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    Scott Adams
    Celiac.com 11/08/2005 - Today a team of scientists at Alba Therapeutics Corporation (Alba) and the University of Maryland School of Medicine reported a direct link between gluten-induced intestinal permeability and zonulin in tissues from patients with celiac disease. The investigators were able to successfully prevent gluten-induced intestinal tissue leak with the administration of the zonulin antagonist FZI/0 (AT-1001). AT-1001 is an orally administered peptide currently under development for the treatment of celiac disease. Published in the November issue of the Scandinavian Journal of Gastroenterology, these results describe the role that leaky gut plays in celiac disease and the role that zonulin plays in establishing the leak. These results are another milestone towards understanding the role of zonulin in celiac disease, says Alessio Fasano, M.D., lead author of the paper, professor of pediatrics, medicine and physiology at the University of Maryland School of Medicine and director of its Center for Celiac Research.
    These results reinforce our conviction that AT-1001 has great therapeutic potential and we look forward to confirming these observations in celiac patients soon, stated Alba CEO Dr. Blake M. Paterson.
    About Zonulin
    Zonulin is a signaling protein that transiently and reversibly opens the tight junctions (tj) between the cells of epithelial and endothelial tissues such as the intestinal mucosa, blood brain barrier and pulmonary epithelia. Zonulin appears to be involved in many diseases in which leakage occurs via paracellular transport across epithelial and endothelial tight junctions (tj),
    and thus may play an important potential role in the treatment of autoimmune diseases.
    About Celiac Disease
    Celiac disease is a T-cell mediated auto-immune disease that occurs in genetically susceptible individuals and is characterized by small intestinal inflammation, injury and intolerance to gluten. According to the National Institutes of Health, celiac disease affects approximately 3 million Americans, although the diagnosis is rarely made. The only treatment for celiac disease is complete elimination of gluten from the diet, which results in remission for some patients.
    About Alba
    Alba Therapeutics Corporation is a privately held biopharmaceutical company based in Baltimore, Maryland. Alba is dedicated to commercializing disease-modifying therapeutics and drug delivery adjuvants based on the zonulin pathway. Albas lead molecule, AT-1001, is targeted towards the treatment of celiac disease and other auto-immune illnesses.
    Contact: Dr. Blake Paterson
    Alba Therapeutics Corporation
    (410) 522-8708

    Scott Adams
    This article appeared in the Winter 2007 edition of Celiac.coms Scott-Free Newsletter.
    Celiac.com 04/26/2007 - My fingernails were shredding and I was a bit out of it mentally, missing obvious things. I’ve had to stop eating many foods because I have intolerances to almost everything I used to eat before I went gluten-free, and I wondered if I had dropped some essential nutrients when I cleared all of those foods out of my diet. So I checked my diet for nutrient deficiencies, using the USDA nutrients database at www.nal.usda.gov/fnic/foodcomp/search. I’m sure there’s software that works with this database but I wrote a little computer program to analyze my diet. I have an electronic food scale, so weighing food is easy.
    The most important thing I found is that I’m low on vitamin D. You can get vitamin D from food, or from a supplement, and from the ultraviolet B in sunlight; many of us, like me, may get almost none from any of those sources. And—this is important for a lot of us—vitamin D deficiency can cause a lot of symptoms including immune system problems! I went looking on Medline and it was mentioned as having anti-inflammatory properties, as preventing cancers such as colon cancer and lymphoma; preventing infections, and helping with autoimmune diseases. Gluten intolerance is less common in the middle east and more common in northern Europe. I’ve seen this explained as the result of evolution, since wheat has been used for longer in the Middle East. But I wonder if people in the north are also more likely to be gluten intolerant (an autoimmune disease) because they don’t get as much vitamin D. It may also explain why people get more colds during the winter season when there’s less sunlight. Vitamin D deficiency is best known for causing rickets in children and osteomalacia (softened bones, muscle weakness and pain, tender sternum) in adults. Osteomalacia is often misdiagnosed as fibromyalgia, because the symptoms are similar. Rickets is increasing in the U.S., especially among black children. Most post-menopausal bone loss in women occurs during the winter. It can take months of increased vitamin D intake to correct the health problems caused by deficiency.
