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Celiac.com 07/01/2021 - We get a lot of questions from celiac community members wondering about various aspects of celiac disease. One question we see a lot is about how genetic makeup influences the odds of developing celiac disease. Specifically, what are the odds of developing celiac disease based on HLA-DQA/DQB genotypes? Here's a breakdown of the odds by genotype combination. The odds of developing celiac disease based on HLA-DQA/DQB genotypes is as follows: DQ2+DQ8 1:7 (14.3%) DQ2+DQ2 OR DQ2 Homozygous DQB1*02 1:10 (10%) DQ8+DQ8 1:12 (8.42%) DQ8+DQ8*02 1:24 (4.2%) Homozygous DQB1*02 1:26 (3.8%) DQ2 only 1:35 (2.9%) DQ8 only 1:89 (1.1%) General Population - Genotypes unknown 1:100 (1%) ½ DQ2*DQB1*02 1:210 (0.5%) ½ DQ2*DQA1*05 1:842 (0.05%) No HLA-DQA/DQB susceptible alleles 1:2518 (0.04%) Testing for celiac disease should be done using FDA-approved HLA test kits. HLA-DQA/DQB genotyping typically provides detection of DQ2 (DQA1*0501, DQA1*0505, and DQB1*0201/*0202) and DQ8 (DQB1*0302) For example: HLA-DQ2(DQA1*05/DQB1*02) Positive or Negative HLA-DQ8(DQA1*03/DQB1*0302) Positive or Negative A testing report typically includes DQ2, DQ8, half DQ2, homozygosity for DQB1*02, and complete DQA and DQB genotypes, along with an easy-to-interpret risk assessment. -
Hi, My HLA DQ2 and DQ8 say no 97% certainty no Celiac. IgA level is high. Yet, the only thing that makes sense for myself, my grandparents, mother, and my children is Celiac based on our symptoms. Anybody else in this boat? Thank you. MDavis -
Celiac.com 06/20/2022 - Doctors currently recommend that first-degree relatives of those with celiac disease also get screened for the disease, but it's been unclear how often doctors should screen, or at what age. A team of researchers recently set out to detect variables influencing the risk of celiac disease development so they can develop and validate clinical prediction models in order to provide individualized screening advice. The research team included Caroline R. Meijer; Renata Auricchio; Hein Putter; Gemma Castillejo; Paula Crespo; Judit Gyimesi; Corina Hartman; Sanja Kolacek; Sibylle Koletzko; Ilma Korponay-Szabo; Eva Martinez Ojinaga; Isabel Polanco; Carmen Ribes-Koninckx; Raanan Shamir; Hania Szajewska; Riccardo Troncone; Vincenzo Villanacci; Katharina Werkstetter; and M. Luisa Mearin. The team analyzed ten years of follow-up data from the PreventCD-birth cohort, which enrolled nearly a thousand genetically predisposed children with celiac-affected first-degree relatives. The researchers combined significant variables for celiac risk to establish a risk score, and performed landmark analyses at different ages to create prediction models using multivariable Cox proportional hazards regression analyses, backward elimination, and Harrell’s c-index for discrimination. They used data from the independent NeoCel cohort to validate their findings. Their results show that the children with celiac-affected first-degree relatives develop celiac disease early in life, and that the main risk factors are gender, age and HLA-DQ genetic markers, which are all important for sound screening advice. According to the researchers children with celiac-affected first-degree relatives should be screened early in life, which should also include HLA-DQ2/8–typing. Anyone genetically predisposed to celiac disease should get more personalized screening advice using the team's Prediction application. Read more in Gastroenterology-
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Celiac.com 11/01/2021 - Globally, there are major regional differences in rates and instances of celiac disease that cannot be explained by HLA genetics alone. To date, more than forty genetic sites outside of the HLA region have been connected with celiac disease. A team of researchers recently set out to investigate the roles of these non-HLA genes in the development of tissue transglutaminase autoantibodies (tTGA) and celiac disease using a large international prospective cohort study. The research team included Ashok Sharma, Xiang Liu, David Hadley, William Hagopian, Edwin Liu, Wei-Min Chen, Suna Onengut-Gumuscu, Ville Simell, Marian Rewers, Anette-G. Ziegler, Åke Lernmark, Olli Simell, Jorma Toppari, Jeffrey P. Krischer, Beena Akolkar, Stephen S. Rich, Daniel Agardh, Jin-Xiong She, and TEDDY Study Group. The team conducted specific HLA genotype screening on nearly 425,000 newborns from the US and European general populations, and first-degree relatives with type 1 diabetes. About 21,500 carried 1 of the 9 HLA genotypes tied to increased risk for type 1 diabetes and celiac disease. The team then followed nearly 8,700 of the children in a 15 year prospective follow-up study. They used the the Illumina ImmunoChip to conduct genotype analyses on just over 6,000 children, and used radio-ligand binding assays to measure tTGA in serum samples. They made diagnoses of celiac