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      Frequently Asked Questions About Celiac Disease   04/07/2018

      This Celiac.com FAQ on celiac disease will guide you to all of the basic information you will need to know about the disease, its diagnosis, testing methods, a gluten-free diet, etc.   Subscribe to Celiac.com's FREE weekly eNewsletter   What are the major symptoms of celiac disease? Celiac Disease Symptoms What testing is available for celiac disease?  Celiac Disease Screening Interpretation of Celiac Disease Blood Test Results Can I be tested even though I am eating gluten free? How long must gluten be taken for the serological tests to be meaningful? The Gluten-Free Diet 101 - A Beginner's Guide to Going Gluten-Free Is celiac inherited? Should my children be tested? Ten Facts About Celiac Disease Genetic Testing Is there a link between celiac and other autoimmune diseases? Celiac Disease Research: Associated Diseases and Disorders Is there a list of gluten foods to avoid? Unsafe Gluten-Free Food List (Unsafe Ingredients) Is there a list of gluten free foods? Safe Gluten-Free Food List (Safe Ingredients) Gluten-Free Alcoholic Beverages Distilled Spirits (Grain Alcohols) and Vinegar: Are they Gluten-Free? Where does gluten hide? Additional Things to Beware of to Maintain a 100% Gluten-Free Diet What if my doctor won't listen to me? An Open Letter to Skeptical Health Care Practitioners Gluten-Free recipes: Gluten-Free Recipes
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    ORIGIN AND IMMUNOPHENOTYPE OF ABERRANT IEL IN PATIENTS WITH REFRACTORY CELIAC DISEASE TYPE II


    Jefferson Adams

    Celiac.com 04/23/2012 - Aberrant intra-epithelial lymphocytes (IELs) are one of the major features of refractory celiac disease type II RCDII. They are categorized as pre-malignant cells, which can give rise to aggressive enteropathy-associated T cell lymphoma (EATL).


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    Photo: CC - audreyjm529A medical research team recently studied the origin and immuno-phenotype of aberrant IEL in RCDII patients. The research team included G.J. Tack, R.L. van Wanrooij, A.W. Langerak, J.M. Tjon, B.M. von Blomberg, D.A. Heideman, J. van Bergen, F. Koning, G. Bouma, C.J. Mulder, and M.W Schreurs. They are affiliated with the Gastroenterology and Hepatology, VU University Medical Center, The Netherlands.

    The team set out to better understand the origin and characteristics of aberrant IELs by scrutinizing T-cell receptor (TCR) rearrangements, and through immunophenotypic analysis of aberrant IELs.

    For their study,  the team looked for TCR delta, gamma, and beta rearrangements in duodenal biopsies from 18 RCDII patients. they also analyzed three RCDII cell lines.

    They also conducted phenotypical analysis on IELs isolated from biopsies taken from RCDII patients.

    They found that aberrant IELs showed an increased expression of granzyme B, along with a reduced expression of PCNA. Biopsies of RCDII patients showed heterogenic TCR rearrangements in the aberrant IEL cells. The researchers suggest that this is likely due to a variation in maturity. Similarly, RCDII cell lines showed a heterogenic TCR rearrangement pattern.

    From their data, the team concludes that aberrant IELs originate from deranged immature T lymphocytes and show clear differentiation to a cytotoxic phenotype.

    Among RCDII patients, aberrant IELs showed different stages of maturity, and only the patients who had the most mature aberrant IEL cells developed an EATL.

    Source:


    Image Caption: Photo: CC--audreyjm529
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    Guest Brian Ferry

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    Thanks for this. But do you think you could write this more in layman's terms?

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    Guest gluten

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    All I know is that I was in lots of pain. Stomach cramps, pains all over, bad headaches, and exhausted! I was so sick and tired that it became hard to get out of bed in the morning.

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    Thanks for this. But do you think you could write this more in layman's terms?

    My thoughts exactly.

