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PubMed2006

Genome-wide linkage analysis of 160 North American families with celiac disease.

Celiac disease (CD) is a common autoimmune disease caused by exposure to the protein gliadin in wheat, and related prolamins in barley and rye. The prevalence of the disease in the US is 1:133. The aim of this study was to identify non-human leukocyte antigen (HLA) loci that predispose to CD. A genome-wide search of 405 microsatellite markers was performed on DNA samples from 160 families with a minimum of two cases of CD. Multipoint, parametric and non-parametric linkage (NPL) analyses were performed. Locations on chromosomes 1q, 3q, 6p, 6q, 7q, 9q and 10q showed linkage statistics (NPL scores or heterogeneity logarithm of the odds (HLOD) scores) of approximately 2.0 or larger. The greatest evidence for linkage outside of chromosome 6 was on 7q and 9q. An NPL score of 2.60 occurred at position 151.0 on 7q and a HLOD score of 2.47 occurred at position 144.8 on 9q under a recessive model. As expected, there was highly significant linkage to the HLA region on 6p, with NPL and HLOD scores exceeding 5.50. In conclusion, this genome-wide linkage analysis represents one of the largest such studies of CD. The most promising region is a putative locus on 7q, a region reported independently in previous genome-wide searches.

Celiac Disease↗
PubMed1998

Genome search in celiac disease.

Celiac disease (CD), a malabsorption disorder of the small intestine, results from ingestion of gluten. The HLA risk factors involved in CD are well known but do not explain the entire genetic susceptibility. To determine the localization of other genetic risk factors, a systematic screening of the genome has been undertaken. The typing information of 281 markers on 110 affected sib pairs and their parents was used to test linkage. Systematic linkage analysis was first performed on 39 pairs in which both sibs had a symptomatic form of CD. Replication of the regions of interest was then carried out on 71 pairs in which one sib had a symptomatic form and the other a silent form of CD. In addition to the HLA loci, our study suggests that a risk factor in 5qter is involved in both forms of CD (symptomatic and silent). Furthermore, a factor on 11qter possibly differentiates the two forms. In contrast, none of the regions recently published was confirmed by the present screening.

Celiac Disease↗
PubMed2001

Molecular dissection of the tissue transglutaminase autoantibody response in celiac disease.

Celiac disease (CD) is an intestinal malabsorption characterized by intolerance to cereal proteins accompanied by immunological responses to dietary gliadins and tissue transglutaminase, an autoantigen located in the endomysium. Tissue transglutaminase belongs to the family of enzymes that catalyze protein cross-linking reactions and is constitutively expressed in many tissues as well as being activated during apoptosis. The role of gliadins in eliciting the immune response in CD and how transglutaminase is linked to the primary reaction are still unclear. In this work, we report the production and analysis of six phage Ab libraries from the peripheral and intestinal lymphocytes of three CD patients. We were able to isolate Abs to transglutaminase from all intestinal lymphocytes libraries but not from those obtained from peripheral lymphocytes. This is in contrast to Abs against gliadin, which could be obtained from all libraries, indicating that the humoral response against transglutaminase occurs at the local level, whereas that against gliadin occurs both peripherally and centrally. Abs from all three patients recognized the same transglutaminase epitopes with a bias toward the use of the V(H)5 Ab variable region family. The possible role of these anti-transglutaminase Abs in the onset of CD and associated autoimmune pathologies is discussed.

Adult↗
PubMed2003

IL12B and IRF1 gene polymorphisms and susceptibility to celiac disease.

Celiac disease (CD) is a common gastro-intestinal disorder resulting from permanent intolerance to wheat gliadins and related proteins in rye and barley. In addition to the strong genetic association with HLA-DQ2 and HLA-DQ8, a genetic region on chromosomes 5 (CELIAC2) has been identified that harbours a susceptibility gene for CD. The gene(s) responsible for this association, however, remains to be identified. In the present study we evaluated polymorphisms in the genes encoding interleukin-12 p40 (IL12B) and interferon regulatory factor 1 (IRF1). Both genes are located in the celiac2 region, and have key roles in inducing interferon (IFN)-gamma secreting T helper 1 (Th1) cells, one of the immunological hallmarks of CD. The frequencies of a TaqI gene polymorphism in the 3' UTR of IL12B and a HinfI gene polymorphism in the 3' UTR of IRF1 were studied in 258 Dutch CD patients and 237 ethnically matched healthy controls. The transmission of the polymorphic variants from parents to affected child was determined in 123 families with at least one affected child. The frequencies of the IL12B TaqI gene polymorphism and the IRF1 HinfI gene polymorphism did not differ significantly between patients and controls. In addition, in the family study, no deviation from the expected transmission from parents to affected child of any of the polymorphic variants was found. The IL12B TaqI and the IRF1 HinfI gene polymorphisms do not appear to be involved in susceptibility to CD. Further studies on the factors that drive the Th1 immunopathology in CD are required.