disease based on persistent detection of tTGA and biopsy analysis. They used Cox proportional hazards ratios to analyze the data. Their analyses of time to celiac disease showed 54 single-nucleotide polymorphisms (SNPs) in the TAGAP, IL18R1, RGS21, PLEK, and CCR9 genes that are connected with celiac disease. Outside of regions previously associated with celiac disease, the team found 10 SNPs in 8 regions that are potentially associated with celiac disease. The SNP rs117128341, near PKIA, and the SNP rs117139146,near PFKFB3 both reached the genome-wide association threshold in subjects from Sweden. The team's analyses of time to detection of tTGA showed twenty-nine SNPs in the CTLA4, LPP regions previously connected with celiac disease, along with six SNPs in five regions not previously connected with celiac disease. The data show that non-HLA genes are play a role in tTGA development, and demonstrate celiac disease development in five non-HLA regions previously associated with the disease, and eight regions not previously associated with celiac disease. Read more at PLoS One. 2016; 11(3): e0152476. The researchers in this study are variously affiliated with the Center for Biotechnology and Genomic Medicine, Georgia Regents University in Augusta, Georgia; the Pediatric Epidemiology Center, Department of Pediatrics, University of South Florida, Tampa, Florida; the Division of Population Health Sciences and Education, St George's University of London, London, United Kingdom; the Pacific Northwest Diabetes Research Institute, Seattle, WA, United States of America; the Digestive Health Institute, Children’s Hospital Colorado, University of Colorado Denver, Aurora, CO, United States of America; the Center for Public Health Genomics, University of Virginia, Charlottesville, VA, United States of America; the Department of Pediatrics, University of Turku, Turku, Finland; the Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora, CO, United States of America; the Institute of Diabetes Research, Helmholtz Zentrum München, and Klinikum rechts der Isar, Technische Universität München, and Forschergruppe Diabetes e.V., Munich-Neuherberg, Germany; the Department of Clinical Sciences, Lund University/CRC, Malmö, Sweden; the National Institutes of Diabetes and Digestive and Kidney Disorders, National Institutes of Health, Bethesda, MD, United States of America; the Diabetes and Celiac Disease Unit, Lund University, Malmo, Sweden; the National Taiwan University, TAIWAN -
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Celiac.com 10/18/2021 - Researchers and clinicians have promoted family screening as a way to reduce the significant under-diagnosis of celiac disease. However, good data for calculating the exact risk of the disease in relatives, and the effects of individual patient- and relative-related factors, remains scarce. A team of researchers recently set out to investigate the individual risk of celiac disease among relatives of celiac patients. The research team included Saana Paavola, Katri Lindfors, Laura Kivelä, Juliana Cerqueira, Heini Huhtala, Päivi Saavalainen, Riku Tauschi, Katri Kaukinen, and Kalle Kurppa. They are variously affiliated with the Faculty of Medicine and Health Technology at the University of Tampere and Tampere University Hospital in Tampere, Finland; the Faculty of Social Sciences at the University of Tampere in Tampere, Finland; the Translational Immunology Research Program, and Department of Medical and Clinical Genetics, University of Helsinki, Helsinki, Finland; and the University Consortium of Seinäjoki, Seinäjoki, Finland. The team assessed nearly three-thousand relatives of 624 index patients for evidence of prior celiac disease, or else screened for the disease. For each subject, the team was able to determine the celiac-associated human leucocyte antigen (HLA) genotype. They then used logistic regression to assess the connection between individual factors and new screening positivity. They found 229 previously diagnosed non-index relatives with celiac disease and 2,714 non-affected (2,067 first-degree, 647 more distant) relatives. Of these 2,714 relatives, 129 (nearly 5%) screened positive, with 5.1% of first-degree, 3.6% of second-degree, and 3.5% of more distant relatives. The combined rate of the previously diagnosed and now detected cases in relatives was just over 12%, and was evenly divided at about 6% for both clinically detected and screen-detected. Univariate analysis showed the main risk factors associated with screening positivity to be: under age 18 years at diagnosis, age 41–60 years, being a sibling, and having the high-risk genotype (3.22, 2.01–5.15 DQ2.5/2.5 or DQ2.5/2.2 vs other risk alleles) in relatives. Multivariable analysis showed that only high-risk HLA remained significant. From this study, the team concludes that unrecognized celiac disease is common for at-risk relatives, and also in relatives beyond first-degree, even where active case-finding prevails. By far, the most important predictor for screening positivity was the presence of the high-risk HLA genotype: 3.22, 2.01–5.15 DQ2.5/2.5 or DQ2.5/2.2. Read more in Aliment Pharmacol Ther. 2021;54(6):805-813. -
