• Join our community!

    Do you have questions about celiac disease or the gluten-free diet?

  • Ads by Google:
     




    Get email alerts Subscribe to Celiac.com's FREE weekly eNewsletter

    Ads by Google:



       Get email alertsSubscribe to Celiac.com's FREE weekly eNewsletter

  • Member Statistics

    77,274
    Total Members
    3,093
    Most Online
    GFsista
    Newest Member
    GFsista
    Joined
  • 0

    Are Doctors Missing 90% of Celiac Disease Cases?


    Jefferson Adams


    • If a new study by Canadian nutrition researchers is any indication, most cases of celiac disease remain undiagnosed.


    Image Caption: Is Celiac Disease Seriously Under-Diagnosed? Photo: CC--US Army

    Celiac.com 10/20/2017 - Are doctors even getting close to diagnosing the actual number of cases of celiac disease? Or are they missing the vast majority?


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    Researchers have said for some time that there are far more people with celiac disease than are being diagnosed, and that the vast majority of cases go undiagnosed.

    So, just how far are we from the actual number? Well, if a new study by Canadian nutrition researchers is any indication, doctors are very far from diagnosing most cases.

    The team studied the blood work of nearly 3,000 people, and their conclusions are stunning. They say that ninety percent of celiac cases go undiagnosed.

    How could this be? One reason is that even classic celiac disease symptom, such as abdominal pain, bloating, gas, diarrhea, anemia and weight loss can mimic other conditions. Less classic symptoms such as fatigue, low vitamin C, D and calcium levels can be misleading.

    Ahmed El-Sohemy, a professor of nutritional science at the University of Toronto, wanted to see whether celiac disease results in subpar nutrition because of poorer absorption of vitamins and minerals. But to find out, he needed Canadian data on the frequency of undiagnosed celiac disease.

    To that end, El-Sohemy and his colleagues checked blood samples from more than 2,800 individuals in Toronto. One group had an average age of 23, and the other 45. Among their findings is likely ~1%, with 87% of cases being undiagnosed. These findings suggest the need for better screening in high genetic risk groups.

    Source:


    0


    User Feedback

    Recommended Comments

    Guest SadCeliac

    Posted

    There really is no excuse for the percentage of undiagnosed individuals to be so high. There is a simple blood test out there that measures the certain antibody found in persons with celiac. I was one of those persons. It took 10 years for a doctor to finally give me this test. I think anyone who goes to a doctor complaining of chronic diarrhea should be given this lab test to rule out celiac.

    Share this comment


    Link to comment
    Share on other sites
    Guest Jacqueline

    Posted

    Do you have to have another endoscopy after 5 years of celiac diagnosis? My blood work is normal.

    Share this comment


    Link to comment
    Share on other sites
    Guest Sabrina S.

    Posted

    Unfortunately from what I have read and been told by doctors, the test only yields a positive result for less than 50 percent of people who have celiac, as in my case. It took 24 years of doctors and specialists not being able to diagnose me and my having to self diagnosis. I came to the diagnosis after researching my celiac related skin condition, dermatitis herpetiformis, explained my observations to a GI celiac specialist and two dermatologist, one of whom has celiac and the same skin condition. I agree that it should not be so difficult to diagnose celiac disease. There is also a great need for awareness campaigns; I'm tired of people deriding my need to eat a gluten-free diet as a fad.

    Share this comment


    Link to comment
    Share on other sites

    Damn rights! I went to my doctor as a teenager, trying to explain my symptoms, which would have been the brain fog that would wham my head. She ended saying she would send me to a psychiatrist. b%$@#! 30 years later my sister figures the gluten/Celiac disorder. I spent 30 years with gluten ruining my life. After my sister's diagnosis, I get genetic testing done and there it was in black and white.

    Share this comment


    Link to comment
    Share on other sites

    I have a friend in Australia in the medical field and she says they test for celiac disease first with symptoms of diarrhea, skin conditions, etc. It's American doctors that are behind the times. BTW, I self diagnosed my celiac disease. I once told a doctor that if I had waited for a doctor to diagnose me I'd be dead by now.

    Share this comment


    Link to comment
    Share on other sites
    There really is no excuse for the percentage of undiagnosed individuals to be so high. There is a simple blood test out there that measures the certain antibody found in persons with celiac. I was one of those persons. It took 10 years for a doctor to finally give me this test. I think anyone who goes to a doctor complaining of chronic diarrhea should be given this lab test to rule out celiac.

    My problem was not chronic diarrhea; it was being deferred from blood donations due to anemia. But once I was diagnosed, I realized the only reason I had called in sick for work for several years was due to diarrhea. It just wasn't that often. The problem is that there are also people who don't have the most common symptoms, but they do still have celiac, which makes it even harder to diagnose.

