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    Screening for Celiac Disease Recommended During Pregnancy


    Scott Adams

    Gut 2000;46:332-335


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    (Celiac.com 03/17/2000) In the latest issue of Gut, Italian researchers propose that celiac disease is more common than previously thought, and that pregnant women should be screened for celiac disease. They conclude that a screening could help women to avoid negative outcomes and miscarriages. Dr. L. Greco and his colleagues from the University of Naples Federico II screened blood samples from 845 pregnant women in an effort to determine the prevalence of celiac disease. They looked for elevated levels of endomysial antibodies against tissue transglutaminase to determine how many of them had celiac disease. Out of the 845, women 12 had celiac disease (1.4%), and only three of the 12 had been previously diagnosed and were not following a gluten-free diet. The other nine women underwent a small intestinal biopsy to confirm their diagnosis. Out of the 12 diagnosed women, seven had either a pre-term delivery, or their babies were smaller than normal. Out of the remaining five women, four had had at least one miscarriage. Three of the babies died.

    When following up with 11 of the women, eight had another pregnancy and seven of them had reached term at the time of publication. Out of the eight women, five followed a gluten-free diet, and six of their babies turned out healthy. According to the researchers: Coeliac disease is considerably more common than most of the diseases for which pregnant women are routinely screened. The authors conclude: Consideration should be given to screening for coeliac disease in pregnancy, because of the high incidence of avoidable outcomes and the chance of reversibility through consumption of a gluten-free diet.

