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Celiac.com 08/23/2023 - Distal gastrectomy has been a common treatment for peptic ulcers and gastroesophageal reflux disease. However, questions have arisen about its impact on gastric mucosa. A team of researchers recently looked into the connection between distal gastrectomy and Helicobacter pylori infection, as well as celiac disease. The research team included Kubilay Issever, Ersin Kuloglu, Demet Sengul, Ali Muhtaroglu, and Ahmet Cumhur Dulger. They are variously affiliated with the departments of Internal Medicine, Pathology, and General Surgery at Giresun University Medical Faculty in Giresun, Turkey. Observational Retrospective Study Focused on Two Groups of Dyspepsia Patients Conducted at Giresun University Faculty of Medicine, the observational retrospective study focused on two groups of patients with dyspepsia. The first group, termed the antrectomy group, consisted of 35 individuals who had undergone distal gastrectomy for benign causes. The second, the control group, included 50 dyspepsia patients who had not undergone gastrectomy. Results showed that the antrectomy group had a higher proportion of older male patients. Lab parameters revealed significant differences: platelets, lymphocytes, and albumin levels were lower in the antrectomy group, while urea, creatinine, and antibodies like anti-Endomisium Ig A (anti-EMA) and anti-tissue transglutaminase IgA (anti-tTGA) were higher. Gastric biopsy results unveiled greater instances of Helicobacter pylori infection, tissue atrophy, neutrophil, and lymphocyte infiltration in the antrectomy group compared to the control group. Further analysis showed correlations of note. An inverse relationship was found between albumin levels and the presence of anti-EMA antibodies or tissue atrophy. Conversely, a positive correlation existed between anti-EMA antibody presence and both Helicobacter pylori infection and tissue atrophy. Distal Gastrectomy for Dyspepsia Patients More Likely to Have Helicobacter Pylori Infection and Celiac Disease The study's implications are significant. People who have undergone distal gastrectomy for dyspepsia may be more susceptible to complications tied to Helicobacter pylori infection and celiac disease. The potential for Helicobacter pylori infections to progress into malignancies raises concerns. As a result, routine screening and interventions to eliminate Helicobacter pylori infections are paramount to prevent malignant transformations in the remaining gastric tissue. This study underscores the potential risks stemming from distal gastrectomy, especially its association with Helicobacter pylori infection and celiac disease. This knowledge will help medical practitioners to better navigate post-gastrectomy care, more effectively manage potential complications, and better plan preventive measures. This study does not indicate whether the increased celiac disease risk was a result of the distal gastrectomy, or whether the patients who underwent a distal gastrectomy may have had undiagnosed celiac disease before this treatment. Logically the results of this study might indicate that routine screenings for celiac disease should be done before any distal gastrectomy surgery to rule it out. Read more at Cureus.com

Celiac.com 08/15/2022 - In a significant finding, a celiac disease registry at University of Alabama reveals significant issues in accurately testing Black people for celiac disease using the TTG antibody test. The new registry of celiac disease patients at the University of Alabama at Birmingham is the work gastroenterologist Dr. Amanda Cartee, MD, and fellow colleagues at UAB. Among the most important findings, the registry reveals that Black people with biopsy confirmed celiac disease are exponentially more likely than non-Hispanic whites to show negative results on the most common diagnostic celiac disease blood test. For people with celiac disease, a positive TTG antibody test is the most common path to an endoscopy and biopsy to confirm or negate celiac disease. For most people with celiac disease, especially non-Hispanic whites, a positive TTG test is highly predictive of celiac disease, hence the routine endoscopy and biopsy to follow-up a