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Differentiation between Celiac Disease, Nonceliac Gluten Sensitivity, and Their Overlapping with Crohn’s Disease: A Case Series  [PDF]
Aristo Vojdani,David Perlmutter
Case Reports in Immunology , 2013, DOI: 10.1155/2013/248482
Abstract: Celiac disease (CD) and nonceliac gluten sensitivity (NCGS) are two distinct conditions triggered by the ingestion of gliadin. Although symptoms of nonceliac gluten sensitivity may resemble those of celiac disease, due to the lack of objective diagnostic tests, NCGS is associated with overlapping symptomatologies of autoimmunities and Crohn’s disease. Furthermore, a gluten-free diet is only recommended for those who meet the criteria for a diagnosis of CD. Unfortunately, that leaves many nonceliac gluten-sensitive people suffering unnecessarily from very serious symptoms that put them at risk for complications of autoimmune disorders that might be resolved with a gluten-free diet. Thus, a new paradigm is needed for aid in diagnosing and distinguishing among various gut-related diseases, including CD, NCGS (also known as silent celiac disease), and gut-related autoimmunities. Herein, we report three different cases: the first, an elderly patient with celiac disease which was diagnosed based on signs and symptoms of malabsorption and by a proper lab test; second, a case of NCGS which was initially misdiagnosed as lupus but was detected as NCGS by a proper lab test with its associated autoimmunities, including gluten ataxia and neuromyelitis optica; third, a patient with NCGS overlapping with Crohn’s disease. The symptomatologies of all three patients improved significantly after 12 months of gluten-free diet plus other modalities. 1. Introduction Wheat allergy, celiac disease (CD), and nonceliac gluten sensitivity (NCGS) are three distinct conditions that are triggered by the ingestion of wheat gliadin [1–3]. In these conditions, the reaction to gluten is mediated by both cellular and humoral immune responses, resulting in the presentation of different symptomatologies. For example, in wheat allergy a specific sequence of gliadin peptides cross-links two IgE molecules on the surface of mast cells and basophils that trigger the release of mediators such as histamines and leukotrienes [4]. Celiac disease (CD) is an autoimmune condition with known genetic makeup and environmental triggers, such as gliadin peptides. CD affects between 1-2% of the general population. Markers for confirming a diagnosis of this disorder are IgA against native, deamidated gliadin peptides, and IgA antitissue transglutaminase (tTg) autoantibody. In comparison with CD, nonceliac gluten sensitivity (NCGS) may affect from 6 to 7% of the population, [5–7]. According to two articles published in 2010 and 2011 by Sapone et al. [5, 6], symptoms in GS may resemble some of the
Markers of Celiac Disease and Gluten Sensitivity in Children with Autism  [PDF]
Nga M. Lau, Peter H. R. Green, Annette K. Taylor, Dan Hellberg, Mary Ajamian, Caroline Z. Tan, Barry E. Kosofsky, Joseph J. Higgins, Anjali M. Rajadhyaksha, Armin Alaedini
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0066155
Abstract: Objective Gastrointestinal symptoms are a common feature in children with autism, drawing attention to a potential association with celiac disease or gluten sensitivity. However, studies to date regarding the immune response to gluten in autism and its association with celiac disease have been inconsistent. The aim of this study was to assess immune reactivity to gluten in pediatric patients diagnosed with autism according to strict criteria and to evaluate the potential link between autism and celiac disease. Methods Study participants included children (with or without gastrointestinal symptoms) diagnosed with autism according to both the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview, Revised (ADI-R) (n = 37), their unaffected siblings (n = 27), and age-matched healthy controls (n = 76). Serum specimens were tested for antibodies to native gliadin, deamidated gliadin, and transglutaminase 2 (TG2). Affected children were genotyped for celiac disease associated HLA-DQ2 and -DQ8 alleles. Results Children with autism had significantly higher levels of IgG antibody to gliadin compared with unrelated healthy controls (p<0.01). The IgG levels were also higher compared to the unaffected siblings, but did not reach statistical significance. The IgG anti-gliadin antibody response was significantly greater in the autistic children with gastrointestinal symptoms in comparison to those without them (p<0.01). There was no difference in IgA response to gliadin across groups. The levels of celiac disease-specific serologic markers, i.e., antibodies to deamidated gliadin and TG2, did not differ between patients and controls. An association between increased anti-gliadin antibody and presence of HLA-DQ2 and/or -DQ8 was not observed. Conclusions A subset of children with autism displays increased immune reactivity to gluten, the mechanism of which appears to be distinct from that in celiac disease. The increased anti-gliadin antibody response and its association with GI symptoms points to a potential mechanism involving immunologic and/or intestinal permeability abnormalities in affected children.