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Celiac.com 05/06/2021 - Gluten neuropathy is the term used to describe peripheral neuropathy that occurs in patients with gluten sensitivity or celiac disease in the absence of other risk factors. A team of researchers recently set out to describe the neurophysiological progression rate of gluten neuropathy across time and look into the potential role of genetic susceptibility in its development. The research team included Panagiotis Zis, Ptolemaios Sarrigiannis, Artemios Artemiadis, David S. Sanders & Marios Hadjivassiliou. They are variously affiliated with the Academic Directorate of Neurosciences, and the Academic Unit of Gastroenterology at Sheffield Teaching Hospitals NHS Foundation Trust in Sheffield, UK, and with the Medical School, University of Cyprus in Nicosia, Cyprus. The team looked at a group of 45 patients with gluten neuropathy for an average follow-up period of 8 ± 5 years. They gathered clinical and neurophysiological data, along with HLA-DQ genotype information. Average patient age at diagnosis was 60 ± 12 years. More than 75% of patients had a length-dependent neuropathy, while the rest had sensory ganglionopathy. Sixty percent of patients with positive DQA1*02 suffered from sensory ganglionopathy compared to just under 14% of DQA1*02-negative patients. The team also noted a statistically significant detail regarding the DQB1*06 allele and the DQA1*01/DQB1*06 haplotype, which were found more frequently in patients with gluten neuropathy than in healthy control subjects. The team found a linear effect of time on the neurophysiological findings, with radial sensory nerve action potential decreasing nearly 2% annually, sural sensory nerve action potential decreasing 3%, and tibial nerve motor compound action potential decreasing 6.5%, independently of age or gender. Gluten neuropathy is a late manifestation of gluten sensitivity and celiac disease. The majority of patients with gluten neuropathy suffer from length-dependent neuropathy with a linear deterioration over time. To help spot patients at risk for developing sensory ganglionopathy, the team recommends HLA genotyping for patients with gluten sensitivity or celiac disease who present with neuropathic symptoms. Read the full report in the Journal of Neurology volume 268, pages199–205(2021) -
Celiac.com 10/23/2019 - Autoimmune therapy company ImmunoMolecular Therapeutics (IM Therapeutics) has received $10 million in Series A financing to support its new HLA-targeted treatment approach to autoimmune diseases, and to develop its lead HLA-targeted drug candidate for type 1 diabetes. Founded by physician scientists at the University of Colorado's Barbara Davis Center for Diabetes, IM Therapeutic creates personalized therapies for autoimmune diseases. The company's research has shown that blocking certain high risk human leukocyte antigen (HLA) genes also blocks the subsequent autoimmune response, which offers a possible way to prevent autoimmune triggering in a number of autoimmune diseases. Based on that research, the company is creating personalized therapies against HLA targets in various autoimmune diseases, including type 1 diabetes and celiac disease. The company has clinically proven that treating patients based on HLA-DQ8 status can reduce the autoimmune response in type 1 diabetes. With a technology platform that integrates computational chemistry, bioassays, and rational drug design, IM Therapeutics is developing a series of HLA targets for a number of autoimmune diseases. IM Therapeutics' personalized therapy approach to treating autoimmune disorders has proven effective in a Phase 1b human study of recently diagnosed type 1 diabetes patients who were positive for the HLA DQ8 variant. The Company is moving forward on its lead oral drug, IMT-002, through IND development for type 1 diabetes, and expanding its therapeutic HLA blocking treatments to other targets of autoimmune disorders, including celiac disease. IM Therapeutics’ HLA is currently focused on HLA-DQ8 and DQ2 gene variants, which are known to greatly increase individual risk to both type 1 diabetes and celiac disease. HLA-DQ8 is present in three out of five type 1 diabetes patients, and in one out of ten celiac disease patients. However, about 90% of celiac patients have DQ2, and nearly 100% of celiac patients have DQ2 and/or DQ8. “Our value has been clear since day one – getting to the root cause of autoimmunity with a targeted therapy approach and making an impact on diseases such as type 1 diabetes,” said Nandan Padukone, Ph.D., CEO of IM Therapeutics. Read more at Businesswire.com -