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    admin

    The following post is from Dr. Joseph Murray, one of the leading USA physicians in the diagnosis of celiac disease (celiac disease) and dermatitis herpetiformis (DH). Dr. Murray (murray.joseph@mayo.edu) of the Mayo Clinic Rochester, MN, is a gastroenterologist who specializes in treating Celiac disease:
    A recent poster asked about refractory celiac disease. This is a highly complex area and is the most challenging in dealing with celiac disease. While refractory celiac disease can be defined as a patient with celiac disease whose symptoms do not respond to a gluten-free diet there are several important questions and issues in coming to the determination that the patient is really suffering from true refractory disease. To make the diagnosis conclusively, first one must be satisfied that there is not another cause for the problem. Though rare, there are other conditions that can mimic, or coexist with celiac disease, and cause continued problems. The second issue is whether the patient is truly gluten-free, and have they been so long enough to conclude that there has been a failure with the diet? To make this determination I have the patient keep a complete and detailed dietary record for 3-4 weeks listing every single item they ate and have them save the wrapper or carton for review. If the dietitian or myself feel that there is any possibility of contamination then we exclude that item and wait longer. Sometimes the patient is exposed to a higher risk of gluten contamination by eating out a lot, where they do not have true control over the food preparation. We also check medications that the patient takes regularly. I also check the endomysial antibodies and gliadin antibodies. These should be negative if the patient has been gluten free for at least 6 months. The gliadin IgG may persist longer but usually its levels drop. If these are positive, this makes me think that they have had significant gluten in the diet in the recent past (Note: there still may be gluten in the diet if the test is negative). The original and follow-up biopsies should be compared to see if there has been any improvement. Assuming that these criteria are met, then one can proceed to consider the patient to have refractory disease. At that point it is important to check for complications such as lymphoma, lymphocyctic colitis and possibly pancreatic insufficiency. I treat the patient with a course of antibiotics and consider adding in pancreatic supplements to see if that will help the patients symptoms. It is only at this point that I consider some suppression of the immune system, such as with steroids or some other agent. Rarely will the patient be so ill that one must accelerate the decision to treat with steroids. Steroids are powerful medicines that can be very helpful, and even lifesaving in many cases, but have attendant risks that should be discussed prior to use. This is not medical advice and should not be used as such.

    Jefferson Adams
    Celiac.com 12/28/2009 - A team of researchers recently set out to compare continual monitoring of intraepithelial lymphocyte immunophenotype and clonality against snapshot analysis in the surveillance of refractory celiac disease. The research team was made up of H. Liu, R. Brais, A. Lavergne-Slove, Q. Jeng, K. Payne K, H. Ye, Z. Liu, J. Carreras, Y. Huang, C. M. Bacon, R. Hamoudi, V. Save, L. Venkatraman, P. G. Isaacson, J. Woodward, and M. Q. Du of Addenbrooke's Hospital, Cambridge, UK.
    Often, people with refractory celiac disease suffer from abnormal immunophenotype and monoclonality of intraepithelial lymphocytes (IELs). No good studies have been done to compare the utility of continual monitoring of IEL immunophenotype and clonality in monitoring refractory celiac disease (RCD).
    To address this deficiency, and to gather some data for comparison, the team used CD3e/CD8 double immunohistochemistry and PCR-based clonality analysis of the rearranged TCR genes to evaluate diagnostic and follow-up biopsies from 33 people with proven celiac disease, 7 with suspected refractory celiac disease, 41 with proven refractory celiac disease, and 20 with enteropathy associated T-cell lymphoma (including 11 evolved from RCD).
    The team found aberrant immunophenotype (CD3epsilon(+)CD8(-) IEL >/=40%) and monoclonality in occasional celiac disease biopsies, either transiently in celiac patients not following a gluten free diet, or in those who later developed refractory celiac disease, suspected RCD, or enteropathy associated T-cell lymphoma (EATL). By comparison, they found aberrant immunophenotype and monoclonality respectively in 30 of 41 (73%) and 24 of 37 (65%) biopsies at the time of diagnosis for refractory celiac disease.
    Among the patients with refractory celiac disease showed no such abnormalities in their diagnostic biopsies, 8 of 10 (80%) and 5 of 11 (45%) cases showed aberrant immunophenotype and monoclonality respectively upon follow-up. Whether found in initial or follow-up biopsies, the ongoing development of both aberrant immunophenotype and monoclonality is a common facet of refractory celiac disease.
    One key point was that the presence of both persistent monoclonality and aberrant immunophenotype, especially <>/=>80% CD3epsilon(+)CD8(-) IEL, was a strong predictor of enteropathy associated T-cell lymphoma development in patients with RCD (P=0.001).
    From these findings, the team found concludes that the continual monitoring of both immunophenotype and clonality of IEL is superior to snapshot analysis for diagnosis and follow-up of refractory celiac disease, and could provide a useful tool for surveillance of patients at risk of developing EATL.
    Source:
    Gut. 2009 Dec 8.

