• 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

    77,411
    Total Members
    3,093
    Most Online
    Liza Wolfe
    Newest Member
    Liza Wolfe
    Joined
  • 0

    Rapid Gluten Detection Test for Food Products Promises Better Product Labeling, Easier Gluten-Free Shopping


    Jefferson Adams

    Celiac.com 11/19/2008 - In a development that could benefit people with celiac disease and gluten intolerance, a team of researchers based in Spain and the U.K. has developed a faster, easier way to test food products for the protein that triggers the adverse reactions associated with celiac disease.


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    Such a rapid gluten detection test for food products could help millions of people avoid the indigestion, diarrhea, bloating, and other symptoms that arise when they accidentally consume foods that contain gluten.

    The research team was made up of Alex Fragoso, Ciara O'Sullivan and other colleagues, and their results will appear in the December 15 issue of the journal Analytical Chemistry.

    Their development centers on the creation of a new sensor that detects antibodies to the protein gliadin, a component of the gluten found in wheat, rye, and barley. Laboratory tests showed that the new sensor is both highly accurate and far faster than the enzyme-linked immunosorbent assay (ELISA), which is the current standard test for gliadin. The new test can detect gliadin in amounts as small as the parts per billion range, while an ELISA test requires a full 8 hours to do the same thing.

    Avoiding gluten enables people with celiac disease to avoid symptoms commonly associated with celiac disease and gluten intolerance. However, since gluten can hide in so many seemingly safe foods, such as soy sauce, canned soups, and licorice candy, it can be difficult to know for certain whether foods are in fact free of gluten free. A number of prepared foods clearly list gluten ingredients on their labels, but spotting its presence can be challenging at best, and is often outright hit or miss.

    A rapid, highly accurate test that can reliably spot gluten in food products promises to make it easier for manufacturers to label their products, and for people with celiac disease and gluten intolerance to avoid gluten and thereby enjoy better health.

    0


    User Feedback

    Recommended Comments

    Sounds like a very promising development, but I am a bit skeptical about exactly how the results will be used. It sounds to me like items passing the test are fine for typical Celiacs, but what about those who have other gluten problems? And what about the presence of things like oats to which some are very sensitive?

    Share this comment


    Link to comment
    Share on other sites

    Somewhat out dated article. The Elisa test claims a 10 minute

    turnover time now. Florida based. down to as low as 5 ppm.

    Time for an update eh!

    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   19 Members, 0 Anonymous, 1,176 Guests (See full list)

  • Related Articles

    Scott Adams
    Scand J Caring Sci. 2003 Sep;17(3):301-7
    Celiac.com 09/03/2003 - A recent study published in the Scandinavian Journal of Caring Sciences looked at the differences in how men and women cope with celiac disease. The study concludes that gender should be taken into account in the treatment of celiac disease to improve its outcome. The biggest flaw in this study is with the number of people in it—only 10. I think that it is difficult to draw such conclusions using such a small sample of people, and that a larger study of this type needs to be done to draw more solid conclusions. Additionally, the poorer outcome for women in this study may be due to the fact that they experienced more bowel-related symptoms than did the men, which may not be due at all to their "emotionally oriented strategy" of coping. It could just be a fact that women with celiac disease experience more real health problems than men, which is also in need of further study. - Scott Adams
    Here is the abstract:

    "Perceptions of health-related quality of life of men and women living with coeliac disease."
    Hallert C, Sandlund O, Broqvist M.
    Coeliac Centre, Faculty of Health Sciences, Linkoping University, Linkoping, Sweden.
    "Women with long-standing coeliac disease express poorer health-related quality of life (HRQoL) than men do for unclear reasons. This led us to explore differences in their understanding of HRQoL using a phenomenographic approach. We interviewed 10 coeliac subjects (mean age 57 years, range 35-73) who had been on a gluten-free diet for 10 years and had scored either high or low in the Short Form 36 Health Survey (SF-36) General Health and Vitality scales. Three dimensions were revealed that pertained to their perception of HRQoL: bodily sensations, social consequences and coping strategies. Within these, the women experienced more bowel symptoms than men did, despite keeping to a strict diet. This item was the only one predicting the SF-36 scores. The women also described more distress caused by the restrictions in daily life, closely related to their controlling of food contents. The coeliac men took advantage of using a problem-oriented coping approach while the women seeking an emotionally oriented strategy showed less satisfaction with the outcome. We conclude that the intriguing difference in HRQoL between coeliac men and women may have some of its origin in the way living with the disorder is conceptualized and coped with. The results imply that in the management of coeliac patients, gender-related aspects need to be taken into account to improve treatment outcome."