positive test. In fact, less than ten percent of non-Hispanic whites with biopsy-proven celiac disease have a "negative" TTG test. However, according to the registry data, high percentages of Black people with celiac disease are testing negative for TTG antibodies, and so being denied a swift and properly diagnosis, simply because they never meet themes common threshold for biopsy. It's the TTG threshold currently used to determine the definition of positive and negative TTG that might just be at the heart of the problem. That's because the numbers are nearly reversed for Black people. While less than ten percent of non-Hispanic whites with celiac disease show negative TTG results, the registry data shows that a whopping eighty percent of Black people with biopsy-proven celiac disease have a "negative" TTG test. The means that these folks were unlikely to have gotten a biopsy as quickly as someone with a positive TTG test. It also means they may have had to suffer longer, and/or self diagnose. And those facts are also borne out by the registry data, which point to longer times to diagnosis and less biopsy-driven diagnoses for Black celiac patients. Black patients were also much less likely to have received genetic testing for celiac-associated genes. There is limited data on celiac disease and Black people, said Dr. Cartee, noting that only a single study with the primary goal of investigating the clinical characteristics of celiac disease and Black people has been done. While the registry revealed differences in TTG test results and BMI, it showed similarities in celiac disease diagnosis for non-Hispanic white and Black patients. These included symptoms as the primary cause for testing, length of time to diagnosis, and a diagnosis that did not include recommended blood tests and a biopsy. Basically, the data show that TTG tests will be negative in the vast majority of Black patients with biopsy-proven celiac disease. That means further study is needed to determine whether the TTG test is useful for Black patients, and more research needs to be done to figure out how to make sure they can get quickly and properly diagnosed. Stat tuned for more on this and related stories regarding celiac disease testing, screening, and diagnosis in Black people, and in other ethnic populations. Read more about the celiac registry data and findings presented by UAB gastroenterologist Dr. Amanda Cartee, MD, at Digestive Disease Week.

Celiac.com 11/26/2021 - Celiac disease has a prevalence of 1/100. Between 90-99% of celiacs are HLA DQ2 and/or DQ8 positive. Every individual has two DQ serotypes. Because the molecular HLA nomenclature can be confusing DQ serotyping is a method for simplifying the results. There are four major types and 5 subtypes: HLA DQ1, DQ2, DQ3 and DQ4; DQ1 has two subtypes; DQ5 and DQ6 whereas DQ3 has three subtypes; DQ7, DQ8 and DQ9. Each individual has two copies of HLA DQ. One DQ type is inherited from each parent. Though 35-45% of individuals of Northern European ancestry are DQ2 and/or DQ8 positive only 1% has classic celiac disease as defined by abnormal blood tests and small intestinal biopsies. Several autoimmune conditions also occur more frequently in DQ2 and DQ8 positive individuals. There is accumulating scientific evidence that many individuals are gluten sensitive and respond to a gluten free diet though they have normal blood tests and/or normal intestinal biopsies (fail to meet strict criteria for celiac disease). This is commonly being referred to as non-Celiac gluten sensitivity (NCGS). Many individuals who have NCGS are relatives of confirmed celiacs and were previously referred to as latent celiacs. Electron microscopy and immunohistochemistry studies of individuals with normal biopsies but suspected of or at risk (1st degree relatives of celiacs) have revealed ultrastructural abnormalities of the intestine and those who chose a gluten free diet usually responded and many who did not ultimately developed abnormal biopsies on long term follow-up. Seronegative celiac has also been recognized. That is, blood tests are negative, but the biopsy reveals classic abnormalities of celiac and the individual responds to a gluten free diet. Fecal antibody testing for gliadin (AG) and tissue transglutaminase (tTG) by Enterolab in Dallas has revealed elevations in 100% of celiacs tested and up to 60% of symptomatic individuals without Celiac disease (NCGS) even if not DQ2 or DQ8 positive. (Fine, K unpublished data). The only DQ pattern he found not associated with gluten sensitivity is DQ4/DQ4, a pattern typically found in non-Caucasians who are known to have a low prevalence of Celiac disease. Testing for DQ2/DQ8 has been suggested as a way to exclude celiac disease. That is, if you are negative for DQ2 and DQ8, then you are very unlikely to have celiac disease. However, well documented cases of celiac disease and Dermatitis Herpetiformis (DH) have been confirmed in DQ2 and DQ8 negative individuals. Moreover, we now have the clinical experience that other DQ patterns predispose to gluten sensitivity because these individuals frequently have elevated fecal antibodies to AG or tTG and respond to a gluten free diet. Why some people develop celiac disease or become sensitive to gluten is not well understood. Risk factors include onset of puberty, pregnancy, stress, trauma or injury, surgery, viral or bacterial infections including those of the gut, medication-induced gut injury or toxicity (e.g. NSAIDs), immune suppression or autoimmune diseases, and antibiotic use resulting in altered gut flora (dysbiosis). The severity of the sensitivity is related to the DQ type, pre-existing intestinal injury, degree of exposure to gluten (how frequent and large a gluten load an individual is exposed to), and immune status. Once initiated, gluten sensitivity tends to be life-long. True celiac disease requires life-long, complete gluten avoidance to prevent serious complications, cancers, and early death. Serotypes can be determined from blood or buccal mucosal cells obtained by oral swab from several commercial labs including Prometheus, Labcorp, Quest, The Laboratories at Bonfils, and Enterolabs. Fecal IgA anti-gliadin and IgA tissue transglutaminase antibody testing is only available commercially in the U.S. through Enterolabs. The fecal AG and tTG testing may be helpful to those with normal blood tests for celiac and/or a normal small bowel biopsy but suspected of being gluten sensitive. Though the fecal antibody results are not widely accepted by many “celiac experts” numerous testimonials of individuals testing positive only on fecal tests who have responded to a gluten free diet can be found in support groups, web postings, personal communication from Dr. Fine, and this physician’s clinical experience. References: Abrams et.al. Seronegative celiac disease:increased prevalence with lesser degrees of villous atrophy. Dig Dis Sci 2004;49:546-550. Alaedini A. and Green P.H.R. Narrative Review: Celiac Disease: Understanding a Complex Autoimmune Disorder. Ann Intern Med. 2005;142:289-298. Arranz et. al. Jejunal fluid antibodies and mucosal gamma/delta IEL in latent and potential coeliac disease. Adv Exp Med Biol. 1995; 371B:1345-1348. Dewar D. and Ciclitira P. Clinical Features and Diagnosis of Celiac Disease. Gastroenterology 2005;128:S19. Kappler et.al. Detection of secretory IgA antibodies against gliadin and human tissue transglutaminase in stool to screen for coeliac disease in children:validation study. BMJ 2006; 332:213-214. Kaukinen et.al. HLA-DQ Typing in the Diagnosis of Celiac Disease. Am J Gastroenterol. 2002;97(3):695-699. Fine KD and Rostami K. Don’t throw the baby out with the bath water. BMJ February 13, 2006 rapid response editorial. Fine K. Early diagnosis of gluten sensitivity before the villi are gone. Transcript of presentation to Greater Louisville Celiac Support Group, June 2003. Picarelli et.al. Antiendomysial antibody detection in fecal supernatants: in vivo proof that small bowel mucosa is the site of antiendomysial antibody production. Am J Gastroenterol. 2002 Jan;97(1):95-98. Sbartati A. et.al. Gluten sensitivity and “normal” histology: is the intestinal mucosa really normal? Dig Liver Dis 2003;35:768-773. Sollid L. and Lie B. Celiac Disease Genetics:Current Concepts and Practical Applications. Clinical Gastroenterology and Hepatology 2005;3:843-851. WGO-OMGE Practice Guideline Celiac Disease. World Gastroenterology News. 2005;10(2):supplement 1-8.