Value of Gluten Patch Test in Diagnosis of Celiac Disease
Hosein Saneian,Fariborz Zandieh,Paria Akhavan,Rouzbeh Taherian
Iranian Journal of Pediatrics , 2011,
Abstract: Objective: Celiac disease is an intestinal disorder identified by mucus inflammation, villous atrophy and crypt hyperplasia. This disorder can be controlled by elimination of gluten from daily diet. Patients with celiac disease are at greater risk of gastrointestinal malignancy and non-Hodgkin lymphoma than are the general population. This study tries to present the value of gluten patch test for diagnosis of celiac disease.Methods: In this investigation, the study population was divided into case and control groups. The case group consisted of patients with celiac disease. The control group were patients involved in celiac disease but suffering from other gastrointestinal disorders. Both gluten patch and placebo patch were attached to the skin between the scapulas. The results were read twice: 48 hours and 96 hours after the patch was applied. Patients who showed irritation reactions were withdrawn from this study. The results were analysed by SPSS software, Spearman's test, chi square, and Mann-Whitney tests. Findings: The value obtained from the gluten patch test after 96 hours are as follows: specification at 95%, sensitivity at 8%, positive prediction value at 67%, and negative prediction value at 43%. Conclusion: It can be concluded that the gluten patch test is not an efficient test for screening of celiac disease, however, it can be useful for diagnosis of celiac disease if employed and studied with clinical symptoms and serologic and biopsy tests. Furthermore, we should doubt our judgment if the result of gluten patch test for the patient with celiac disease is positive.
Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity
Anna Sapone, Karen M Lammers, Vincenzo Casolaro, Marcella Cammarota, Maria Giuliano, Mario De Rosa, Rosita Stefanile, Giuseppe Mazzarella, Carlo Tolone, Maria Russo, Pasquale Esposito, Franca Ferraraccio, Maria Cartenì, Gabriele Riegler, Laura de Magistris, Alessio Fasano
BMC Medicine , 2011, DOI: 10.1186/1741-7015-9-23
Abstract: CD, GS and healthy, gluten-tolerant individuals were enrolled in this study. Intestinal permeability was evaluated using a lactulose and mannitol probe, and mucosal biopsy specimens were collected to study the expression of genes involved in barrier function and immunity.Unlike CD, GS is not associated with increased intestinal permeability. In fact, this was significantly reduced in GS compared with controls (P = 0.0308), paralleled by significantly increased expression of claudin (CLDN) 4 (P = 0.0286). Relative to controls, adaptive immunity markers interleukin (IL)-6 (P = 0.0124) and IL-21 (P = 0.0572) were expressed at higher levels in CD but not in GS, while expression of the innate immunity marker Toll-like receptor (TLR) 2 was increased in GS but not in CD (P = 0.0295). Finally, expression of the T-regulatory cell marker FOXP3 was significantly reduced in GS relative to controls (P = 0.0325) and CD patients (P = 0.0293).This study shows that the two gluten-associated disorders, CD and GS, are different clinical entities, and it contributes to the characterization of GS as a condition associated with prevalent gluten-induced activation of innate, rather than adaptive, immune responses in the absence of detectable changes in mucosal barrier function.Gluten is the structural protein component of the grains wheat, rye and barley, which are the basis for a variety of flour- and wheat-derived food products consumed throughout the world. Possibly, the introduction of gluten-containing grains, which occurred about 10,000 years ago with the advent of agriculture, represented a "mistake of evolution" that created the conditions for human diseases related to gluten exposure, the best known of which are mediated by the adaptive immune system: wheat allergy and celiac disease (CD). In both conditions, the reaction to gluten is mediated by T-cell activation in the gastrointestinal mucosa. However, in wheat allergy, it is the cross-linking of immunoglobulin E (IgE) by repea
Neurological Manifestations, Diagnosis, and Treatment of Celiac Disease: A Comprehensive Review  [cached]
Shahriar Nikpour
Iranian Journal of Neurology , 2012,
Abstract: Celiac disease or gluten sensitivity may initially present asone or more neurological signs and/or symptoms. On the other hand, it may be associated with or complicated by neurological manifestations. Neurological presentations are rare in children but as many as 36% of adult patients present with neurological changes. With severe malnutrition after progression of celiac disease, different vitamin deficiencies may develop. Such problems can in turn overlap with previous neurological abnormalities including ataxia,epilepsy, neuropathy, dementia, and cognitive disorders. Inthis study, we aimed to review the neurological aspects of celiac disease. Early diagnosis and treatment could prevent related disability in patients with celiac disease.