    There are only a few significant dietary sources of vitamin D. In the U.S., almost all milk is fortified with vitamin D to 100 IU per cup, so you should get the recommended daily intake of 400 IU if you drink 4 cups of milk per day. However, milk often doesn’t have as much vitamin D as is claimed on the label. Some cereals, like Kellogg’s Cornflakes, have small amounts of added vitamin D. Typically, 10 cups of fortified cereal would give you the RDI. The government encourages fortification of milk and cereal so that fewer children will develop rickets. Otherwise—you would get the RDI from nine oysters, or about 4 ounces of fatty fish like salmon or tuna, or a teaspoon of cod liver oil. Many other kinds of fish have only small amounts. You’d have to eat 2 pounds of cod to get the RDI. The only natural vegan source of vitamin D is Shiitake mushrooms. Just like people, mushrooms make vitamin D when they’re exposed to ultraviolet. About 13 sun-dried shiitake mushrooms contain the RDI. And that’s it. Many of us on gluten-free diets are also not eating dairy or fortified cereals, so unless we have a passionate love-affair with fish or oysters or shiitake, we would be getting almost no vitamin D from food.
    You can get vitamin D the natural way, from the sun. It takes exposure to sunlight outside (not under glass) on your hands and feet for about fifteen minutes a day. I was not sure what was meant by “direct sunlight”. I read someplace that ultraviolet is scattered over the whole sky. Unlike visible light, the whole sky shines with ultraviolet. Clouds would filter out some of it. People with dark skin require more time in the sun, so many black people develop a deficiency. Using even low-SPF sunscreen prevents your body from making vitamin D. The farther from the equator you live, the less UVB there is in the winter sunlight, because the sun is closer to the horizon in the winter and the sunlight filters through more atmosphere before it gets to you. At the latitude of Boston, and near sea level, there isn’t enough UVB radiation between November and February for one’s body to make vitamin D.
    You have probably heard the public health advice to wear sunscreen—the same ultraviolet B that generates vitamin D in your body also causes skin cancer and ages skin. The small amount of exposure to sunlight required is probably only a very small cancer risk and would cause little photo-aging of the skin. Unfortunately I wasn’t able to find quantitative information about how carcinogenic fifteen minutes’ daily sun exposure would be. There are also vitamin D lights, which are probably also a healthful choice.
    I have severe immune system problems. I tested positive for 53 inhalant allergies—my body had developed allergies to almost all the allergens around. I get sick for days if I eat almost any of the foods that I ate while I was eating gluten. I even get sick from a couple of foods that, so far as I can remember, I only started eating on a gluten-free diet. So I live on an exotic-foods diet. I’ve had a hellish time trying to get allergy shots. At a concentration of 1 part in 10 million they make me sick for a couple of days while the normal starting concentration for allergy shots is 1 in 100,000. I’m plagued by bladder infections. With cranberries being one of my intolerances, I can’t even use them to help prevent the infections.
    I’ve certainly been short of vitamin D. I live in the north, and I’m always careful to use high-SPF sunscreen when I go outdoors. I can’t eat milk, fish, shellfish or mushrooms, so I can’t get a significant amount of vitamin D from food. I haven’t been taking any vitamin supplements, because almost all have traces of protein from some food that makes me sick. It would be lovely if vitamin D deficiency turned out to be part of the cause of my very burdensome immune problems. I’m skeptical because I was getting vitamin D from a supplement and/or from my diet up until 2 years ago, when I found I had a vast number of hidden food intolerances, and I started having reactions to vitamin pills. Fortunately there is a vitamin D supplement that I can take—vitamin D3 made by Pure Encapsulations. The ingredients in the capsule are made from wool and pine trees. I’ll find out if it helps over the next few months.