    Share this comment


    Link to comment
    Share on other sites


    Your content will need to be approved by a moderator

    Guest
    You are commenting as a guest. If you have an account, please sign in.
    Add a comment...

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoji are allowed.

    ×   Your link has been automatically embedded.   Display as a link instead

    ×   Your previous content has been restored.   Clear editor

    ×   You cannot paste images directly. Upload or insert images from URL.


  • Popular Contributors

  • Ads by Google:

  • Who's Online   20 Members, 1 Anonymous, 1,135 Guests (See full list)

  • Related Articles

    Jefferson Adams
    Celiac.com 07/13/2017 - Until recently, duodenal biopsy was considered the gold standard for diagnosing celiac disease, but that is changing.
    A number of studies have shown that celiac disease can be diagnosed using serological tests alone, but many clinicians have yet to embrace this approach.
    In both retrospective and prospective studies, one research team showed that certain IgA-tissue transglutaminase antibodies levels can predict celiac disease in adults 100% of the time.
    After making some adjustments to the analytical method for measuring the antibody, a team of researchers recently set out to to determine whether such serum tests can reliably diagnose celiac disease in large numbers adult patients without the need for small bowel biopsy.
    The research team included GKT Holmes, JM Forsyth, S Knowles, H Seddon, PG Hill, and AS Austin.
    They are variously associated with the Royal Derby Hospital, the Department of Pathology, and the Derby Digestive Diseases Centre at the Royal Derby Hospital in Derby, UK.
    For their study, the team conducted a retrospective analysis in an unselected series of 270 adult patients who underwent small bowel biopsies and the measurement of serum IgA-tissue transglutaminase antibody levels from 2009 to 2014.
    At an IgA-tissue transglutaminase antibody cut-off greater than 45 U/ml (>8×upper limit of normal+2SDs) the positive predictive value for celiac disease in this cohort was 100%; 40% of cases were above this cut-off.
    The team found that they could use IgA-tissue transglutaminase antibody levels to reliably diagnose celiac disease in a high proportion of these adult patients.
    This study adds to the growing body of evidence that supports the diagnosis of celiac disease without a mandatory small bowel biopsy.
    As a realist of these findings, the study team has changed the diagnostic guidelines for their center, and will now make celiac diagnosis based on cut-off levels of IgA-tissue transglutaminase.
    This is exciting news. For many, many years, the biopsy was considered the gold standard for diagnosing celiac disease.
    By eliminating biopsies in favor of IgA-tissue transglutaminase levels, diagnosing celiac disease could become much easier and even cheaper.
    Do you have celiac disease? Did you receive a biopsy for diagnosis? How do you feel about celiac diagnosis without biopsy? Share your thoughts below.
    Source:
    Eur J Gastroenterol Hepatol. 2017 Jun;29(6):640-645. doi: 10.1097/MEG.0000000000000841.

    Jefferson Adams
    Celiac.com 09/27/2017 - Patients who have clinical, genetic and histological signs of celiac disease, but no serological markers, present a challenge when it comes to making a diagnosis. If the patient doesn't have elevated antibodies, what signs do doctors look for? What's the best way to evaluate the patient's natural history and response to a gluten-free diet?
    A team of researchers recently set out to outline a specific profile, and to evaluate the natural history and response to a gluten-free diet of patients with seronegative celiac disease.
    The research team included Maria Pina Dore; Giovanni Mario Pes; Ivana Dettori; Vincenzo Villanacci; Alessandra Manca and Giuseppe Realdi. They are variously affiliated with the Internal Medicine Section, Department of Clinical and Experimental Medicine, University of Sassari, Sassari, Italy, with the Baylor College of Medicine, Michael E. DeBakey VAMC, Houston, TX, USA, the Pathology Section, Department of Molecular and Translational Medicine, Spedali Civili and University of Brescia, Brescia, Italy, and with the Pathology Section, Department of Clinical and Experimental Medicine, University of Sassari in Sassari, Italy.
    Patients with duodenal mucosa damage Marsh I, II and III stages, HLA DQ2/DQ8 haplotype and clinical features suggestive of celiac disease, but with negative celiac serology, were defined as seronegative celiac patients.
    The team excluded other common causes of duodenal mucosa damage. They the compared HLA–DR and DQ genotype/haplotype between all Marsh stages of patients with seronegative and seropositive celiac disease. They then assessed clinical features, lab tests and histological findings after a gluten-free diet and a gluten re-challenge. The group provided the team with a long follow-up period to gather data.
    The researchers enrolled a total of 48 patients who fulfilled diagnostic criteria over a 4-year period. Patients with seronegative and seropositive celiac disease showed similar clinical phenotype and HLA−DR and DQ frequencies. However, Marsh I stage was seen in 42% of seronegative patients (42% vs 22%; p<0.05).
    After a 1-year gluten-free diet trial, clinical symptoms, histological features and laboratory testing improved in 40 patients and worsened in those who underwent a 6-months gluten challenge. Five patients with seronegative celiac disease (25%) experienced the occurrence of autoimmune diseases during an average follow-up of about 11 years.
    Patients with seronegative celiac disease did not show any specific profile, but they did see benefits from a gluten-free diet similar to seropositive patients.
    In the absence of more sensitive serological markers, diagnosing seronegative celiac disease remains an often confusing and challenging process of excluding various other possibilities.
    Source:
    BMJ Open Gastro. 2017;4(1):e000159