A Non-Human Primate Model for Gluten Sensitivity  [PDF]
Michael T. Bethune, Juan T. Borda, Erin Ribka, Michael-Xun Liu, Kathrine Phillippi-Falkenstein, Ronald J. Jandacek, Gaby G. M. Doxiadis, Gary M. Gray, Chaitan Khosla, Karol Sestak
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0001614
Abstract: Background and Aims Gluten sensitivity is widespread among humans. For example, in celiac disease patients, an inflammatory response to dietary gluten leads to enteropathy, malabsorption, circulating antibodies against gluten and transglutaminase 2, and clinical symptoms such as diarrhea. There is a growing need in fundamental and translational research for animal models that exhibit aspects of human gluten sensitivity. Methods Using ELISA-based antibody assays, we screened a population of captive rhesus macaques with chronic diarrhea of non-infectious origin to estimate the incidence of gluten sensitivity. A selected animal with elevated anti-gliadin antibodies and a matched control were extensively studied through alternating periods of gluten-free diet and gluten challenge. Blinded clinical and histological evaluations were conducted to seek evidence for gluten sensitivity. Results When fed with a gluten-containing diet, gluten-sensitive macaques showed signs and symptoms of celiac disease including chronic diarrhea, malabsorptive steatorrhea, intestinal lesions and anti-gliadin antibodies. A gluten-free diet reversed these clinical, histological and serological features, while reintroduction of dietary gluten caused rapid relapse. Conclusions Gluten-sensitive rhesus macaques may be an attractive resource for investigating both the pathogenesis and the treatment of celiac disease.
Hepatobiliary Disorders in Celiac Disease: An Update  [PDF]
Kaushal K. Prasad,Uma Debi,Saroj K. Sinha,Chander K. Nain,Kartar Singh
International Journal of Hepatology , 2011, DOI: 10.4061/2011/438184
Abstract: This communication reviews recent literature and summarizes hepatobiliary abnormalities that may complicate the clinical course of celiac disease. A wide spectrum of hepatobiliary diseases has been described, including asymptomatic elevations of liver enzyme levels, nonspecific hepatitis, nonalcoholic fatty liver disease, and autoimmune and cholestatic liver disease. Moreover, in the majority of patients, liver enzyme levels will normalize on a gluten-free diet. In addition, celiac disease may be associated with rare hepatic complications, such as hepatic T-cell lymphoma. Because many celiac patients do not have overt gastrointestinal symptoms, a high index of suspicion is required. Simple methods of detecting celiac disease such as serum antibody tests help in the early identification of the disease, thus preventing serious complications of the disorder. The IgG DGP antibody test and IgA tTG antibody test used in combination are an excellent screening test for suspected cases of celiac disease. 1. Introduction Celiac disease (CD), or gluten-sensitive enteropathy (GSE), is an autoimmune disorder characterized by reversible small bowel mucosal inflammation with villous atrophy affecting patients with a specific genetic predisposition (HLA DR3-DQ2 and HLA DR4-DQ8). The mucosal lesion develops after ingestion of dietary gluten and recovers when gluten-containing cereals, wheat, rye, and barley, are withdrawn from the diet [1]. In untreated CD, the characteristic abnormalities in the small bowel mucosa are villous atrophy, crypt hyperplasia, and an increased density of inflammatory cells in the epithelium and lamina propria [2–4]. The small bowel lesion of CD is a dynamic process whereby mucosal damage to the small intestine develops in three subsequent phases: (a) infiltrative phase, characterized solely by an increased number of intraepithelial lymphocytes; (b) hyperplastic phase, characterized by crypt hypertrophy; (c) destructive phase, which is characterized by progressive villous atrophy ultimately leading to the flattening of the mucosa [5]. Abnormal immune response to gliadin, genetic, and environmental factors plays a role in the pathogenesis of CD. Infectious agents have been implicated in the pathogenesis of many autoimmune disorders. Transient infections or increased permeability of the mucosa may facilitate disease onset induced by the uptake of gluten peptides into a microenvironmental milieu in the small intestinal mucosa [6]. An environmental factor, such as an infectious agent, is thought to precipitate the disease via various pathogenic
A Case of Multiple Sclerosis and Celiac Disease  [PDF]
H. Z. Batur-Caglayan,C. Irkec,I. Yildirim-Capraz,N. Atalay-Akyurek,S. Dumlu
Case Reports in Neurological Medicine , 2013, DOI: 10.1155/2013/576921