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    Dr. Fine: Yes, I've got two organizations. One is a purely educational, non-profit public organization, called the Intestinal Health Institute. My lecturing, for about 12 years now, is aimed at trying to bring about greater awareness of the health problems caused by gluten and other foods, plus intestinal and overall health. Several years ago when talking about gluten sensitivity, it was almost like getting people to see that the emperor didn't have clothes on. That has improved lately, because public and medical beliefs are changing.  
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    Ron: How did you get started on your own?
    Dr. Fine: I made the transition in 2000, so our anniversary is April 1st, 2000. This is our 13th year. If you've hung around 13 years, I think, that also makes a statement.  EnteroLab.com was born because I knew that what I had discovered was, well, what we're really talking about is an epidemic.  At that time, I didn't know anything about the "why" or even the "what".  I just knew it was a massive problem I had discovered. Maybe I could call myself the Paul Revere of gluten sensitivity. I had to be the one to get on the horse and say "gluten sensitivity is coming".     
    I converted my academic career, which was stellar at the time.... it was very traditional.... 40 publications by the time I was 35 and I worked with what would arguably be one of the most successful researchers in the world, Dr. John Fordtran. And I went out on a limb and put my entire professional reputation and career in jeopardy because I knew this had to be brought to the world.  I knew there would be a controversy. The idea, which had been in the medical literature for years..... non-celiac gluten sensitivity can be traced back to at least 1980, so we were already 20 years into that. And I thought if I bring the idea directly to the public, then, because it's a dietary treatment, they can proceed in getting better while we wait 15 to 20 years for the doctors to catch on. What I didn't know at the time is that there's a whole subset of practitioners, like chiropractors, nutritionists, and nurse practitioners, who don't seem to feel so threatened by some major new idea.  They caught on quickly. They're the early adopters.  
    Ron: You have traveled a long way since 2000
    Dr. Fine: Here's the way I'm looking at what's going on now versus where we started. My observation is that every new idea, every revolutionary finding, seems to happen in two places on opposite sides of the globe. Having happened in Christchurch, New Zealand and in Dallas, Texas would qualify for that. I think Dr. Rodney Ford and I got on the track at about the same time.
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    Ron: Is there more mainstream research that supports your findings?
    Dr. Fine: Well, I found a rate of about 11% serum IgG or IgA  among people at a shopping center in Dallas.  Dr. Marios Hadjivassiliou found IgG antibodies in about 12%  of the population, and Dr. Rodney Ford tells me that he has found a rate of about 10% who are gluten sensitive. These are all congruent findings.
    Fecal Antibodies at 25% of asymptomatic and 60 to 75% of symptomatic people, depending on what disease or symptom you're talking about and then, because those problems are so common, the overall average, from my calculations is 50% overall...... mostly adults. Theoretically, it might be less frequent in children, but I don't have enough children's data to know.  
    Ron: Is your testing similar to Dr. Marsh's rectal challenge testing for celiac disease?
    Dr. Fine: Yes. I identify one of his references in my manuscript where even siblings without DQ2 or DQ8 can be positive for a rectal challenge, even though they don't have celiac genes or get celiac disease. That's another proof that you don't have to be celiac to be gluten reactive. He did studies on that, a sibling study which was really interesting.
    What is your vision for future testing & treatment of celiac disease and non celiac gluten sensitivity?
    Dr. Fine: My lab and myself are just about finding the facts and then helping people to understand those facts. Frankly, to use a metaphor, your vision is only as good as your eyes and your glasses. If your eyes aren't good, good glasses can make your vision perfect. But if you are using the wrong glasses, ie: the wrong test, or the wrong paradigm, then you might be seeing farther than you used to see, but you are not really seeing the truth yet.
    Ron: Would you care to comment on the whole oats controversy?
    Dr. Fine: I've got a feel on oats that is a departure from the general view. We have a new test for oat protein sensitivity and it is really showing to be very helpful. We launched a more extensive food sensitivity test panel, 2 years ago, and oats is one of the antigens we included, along with rice and corn and a few meats and nuts and potatoes.  What we are seeing sometimes, is people who don't have a reaction to any foods and their oats are through the roof and they are gluten sensitive.  I don't know why. Just like it was all or none  with celiac.... you could have something in the middle, right? Oats is the same way. It's not all or nothing. Some people are sensitive, and some people are not. We know it's the least stimulating of the four grains. That makes sense because of the biochemistry of the prolamine and glutamine residues, and a lot of antigenic glutens.  
    However, logically, you cannot do a study of tolerating oats in anyone who doesn't tolerate oats. So anyone doing a study where the subject has to consume oats for long periods of time, that could never include someone who is sensitive to oats. The truth about studies that make this claim is that there is a very large withdrawal rate and a large component that can't qualify for the study because it made them vomit or sick in other ways. So the only thing you can conclude is that among the people who can symptomatically tolerate oats, over long periods of time, oats don't seem to cause the villous atrophy of celiac disease, which isn't the best measure anyway, to my thinking. But that does not mean that anybody with celiac disease can tolerate oats and that seems to be the message that has come down to us.