3' Untranslated Regions↗
PubMed1999

Management of celiac disease.

Celiac disease (CD), perceived as a rare cause of chronic diarrhea three decades ago, was diagnosed as a cause of diarrhea in 60 (7.5%) post weaned children among 800 cases of chronic diarrhea. The diagnosis was established on the basis of a detailed clinical history, histopathological studies on small bowel mucosa and a complete recovery on gluten free diets. Thirty four children were followed up for a period of 0.3 to 8.2 years (mean 3.45 +/- 2.28). Catch up growth was seen in all. A rapid gain in height and weight was observed in first year following exclusion of gluten from the diet. However, on subsequent follow up, flattening of growth curve was seen in 9 subjects which was attributed to non-compliance of gluten free diets and dietary inadequacies. Strict dietary compliance is difficult to adhere to with wheat being a staple cereal in India. Other factors affecting compliance include lack of awareness and non availability of gluten free diets as well as contamination of other items with wheat at grocery shops. A few cases may present as celiac crisis which is a medical emergency requiring aggressive management including use of corticosteroids to improve survival in this otherwise life threatening situation. Effective management of CD requires intense family cooperation as well as concerted national efforts to provide these patients easy access to gluten free diets. The evolution of Celiac Societies, and widespread dissemination of knowledge through all available media will greatly help in management of patients with this chronic disease.

Celiac Disease↗
PubMed2005

Tissue transglutaminase-mediated formation and cleavage of histamine-gliadin complexes: biological effects and implications for celiac disease.

Celiac disease is an HLA-DQ2-associated disorder characterized by an intestinal T cell response. The disease-relevant T cells secrete IFN-gamma upon recognition of gluten peptides that have been deamidated in vivo by the enzyme tissue transglutaminase (transglutaminase 2 (TG2)). The celiac intestinal mucosa contains elevated numbers of mast cells, and increased histamine secretion has been reported in celiac patients. This appears paradoxical because histamine typically biases T cell responses in the direction of Th2 instead of the Th1 pattern seen in the celiac lesions. We report that histamine is an excellent substrate for TG2, and it can be efficiently conjugated to gluten peptides through TG2-mediated transamidation. Histamine-peptide conjugates do not exert agonistic effects on histamine receptors, and scavenging of biologically active histamine by gluten peptide conjugation can have physiological implications and may contribute to the mucosal IFN-gamma response in active disease. Interestingly, TG2 is able to hydrolyze the peptide-histamine conjugates when the concentrations of substrates are lowered, thereby releasing deamidated gluten peptides that are stimulatory to T cells.

Amino Acid Sequence↗
PubMed2003

Autoimmune thyroid disease and celiac disease in children.

BACKGROUND: Celiac disease (CD) may be associated with other immunologic disorders in adults and children. Previous studies linking CD and autoimmune thyroid disease in children have included very few patients with limited biochemical and immunologic screening tests. The aim of this multicenter study was to establish the prevalence of autoimmune thyroid involvement in a large series of pediatric patients with CD. METHODS: Five hundred seventy-three consecutive pediatric patients were enrolled from clinics in Torino, Bologna, Foggia, Rome (two clinics), Naples, and Bari. Three hundred forty-three patients with CD were studied, 230 girls and 113 boys (median age, 8.5 years). Two hundred fifty-six of the patients with CD (median age, 9 years) had been following a gluten-free diet for 3 months to 16 years; 87 patients were untreated (median age, 6.2 years). The diagnosis of CD was made using the European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) criteria. A control group of 230 subjects (median age, 8.3 years) was enrolled. Serum free triiodothyronine, free thyroxine, and thyroid-stimulating hormone (TSH), antithyroperoxidase, antithyroglobulin, anti-TSH receptor antibodies, and thyroid echographic pattern were considered. RESULTS: Autoimmune thyroid disease was found in 90 of 343 (26.2%) patients with CD (62 on a gluten-free diet) and in 20 (10%) of the control subjects (P = 0.001). Fifty-four (15.7%) patients with CD and autoimmune markers had normal thyroid function (euthyroidism) as did 12 (6.0%) of the control subjects; hypothyroidism was observed in 28 (8.1%) patients with CD and in 7 (3.5%) of the control subjects. Hyperthyroidism was diagnosed in four patients with CD and in none of the control subjects with autoimmune markers. An abnormal echographic pattern was seen in 37 patients with CD (16.8%) and only in 1 (1.6%) of the control subjects (P = 0.002). CONCLUSIONS: The high frequency of autoimmune thyroid disease found among patients with CD, even those on a gluten-free diet, may justify a thyroid status assessment at diagnosis and at follow-up evaluation of children with CD.