Celiac.com 10/19/2021 - There is some data to indicate a connection between celiac disease and IgA nephropathy (IgAN). In celiac disease IgA-class tissue transglutaminase (tTG) autoantibodies are seen in the small bowel mucosa and extraintestinal organs, in addition to circulating in serum. A team of researchers recently studied whether celiac disease-type IgA-tTG deposits occur in kidney biopsies in a case series of IgAN patients with or without celiac disease. The research team included Rakel Nurmi, Ilma Korponay-Szabó, Kaija Laurila, Heini Huhtala, Onni Niemelä, Jukka Mustonen, Satu Mäkelä, Katri Kaukinen, and Katri Lindfors. They are variously affiliated with the Celiac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University in Tampere, Finland; the Celiac Disease Center, Heim Pál National Pediatric Institute in Budapest, Hungary; the Department of Pediatrics, Faculty of Medicine and Clinical Center, University of Debrecen in Debrecen, Hungary; the Faculty of Social Sciences, Tampere University in Tampere, Finland; the Medical Research Unit, Seinäjoki Central Hospital in Seinäjoki, Finland; and the Department of Internal Medicine, Tampere University Hospital in Tampere, Finland The team looked at nine IgAN patients, four of whom had celiac disease. The team measured serum tTG autoantibodies at the time of the diagnostic kidney biopsy, and looked at colocalization of IgA and tTG in the frozen kidney biopsies. The results showed IgA-tTG deposits in the kidneys of three IgAN patients with celiac disease though two patients had been diagnosed with celiac disease years later. They fund no deposits in a known celiac disease patient who was following a gluten-free diet. Of the five non-celiac IgAN patients, three showed IgA-tTG deposits in their kidneys. From their small study, the team concludes that tTG-targeted IgA deposits can be found in the kidney biopsies of gluten-consuming IgAN patients, but they likely won't be much help in spotting celiac disease, due to limited specificity. Read more in Nutrients

Celiac.com 09/06/2021 - Antibodies specific for peptides bound to human leukocyte antigen (HLA) molecules are valuable tools for studies of antigen presentation, and may have therapeutic potential. Human T cell receptor (TCR)–like antibodies that block immunodominant epitope recognition have potential as personalized medicine treatments for blunting gluten-activated T cell responses without compromising effector functions provided by other T cells. A team of researchers recently set out to generate human T cell receptor (TCR)–like antibodies toward the immunodominant signature gluten epitope DQ2.5-glia-α2 in celiac disease (CeD). Consuming gluten in food triggers the gastrointestinal symptoms of celiac disease in patients with CD4+ T cells specific for deamidated gluten peptides presented by disease-associated HLA-DQ class II MHC molecules. Frick and colleagues used phage display technology to look for TCR-like antibodies specific for an immunodominant gluten peptide bound by HLA-DQ2.5. By using phage display selection combined with secondary targeted engineering, the team was able to obtain highly specific antibodies with picomolar affinity. The team's antibody engineering improved affinity and binding stability, producing a superior TCR-like antibody that structurally mimicked the TCR interface with gluten peptide–MHC complexes. These TCR-like antibodies prevented triggering and expansion of gluten-responsive human CD4+ T cells both in vitro and in DQ2.5 transgenic mice. The binding geometry and interaction mode of the crystal structure of a Fab fragment of the lead antibody 3.C11 in complex with HLA-DQ2.5:DQ2.5-glia-α2 were very similar to prototypic TCRs specific for the same complex. Evaluation of celiac biopsy material confirmed celiac specificity and supports the idea that plentiful plasma cells present antigen in the inflamed gut of a celiac patient. Moreover, 3.C11 specifically blocked activation and proliferation of gluten-specific CD4+ T cells in vitro and in HLA-DQ2.5 humanized mice, suggesting that celiac disease mechanisms can potentially be blocked without weakening patient immunity. Read more in Science Immunology The research team included Rahel Frick, Lene S. Høydahl, Jan Petersen, M. Fleur du Pré, Shraddha Kumari, Grete Berntsen, Alisa E. Dewan, Jeliazko R. Jeliazkov, Kristin S. Gunnarsen, Terje Frigstad, Erik S. Vik, Carmen Llerena, Knut E.A. Lundin, Sheraz Yaqub, Jørgen Jahnsen, Jeffrey J. Gray, Jamie Rossjohn, Ludvig M. Sollid, Inger Sandlie and Geir Åge Løset. They are variously affiliated with the Centre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital-Rikshospitalet, Oslo, Norway; the Centre for Immune Regulation and Department of Biosciences, University of Oslo, Oslo, Norway; the KG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway; the Infection and Immunity Program, Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia; the Australian Research Council Centre of Excellence for Advanced Molecular Imaging, Monash University, Clayton, Victoria, Australia; Nextera AS, Oslo, Norway; the Program in Molecular Biophysics, Johns Hopkins University, Baltimore, MD, USA; the Department of Gastroenterology, Oslo University Hospital-Rikshospitalet, Oslo, Norway; the Department of Gastrointestinal Surgery, Oslo University Hospital-Rikshospitalet, Oslo, Norway; the Institute of Clinical Medicine, University of Oslo, Oslo, Norway; the Department of Gastroenterology, Akershus University Hospital, Lørenskog, Norway; the Department of Chemical and Biomolecular Engineering and Institute of NanoBioTechnology, Johns Hopkins University, Baltimore, MD, USA; the Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD, USA; and the Institute of Infection and Immunity, Cardiff University School of Medicine, Heath Park, Cardiff, UK.