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    A person who doesn't eat gluten-free cannot know what an insider knows. And, they have a different agenda. They're clearly exclusively a professional. It's kind of like somebody making policy on health food who eats a horribly unhealthy diet.  So I see these jaws drop in my lectures when people find out that you can't just automatically assume that you can tolerate oats. You might be able to, but you might not, and there's no way someone can
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    Dr. Fine: I don't know. That's a good question. The good thing about the stool test is that the antibodies last a lot longer. You can be gluten-free for one or two years and still we can find antibodies to the wheat gliadin in the stool. I guess that it would be the same for oats.  I definitely abhor the idea of a gluten challenge for celiac disease.... especially the biopsy. I mean, the biopsy may not become abnormal for 5 years and they could still be sick.
    Ron: You mentioned that you follow a gluten-free diet. Can you tell me why?
    Dr. Fine: I've had spondyloarthropathy since I was about 14.  I manage it without drugs and I have no pain. I control it just with diet.
    Ron: Does your lab do genetic testing?
    Dr. Fine:  Yes, and the gene test that EnteroLab.com offers actually types the gene at the HLA locus, which means our reports indicate "this is the gene you have at the HLA-DQB1 locus".; we don't just say "yes you have the celiac  gene", or "no you don't".  There is data in the literature, including research I have published that identifies HLA-DQB1*0301, 0303, which are the DQ7 and DQ9 genes, respectively, and DQ1, and we know from Dr. Hadjivassiliou's research that DQ1 (including 05xx and 06xx subtypes) reacts with gluten and represent gluten sensitive genes. Of course, DQ2 and DQ8 are the main celiac HLA-DQB1 genes. The interesting thing is that, in America, it's very rare not to have one of these.  Almost everybody does, actually. It just comes down to how many do you have? Which one/ones do you have? Do you have one that seems to be a more reactive one or a less reactive one? And, do you have a celiac gene or two celiac genes? Which is going to mean, if you have two celiac genes or two gluten-sensitive genes, or a celiac gene and a gluten-sensitive gene that every child you have will have at least one of them.    So, we prefer our gene test over that of others that merely answers the question “ Do I or do I not have a celiac gene.” Not only is it inexpensive, at about half the price of the other lab that does it, we give you more data.
    I was doing genetic studies in the 90s, to figure all this information out. For instance, I met Dr. Hadjivassiliou at the International Conference on Celiac Disease at the University of Maryland in August of 2000. Dr. Fasano hosted it. I spoke before Dr. Hadjivassiliou and I showed this association with DQ1,7, or I called it 1,3 with 7 being a subtype primarily but also 9, and so he came to me and said "Well, I've seen associations with my neurologic disease with DQ1, so I'm glad someone else is finding this." So, again, it's not just the antibodies, and it's not just non-celiac gluten sensitive genes, and as far as I know, no other lab is dealing with that except us.  
    The abnormal permeability, in my opinion, is an effect of the immune arrays going on and the primary reaction is the immune response to gluten. You could possibly say that you get altered permeability first and then you get the gluten reaction, but I don't think so. I used to study permeability in humans in vivo. You can look at my CV or go to PubMed.com and put Fine KD and you'll see some early studies about permeability where we used to measure permeability in live human subjects and it was just a given, to me, that abnormal permeability in inflammatory disorders is primarily due to the inflammation and the disruption of tissue, architecture, and the like. I think that the permeability follows the inflammation.
    Ron: I have dermatitis herpetiformis (DH) and I find that my skin reacts more to oats than other grains. If I eat something that is labeled “gluten-free” but contains oats, I soon find that my DH flares up. I know others with celiac disease and DH who say the same thing. I mention this oats connection in the hope that you might someday do some research to explore that connection.
    Dr. Fine: We are just about to launch our oat sensitivity fecal IgA test as part of a gluten sensitivity panel because it is playing a little bit different role than testing for other non-gluten foods. It's like when a sophomore seems to be stellar on a football team, they pull him up to the varsity team.  So we're pulling the oat test out of the sophomore squad and putting it on the varsity because it was showing up a lot more often and I think it's in the same paradigm as the wheat gliadin separate from other foods. Even though we like to look at it as "other grains". We are seeing a lot of rice sensitivity, some corn sensitivity.  Many seem to react to other grains, as I do personally.
    The news is that we'd like to use April 1st, 2013 as the launch date for our new gluten sensitivity panel because it is an anniversary date for us. We hope to have that new panel available about April 1st, along with a tTG test, and an anti- gliadin fecal IgA test, and maybe even another test for another dietary food antigen, which is an ASCA (anti-Saccharomyces cerevisiae antibodies). It's been associated with Crohn's disease. It's like the diagnostic screening blood test for Crohn's, but more sensitive.
    We and some other people have looked at it in the stool, so that's just another test that we might put in the panel to make it affordable to get all 4.
    Ron: Thank you for taking the time to provide our readers with such a comprehensive discussion of your  work and the exciting new tests that will soon be available at your lab.
    Dr. Fine: You are very welcome. It was nice chatting with you. And thank you for the pioneering work that you have done as well!