    Jefferson Adams
    Celiac.com 12/22/2010 - A recent evaluation of the safety and efficacy of small intestinal release mesalamine (SIRM) for symptom relief in refractory celiac disease (RCD) shows that SIRM seems to be a safe and effective treatment option, though larger tests are needed to know for certain.
    The research team conducting the evaluation included Shailaja Jamma, MD, Daniel A. Leffler, MD, Melinda Dennis, RD, Robert M. Najarian, MD, Detlef B. Schuppan, MD, Sunil Sheth, MD, and Ciaran P. Kelly, MD,
    They set out to evaluate the safety and efficacy of small intestinal release mesalamine (SIRM) for symptom relief in refractory celiac disease.
    There are currently no adequate clinical therapies for patients with refractory celiac disease and corticosteroid and/or immunosuppressants treatments are of limited use due to side effects. SIRM has been shown to reduce local inflammation, and it is well tolerated.
    For the study, the team looked at records of the refractory celiac disease patients who received SIRM in an open-label therapeutic trial. Data included patient demographics, disease characteristics, dose and duration of SIRM therapy, and patient response.
    The team then categorized each response as complete, if symptoms resolved completely, partial if symptoms improved at least 50%, and non-responsive if symptoms improved less than 50%.
    The team treated four patients with SIRM alone and six patients with a combination of SIRM and oral budesonide. After four weeks, half of the patients showed complete response, while 10% showed a partial response. Two of the six patients were able to discontinue budesonide. One patient discontinued SIRM after complaining of headaches.
    These initial results indicate that SIRM seems to be a safe and efficacious treatment option in patients with refractory celiac disease, though a larger, more comprehensive study is needed to confirm these results.
    Source:

    J Clin Gastroenterol 2010 Sep 24. doi: 10.1097/MCG.0b013e3181f42401


    Jefferson Adams
    Celiac.com 03/25/2011 - A group of researchers recently set out to evaluate cladribine [2-chlorodeoxyadenosine (2-CdA)] therapy in refractory celiac disease (RCD) â…¡.
    The team included Greetje J. Tack, Wieke H. M. Verbeek, Abdul Al-Toma, Dirk J. Kuik, Marco W. J. Schreurs, Otto Visser, Chris J. J. Mulder of the Department of Gastroenterology and Hepatology,  at VU University Medical Center, Amsterdam, The Netherlands.
    Between 2000 and 2010, the research team conducted an open-label cohort-study of RCD â…¡ patients treated with 2-CdA. They assessed survival rate, enteropathy associated T-cell lymphoma (EATL) occurrence, clinical course, and histological and immunological response rates.
    The study followed a total of  32 patients over an average 31-month period. Eighteen patients responded well to 2-CdA. Patients responsive to 2-CdA showed markedly higher survival rates, compared to unresponsive patients.
    The responder group showed an 83% survival rate at the 3- and 5-year mark, compared to rates of 63% and 22% in the non-responder group. The responder group showed an 81% clinical, histological and immunological response rates at the 2-year mark, compared to rates of 47% and 41% in the non-responder group. 16% of non-responsive patients progressed into EATL, and all of these patients died.
    Because 2-CdA shows excellent clinical and histological response rates, and probably less frequent transition into EATL, it looks like a promising treatment for RCD II.
    Source:

    World J Gastroenterol. 2011 January 28; 17(4): 506–513. doi: 10.3748/wjg.v17.i4.506.

    Jefferson Adams
    Celiac.com 09/21/2012 - Refractory celiac disease type II (RCDII) is a severe complication of celiac disease that occurs when symptoms and intestinal damage continue even when the patient adopt a gluten-free diet. Refractory celiac disease marked by abnormal intraepithelial lymphocytes (IELs) of unknown origin that display an atypical CD3(-)CD7(+)icCD3(+) phenotype. About 40% of patients with RCDII lymphocytes develop a dangerous and invasive lymphoma.
    A team of researchers recently sought to identify possible origins of abnormal intraepithelial lymphocytes in refractory celiac disease type II.
    The research team included F. Schmitz; T.M. Tjon, Y. Lai; A. Thompson; Y. Kooy-Winkelaar; R.J. Lemmers; H.W. Verspaget; M.L. Mearin; F.J. Staal; M.W. Schreurs; T. Cupedo; A.W. Langerak; C.J. Mulder; J. van Bergen; and F. Koning.
    In their study, the researches sought to find the physiological counterpart of these abnormal intraepithelial lymphocytes cells.
    To do so, they used microarray analysis, real-time quantitative PCR and flow cytometry to compare RCDII cell lines with T-cell receptor positive (TCR(+)) IEL (T-IEL) lines. They then used their data to identify cells with an RCDII-associated phenotype in duodenal biopsies from non-refractory individuals by multicolor flow cytometry.
    They found that RCDII cell lines were distinct from T-IEL lines and showed higher levels of multiple natural killer (NK) cell receptors.
    In addition to the CD3(-)CD7(+)icCD3(+) phenotype, the RCDII lines showed an absence of CD56, CD127 and CD34, compared with other lymphocyte subsets.
    Moreover, they found cells matching this surface lineage-negative (Lin(-)) CD7(+)CD127(-)CD34(-) phenotype that showed a functional interleukin-15 (IL-15) receptor and comprised a substantial portion of IELs in duodenal specimens of patients without celiac disease, particularly children. They also found cells of this kind in the thymus.
    For patients without celiac disease, the Lin(-)CD7(+)CD127(-)CD34(-) subset was one of four subsets within the CD3(-)CD7(+)icCD3(+) population that showed a differential expression of CD56 and/or CD127.
    The results indicate that the CD3(-)CD7(+)icCD3(+) population is heterogeneous and show the existence of a Lin(-) subset that is different from T, B, NK and lymphoid tissue inducer cells.
    The team hypothesizes that the IL-15 cells are the counterpart of abnormal cells that are expanded in RCDII and transformed in RCDII-associated lymphoma.
    Source:
    Gut. 2012 Jul 6.