    Jefferson Adams
    Celiac.com 09/25/2017 - There are currently several efforts underway to develop successful commercial enzyme treatments for celiac disease. Efforts include looking at the digestive enzymes in plants, such as the papaya and star fruits, including such predatory plants, such as the pitcher plant.
    One focus has been on developing enzymes that can break down gluten before it can trigger an immune reaction. This could prove helpful to many people with celiac disease.
    One such enzyme under development is Latiglutenase, formerly known as ALV003. Latiglutenase is a new name for an enzyme therapy designed to be taken with meals.
    The idea is that a person with celiac disease would take an enzyme tablet with a meal. If the meal had mild gluten contamination, the enzyme’s two recombinant proteins would break gluten into fragments that are not toxic to the immune system, thereby preventing exposure, and symptoms.
    But the stomach is a notoriously difficult environment to work in, so what seems like a simple idea quite a challenge from a science and biology perspective.
    Seeking to explore the ability of Latiglutinase to improve symptoms, a team of researchers recently set out to test latiglutenase on celiac patients who are seropositive despite following a gluten-free diet.
    The research team included Jack A. Syage, Joseph A. Murray, Peter H. R. Green and Chaitan Khosla. They are variously affiliated with the Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester USA, the Celiac Disease Center at Columbia University, New York, USA, the Departments of Chemical Engineering and Chemistry, Stanford University, USA, and with ImmunogenX, Newport Beach, USA.
    "Though the ALV003-1221 trial was inconclusive regarding histologic improvement from latiglutenase, the evidence for symptom benefit, which is more quickly achieved, is quite convincing and clinically relevant," Joseph Murray, MD, of the Mayo Clinic in Rochester, Minn., said in a press release.
    In these trials, patients with celiac disease who were seropositive despite following a gluten-free diet saw major improvement in symptoms when taking latiglutenase with meals, according to a post hoc analysis of the CeliAction study.
    The team was really hoping to see histological improvement, but they feel satisfied that this trial shows, says Dr. Murray, that a "therapy to help patients struggling with symptoms due to celiac disease is now within reach."
    Stay tuned for more on efforts to develop effective enzyme treatments for celiac disease.
    Read more: Dig Dis Sci. 2017 Doi:10.1007/s10620-017-4687-7.

    Jefferson Adams
    Celiac.com 10/02/2017 - For anyone following the efforts by ImmusanT to develop a vaccine for celiac disease, the company's recent presentations at the 2017 International Celiac Disease Symposium (ICDS) in New Delhi, India, were welcome news.
    Nexvax2® is a therapeutic vaccine intended to protect against the effects of gluten exposure while maintaining a gluten-free diet in HLA-DQ2.5+ patients with celiac disease.
    The company announced at ICDS 2017 that it has presented data showing the immunologic basis for the early clinical effects of gluten in celiac disease.
    Presented in two poster presentations and an oral presentation, the company says its data show that "early cytokine changes in blood following gluten ingestion could provide the basis for a new diagnostic for celiac disease in patients on a gluten free diet with an uncertain diagnosis," said Robert Anderson, MBChB, Ph.D., Chief Scientific Officer of ImmusanT.
    The company says its results are "significant" because celiac disease sufferers often adopt a gluten-free diet prior to being diagnosed by a doctor. This can cause problems and lead to unreliable or misleading results with current diagnostic tests.
    ImmusanT says that their data demonstrate that early changes in circulating cytokines after a single gluten exposure may offer a clinical way to assess celiac disease activity.
    The company says that the data, along with the potential to differentiate between celiac disease and non-celiac gluten sensitivity (NCGS) by assessing IL-2 levels, support the science behind targeted immunotherapies such as Nexvax2®.
    Read more at BusinessWire.com

  • 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.