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Celiac.com 07/29/2019 - Gluten and related prolamines trigger celiac disease in people who are genetically susceptible. The role of HLA-DQ genotypes is not well understood. A team of researchers recently set out to investigate the influence of HLA-DQ genotypes in clinical, serological and histological features related to celiac disease. The research team included Eva Martínez-Ojinaga, Marta Fernández-Prieto, Manuel Molina, Isabel Polanco, Elena Urcelay and Concepción Núñez. They are variously affiliated with the Servicio de Gastroenterología y Nutrición Pediátrica, Hospital Universitario La Paz in Madrid, Spain; and the Laboratorio de investigación en Genética de enfermedades complejas, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC) in Madrid, Spain. The researchers conducted a retrospective observational study that included 463 Spanish patients with biopsy-proven celiac disease. The team collected clinical, serological, histological and HLA-DQ genetic data from each patient. They considered each patient's family history of celiac disease. They analyzed the data using chi-square tests or the Fisher’s exact test, along with multivariate logistic regression (after adjusting for age and sex) to assess the association between clinical and laboratory parameters with HLA-DQ. The team's sample group was 62% females, with 86% showing classical clinical celiac presentation, and 99% showing positive anti-transglutaminase 2/endomysium antibodies. Patients averaged about 30 months old at disease onset. This study puts the rate of celiac disease in first-degree relatives at about five percent of total patients, while HLA-DQ genetics showed increased homozygosity of HLA-DQ2.5 and HLA-DQ8. In the non-celiac disease family history group, an association between delayed disease onset and HLA-DQ8 carriage was observed (p < 0.001), besides an influence of HLA-DQB1*02 gene dosage on clinical presentation and severity of histological damage (after adjusting for age and sex, p = 0.05 and p = 0.02, respectively) and a trend towards presence of specific antibodies (p = 0.09). Due to the small sample size, these associations could not be properly assessed in the group of patients with affected first-degree relatives. For people with celiac disease, HLA-DQ genotypic frequency varies depending on the close family history of the disease. For people who do not have first-degree relatives with celiac disease, carrying the HLA-DQ2.5 gene with double dose of HLA-DQB1*02 seems correspond to classical clinical celiac presentation and more severe gut damage. Clearly more study is needed to get a better picture of the connections between HLA-DQ genotypes and particular manifestations of celiac disease. However, this study offers one more piece of the celiac disease and genetics puzzle. Stay tuned as more information becomes available. Read more in BMC Gastroenterology 201919:91 -
Celiac.com 03/07/2019 - Researchers don’t have much good data on the distribution of the related alleles in the type 1 diabetes Iranian population. In an effort to generate better data, a team of researchers recently set out to assess the frequency of HLA DQ2 and DQ8 haplotypes in patients with type 1 diabetes, with and without celiac disease, and to compare them to the healthy population. The research team included Ali Moheb-Alian, Flora Forouzesh, Amir Sadeghia, Kamran Rostami, Elham Aghamohammadi, Mohammad Rostami-Nejad, Mostafa Rezaei-Tavirani, and Mohammad Reza Zali. The team looked at 70 type 1 diabetes patients who did not have celiac disease, 60 type 1 diabetes cases with celiac disease, and compared them with 150 healthy individuals. They collected ten milliliter Gheparinized blood samples, extracted genomic DNA, and genotyped alleles in Real-time PCR using SYBR Green as a low-resolution method. They found HLA-DQ2 genotypes in 51% of type 1 diabetes patients without celiac disease, and HLA-DQ8 in 23% of such patients. Just over twenty percent of those patients carried both alleles, while 5% carried neither allele. More than 70% of type 1 diabetes patients with celiac disease had DQ2, while nearly 12% carried DQ8. Compared to diabetes patients without celiac disease and the control group, 14% carry both alleles, and 3% carrying neither allele. The frequencies of DQ2 and DQ8 alleles in Iranian healthy population were 19 and 5% respectively. The similarities in genetic background for celiac disease and type 1 diabetes show that HLA-typing can be serve as a helpful tool for spotting celiac disease in people with type one diabetes. Read more in the Journal of Diabetes and its Complicationshttps://doi.org/10.1016/j.jdiacomp.2018.10.001 The researchers are variously affiliated with the Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran; the Department of Genetics, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran; the Department of Gastroenterology MidCentral District Health Board, Palmerston North Hospital, New Zealand; the Basic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran; and the Proteomics Research Center, Faculty of Paramedical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. -