    Jefferson Adams
    Celiac.com 10/25/2012 - Abnormal intraepithelial lymphocytes (IELs) are the main feature of refractory celiac disease type II (RCDII). However, researchers still don't know exactly how these abnormal IELs originate.
    A pair of researchers recently commented on efforts to learn how these abnormal IELs might come about.
    The pair were Victor F. Zevallos, and Detlef Schuppan, of the center for Molecular and Translational Medicine, Department of Medicine I at the University Medical Center of Johannes Gutenberg University Mainz, in Mainz, Germany.
    Their commentary focuses on efforts by a separate research team, Schmitz, et al., which had already used a broad spectrum of cell specific markers, RNA array and immunological techniques, to explore abnormal IEL cell lines from four RCDII patients, and compare them with IELs from the fetal intestine, the intestine of children and adults and the thymus.
    IELs are highly varied lymphocytes cells with innate and adaptive features that live in the small and large intestine. IELs play an important role in maintaining gut tolerance to common food antigens versus defense against pathogens.
    A number of nutritional factors influence the development and spread of IELs, especially vitamins and their active metabolites, such as retinoic acid, and phytochemicals such as ligands of the aryl hydrocarbon receptor from cruciferous vegetables.
    However, when IELs activate and expand uncontrollably in response to chronic inflammatory conditions in the gut, they trigger mucosal damage, which can lead to celiac disease, and in some cases, to malignant cancers.
    Up to 5% of people with celiac disease, especially those who are over fifty years old when diagnosed, continue to suffer from clinical symptoms and villous atrophy even when following a gluten-free diet.
    After excluding ongoing gluten consumption and other potential underlying diseases, all four patients studied by Schmitz could be diagnosed with RCD, which is classically classified as type I or type II, based on the histological co-expression of CD3 and CD8 in RCDI, or absence of such co-expression in RCDII.
    Read the entire report in Gut.
    Source:
    Gut doi:10.1136/gutjnl-2012-303030

    Jefferson Adams
    Celiac.com 03/12/2014 - Researchers and clinicians consider refractory celiac disease (RCD) to be rare, but they don't actually have solid, reliable information about how common the condition actually is.
    A team of researches recently set out to establish rates of refractory celiac disease, and to identify corresponding risk factors in a Finnish population with high rates of clinically diagnosed celiac disease.
    The research team included T. Ilus, K. Kaukinen, L. J. Virta, H. Huhtala, M. Mäki, K. Kurppa, M. Heikkinen, M. Heikura, E. Hirsi, K. Jantunen, V. Moilanen, C. Nielsen, M. Puhto, H. Pölkki, I. Vihriälä, and P. Collin.
    For their study, the team looked at data on 44 treated RCD patients, 12,243 clinically diagnosed celiac disease patients, and a compared results against a control group of 1.7 million adult inhabitants.
    Specifically, the team compared clinical characteristics upon celiac disease diagnosis between the RCD patients and patients with uncomplicated disease.
    RCD affected 0.31% of diagnosed celiac disease patients, but just 0.002% in the general population.
    Of the enrolled 44 RCD patients, 68% showed type I RCD, 23% type II RCD, and 9% remained undetermined.
    Compared with the 886 patients with uncomplicated celiac disease, the 44 patients who developed RCD later in life were, when first diagnosed for celiac disease, significantly older (median 56 vs 44 years, P < 0.001), more likely to be male (41% vs. 24%, P = 0.012) and largely seronegative (30% vs. 5%, P < 0.001).
    More patients with evolving RCD showed severe symptoms upon celiac disease diagnosis, including weight loss in 36% (vs. 16%, P = 0.001) and diarrhea in 54% (vs. 38%, P = 0.050).
    These results show that refractory celiac disease is very rare in the general population.
    However, patients who are male, older, who experience severe symptoms or seronegativity when first diagnosed with celiac disease have a higher risk of developing refractory celiac disease. These patients should be closely monitored over time..
    Source:
    Alimentary Pharmacology & Therapeutics Volume 39, Issue 4, pages 418–425, February 2014. DOI: 10.1111/apt.12606

