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Celiac.com 06/06/2024 - Microscopic colitis is a type of chronic inflammatory bowel disease characterized by persistent watery diarrhea, abdominal pain, cramps, bloating, weight loss, nausea, fecal incontinence, and dehydration. It comprises two distinct sub-types: collagenous colitis and lymphocytic colitis, both leading to non-bloody watery diarrhea. In contrast, celiac disease is an autoimmune disorder triggered by gluten consumption, resulting in damage to the small intestine. Despite their differences, recent studies have hinted at a potential association between microscopic colitis and celiac disease, necessitating further investigation. Utilizing National Inpatient Data for Analysis This study utilized the National Inpatient Sample (NIS) database spanning four years (2016–2019) to conduct a comprehensive analysis of the relationship between microscopic colitis and celiac disease. Through specified International Classification of Diseases, 10th Edition (ICD-10) codes, patients with and without microscopic colitis, along with the presence or absence of coexisting celiac disease, were identified. Statistical analyses, including univariate and multi-variate methods, were employed to assess the association while adjusting for various confounding factors. The study encompassed a vast dataset of over 26 million patients, providing robust insights into this intriguing link. Key Findings and Clinical Implications The analysis revealed a significant association between microscopic colitis and celiac disease, supported by both univariate and multi-variate analyses. Interestingly, celiac disease emerged as an independent risk factor for increased mortality among microscopic colitis patients, although it did not significantly impact the mean hospital stay. These findings underscore the need for heightened awareness and clinical vigilance in managing patients with coexisting microscopic colitis and celiac disease. Moreover, the study's large-scale approach and comprehensive analysis contribute valuable insights into the complex interplay between these gastrointestinal disorders, paving the way for more targeted treatments and improved patient outcomes. This study delved into the intriguing association between microscopic colitis and celiac disease using extensive population-based data from the National Inpatient Sample (NIS) database spanning four years (2016–2019). The investigation aimed to elucidate this relationship with robust statistical analyses while controlling for various confounding factors. Here's a detailed summary of the study's key aspects and findings: Exploring the Link Between Microscopic Colitis and Celiac Disease The study analyzed data from over 26 million patients, identifying those with and without microscopic colitis and assessing the presence or absence of coexisting celiac disease. Statistical analyses, including univariate and multi-variate methods, were employed to evaluate the association while adjusting for confounding factors such as age, race, hospital characteristics, and comorbidities. Association and Impact The analysis revealed a significant association between microscopic colitis and celiac disease, supported by both univariate and multi-variate analyses. Interestingly, celiac disease emerged as an independent risk factor for increased mortality among microscopic colitis patients. However, there was no significant impact on the mean hospital stay. Clinical Implications These findings highlight the clinical relevance of understanding the link between microscopic colitis and celiac disease, emphasizing the need for vigilant monitoring and appropriate management for patients with coexisting conditions. The study's population-based approach and comprehensive analysis contribute valuable insights for informed decision-making in healthcare. Future Directions The study sets the stage for further research focusing on mechanistic aspects, prospective studies to establish causality, and exploring therapeutic interventions. Addressing limitations related to data accuracy and histologic subtypes is crucial for refining our understanding and improving clinical management. This study establishes a probable association between microscopic colitis and celiac disease, backed by rigorous statistical analyses. It also identifies celiac disease as an independent risk factor for increased mortality among microscopic colitis patients. These findings provide a foundation for future research and clinical considerations, aiming to optimize patient care and outcomes in the realm of gastrointestinal health. Source: journals.lww.com
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Celiac.com 07/03/2023 - Celiac disease is an autoimmune disorder caused by eating gluten, which damages the small intestine. We know that the immune system plays a crucial role in the development of the disease, which involves various types of immune cells. In a recent study, researchers Nader Atlasy, Anna Bujko of the Department of Molecular Biology, Faculty of Science, Radboud University, Nijmegen, The Netherlands, examined the immune cells in the small intestine of individuals with celiac disease to understand their role in the disease. Macrophages are Reduced in Celiac Disease Patients Increasing Inflammation Their study found that certain immune cells called macrophages were reduced in celiac disease. These cells showed changes in their gene activity in response to a signaling molecule called interferon-gamma (IFNg). This signaling pathway may contribute to the accumulation of pro-inflammatory macrophages in celiac disease. The study also observed differences in the gene activity of mast cells, which are involved in the immune response, between individuals with celiac disease and those following a gluten-free diet. New Genetic Markers Identified May Trigger Celiac Disease The number of CD3+ T cells, a type of immune cell, was increased in celiac disease. The gene activity of CD4+ and CD8+ T cells, subtypes of CD3+ T cells, was significantly