy and biopsy.
    It was important for the team to exclude celiac disease for several reasons, including the fact that although it was safe to use gluten to test people who may have an intolerance, it could harm people with celiac disease.
    "If you go back on gluten while you have celiac disease - even if you only eat a few pieces of bread - you will damage your body and undo many months of healing," Professor Gibson said.
    For that reason, and also to prove gluten intolerance alone was the symptom cause, the team recruited people  clinically proven to be free of celiac disease, and who were already on gluten-free diets.
    For those patients with irritable bowel syndrome, excluding celiac disease, who were symptomatically controlled on a gluten-free diet, the team crafted a double-blind, randomized, placebo-controlled re-challenge trial.
    Participants received either gluten or placebo in the form of two bread slices plus one muffin per day with a gluten-free diet for up to 6 weeks. The team evaluated symptoms using a visual analog scale and markers of intestinal inflammation, injury, and immune activation monitoring.
    A total of 4 men and 30 women between the ages of 29–59-years old completed the study as per protocol. Overall, 56% showed human leukocyte antigen (HLA)-DQ2 and/or HLA-DQ8. Adherence to diet and supplements was very high.
    Of 19 patients (68%) in the gluten-consuming group, 13 reported that symptoms were not adequately controlled compared with 6 of 15 (40%) on placebo (P=0.0001; generalized estimating equation).
    On a visual analog scale, patients were significantly worse within one week of consuming gluten for overall symptoms (P=0.047), pain (P=0.016), bloating (P=0.031), satisfaction with stool consistency (P=0.024), and tiredness (P=0.001).
    In no cases did gluten-consumption trigger anti-gliadin antibodies. Moreover, there where were no significant changes in fecal lactoferrin, levels of celiac antibodies, highly sensitive C-reactive protein, or intestinal permeability. There were no differences in any end point in individuals with the DQ2/DQ8 and those without.
    Gibson calls the general lack of research into gluten intolerance "almost unbelievable." He plans to now investigate the prevalence of non-celiac gluten intolerance, why it occurs and whether low levels of gluten can be eaten safely.

    Source:

    American Journal of Gastroenterology: 11 January 2011. doi: 10.1038/ajg.2010.487

    Jefferson Adams
    Celiac.com 03/30/2011 - A team of medical researchers set out to compare gut permeability and mucosal immune gene expression in celiac disease and gluten sensitivity.
    The research team included Anna Sapone, Karen M Lammers, Vincenzo Casolaro, Marcella Cammarota, Maria T Giuliano, Mario De Rosa, Rosita Stefanile, Giuseppe Mazzarella, Carlo Tolone, Maria I Russo, Pasquale Esposito, Franca Ferraraccio, Maria Carteni, Gabriele Riegler, Laura de Magistris  and Alessio Fasano.
    People with celiac disease suffer an adverse autoimmune reaction when they consume gluten. People with gluten-sensitivity cannot tolerate gluten and may develop gastrointestinal symptoms similar to those in celiac disease.
    However, for people with gluten intolerance, the overall clinical picture is usually less severe, and is not accompanied by the concurrence of tissue transglutaminase autoantibodies or autoimmune comorbidities.
    By examining and comparing mucosal expression of genes associated with intestinal barrier function, along with innate and adaptive immunity the team sought to better understand the similarities and differences between celiac disease and gluten sensitivity.
    For their study, the team enrolled a group of subjects with celiac disease, a group with gluten sensitivity, and a control group of healthy, gluten-tolerant individuals.
    They assessed intestinal permeability using a lactulose and mannitol probe, and collected mucosal biopsy specimens to study the expression of genes involved in barrier function and immunity.
    They found that gluten sensitivity, unlike celiac disease, is not associated with increased intestinal permeability.
    In fact, subjects with gluten sensitivity showed significantly reduced intestinal permeability compared with controls (P = 0.0308). This was accompanied with significantly increased expression of claudin (CLDN) 4 (P = 0.0286).
    Relative to controls, subjects with celiac disease expressed higher levels of adaptive immunity markers interleukin (IL)-6 (P = 0.0124) and IL-21 (P = 0.0572), while those with gluten sensitivity showed no higher levels.
    Subjects with gluten intolerance showed increased expression of the innate immunity marker Toll-like receptor (TLR) 2, but subjects with celiac disease showed no such increase (P = 0.0295).
    Finally, subjects with gluten intolerance showed significantly reduced expression of the T-regulatory cell marker FOXP3 relative to controls (P = 0.0325) and celiac subjects (P = 0.0293).
    This study supports the existence of gluten sensitivity and celiac disease as two clinically different gluten-associated disorders.
    The study also supports the characterization of gluten sensitivity as a condition associated with prevalent gluten-induced activation of innate, rather than adaptive, immune responses in the absence of detectable changes in mucosal barrier function.
    Source:

    BMC Medicine 2011, 9:23 doi:10.1186/1741-7015-9-2

    Jefferson Adams
    Celiac.com 05/14/2012 - Should gluten sensitivity be thought of as “celiac light,” as just one of the milder manifestations within the wider spectrum of celiac disease? Some doctors and researchers think so.
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    In a recent letter to the editors of the American Journal of Gastroenterology, doctors Courtney C. Ferch and William D. Chey of the Division of Gastroenterology at the University of Michigan Health System in Ann Arbor, Michigan, comment at length on the latest findings regarding Irritable Bowel Syndrome and gluten sensitivity without celiac disease.
    Ferch and Chey note that gluten sensitivity is one of the most rapidly growing sectors in the food industry, with gluten-free products accounting for $1.31 billion in U.S. sales alone in 2011. Those sales are expected to exceed $1.6 billion by 2015.
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    Unlike celiac disease, there are no accepted biomarkers for gluten-sensitivity. Doctors diagnose the condition mainly by looking at the connection between eating gluten and the presence adverse symptoms.
    Numerous studies on gluten sensitivity suffer have included small sample size, a lack of adequate controls, a lack of blinding, and the use of non-validated outcome measures. Even with these limitations, Ferch and Chey say there are several studies worthy of further consideration.
    One of the studies discussed in the Ferch and Chey was a double-blind, placebo-controlled, dietary re-challenge trial performed by Biesiekierski et al. The study sought to better understand the role of gluten ingestion in the development of gastrointestinal (GI) and non-GI symptoms in patients diagnosed with IBS.
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    Over a six week double-blind randomization phase, study participants followed either a gluten-free or gluten-containing diet that was assigned at random. Nineteen of the 34 patients ate food containing 16 g of gluten per day. The other 15 patients ate gluten-free bread and mufï¬ns. Gluten used in the study was free of fermentable oligo-, di-, monosaccharides and polyols, and its protein distribution included 2.3% nongluten, 45.7% glutenin, and 52% gliadin.
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    Meanwhile, high-sensitivity C-reactive protein levels remained normal before and after the dietary intervention.
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    In their letter, Ferch and Chey also comment on several side issues.
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    Secondly, they note that there has been much recent discussion around the potential role of food in IBS symptoms that has focused on celiac disease. However, they point out that much has been made over the possible role of food, and possibly celiac disease, in IBS symptoms. However, they note that data from US studies show no higher risk for celiac disease among patients with IBS symptoms and no warning signs.
    Although these results are certainly intriguing and hypothesis generating, they require validation in larger, randomized, controlled trials in other parts of the world.
    What is clear and important for providers to understand is that gluten sensitivity is here to stay and signiï¬cantly more likely for them to encounter in day-to-day practice than celiac disease.
    Read the full letter by Ferch and Chey at the website for the  American Journal of Gastroenterology.
    Source:
    Am J Gastroenterol 2011;106:508 –514

    Jefferson Adams
    Celiac.com 06/16/2014 - Differentiating between celiac disease and non-celiac gluten sensitivity (NCGS) is important for appropriate treatment, but is often challenging.
    A team of researchers recently set out to assess the best way to distinguish between celiac disease and non-gluten sensitivity. The research team included Toufic A Kabbani, Rohini R Vanga, Daniel A Leffler, Javier Villafuerte-Galvez, Kumar Pallav, Joshua Hansen, Rupa Mukherjee, Melinda Dennis and Ciaran P Kelly.
    For their study, the team reviewed records for 238 patients who were assessed for symptoms responsive to gluten restriction without having celiac disease ruled in or out. For each patient, clinicians noted the demographic information, presenting symptoms, serologic, genetic, and histologic data, nutrient deficiencies, personal history of autoimmune diseases, and family history of celiac disease.
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    In addition, the patients with celiac disease were far more likely to have a family history of celiac disease (P=0.004), personal history of autoimmune diseases (P=0.002), or nutrient deficiencies (P<0.0001).
    The positive likelihood ratio for celiac disease diagnosis of a >2× upper limit of normal IgA trans-glutaminase antibody (tTG) or IgA/IgG deaminated gliadan peptide antibody (DGP) with clinical response to a gluten-free diet was 130 (confidence interval (CI): 18.5–918.3).
    The positive likelihood ratio of the combination of gluten-responsive symptoms and negative IgA tTG or IgA/IgG DGP on a regular diet for NCGS was 9.6 (CI: 5.5–16.9).
    When individuals with negative IgA tTG or IgA/IgG DGP also lacked symptoms of malabsorption (weight loss, diarrhea, and nutrient deficiencies) and celiac disease risk factors (personal history of autoimmune diseases and family history of celiac disease), the positive likelihood ratio for NCGS increased to 80.9.
    Based on their findings, the team developed a diagnostic algorithm to distinguish celiac disease from NCGS.
    People with negative celiac blood tests (IgA tTG or IgA/IgG DGP, who are eating a regular gluten-containing diet, are unlikely to have celiac disease.
    Those with negative serology who show no clinical signs of malabsorption, and show no celiac disease risk factors, are highly likely to have NCGS and may not require further testing. Those with positive blood tests should undergo HLA typing to determine the need for biopsy.
    Source:
    The American Journal of Gastroenterology 109, 741-746 (May 2014) doi:10.1038/ajg.2014.41

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    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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    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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    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.