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I was wondering if anyone is familiar with genetic test results. I was tested through Prometheus over a year ago due to many celiac symptoms. My test came back positive DQ2.2 and DQ2.5, putting me in their "very high" risk category. Because of these results, my doctor also ordered a genetics screening for my daughter, 10 at the time. Her results ended up being processed through Quest instead and had a very different type of report. It showed the following: HLA-DQ2 Negative HLA-DQ8 Negative HLA-DQA1* 02 HLA-DQA1* 02 HLA-DQB1* 0202 HLA-DQB1* 0202 According to the notations on the test results, she "did not have the HLA-DQ variants associated with celiac disease." I left it at that thinking she could not develop celiac. Fast forward a year and she began developing symptoms - stomach aches that became more and more frequent and reflux after meals with throat clearing and coughing. I looked at these results again, and this is when I noticed the variations that showed positive. I wish I understood genetics more, but I did some research and discovered that these haplotypes form the DQ2.2 gene. Is this correct? If so, I've read studies indicating that being homozygous for DQ2.2 puts you at a moderate risk for celiac - not "no risk." I've also ran her raw DNA through several sites which show she carries genes that put her at risk for celiac. I'm trying to piece all of this together. Am I missing something here? It should be noted that I've since had to go gluten-free, and my husband later did. We've both had dramatic health improvements since. We are seeing her functional MD for this, and also have an appointment with a pediatric GI. Her one doctor reordered tests for both genetics and antibodies and told me I could go through Prometheus with it. It's my understanding that Prometheus offers a more comprehensive genetics screening. -
Beginning a few months ago, I thought I was just gluten intolerant. Then I started to really question what was wrong with me. Since I was a baby, I had intolerance to dairy. They would make us drink milk at school, and they (the government, basically) told us it was essential to our health. Yet, I was always in the health room after lunch in pain. Everyone thought I was faking it because I didn't like being at school. It wasn't until I entered high school that I diagnosed myself as lactose intolerant. I never had those stomach aches, gas, etc. again as long as I didn't consume dairy. Since I was 20, I lost a lot of weight. My BMI is 19.0, but it was 18.2 when it first happened. To maintain my weight, I don't exercise, and I overeat. This is not how things are supposed to be! I miss working out! I don't like worrying about eating when I don't want to. I'm pale, I'm cold, I can't sleep because I get a pins-and-needles feeling all over my body, sometimes I'll lose feeling in a toe, I've been told I look unhealthy, or like a ghost, I have no energy anymore, my anxiety, anger, and other mood issues are through the roof. I developed borderline personality disorder (ironically, probably, and partially stems from the emotional neglect of my parents about my physical and mental health for all those years. Saying it's all in my head, etc. I actually cried 3 times today, first time in months. My mom doesn't believe anythings wrong with me. I stayed up all night interpreting my DNA results to try getting her to believe me. We've been fighting all day. She always tries to minimize my problems and calls me a bypochondriac). My hair is becoming finer and possibly even thinning. I was diagnosed with ADD, bipolar, and psychosis. At about 17, I developed acid reflux - lots of throat-related issues like clearing it a lot, and post-nasal drop. All of this happened at the same time, basically. About 1 year ago. I had a genetic test done. There are two haplogroups related to celiac, I have the HLA DQA1 version (the most common). There are 13 (I believe) SNPs related to celiac disease. I have 12. My cousin had a similar issue and did NRT. And she's never felt better. They didn't give her diagnoses but told her to watch her dairy intake. What are your thoughts? Is it safe to assume I have the disease? I want to be myself again, but I don't know how to do that unless I know what's causing the problem. And please please please don't tell me to see a doctor, because some of us can't afford it, nor can we afford putting another medical issue on our profile. Thank you! -
I was wondering if anyone has ancestors from the present-day region of Alsace, France, or near there, who had celiac disease on that side of the family? This condition and related ones (diabetes) are common in my family on this side. I have traced it up the family tree and am wondering for research purposes.