Celiac.com 09/14/2020 - Researchers understand that celiac disease is marked by robust B cell and antibody responses to gluten, and to the transglutaminase 2 (TG2) autoantigen. In contrast, non-celiac gluten sensitivity (NCGS) is marked by the absence of the physical or testable features of celiac disease. Beyond that, researchers don't know much about NCGS. There are no established biomarkers yet for NCGS, but research shows a state of systemic immune activation together with a compromised intestinal epithelium. Researchers have been homing in on IgG antibody response to gluten as a means of distinguishing non-celiac gluten sensitivity (NCGS ) from celiac disease. A team of researchers recently set out to observed differences in the IgG subclass distribution and relationship with FABP2 release in NCGS versus celiac disease. The team's recent paper describes a contrast in the IgG subclass distribution and relationship with FABP2 release in NCGS versus celiac disease, which, they say, demonstrates differences in the evolution and disease relevance of B cell immune responses in each condition. Pathways involved in this process may make tempting targets for molecular therapy focused on disrupting or blocking the pathway. The team demonstrated that the anti-gluten IgG antibody in NCGS differs substantially from celiac disease in subclass distribution, and in terms of intestinal cell damage. The data suggests a sustained primary B cell response to gluten in celiac patients, despite the condition’s chronicity, and a more advanced and less intense immune response to gluten in NCGS. Based on their data, the team is calling for further study of the evolution of gluten-reactive B cell response and subclass switching in celiac disease and NCGS. In addition, they expect information on other aspects of B cell and antibody variability, including affinity, glycosylation profile, and epitope specificity, to improve the understanding of differences in the immune response to gluten, and its relationship with disease pathophysiology, in the two conditions. Coupled with markers described earlier, these aspects of immune response to gluten will likely offer more biomarkers that may help to clarify potential disease subsets with varying mechanisms, prognoses, and therapeutic efficacy. Researchers are making critical progress in distinguishing celiac disease from NCGS. Their efforts could drive breakthroughs in the diagnosis and treatment of both conditions, so their ongoing study is important. Read more in Gastroenterology The research team included Melanie Uhde, PhD, Giacomo Caio, MD, Roberto De Giorgio, MD, Peter H. Green, MD, Umberto Volta, MD, and Armin Alaedini, PhD. They are variously affiliated with the Department of Medicine, Columbia University Medical Center, New York, NY, USA; the Institute of Human Nutrition, Columbia University Medical Center, New York, NY, USA; the Celiac Disease Center, Columbia University Medical Center, New York, NY, USA; the Department of Medical Sciences, University of Ferrara, Arcispedale St. Anna, Ferrara, Italy; the Celiac Disease Center and Mucosal Immunology and Biology Research Center, Massachusetts General Hospital – Harvard Medical School, Boston, MA, USA; the Department of Medical and Surgical Sciences, University of Bologna, Italy; the Department of Medicine, New York Medical College, Valhalla, NY, USA.