    Jefferson Adams
    Celiac.com 04/07/2014 - Histologically non-responsive celiac disease (NRCD) is a potentially serious condition found in celiac disease patients who suffer persistent villous atrophy despite following a gluten-free diet (GFD).
    Currently, the only way to monitor patient progress rely on invasive and costly serial duodenal biopsies. Looking for better options, a team of researchers recently set out to identify antibody biomarkers for celiac disease patients that do not respond to traditional therapy.
    The research team included B. N. Spatola, K. Kaukinen, P. Collin, M. Mäki, M. F. Kagnoff, and P. S. Daugherty. They are affiliated with the Department of Chemical Engineering, University of California, Santa Barbara in California, the Department of Gastroenterology and Alimentary Tract Surgery and the Center for Child Health Research at the University of Tampere and Tampere University Hospital in Tampere, Finland, with the Department of Medicine at Seinäjoki Central Hospital in Seinäjoki, Finland, and with the Laboratory of Mucosal Immunology in the Departments of Medicine and Pediatrics at the University of California San Diego in La Jolla, California.
    Using flow cytometry to screen bacterial display peptide libraries, the team was able to identify the epitopes specifically recognized by antibodies from patients with NRCD, but not by antibodies from responsive celiac disease patients.
    By comparing ELISA results for sera from 15 NRCD patients and 45 patients with responsive celiac disease, all on a strict GFD for at least 1 year, the team confirmed that deamidated gliadin was the antigen mimicked by library peptides.
    They identified the dominant consensus epitope sequence by unbiased library screening QPxx(A/P)FP(E/D). The epitope sequence was highly similar to reported deamidated gliadin peptide (dGP) B-cell epitopes.
    They also found that anti-dGP IgG measurement by ELISA discriminated between NRCD and responsive celiac disease patients with 87% sensitivity and 89% specificity.
    Most importantly, they found that dGP antibody levels correlated with the severity of mucosal damage, meaning that IgG dGP levels may be useful in monitoring small intestinal mucosal recovery on a GFD in NCRD patients.
    The team found that celiac patients with NRCD can be spotted by their increased levels of anti-dGP IgG antibodies even when the patients are following strict gluten-free diets
    Lastly, they feel that anti-dGP IgG assays may be useful for monitoring mucosal damage and histological improvement in celiac disease patients on a strict GFD.
    Source:
    Aliment Pharmacol Ther. 2014;39(4):407-417.

    Jefferson Adams
    Celiac.com 06/17/2015 - Refractory celiac disease type II (RCDII) and EATL (Enteropathy Associated T-cell Lymphoma) are pre-malignant complications of celiac disease. However, there is scant medical literature and data what role malnutrition and intestinal absorption may play in these conditions.
    With this in mind, a team of researchers set out to conduct a comprehensive assessment of nutritional status and intestinal absorption capacity of patients with RCDII and EATL, and to compare that with data of newly diagnosed celiac disease patients. The research team included N.J. Wierdsma, P. Nijeboer, M.A. de van der Schueren, M. Berkenpas, A.A. van Bodegraven, and C.J. Mulder.
    They are affiliated with the Department of Nutrition and Dietetics, the Department of Gastroenterology, the Celiac Centre Amsterdam, the Department of Nutrition and Dietetics at VU University Medical Centre in Amsterdam, The Netherlands; and with the Department of Internal Medicine, Gastroenterology and Geriatrics at ATRIUM-ORBIS Medical Centre, Sittard, The Netherlands.
    They conducted an observational study in tertiary care setting in for 24 RCDII patients, averaging 63.8 ± 8.2 years of age, 25 EATL patients averaging 62.3 ± 5.7 years of age, and 43 celiac disease patients averaging 45.6 ± 14.8 years of age.
    At diagnosis, the team evaluated anthropometry (BMI, unintentional weight loss, fat-free mass index (FFMI), handgrip strength (HGS), nutritional intake, fecal losses and Resting Energy Expenditure (REE)).
    They found low BMI (<18.5) more often in RCDII patients than in celiac disease or EATL patients (in 33%, 12% and 12%, respectively, p = 0.029). Also, 58% of EATL patients had unintentional weight loss greater than 10% of total weight, compared to 19% of celiac disease patients, and 39% for RCDII patients (p = 0.005/0.082).
    The team found energy malabsorption (below 85%) in 44% of RCDII patients, and in 33% of EATL patients, compared with 21.6% in celiac disease (NS).
    Fecal energy losses were higher in RCDII than in celiac disease patients (589 ± 451 vs 277 ± 137 kcal/d, p = 0.017). REE was lower than predicted, with reulst greater than 10% in 60% of RCDII, 89% of EATL, and 38% of celiac disease patients (p = 0.006).
    Between one third and two thirds of all patients showed Low FFMI and HGS.
    Patients with RCDII and EATL show far worse nutritional profiles than untreated naïve celiac disease patients at presentation. This malnutrition is at least partly due to malabsorption as well as hypermetabolism.
    This study shows the importance of proper diagnosis, and of nutrition in the treatment of these conditions.
    Source:
     Clin Nutr. 2015 Apr 30. pii: S0261-5614(15)00124-7. doi: 10.1016/j.clnu.2015.04.014.