    Vitamin D causes disease when taken in large amounts, so if you think you are deficient, don’t take too much to make up for it. Vitamin D is a hormone—it’s not something to take in mega-doses, any more than, hopefully, one would take a mega-dose of estrogen or testosterone. If your doctor recommends a high dose, they should do regular blood tests to keep track of your vitamin D level. It’s pretty safe to take up to 2000 IU per day on your own. Dr. Michael Holick, a vitamin D researcher at Boston University and author of The UV Advantage, believes that people need about 1000 IU per day. I asked a family doctor, who said they suggest 400-800 IU per day for middle-aged women. However, it might be a good idea for gluten intolerant people to take more, about 1000 - 2000 IU per day, since we may have difficulties absorbing vitamins and celiac disease is an autoimmune disease.
    Vitamin D is very important, just as all the vitamins are. But we are conditioned by the media, and tend to think more about vitamins C and E, which get a lot of attention because they’re antioxidants. Vitamin D was the absolutely last one I looked at. Then I found that it was my most serious deficiency!  And nutrient deficiencies are not a trendy topic, so the possibility of developing deficiencies is something people tend to forget while trying to improve their diets. Many people who avoid gluten also have other food intolerances, or are on some other kind of special diet, and it would be an excellent idea to go to the USDA database and find out whether their new diet is giving them enough vitamins and minerals. It certainly helped me. I feel more cheerful and alert, like my mind woke up on a sunny day.
    It’s best to get as much as possible from one’s diet, too. Whole foods have a lot in them that’s good for the body that research hasn’t yet identified, and if your diet gives you the RDA of  all the vitamins and minerals, it will also be giving you other healthful nutrients that will do you a lot of good. This might also be true of vitamin D. Maybe it’s better to get a small amount of ultraviolet, like an iguana sitting under a UV lamp, instead of taking pills. UVB might be healthy in ways we don’t yet know about.
    Vitamin D is a bit like stored-up sunlight. You can catch it for yourself from the sun when it’s high in the sky, you can eat the sunlight the fish have gathered for you, or you can take a supplement and keep packed sunlight on your shelf.

    Tina Turbin
    This article originally appeared in the Autumn 2010 edition of Journal of Gluten Sensitivity.
    Celiac.com 01/10/2011 - As an author, researcher, and gluten-free advocate, I work hard to raise awareness for celiac disease and gluten issues, particularly when it comes to increasing the diagnosis rate. Part and parcel of improving diagnosis is proper testing. Evidence is mounting that indicates that blood testing may not be the most effective way to test for celiac disease, and I would recommend that people who suspect they have celiac disease to check with their doctors about other testing options.
    Celiac disease, which is essentially an autoimmune reaction to gluten, a protein found in wheat, barley, and rye, affects approximately three million Americans, but according to estimates, only three percent of them have been properly diagnosed with the disease. Once celiac disease is diagnosed, treatment is simple—following a gluten-free diet. With so many American celiacs going without a diagnosis,  this painful and potentially fatal autoimmune disorder, with its easy method of treatment, attention needs to be focused on effective, efficient testing.
    Although awareness of celiac disease and gluten-free living is increasing in the various medical fields, accurate and reliable testing has not been definitively tackled or uniformly implemented by medical practitioners. Currently a popular method of testing is a blood test, but some people with celiac disease can get blood testing many times and the results will nevertheless be negative.
    Although blood testing has been successful in diagnosing some people with celiac disease, this method is inaccurate at least 80 percent of the time, according to Dr. Datis Kharrazian, Blood Chemistry Seminar instructor and the formulator for Apex Energetics, Inc. supplements. To understand how blood testing works, a basic grasp of the workings of the immune system is essential. Antibodies are part of the immune system and designed to attack specific antigens, or invaders, of the body. Tests can be conducted that find an increase of antibodies in the system, which are on the prowl for certain foreign invaders. Specifically, anti-gliadin, or anti-gluten antibodies, can be tested for; when these exist in the system in large amounts, it is a sign of the autoimmune disorder, celiac disease. Although this may sound workable in theory, in practice blood testing is insufficient and inaccurate due to the fact that the autoimmune response doesn’t occur in the blood stream, but in the small intestine, as the immune system attacks this organ’s absorptive finger-like structures called villi which line the inside. Thus, for the sake of reliability, this suggests that testing should be focused on the gut.