Celiac.com 12/11/2019 - While celiac disease affects an estimated 1% of people worldwide, more than 90% of people with the disease remain undiagnosed. Current celiac disease protocols call for screening patients with gastrointestinal symptoms or other autoimmune diseases, along with any first-degree relatives of celiac patients. However, current screening usually involves a trip to the doctor's office for a blood test that measures levels of celiac-specific antibodies. That simple trip can be a barrier to screening, and thus to treatment and healing. Even in more developed countries, more than half of celiacs are unaware of their disease. Rapid diagnosis and treatment of celiac disease is important, because delayed diagnosis often means persistent symptoms even after treatment, along with impaired quality of life. One solution lies in point-of-care (POC) testing, which moves medical testing from central laboratories directly to the place where the patient is receiving care. To assist in rapid and reliable disease screening, researchers from the University of Helsinki have developed a novel diagnostic method coined RFS (Rapid FRET serodiagnostics) for the rapid on-site measurement of antibodies from patient samples. This technology could revolutionize blood screening for microbial, autoimmune and allergic disorders. That same team recently applied their new diagnostic method to celiac disease screening. Fast and Easy Detection of Celiac Antibodies The research team took blood samples from 35 children and 35 adults with celiac disease. They also took samples from healthy control subjects. They measured samples with the new test method, and compared results with two current methods. According to Juuso Rusanen, MD, "The performance of the test was comparable to that of current methods, [which] involves transporting the sample to a central laboratory and a multi-step procedure taking hours." The new method provides accurate results "in less than half an hour by simply combining the sample and a reagent mix, waiting for a while and reading the result." Rusanen says that the team hopes that the new method can "lower the threshold for screening of celiac disease and thus help overcome the vast under-diagnosis of this relatively common condition." This test marks the first time their method has been used for diagnosing an autoimmune disease. The promising results invite the development of similar diagnostic tests aimed at other autoimmune diseases, says Rusanen. Read more at Eurekalert.com

Celiac.com 03/06/2018 - A number of clinicians and researchers have suspected that antibodies against transglutaminase 6 (anti-TG6) play a role in neurological issues in adult patients with genetic gluten intolerance, but it is not known if autoimmunity to TG6 develops after long-term consumption of gluten. A team of researchers recently set out to establish a correlation between these autoantibodies and the duration of gluten exposure by measuring the anti-TG6 in children with celiac disease at diagnosis. The team then investigated a correlation between anti-TG6 and the presence of neurological disorders. The research team included L De Leo, D Aeschlimann, M Hadjivassiliou, P Aeschlimann, N Salce, S Vatta, F Ziberna, G Cozzi, S Martelossi, A Ventura, and T Not. They are variously affiliated with the Institute for Maternal and Child Health-IRCCS "Burlo Garofolo" Trieste, Trieste, Italy; Matrix Biology and Tissue Repair Research Unit, School of Dentistry, and Arthritis Research UK Biomechanics and Bioengineering Centre of Excellence, College of Biomedical and Life Sciences, Cardiff University, Cardiff; the Department of Neurology at the Royal Hallmshire Hospital, Sheffield, UK; and with the University of Trieste in Trieste, Italy. The team used ELISA to measure anti-TG6 (IgA/IgG) in children with biopsy-proven celiac disease and of children experiencing gastrointestinal disorders. Celiac disease patients who tested positive for anti-TG6 were retested after 2 years of gluten-free diet. In all, the team analyzed test results for 274 children with celiac disease, along with 121 control subjects. They found anti-TG6 in 68 out of 274 celiac disease patients and in 19/121 control subjects, though the differences between the two groups was significant. None of the celiac patients or the controls who tested positive for anti-TG6 suffered from neurological disorders. Eleven of 18 celiac disease patients with other autoimmune diseases tested positive for anti-TG6. Among the celiac disease patients, the team found a significant correlation between the gluten exposure before the celiac disease diagnosis and anti-TG6 concentration. The gluten-free diet substantially reduced the anti-TG6 concentrations. The team found no significant correlation between anti-TG6 and anti-TG2 serum concentrations. Anti-TG6 is much more common in children with untreated celiac disease , but with no apparent neurological disorders. The synthesis of the anti-TG6 is associated with longer exposure to gluten prior to celiac diagnosis, while the autoimmunity against TG6 is gluten dependent and disappears with a gluten-free diet. Source: J Pediatr Gastroenterol Nutr. 2018 Jan;66(1):64-68. doi: 10.1097/MPG.0000000000001642.