Adolescent↗
PubMed2003

Seroreactivity against Saccharomyces cerevisiae in patients with Crohn's disease and celiac disease.

AIM: To explore whether there was anti-Saccharomyces cerevisiae antibodies (ASCA) positivity in our patients with biopsy-confirmed celiac disease. METHODS: A cohort of patients with inflammatory bowel diseases (42 patients with Crohn's disease and 10 patients with ulcerative colitis) and gluten sensitive enteropathy (16 patients) from Debrecen, Hungary were enrolled in the study. The diagnosis was made using the formally accepted criteria. Perinuclear antineutrophil cytoplasmic antibodies (pANCA) and anti-Saccharomyces cerevisiae antibodies (ASCA), antiendomysium antibodies (EMA), antigliadin antibodies (AGA) and anti human tissue transglutaminase antibodies (tTGA) were investigated. RESULTS: The results showed that ASCA positivity occurred not only in Crohn's disease but also in Celiac disease and in these cases both the IgG and IgA type antibodies were proved. CONCLUSION: It is conceivable that ASCA positivity correlates with the (auto-) immune inflammation of small intestines and it is a specific marker of Crohn's disease.

Adult↗
PubMed2005

The many faces of celiac disease: clinical presentation of celiac disease in the adult population.

The major modes of presentation of patients with celiac disease are the classic diarrhea-predominant form and silent celiac disease. Those with silent celiac disease lack diarrhea, although they may present with manifestations of celiac disease that include an irritable bowel syndrome, anemia, osteoporosis, neurologic diseases, or malignancy. A significant proportion of patients are diagnosed through screening at-risk groups including relatives of patients and insulin-dependant diabetics. Nondiarrheal presentations now are seen more commonly than those with diarrhea. Patients with celiac disease have a greater burden of disease than the general population because of autoimmune diseases and malignancies. There is a need for screening studies of patients with conditions associated with celiac disease to determine whether the large numbers of people with undiagnosed celiac disease currently are seeking health care.

Adolescent↗
PubMed1999

Celiac disease and markers of celiac disease latency in patients with primary Sjögren's syndrome.

OBJECTIVE: Many autoimmune diseases occur concomitantly with celiac disease. We investigated prospectively the occurrence of celiac disease and small-bowel mucosal inflammation in patients with primary Sjögren's syndrome. METHODS: A total of 34 patients with primary Sjögren's syndrome and 28 controls underwent small bowel biopsy. Villous morphology, jejunal intraepithelial lymphocytes, and mucosal HLA-DR were evaluated and DQA and DQB alleles, serum antiendomysial, and antigliadin antibodies were examined. RESULTS: Five (14.7%) of 34 Sjögren's syndrome patients were found to have celiac disease. The density of jejunal intraepithelial gammadelta+ T cells was increased in all celiac and in four nonceliac patients. All celiac patients, 69% of nonceliac Sjögren's syndrome patients, and 11% of control subjects showed enhanced HLA-DR expression (p < 0.001). HLA DQ2 was present in 19 (56%) patients with Sjögren's syndrome, including all five with celiac disease. CONCLUSIONS: The findings show a close association between Sjögren's syndrome and celiac disease. Even among nonceliac patients with primary Sjögren's syndrome, an ongoing inflammation is often present in the small bowel mucosa.

Autoimmune Diseases↗
PubMed2006

Mechanisms of disease: immunopathogenesis of celiac disease.

Celiac disease is a genetic inflammatory disorder with autoimmune components that is induced by the ingestion of dietary gluten. Refractory sprue and enteropathy-associated T-cell lymphoma are rare but distinctive complications of the disease. Although the importance of the adaptive immune response to gluten has been well established, observations now also point towards a central role for the gluten-induced innate stress response in the pathogenesis of celiac disease and its malignant complications.

Celiac Disease↗
PubMedDate not supplied

Prevalence of celiac disease among siblings of celiac disease patients.