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    First, the team used liquid chromatography-tandem mass spectrometry (LC/MS) to analyze amino acid levels in fasting plasma samples from 141 children with celiac disease and 129 non-celiac disease controls. They then crafted a general linear model using age and experimental effects as covariates to compare amino acid levels between children with celiac disease and non-celiac control subjects.
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    This study shows that amino acids can influence inflammation and may play a role in the development of celiac disease.
    Source:
    PLoS One. 2018; 13(3): e0193764. doi: & 10.1371/journal.pone.0193764

    Jefferson Adams
    Celiac.com 04/18/2018 - To the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service animals.
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    However, many of these animals are not service animals at all. Many of these animals perform no actual service to their owners, and are nothing more than thinly disguised pets. Many lack proper training, and some have caused serious problems for the airlines and for other passengers.
    Now the major airlines are taking note and introducing stringent requirements for service animals.
    Delta was the first to strike. As reported by the New York Times on January 19: “Effective March 1, Delta, the second largest US airline by passenger traffic, said it will require passengers seeking to fly with pets to present additional documents outlining the passenger’s need for the animal and proof of its training and vaccinations, 48 hours prior to the flight.… This comes in response to what the carrier said was a 150 percent increase in service and support animals — pets, often dogs, that accompany people with disabilities — carried onboard since 2015.… Delta said that it flies some 700 service animals a day. Among them, customers have attempted to fly with comfort turkeys, gliding possums, snakes, spiders, and other unusual pets.”
    Fresh from an unsavory incident with an “emotional support” peacock incident, United Airlines has followed Delta’s lead and set stricter rules for emotional support animals. United’s rules also took effect March 1, 2018.
    So, to the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service and emotional support animals.
    Source:
    cnbc.com

    admin
    WHAT IS CELIAC DISEASE?
    Celiac disease is an autoimmune condition that affects around 1% of the population. People with celiac disease suffer an autoimmune reaction when they consume wheat, rye or barley. The immune reaction is triggered by certain proteins in the wheat, rye, or barley, and, left untreated, causes damage to the small, finger-like structures, called villi, that line the gut. The damage occurs as shortening and villous flattening in the lamina propria and crypt regions of the intestines. The damage to these villi then leads to numerous other issues that commonly plague people with untreated celiac disease, including poor nutritional uptake, fatigue, and myriad other problems.
    Celiac disease mostly affects people of Northern European descent, but recent studies show that it also affects large numbers of people in Italy, China, Iran, India, and numerous other places thought to have few or no cases.
    Celiac disease is most often uncovered because people experience symptoms that lead them to get tests for antibodies to gluten. If these tests are positive, then the people usually get biopsy confirmation of their celiac disease. Once they adopt a gluten-free diet, they usually see gut healing, and major improvements in their symptoms. 
    CLASSIC CELIAC DISEASE SYMPTOMS
    Symptoms of celiac disease can range from the classic features, such as diarrhea, upset stomach, bloating, gas, weight loss, and malnutrition, among others.
    LESS OBVIOUS SYMPTOMS
    Celiac disease can often less obvious symptoms, such fatigue, vitamin and nutrient deficiencies, anemia, to name a few. Often, these symptoms are regarded as less obvious because they are not gastrointestinal in nature. You got that right, it is not uncommon for people with celiac disease to have few or no gastrointestinal symptoms. That makes spotting and connecting these seemingly unrelated and unclear celiac symptoms so important.
    NO SYMPTOMS
    Currently, most people diagnosed with celiac disease do not show symptoms, but are diagnosed on the basis of referral for elevated risk factors. 

    CELIAC DISEASE VS. GLUTEN INTOLERANCE
    Gluten intolerance is a generic term for people who have some sort of sensitivity to gluten. These people may or may not have celiac disease. Researchers generally agree that there is a condition called non-celiac gluten sensitivity. That term has largely replaced the term gluten-intolerance. What’s the difference between celiac disease and non-celiac gluten-sensitivity? 
    CELIAC DISEASE VS. NON-CELIAC GLUTEN SENSITIVITY (NCGS)
    Gluten triggers symptoms and immune reactions in people with celiac disease. Gluten can also trigger symptoms in some people with NCGS, but the similarities largely end there.