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I am in Pittsburgh and have been to multiple doctors for stomach issues. I had an endoscopy that showed "villous atrophy indicative of celiac sprue". I had IgG and IgA testing- both came back negative. I had genetic testing and the doctor says it is also negative, but the results say I am positive for: DQB1*03 DQB1*06 DQA1*01 DQA1*03 I have googled and googled with no luck. I guess I have a few questions. Can everything be negative and I still have Celiac disease? Or what else could cause the damage to my intestines? Does anyone know enough about genetics to interpret these positives? I know I shouldn't be seeking medical advice on a forum, but my doctors have been useless. Any advice is appreciated. Should I keep up the hunt for a doctor or is this a true negative? Thanks!
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Can you help me understand these results? Question 1: Do I have Celiac? Question 2: If not, what are chances of developing in future? Question 3: Should I have another test performed? Piotr --------------------------------------------------------------------------------------------------------------------------------------------------- HLA-DQ2 -- Positive HLA-DQ8 -- Negative HLA-DQA1* -- 01 HLA-DQA1* -- 05 HLA-DQB1* -- 0201 HLA-DQB1* -- 0502 TISSUE TRANSGLUTAM AB IGA -- 1 (Range: No Antibody Detected <4) IMMUNOGLOBULIN A -- 193 (Range: 81-463 mg/dL) Also, I have low vitamins deficiencies of B12 and D3 -
I would like some help in understanding my results from the 23andme test. I am being told that I have 2 copies of a genetic variant that was tested. The variants were detected in the HLA-DQA1 gene. "We detected two copies of a variant linked to the HLA-DQ2.5 haplotype." Do do these results mean? In the HLA-DQ2.5 - HLA-DQa1 - rs2187668 - there are two TT. Is this bad? Is this what is mean by having homozygous hla dqa2.5? I am new to all of this and am just looking for some answers. I am concerned about being at risk for celiac disease. Thanks!
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Celiac.com 03/16/2017 - When screening arthritis patients for celiac disease, should HLA be done before serology? During the past decades, an accumulating evidence shows a dramatic rise in the frequency of autoimmune diseases, including rheumatoid arthritis and gastrointestinal conditions, such as celiac disease. HLA genes have been shown to be strongly associated with numerous autoimmune diseases, including rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA) and celiac disease. A team of researchers recently set out to assess the performance of celiac disease associated serology in face of a rheumatologic patient, when gluten enteropaty is suspected. The research team included Hakim Rahmoune, Nada Boutrid, Mounira Amrane, and Belkacem Bioud. They are variously affiliated with the Pediatrics Department and the Biochemistry Department of Setif University Hospital at Setif-1 University in Algeria. The main question they sought to answer was: Should HLA be done prior to the serology? Could unnecessary serial serological celiac disease screening in such rheumatology patient be avoided by performing an HLA typing, as a long-life marker of genetically celiac disease-susceptible patients? Serogenetic screening without the requirement for follow-up small bowel biopsies provides a flexible, cost-effective methodology that could be widely applied to obtain accurate estimates of the prevalence of celiac disease in large group studies. Source: International Journal of Celiac Disease, 2017, Vol. 5, No. 1, xx. DOI:10.12691/ijceliac disease-5-1-2
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