Celiac.com 06/06/2014 - Celiac disease guidelines suggest that some patients with high anti-tTG ab levels might be diagnosed without biopsy. A team of Indian researchers recently reviewed their celiac disease database to determine if anti-tissue transglutaminase (tTG) antibody (ab) titers correlate with severity of villous abnormalities in Indian patients, and to find out a cutoff value of anti-tTG ab fold-rise that might best predict celiac disease. The researchers included P. Singh, L. Kurray, A. Agnihotri, P. Das, A.K. Verma, V. Sreenivas, S. Datta Gupta, and G.K. Makharia. The are affiliated with the Departments of Gastroenterology and Human Nutrition, Pathology, and Biostatistics at the All India Institute of Medical Sciences in New Delhi, India. The team reviewed data on 366 anti-tTG ab-positive individuals who received duodenal biopsies. The team conducted anti-tTG ab screens before patients began a gluten-free diet, and they expressed anti-tTG ab results in terms of fold-rise by calculating ratio of observed values with cutoff value. Celiac disease was diagnosed only in patients with positive serology, villous atrophy greater than Marsh grade 2, and clear response to gluten-free diet. Average anti-tTG fold-rise in groups with Marsh grade ≤2 was 2.6 (±2.5), grade 3a was 4.0 (±3.9), 3b was 5.7 (±5.1), and 3c was 11.8 (±8.0). Overall positive likelihood ratio for diagnosing celiac disease was 15.4 and 27.4 at 12- and 14-fold-rise of anti-tTG ab titer, respectively. The positive predictive value of diagnosis of celiac disease was 100% when anti-tTG ab titer was 14-fold higher over the cutoff value. Fifty-seven (43.9%) patients with anti-tTG titer rise less than 2-fold also had celiac disease. Levels of anti-tTG rise directly with severity of villous abnormality. High anti-tTG ab titers indicate likely villous atrophy. Contrary to emerging wisdom, even patients with anti-tTG ab levels less than 2-times baseline should receive mucosal biopsies, because many patients with celiac disease have such low levels. Source: J Clin Gastroenterol. 2014 Feb 27.

Celiac.com 06/24/2010 - Scientists have previously seen a nuclear fluorescence reactivity (NFR) pattern on monkey esophagus in sections which were exposed to celiac disease patients that were sera positive for anti-endomysium antibodies (EMA). Because of this prior knowledge, scientists created a new study to illustrate the NFR, to study NFR positive results in connection with gluten withdrawal, and also to assess the possible role of NFR in celiac disease follow-up's. For twelve months, scientists closely evaluated twenty untreated celiac patients, eighty-seven treated celiac patients, and fifteen healthy control subjects. Scientists incubated the sera of all 122 patients on monkey esophagus sections. The goal was to evaluate the existence of NFR by indirect immunofluorescence analysis. To asses the rate of NFR in culture supernatants, duodenal mucosa samples from treated celiac patients were challenged with gliadin peptides. Scientists evaluated the reactivity of NFR immunoglobulins (Igs) response to the nuclear extract of human intestinal cells. What they found was that serum NFR was visible in all untreated celiac patients and it persisted for up to 151 +/-37 days from gluten withdrawal. It reappeared in treated celiac patents when they did not stick to their dietary restrictions. Serum NFR was also present in two of the healthy control subjects. NFR presented itself before EMA, in culture supernatants of celiac intestinal mucosa that was challenged with gliadin peptides. The Igs responsible for NFR were labeled as, “IgA2 Subclass”. The NFR had different results than the EMA and anti-nuclear antibodies, although they reacted with two nuclear antigens of 65 and 49 kDa. Thus, a new auto-antibody named NFR, which is related to celiac disease, was depicted. In conclusion, the studies of NFR have demonstrated that NFR detection has potential to be used as a beneficial tool in monitoring compliance of a gluten-free diet, as it has the ability to diagnose slight dietary shifts pertaining to gluten. Source: Clinical and Experimental Immunology