    There are four main differences between celiac disease and non-celiac gluten sensitivity:
    No Hereditary Link in NCGS
    Researchers know for certain that genetic heredity plays a major role in celiac disease. If a first-degree relative has celiac disease, then you have a statistically higher risk of carrying genetic markers DQ2 and/or DQ8, and of developing celiac disease yourself. NCGS is not known to be hereditary. Some research has shown certain genetic associations, such as some NCGS patients, but there is no proof that NCGS is hereditary. No Connection with Celiac-related Disorders
    Unlike celiac disease, NCGS is so far not associated with malabsorption, nutritional deficiencies, or a higher risk of autoimmune disorders or intestinal malignancies. No Immunological or Serological Markers
    People with celiac disease nearly always test positive for antibodies to gluten proteins. Researchers have, as yet, identified no such antobodies or serologic markers for NCGS. That means that, unlike with celiac disease, there are no telltale screening tests that can point to NCGS. Absence of Celiac Disease or Wheat Allergy
    Doctors diagnose NCGS only by excluding both celiac disease, an IgE-mediated allergy to wheat, and by the noting ongoing adverse symptoms associated with gluten consumption. WHAT ABOUT IRRITABLE BOWEL SYNDROME (IBS) AND IRRITABLE BOWEL DISEASE (IBD)?
    IBS and IBD are usually diagnosed in part by ruling out celiac disease. Many patients with irritable bowel syndrome are sensitive to gluten. Many experience celiac disease-like symptoms in reaction to wheat. However, patients with IBS generally show no gut damage, and do not test positive for antibodies to gliadin and other proteins as do people with celiac disease. Some IBS patients also suffer from NCGS.

    To add more confusion, many cases of IBS are, in fact, celiac disease in disguise.

    That said, people with IBS generally react to more than just wheat. People with NCGS generally react to wheat and not to other things, but that’s not always the case. Doctors generally try to rule out celiac disease before making a diagnosis of IBS or NCGS. 
    Crohn’s Disease and celiac disease share many common symptoms, though causes are different.  In Crohn’s disease, the immune system can cause disruption anywhere along the gastrointestinal tract, and a diagnosis of Crohn’s disease typically requires more diagnostic testing than does a celiac diagnosis.  
    Crohn’s treatment consists of changes to diet and possible surgery.  Up to 10% of Crohn's patients can have both of conditions, which suggests a genetic connection, and researchers continue to examine that connection.
    Is There a Connection Between Celiac Disease, Non-Celiac Gluten Sensitivity and Irritable Bowel Syndrome? Large Number of Irritable Bowel Syndrome Patients Sensitive To Gluten Some IBD Patients also Suffer from Non-Celiac Gluten Sensitivity Many Cases of IBS and Fibromyalgia Actually Celiac Disease in Disguise CELIAC DISEASE DIAGNOSIS
    Diagnosis of celiac disease can be difficult. 

    Perhaps because celiac disease presents clinically in such a variety of ways, proper diagnosis often takes years. A positive serological test for antibodies against tissue transglutaminase is considered a very strong diagnostic indicator, and a duodenal biopsy revealing villous atrophy is still considered by many to be the diagnostic gold standard. 
    But this idea is being questioned; some think the biopsy is unnecessary in the face of clear serological tests and obvious symptoms. Also, researchers are developing accurate and reliable ways to test for celiac disease even when patients are already avoiding wheat. In the past, patients needed to be consuming wheat to get an accurate test result. 
    Celiac disease can have numerous vague, or confusing symptoms that can make diagnosis difficult.  Celiac disease is commonly misdiagnosed by doctors. Read a Personal Story About Celiac Disease Diagnosis from the Founder of Celiac.com Currently, testing and biopsy still form the cornerstone of celiac diagnosis.
    TESTING
    There are several serologic (blood) tests available that screen for celiac disease antibodies, but the most commonly used is called a tTG-IgA test. If blood test results suggest celiac disease, your physician will recommend a biopsy of your small intestine to confirm the diagnosis.
    Testing is fairly simple and involves screening the patients blood for antigliadin (AGA) and endomysium antibodies (EmA), and/or doing a biopsy on the areas of the intestines mentioned above, which is still the standard for a formal diagnosis. Also, it is now possible to test people for celiac disease without making them concume wheat products.

    BIOPSY
    Until recently, biopsy confirmation of a positive gluten antibody test was the gold standard for celiac diagnosis. It still is, but things are changing fairly quickly. Children can now be accurately diagnosed for celiac disease without biopsy. Diagnosis based on level of TGA-IgA 10-fold or more the ULN, a positive result from the EMA tests in a second blood sample, and the presence of at least 1 symptom could avoid risks and costs of endoscopy for more than half the children with celiac disease worldwide.