Abstract: Objectives. Multiple sclerosis (MS) is an inflammatory autoimmune disorder of the central nervous system (CNS). Since a correlation between gluten intake and incidence of MS had been reported, the relationship of antigliadin antibodies and MS was debated. Case Report. We report the case of a 45-year-old female MS patient who is under interferon treatment. After seven years of monitoring, during her routine gastroenterological assessment, she was diagnosed with celiac disease. Conclusion. Beside the neurological manifestations that have been demonstrated in about 10% of celiac disease (CD) patients, white-matter abnormalities in brain MRI are uncommon and controversial. But in the literature, MS seems to be associated with CD as in our patient. We suggest that MS patients with gastroenterological complaints should undergo an assessment for CD. 1. Objectives Multiple sclerosis (MS) is an inflammatory autoimmune disorder of the central nervous system (CNS). MS, resembling other autoimmune disorders, has a multifactorial etiology, including environmental, immunological, and genetic factors. MS is sometimes difficult to be differentiated from CNS involvement in systemic autoimmune diseases [1]. Celiac disease is an immune-mediated intestinal disorder with gluten sensitivity which is characterized with villous atrophy and crypt hyperplasia. Celiac disease is well known to be associated with many neurological diseases like cerebellar ataxia, peripheral neuropathy, epilepsy, dementia, and depression. Earlier reports mainly have documented the involvement of the nervous system as a complication of prediagnosed CD. As gluten sensitivity with or without intestinal involvement shows concurrence with neurological manifestations like white-matter lesions, MS has been studied for the association with gluten sensitivity [2–5]. We describe an MS patient who is diagnosed with CD after seven years of followup. 2. Case Report Seven years ago, at the age of 38, a female patient was consulted to our clinic with right leg weakness and paresthesias in her arms and legs. Neurological examination showed right hemiparesis (4/5) and right hemihypoesthesia. Past history was unremarkable except that she had irritable bowel syndrome and iron deficiency anaemia. Routine laboratory investigations revealed haemoglobin of 12,4?g/dL with MCV of 80,8 and serum ferritin 6,36?ng/mL (normal values 7–270?ng/mL) confirming a mild iron deficiency. Detailed biochemical and immunological profiles were normal. Vitamin B12, folate, ANA, anti-dsDNA antibodies, ANCA, ASMA, AMA, and anticardiolipin and
Compliant gluten-free children with celiac disease: an evaluation of psychological distress
Luigi Mazzone, Laura Reale, Massimo Spina, Manuela Guarnera, Elena Lionetti, Serena Martorana, Domenico Mazzone
BMC Pediatrics , 2011, DOI: 10.1186/1471-2431-11-46
Abstract: A total of 100 well-treated and compliant CD patients (65 females/35 males; age mean ± SD: 10.38 ± 2.71) were compared to 100 normal controls (58 females/42 males; age mean ± SD: 11.47 ± 2.61). Emotional and behavioral problems were assessed by the Child Behavior Checklist (CBCL), the Children's Depression Inventory (CDI) and the Multidimensional Anxiety Scale for Children (MASC).Subjects with CD self-reported an increased rate of anxiety and depression symptoms and showed higher scores in "harm avoidance" and "somatic complaints", in the CBCL parent-report questionnaire, as compared to healthy control subjects. Furthermore, gender differences could be observed in the group of CD patients, with males displaying significantly higher CBCL externalizing scores, in social, thought and attention problems, as compared to female, who in turns showed more prominent internalizing symptoms such as depression.The increased rate of emotional and behavioral problems in children and adolescent with CD emphasizes the importance of an early detection of mental health problems in these children.Celiac disease (CD) is an autoimmune enteropathy characterized by intolerance to dietary gluten. The clinical spectrum of celiac disease is extremely wide, varying in onset, duration and severity of the disease, and the compliance to a gluten-free diet is also extremely variable. Besides the classic form, which shows the typical gastrointestinal manifestations, there are also atypical and asymptomatic (silent) forms of celiac disease [1-3].Celiac disease can also be found in association with other autoimmune diseases (i.e. diabetes, thyroiditis of Hashimoto, psoriasis), as well as with extra-intestinal complications such as neurologic and psychiatric disturbances, which may either follow or precede symptoms and diagnosis of the celiac disease [4-6]. Several studies have documented the occurrence of internalizing disorders such as depression, anxiety, and psychoneurotic symptoms in adults with
Effect of the timing of gluten introduction on the development of celiac disease  [cached]
Marco Silano, Carlo Agostoni, Stefano Guandalini
World Journal of Gastroenterology , 2010,
Abstract: Celiac disease (CD) is a permanent auto-immune enteropathy, triggered in genetically predisposed individuals by the ingestion of dietary gluten. Gluten is the alcohol-soluble protein component of the cereals wheat, rye and barley. CD is a multifactorial condition, originating from the interplay of genetic and environmental factors. The necessary environmental trigger is gluten, while the genetic predisposition has been identified in the major histocompatibility complex region on chromosome 6p21, with over 90% of CD patients expressing HLA DQ2 and the remaining celiac patients express DQ8. The fact that only about 4% of DQ2/8-positive individuals exposed to gluten develop CD, has led to the recognition that other genetic and environmental factors are also necessary. In the last few years, several epidemiological studies have suggested that the timing of the introduction of gluten, as well as the pattern of breastfeeding, may play an important role in the subsequent development of CD. Here, we present and review the most recent evidences regarding the effect of timing of gluten introduction during weaning, the amount of gluten introduced and simultaneous breastfeeding, on the development of CD.
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