different from healthy individuals and those on a gluten-free diet. These T cells expressed genes related to infections, suggesting a potential link between altered intestinal bacteria and celiac disease. The study identified a population of CD4+ T cells with regulatory properties, indicated by the expression of TIGIT and IKZF2 (Helios). CD4+ T cells in celiac disease displayed a mixed phenotype of activated cells and cells with regulatory properties. CD8+ T cells in the gut also showed an activated gene activity pattern, suggesting their involvement in celiac disease. Furthermore, the study identified a distinct population of intraepithelial lymphocytes (IELs) in the small intestine. This population was reduced in people with celiac disease, and only partially restored in individuals following a gluten-free diet. The decrease in this population may contribute to the development of celiac disease. The findings also suggested a potential role of viral or bacterial stimuli in celiac disease, as certain pathways associated with viral and bacterial responses were upregulated in immune cells of individuals with the disease. Read more in Nature Communications volume 13, Article number: 4920 (2022)
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Celiac.com 06/15/2010 - A clinical team conducted a functional analysis of celiac risk loci, and found that SH2B3 offers protection against bacterial infection. The team included Alexandra Zhernakova, Clara C. Elbers, Bart Ferwerda, Jihane Romanos, Gosia Trynka, Patrick C. Dubois, Carolien G.F. de Kovel, Lude Franke, Marije Oosting, Donatella Barisani, Maria Teresa Bardella, the Finnish Celiac Disease Study Group, Leo A.B. Joosten, Paivi Saavalainen, David A. van Heel, Carlo Catassi, Mihai G. Netea, and Cisca Wijmenga. Celiac disease has a fairly high morbidity, yet it is prevalent in Western populations at rates of of 1%–2%. So far, scientists don't understand why the celiac disease phenotype is so common despite its obvious negative impact on human health. This is especially true when one considers that doctors only developed a gluten-free diet to treat celiac disease in the 1950's. The research team scientists hypothesize that the high prevalence of celiac disease might suggest that the process of natural selection favors genes that trigger celiac disease, and thus, that the gene may convey some evolutionary advantage to those who inherit them. The study group included 8,154 controls from four European populations, and 195 individuals from a North African population. By examining haplotype lengths using the integrated haplotype score (iHS) method, the team looked at selection signatures for ten confirmed celiac-associated loci in several genome-wide data sets. They found consistent indications of positive selection for celiac-associated derived alleles in three loci: IL12A, IL18RAP, and SH2B3. For the SH2B3 risk allele, they also found a variation in allele frequency distribution (Fst) between HapMapphase II populations. Functional investigation of the effect of the SH2B3 genotype in response to lipopolysaccharide and muramyl dipeptide showed that carriers of the SH2B3 rs3184504*A risk allele provided more robust triggering of the NOD2 recognition pathway. This suggests that SH2B3 plays a role in protection against bacteria infection, and it provides a possible explanation for the selective sweep on SH2B3, which occurred sometime between 1,200 and 1,700 years ago. Source: AJHG - 2010, 04 May. doi:10.1016/j.ajhg.2010.05.004
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Celiac.com 12/26/2012 - Currently, researchers have found forty separate gene sites that they associate with celiac disease. They classify all of these sies as "low-penetrance," with the exception of the high-risk genotypes in the HLA-DQA1 and HLA-DQB1 genes, which are necessary, but not sufficient to cause the disease. So far, their efforts to find more such sites have been prevented by the strong effects from the known HLA loci and the genetically complex nature of the major histocompatibility complex (MHC). A research team wanted to test the hypothesis that additional celiac disease gene sites exist within the extended major histocompatibility complex (xMHC). The research team included Richard Ahn, Yuan Chun Ding, Joseph Murray, Alessio Fasano, Peter H. R. Green, Susan L. Neuhausen, and Chad Garner. They are variously affiliated with the Department of Epidemiology, University of California Irvine, Irvine, California, the Department of Population Sciences at eh Beckman Research Institute of City of Hope in Duarte, California, the Department of Medicine and Immunology at The Mayo Clinic in Rochester, Minnesota, the Center for Celiac Research at the University of Maryland School of Medicine in Baltimore, Maryland, and the Celiac Disease Center at Columbia University in New York, New York. To follow up on the hypothesis, they looked at a collection of single nucleotide polymorphisms, frequently called SNPs (pronounced “snips”), which are the most common type of genetic variation among people. For their study, the research team analyzed a set of 1898 SNPs for association across the 7.6 Mb xMHC region in 1668 patients with confirmed celiac disease, and 517 non-celiac control subjects. The researchers used what is called conditional recursive partitioning to create a marker of known HLA-DQA1 and HLA-DQB1 high-risk genotypes that was included in the association analysis to account for their effects. After accounting for the known effects, they used a linkage disequilibrium-based grouping procedure to estimate the number of independent celiac disease loci present in the xMHC. They found strong statistical evidence for four new independent celiac disease loci within the classic MHC region. This was the first time researchers have conducted a comprehensive association analysis of the xMHC in celiac disease that specifically accounts for the known HLA disease genotypes and the genetic complexity of the region. Source: PLoS One. 2012;7(5):e36926. Epub 2012 May 17.