    Jefferson Adams
    Celiac.com 07/10/2007 - A study published recently in the American Journal of Gastroenterology tracks the appearance and disappearance of antibodies associated with childhood risk celiac disease, and suggests that key antibodies often disappear even when gluten is still present in the diet.
    A team of Finnish doctors set out to evaluate the natural history of antibodies versus tissue transglutaminase (TGA), endomysium (EMA), reticulin (ARA), and gliadin (AGA-IgG and AGA-IgA). They looked at data for children genetically at risk for celiac disease, specifically, children who carried HLA-conferred risk of celiac disease who had been monitored frequently since birth. The research team was made up of S. Simell, S. Hoppu, A. Hekkala, T. Simell, M.R. Ståhlberg, M. Viander, H. Yrjänäinen, J. Grönlund, P. Markula, V. Simell, M. Knip, J. Ilonen, H. Hyöty, O. Simell.
    The team looked at serum samples from 1,320 children who were genetically at risk for celiac disease. Serum samples taken between 2000 and 2003 were assessed for TGA. Samples testing positive for TGA were evaluated for all five antibodies. Also, all future samples for the given patient were similarly evaluated. Also, positive TGA patients were encouraged to have a duodenal biopsy.
    The assessment was completed in August 2004. At that time, the test subjects ranged in age from 1 year to 9.5 years, with a mean age of 4.1 years. In all, 49 children (3.7%) were TGA positive. 26 of these TGA positive children submitted to biopsy. Celiac disease was diagnosed by biopsy in 20 of the 26. Of the 49 children who tested TGA positive, AGA-IgA surfaced at an average age of 2 years (+/- 1.5 over a range of 0.5 to 6.6 years for subjects). Compared to AGA-IgA, TGA, EMA, and ARA all surfaced together about 1 year later (TGA at 3.2 +/- 1.5, 1.0-7.0 yr, P < 0.001).
    Key Antibodies Can Vanish Early in Childhood Celiac Disease
    Even with ongoing gluten consumption, positive TGA values disappeared in 49%, EMA values disappeared in 49%, ARA values disappeared in 43%, AGA-IgA values disappeared in 41%, and AGA-IgG in 32%.
    The research team concluded that there are likely potential triggers for celiac disease that are active before AGA-IgA surfaces, or about 3 months earlier on average than when the TGA-associated antibodies appear.
    In a significant number of children, antibodies vanish spontaneously. This indicates that in many cases, conditions allow the regulatory immune phenomena to eliminate incipient celiac disease in genetically at-risk children even when gluten is still significant part of the diet.
    Am J Gastroenterol 2007;102:1–10
     

    Jefferson Adams
    A team of researchers has announced what they are calling a 'pivotal advance' regarding the differential influence of bifidobacteria and gram-negative bacteria on immune responses to inflammatory triggers in celiac disease.
     
    Their study provides strong evidence that various intestinal bacteria in celiac patients can influence inflammation, and that dietary probiotics and prebiotics can help improve the quality of life for patients with celiac and other associated diseases, such as type 1 diabetes and various autoimmune disorders.
    To conduct their study, they the team used cultures of human peripheral mononuclear cells (PBMCs) as in vitro models. This was possible because blood monocytes constantly replenish intestinal mucosal monocytes, and accurately represent an in vivo situation.
    To duplicate the intestinal environment surrounding celiac disease, researchers exposed cell cultures to Gram-negative bacteria and bifidobacteria they had isolated from celiac patients, both alone and in the presence of disease triggers.
    They then assessed the effects on surface marker expression and cytokine production by PBMCs. Gram-negative bacteria induced higher pro-inflammatory cytokines than did bifidobacteria.
    The Gram-negative bacteria also up-regulated expression of cell surface markers involved in inflammatory aspects of the disease, while bifidobacteria up-regulated the expression of anti-inflammatory cytokines.
    Research team still need to confirm the results in clinical trials on people, but the findings offer the first support for new treatment options that may change how celiac disease is treated and possibly prevented.
    In the same way the certain foods may contribute to poor health, notes Louis Montaner, D.V.M., M.Sc., D.Phil. Editor-in-Chief of the Journal of Leukocyte Biology, "others can have positive effects. For people with celiac disease, this opens a line of research into new therapies that may be as accessible as a grocer's shelf."
    SOURCE: Journal of Leukocyte Biology. 2010;87:765-778.


  • Recent Articles

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    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