    WHY A GLUTEN-FREE DIET?
    Currently the only effective, medically approved treatment for celiac disease is a strict gluten-free diet. Following a gluten-free diet relieves symptoms, promotes gut healing, and prevents nearly all celiac-related complications. 
    A gluten-free diet means avoiding all products that contain wheat, rye and barley, or any of their derivatives. This is a difficult task as there are many hidden sources of gluten found in the ingredients of many processed foods. Still, with effort, most people with celiac disease manage to make the transition. The vast majority of celiac disease patients who follow a gluten-free diet see symptom relief and experience gut healing within two years.
    For these reasons, a gluten-free diet remains the only effective, medically proven treatment for celiac disease.
    WHAT ABOUT ENZYMES, VACCINES, ETC.?
    There is currently no enzyme or vaccine that can replace a gluten-free diet for people with celiac disease.
    There are enzyme supplements currently available, such as AN-PEP, Latiglutetenase, GluteGuard, and KumaMax, which may help to mitigate accidental gluten ingestion by celiacs. KumaMax, has been shown to survive the stomach, and to break down gluten in the small intestine. Latiglutenase, formerly known as ALV003, is an enzyme therapy designed to be taken with meals. GluteGuard has been shown to significantly protect celiac patients from the serious symptoms they would normally experience after gluten ingestion. There are other enzymes, including those based on papaya enzymes.

    Additionally, there are many celiac disease drugs, enzymes, and therapies in various stages of development by pharmaceutical companies, including at least one vaccine that has received financial backing. At some point in the not too distant future there will likely be new treatments available for those who seek an alternative to a lifelong gluten-free diet. 

    For now though, there are no products on the market that can take the place of a gluten-free diet. Any enzyme or other treatment for celiac disease is intended to be used in conjunction with a gluten-free diet, not as a replacement.

    ASSOCIATED DISEASES
    The most common disorders associated with celiac disease are thyroid disease and Type 1 Diabetes, however, celiac disease is associated with many other conditions, including but not limited to the following autoimmune conditions:
    Type 1 Diabetes Mellitus: 2.4-16.4% Multiple Sclerosis (MS): 11% Hashimoto’s thyroiditis: 4-6% Autoimmune hepatitis: 6-15% Addison disease: 6% Arthritis: 1.5-7.5% Sjögren’s syndrome: 2-15% Idiopathic dilated cardiomyopathy: 5.7% IgA Nephropathy (Berger’s Disease): 3.6% Other celiac co-morditities include:
    Crohn’s Disease; Inflammatory Bowel Disease Chronic Pancreatitis Down Syndrome Irritable Bowel Syndrome (IBS) Lupus Multiple Sclerosis Primary Biliary Cirrhosis Primary Sclerosing Cholangitis Psoriasis Rheumatoid Arthritis Scleroderma Turner Syndrome Ulcerative Colitis; Inflammatory Bowel Disease Williams Syndrome Cancers:
    Non-Hodgkin lymphoma (intestinal and extra-intestinal, T- and B-cell types) Small intestinal adenocarcinoma Esophageal carcinoma Papillary thyroid cancer Melanoma CELIAC DISEASE REFERENCES:
    Celiac Disease Center, Columbia University
    Gluten Intolerance Group
    National Institutes of Health
    U.S. National Library of Medicine
    Mayo Clinic
    University of Chicago Celiac Disease Center

    Jefferson Adams
    Celiac.com 04/17/2018 - Could the holy grail of gluten-free food lie in special strains of wheat that lack “bad glutens” that trigger the celiac disease, but include the “good glutens” that make bread and other products chewy, spongey and delicious? Such products would include all of the good things about wheat, but none of the bad things that might trigger celiac disease.
    A team of researchers in Spain is creating strains of wheat that lack the “bad glutens” that trigger the autoimmune disorder celiac disease. The team, based at the Institute for Sustainable Agriculture in Cordoba, Spain, is making use of the new and highly effective CRISPR gene editing to eliminate the majority of the gliadins in wheat.
    Gliadins are the gluten proteins that trigger the majority of symptoms for people with celiac disease.
    As part of their efforts, the team has conducted a small study on 20 people with “gluten sensitivity.” That study showed that test subjects can tolerate bread made with this special wheat, says team member Francisco Barro. However, the team has yet to publish the results.
    Clearly, more comprehensive testing would be needed to determine if such a product is safely tolerated by people with celiac disease. Still, with these efforts, along with efforts to develop vaccines, enzymes, and other treatments making steady progress, we are living in exciting times for people with celiac disease.
    It is entirely conceivable that in the not-so-distant future we will see safe, viable treatments for celiac disease that do not require a strict gluten-free diet.
    Read more at Digitaltrends.com , and at Newscientist.com