AIMS: To determine the prevalence of celiac disease (CD) in siblings of patients with this disease in Punjab, where wheat is the staple diet. METHODS: Families of 80 patients with CD diagnosed as per modified ESPGAN criteria were offered family screening. Their siblings aged 2-15 years were tested for serum IgA anti-tissue transglutaminase antibody (anti-tTG) antibody. Those with positive or borderline test and some of those with negative test underwent endoscopic duodenal biopsy. Siblings with characteristics histological findings and showing improvement on follow-up were labeled as having celiac disease. RESULTS: Of the 63 siblings of 48 index cases studied, 15 tested positive for anti-tTG; of these 13 had celiac disease. Three tested borderline for anti-tTG; none of them had CD. Of the 45 anti-tTG-negative subjects, two agreed to undergo biopsy; one of these had features of CD. Overall, 14 of 63 (22%) siblings had CD, including 8 who had no symptoms suggestive of CD. CONCLUSIONS: CD is common among siblings of patients with CD in Punjab and may be asymptomatic.

Adolescent↗
PubMed2004

[Diabetes and celiac disease].

Celiac sprue is permanent lifelong intolerance of gluten which in some sensitive individuals leads to an inflammation of various grades followed by atrophy of jejunum mucosa. Diagnosis of celiac sprue is based on proof of histopathological changes in jejunum mucosa as a result of presence of gluten in food. In recent years, serum endogenous myosin and tissue transglutaminase antibodies were used in a diagnostic algorithm. We distinguish active, silent, latent, and potential celiac sprue. Simultaneous incidence of type I diabetes mellitus and celiac sprue has been documented in a range of studies. Both diseases have common immunology and genetic characters. Prevalence of celiac sprue in patients with type I diabetes is several times higher compared to prevalence of this disease in the population. There is the prevalence of celiac sprue 3.6-5.1% in children with type I diabetes mellitus in the Czech Republic, silent form of the disease is the most frequent one. An effect of a strict gluten free diet on a metabolic control of diabetes has not been proved. It is necessary to assess (at least once per two years) actively and on regular basis endogenous myosin and/or tissue transglutaminase antibodies in patients with type I diabetes.

Celiac Disease↗
PubMed2007

Celiac disease and antibodies associated with celiac disease in patients with inflammatory myopathy.

Celiac disease is usually associated with autoimmune disorders and has occasionally been reported in patients with inflammatory myopathies. Our aim was to determine the presence of celiac disease and antibodies associated with celiac disease in patients with inflammatory myopathies and to investigate their relationship. Serum antigliadin, anti-tissue transglutaminase, and antiendomysial antibodies were determined in 51 patients with inflammatory myopathies. HLA-DQ2 and -DQ8 alleles were studied to assess their complementary diagnostic value. Jejunal biopsy was performed in patients with moderate to high levels of antigliadin antibodies. Patients with jejunal histology consistent with celiac disease initiated a gluten-free diet. Seventeen patients (31%) were positive for antigliadin antibodies, which were significantly more frequent in patients with inclusion-body myositis than dermatomyositis (P < 0.001). Positive status to HLA-DQ2 and/or -DQ8 did not differ between antigliadin-positive (75% and 12.5%) or -negative (60% and 15%) patients. Three of five jejunal biopsies were diagnostic for celiac disease with histological normalization after a gluten-free diet. Thus, celiac disease is more prevalent in patients with inflammatory myopathies than in the general population. Positive status to HLA-DQ2 allele, which is known to be more frequent in patients with inflammatory myopathies, could explain the high prevalence of antigliadin antibodies in this population. The diagnostic value of HLA-DQ2 or -DQ8 haplotypes to detect celiac disease in patients with inflammatory myopathy is limited.

Adult↗
PubMed2004

[When gastrointestinal symptoms present, consideration should always be given to celiac disease].

Celiac disease/nontropical sprue is diagnosed too rarely and often too late. In the routine clinical setting, therefore, it should receive more consideration. In patients with gastrointestinal symptoms that prompt gastroscopy, a small bowel biopsy should always be obtained, for it alone detects sprue. Despite the high level of accuracy of antibody determination, there is no substitution for the demonstration of atrophic villi in biopsy material. In the absence of a diagnosis, a gluten-free diet should not be recommended, since in patients who actually have the disease, mucosal changes will regress, and confirmation of the diagnosis is no longer possible. Once the diagnosis has been confirmed, treatment comprises a life-long gluten-free diet, which not only leads to an improvement of the symptoms, but also eliminates the increased lymphoma risk.

Celiac Disease↗
PubMed2005

[Definitions of celiac disease--statement of an expert group from the German Society for Celiac Disease].

Celiac disease may have different manifestations and the clinical course can be very heterogeneous. Thus, management and treatment of celiac disease can be difficult and therefore requires individual patient care. In this article an expert group from the German Society for Celiac Disease (Deutsche Zöliakie-Gesellschaft) defines the different manifestations of celiac disease. In the past these definitions were often used differently. The consequent usage of these definitions may diminish uncertainties in clinical practice and lead to a more standardized management of the disease which is likely to improve patient care.

Adult↗