    Yvonne (Vonnie) Mostat
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    signs to look for in their own bodies regarding celiac disease. The Celiac Awareness Month campaign runs right through until May 31st, and YOU can help inform people about gluten sensitivity and celiac disease. It is also a time for you to reach out to other people in the celiac community, share your recipes and what you have learned living the celiac life.
    ONE IDEA: Approach your local bakeries and restaurants. Ask at the bakeries whether they carry gluten-free foods. If they look confused, explain celiac disease to them and how difficult it often is to get really safe gluten-free food. If they point to items that they have that are gluten free, and not wrapped up or kept separate, explain nicely about cross-contamination and how strict you need to be with your diet.
    If you have Dermatitis Herpetiformis, which also requires a totally gluten-free diet, and is often thought to be stress-related, and the bakery assistant appears to be interested and has the time to listen, tell them how you suffer when an outbreak occurs. If you are gluten sensitive you can explain how gluten sensitive does not necessarily mean you have celiac disease, (between one and three percent of the population may be gluten sensitive according to the University of Chicago's Celiac Disease Center).
    If you are gluten sensitive it makes sense to avoid ingesting gluten as much as possible. If you continue eating something that makes you sick, bloated, and all the other symptoms that go along with gluten sensitivity do not continue challenging your body with something that makes you feel unwell why keep challenging your body? Again, according to the Chicago Celiac Disease Center, you are on a crash course for full blown celiac disease.
    My husband and I have had "Fun" this month going to stores and asking where their gluten-free foods are. Often they are mixed up with other foods such as a gluten-free cereal with all the other cereals. But many times these same stores have a specialty aisle devoted to the diabetic, those with celiac disease and those on special diets, such as "Heart Healthy" foods for the person with high cholesterol, or "low salt" foods for those with high blood pressure.
    We went to Granville Island in Vancouver last week. This is a big market with numerous bakeries. Many said they had gluten-free cookies, or breads but they were sold out by noon. My husband smiles charmingly and says, "I think that indicates you need to make more gluten-free foods. Celiac disease is becoming extremely common. My husband, who is not the celiac, even had the nerve to ask a young woman if she knew what foods a celiac could not eat; (he has quite the nerve). She listed flour, but also said potatoes!
    For us the most exciting thing to occur this month was something we were able to do ourselves. I wrote to the two Langley free newspapers, the Langley Times and the Langley Advance, and mentioned that May was Celiac Awareness Month in the United States and Canada and would they accept an article from me listing just what celiac disease and gluten sensitivity was and how they could inform the public. I received positive results and was very excited. I was able to give them the statistics regarding how long it takes for a celiac to be diagnosed, how some physicians are not even aware of all the symptoms, and how they differ from person to person. I was able to give them the statistics from 2010, and how the auto immune disease has increased yearly in the United States and Canada. Listing the local chapter and the U.S. and Canadian Celiac Associations web pages I crossed my fingers and hoped that at least most of the information would get into the local newspapers.
    It was a triumph when it appeared, and managing to switch the wording around from paper to paper they left out little. YOU CAN DO IT TOO. You may be too late for this year, but maybe not. You can STILL write to your local paper and tell them that this year has been the best advertised and informed year for celiac disease and the gluten sensitive, and next year you hope to do even better.
    It is when Fox News and U.S. news get involved in mentioning that May is Celiac Awareness Month that you feel we have arrived, (or almost). After contacting the main grocery stores in the lower mainland it almost made me quite teary to find inserts sheets in some of the grocery sales fliers listing their sales on gluten-free products. Wow! The bread is so expensive and to receive coupons with even .75 cents off, or $1.00 off is like gold to us! Progress is going into the Safeway bakery and see their frozen food section (fully expecting to find frosted bread and some muffins), and find that they have decorated cakes, cheesecakes and these fancy little decorated cupcakes all certified gluten-free. I was like a child in a candy shop. My husband did slow me down a little, and he did ask if they had considered the icing sugar and the decorations and whether they were also gluten-free.
    CHALLENGE YOURSELF until the end of this month. Every time you go grocery shopping ask the bakery assistants for the gluten-free section, and be sure to look very disappointed when you find out they do not carry any gluten-free foods. It does not happen as often now because we are learning, just like the peanut allergy people have had to do—we also need to eat and not get sick.
    AND we need to unite and fight for the right to be able to trust the gluten-free foods without getting out our magnifying glass and reading every label and box.
    I did mention the certification logo we have for guaranteed gluten-free, the two wheat sheaves crossed, and hope next year to be even bolder, contacting the Vancouver Chapter, the Victoria Chapter, Washington Chapter at the beginning of April to see if we can unite and advertise to a broader section of local communities this under-diagnosed, under-recognized auto-immune disorder.

  • 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.  doi: 10.1136/gutjnl-2015-310148.