    So what method can we turn to? Fortunately, there is another method apart from an intestinal biopsy, which is an invasive as well as expensive procedure. It turns out that the immune cells which surround the gut also can be located in large numbers in the stool, making a stool anti-gliadin antibody test a reliable alternative to blood testing.
    Stool testing may be more accurate than blood testing and is more convenient. One doesn’t need a doctor’s prescription for the test, which can be conducted in the privacy of one’s own home with an online-ordered kit from EnteroLab, which according to its website, is “a registered and fully accredited clinical laboratory specializing in the analysis of intestinal specimens for food sensitivities.”
    Enterolab offers the Anti-Gliadin Antibodies Stool Test as well as additional tests which can be ordered may be important diagnostic tools for people who have celiac disease or gluten-sensitivity. These additional tests include the Tissue Transglutaminase Stool Test, which tests whether gluten is actively attacking the intestine and other tissues, the Malabsorption Test, used to determine whether the intestine is malabsorbing nutrients due to the autoimmune reaction to gluten, or the Celiac and Gluten-Sensitivity Gene Test. The lab also offers a Milk Sensitivity Test, which tests for reactions to casein, a milk protein
    With millions of celiac Americans living with their disease undiagnosed, we can’t afford to waste time with inaccurate and inefficient testing. The anti-gliadin antibodies stool test, so easily available to the public, is a great stride forward for the celiac community.
    Talk with your health care provider today about this alternative to celiac blood testing.


    Jefferson Adams
    Celiac.com 04/18/2011 - In an effort to improve diagnosis of celiac disease in patients already on a gluten-free diet, a team of researchers recently evaluated HLA-DQ2-gliadin tetramers for detection of gluten-specific T cells in peripheral blood and histological changes in the duodenum after a short gluten challenge as a diagnostic tool.
    The study team included Margit Brottveit MD, Melinda Ráki MD, PhD, Elin Bergseng MScPharm, PhD, Lars-Egil Fallang MSc, PhD, Bjørg Simonsen BLS, Astrid Løvik MSc, Stig Larsen MSc, PhD, Else Marit Løberg MD, PhD, Frode L Jahnsen MD, PhD, Ludvig M Sollid MD, PhD, and Knut EA Lundin MD, PhD.
    They are associated variously with the Department of Gastroenterology, the Department of Medicine, and the Department of Pathology at Oslo University Hospital in Ullevål, Norway, the Centre for Immune Regulation at the Institute of Immunology at the University of Oslo and Oslo University Hospital, the Department of Pathology at Oslo University Hospital in Rikshospitalet, Norway, and the Norwegian School of Veterinary Medicine, Oslo, Norway.
    For their study, the team evaluated HLA-DQ2+ individuals on a gluten-free diet for at least 4 weeks. 35 patients had uncertain diagnosis, 13 patients had celiac disease, and 2 healthy subjects served as disease controls.
    The team challenged each participant with four slices of gluten-containing white bread per day for 3 days (d1–d3). The team took biopsy samples via esophagogastroduodenoscopy on d0 and d4, and scored the biopsies using Marsh criteria.
    On d0 and d4,  team isolated peripheral blood celiac disease 4+ T cells, stained them with HLA-DQ2-gliadin peptide tetramers, and analyzed the results using flow cytometry.
    After the gluten challenge, 11 of the 13 celiac disease patients showed a positive tetramer test, while four of them also showed typical histological changes on biopsy.
    Of the 35 patients with uncertain celiac diagnosis, 3 were found to have celiac disease. Two of these three patients showed both positive tetramer stains and histological changes in biopsies after  gluten challenge.
    Overall, the team found celiac disease in about ten percent of the group with self-prescribed gluten-free diet.
    From these results, the team concluded that tetramer staining for gluten-specific T cells is a sensitive method in detecting an immune response in celiac disease patients after a short gluten challenge.

    SOURCE:
    Am J Gastroenterol advance online publication 1 March 2011;    doi: 10.1038/ajg.2011.23


  • 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.