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Celiac.com 06/23/2010 - A team of researchers evaluated the possibility of diagnosing celiac disease using quantitative analysis of videocapsule endoscopy images. The team included Edward J. Ciaccioa, Christina A. Tennysonb, Suzanne K. Lewisb, Suneet, Krishnareddy, Govind Bhagat, and Peter H.R. Green. They are variously associated with the Department of Pharmacology, Department of Medicine, Department of Pathology, Columbia University College of Physicians and Surgeons in New York. Images taken with videocapsule endoscopy can be useful for diagnosing celiac disease, but their interpretation is highly subjective. Quantitative disease markers might help to determine the degree of villous atrophy and efficacy of treatment. The team gathered capsule endoscopy images from a group of 11 celiac patients with small bowel pathology, and from a group of 10 control patients. Images had a resolution of 576×576 pixels, with 256 grayscale tones, and a frame-rate of 2 s−1. The team measured over 10×10 pixel sub-images for pixel brightness and image texture. They then averaged the results for for 56×56 sub-images per frame. For each patient, the team took measurements at from five locations in the proximal to distal small intestine. At each location, they figured measurements using 200 consecutive image frames (100 s). For classification with a nonlinear discriminant function, they computed mean frame-to-frame pixel brightness, image texture, periodicity in brightness, and estimated wall motion or intestinal motility. By pooling the data, the team found that images from the celiac group showed greater texture than did images from control group (p < 0.001). Images from the celiac disease group exhibited more frame-to-frame brightness variation as well (p = 0.032). Celiac patients showed longer dominant period of brightness in celiacs (p = 0.001), which may indicate reduced motility. Markers for three-dimensional nonlinear classification of celiacs versus controls showed sensitivity of 92.7% and specificity of 93.5%. Both celiac patients and control subjects showed an approximately linear association between dominant period and small intestinal transit time (r2 = 0.42 and r2 =0 .55, respectively). The results show that videocapsule images can be used to reveal villous atrophy throughout the small intestine, and to distinguish individuals with celiac disease from individuals without mucosal atrophy. Source: Science Direct. doi:10.1016/j.cmpb.2010.02.005
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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.
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Celiac.com 09/25/2008 - Mucosal inflammation of the small intestine, coupled with damage to intestinal villi, is a classic indication of celiac disease. Recently, doctors have begun to embrace the idea that some patients with positive celiac blood tests may have mucosal lesions that are too small to appear on routine histopathological analysis. In the first study of its kind, a team of researchers based in Ireland set out to analyze enterocyte morphology and cytoskeletal structures using a high content analysis technology. The research team was made up of doctors Bashir M. Mohamed, Conleth Feighery, Yvonne Williams, Anthony Davies, Dermot Kelleher, Yuri Volkov, Jacinta Kelly and Mohamed Abuzakouk. The team examined duodenal biopsies from 14 untreated and 10 treated celiac patients and from 20 non-celiac control subjects. They also investigated tissue sections from six study group subjects before and after the development of gluten-sensitive enteropathy. The research team used an anti-α-tubulin antibody to conduct immunohistochemical studies on paraffin-embedded tissue sections. They found important differences in enterocyte morphology and intracellular cytoskeletal structures in the patients with proven celiac disease and those in the study group. Moreover, the team observed that these changes existed in the study group prior to any indication of enteropathy, as determined by standard microscopy. This is the first time researchers have used high content analysis to show specific details of enterocyte morphology. Such an approach permits doctors to quantitatively analyze enterocyte intracellular structure from standard biopsy samples and allows for detection of minute changes that develop before the classic histological lesion. This process could become important for improving the diagnosis of celiac disease. If doctors can spot celiac-related intestinal lesions before they develop, they can begin to prevent celiac disease before it develops and thereby save lives. Central European Journal of Biology Volume 3, Number 3 / September, 2008
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