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PubMed2004

Strongly positive tissue transglutaminase antibody assays without celiac disease.

Celiac disease is a small bowel disorder characterized by flattened villi and crypt hyperplasia, often with malabsorption. Improvement occurs with a gluten-free diet. Sensitive and specific assays (eg, immunoglobulin A antibodies to tissue transglutaminase [tTG]) that can be quantified appear to be valuable tools for population screening studies. In addition, their use is expanding widely in the clinical practice arena, being employed as a method of case finding. In this evaluation, clinical use of a commercially available test kit was explored. Of 1330 samples submitted to our hospital laboratory by physicians in British Columbia, Alberta and the Yukon Territory (from 1999 to 2003, inclusive), 96 patients (7%) had increased values (normal range greater than 20 units) and markedly increased levels greater than 100 units were detected in 36 patients (3%). Of these, 14 patients (almost 40%) were referred to gastroenterologists in our hospital and all 14 had small intestinal biopsies. Of these, three patients (more than 20%) did not have celiac disease. Two had normal small bowel biopsies and one had unclassified sprue or 'sprue-like' intestinal disease that failed to respond to a gluten-free diet. The other 11 had biopsy-defined celiac disease. While the tTG assay may be a useful predictor of celiac disease, small intestinal biopsy is still required to confirm the diagnosis. In clinical practice, even strongly positive tTG results are not specific in individual patients, do not necessarily correlate with the degree of severity of biopsy change and, as a result, are also unlikely to be useful for monitoring diet compliance.

Adult↗

PubMed2002

HLA DQA1-DQB1 genotypes in Bedouin families with celiac disease.

Celiac disease (CD) has a strong genetic association with human leukocyte antigens (HLA). The primary susceptibility for CD is HLA-DQA1*05 DQB1*02 (also known as DQ2), with the remainder of cases primarily HLA-DQA1*03 DQB1*03 (also known as DQ8). In a set of nine Bedouin multiplex celiac disease families and one simplex, we genotyped DNA samples at HLA DQA1 and DQB1. Nineteen celiac disease patients had at least one DQA1*05 DQB1*02 genotype (= DQ2), 4 affecteds had the second most common genotype of DQA1*03 DQB1*0302 (= DQ8), 9 were DQ2 and DQ8, and 4 had at least one copy of DQB1*02 without the DQA1*05 genotype. Using transmission disequilibrium testing, we observed a significant over-representation in affecteds of the DQA1*05 DQB1*02 genotype (p = 0.0089), as well as over-representation of the DQA1*03 DQB1*0302 genotype (p = 0.078). The HLA DQA1 DQB1 high-risk genotypes associated with celiac disease are similar in these Bedouin families with CD to what is observed in Northern and Southern Europeans.

Alleles↗

PubMed1998

New clinical issues in celiac disease.

Celiac disease is a chronic disorder of gluten sensitivity associated with a spectrum of mucosal lesions termed preinfiltrative, infiltrative, hyperplastic, destructive, and atrophic. The symptoms are not related to the degree of mucosal pathology but to the extent of the mucosal lesion. Neoplasms constitute the major complication of celiac disease, and EATCL is the most common neoplasm in this category. There is evidence that a strict gluten-free diet is protective against the complications of celiac disease; hence it is important that even the subclinical forms be diagnosed early. Small bowel biopsy remains the gold standard for diagnosis of celiac disease; however, antibody tests are a useful adjunct in deciding whom to biopsy and for screening groups at high risk before initiating a lifelong gluten-free diet.

Celiac Disease↗

PubMed1994

A mathematical model describing catch-up growth in celiac disease.

Celiac disease may lead to various degrees of growth retardation. In general, catch-up growth is completed in the first 2 years after the start of therapy. A mathematical model for catch-up growth in celiac disease can be useful as a reference to which the growth pattern observed during treatment of other conditions can be compared. In this study we performed a non-linear regression analysis on individual growth data of 16 celiac disease patients using a monomolecular growth function. The goodness of fit was significant in all cases (p < 0.05), which illustrates that this function adequately describes catch-up growth in individuals with celiac disease. From the individual models we have composed a cross-sectional curve and a longitudinal description of the pattern of catch-up growth for the entire population.

Celiac Disease↗

PubMed2006

Extraintestinal manifestations of celiac disease.

Celiac disease is an autoimmune disorder that occurs in genetically predisposed individuals as the result of an immune response to gluten. It is present in approximately 1% of the population. Diarrhea has become a less common mode of presentation (<50% of cases) than it once was. Other presentations include iron-deficiency anemia, osteoporosis, dermatitis herpetiforme, and neurologic disorders, mainly peripheral neuropathy and ataxia. Arthritis is commonly found in patients with celiac disease when systematically sought. Overall, autoimmune diseases occur more frequently (three to ten times more) in those with celiac disease than in the general population. A gluten-free diet is the standard of treatment, although its effect on some of the extraintestinal manifestations remains to be determined.

Anemia, Iron-Deficiency↗

PubMed1985

Specificity of antigliadin antibody in celiac disease.

Celiac disease is activated in genetically susceptible individuals by the dietary ingestion of wheat gluten and similar proteins in other grains. Gliadins are a complex mixture of proteins that contain at least 40 different components in a single variety of wheat. We have purified the four major electrophoretic fractions of wheat gliadin and examined the specificity of antigliadin antibody for those fractions by radioimmunoassay in 30 patients with celiac disease and 30 matched controls. All patients had been on a gluten-free diet for more than 18 mo and were clinically asymptomatic at the time of study. Seventeen of 30 patients had increased antibody levels to one or more of the gliadin fractions. Twelve of 17 patients had elevated antibody to A or 6D alpha-gliadin, 9 of 17 to beta-gliadin, 10 of 17 to gamma-gliadin, and 8 of 17 to omega-gliadin. Of the 17 subjects, 5 had increased antigliadin antibody levels to one gliadin fraction only, whereas 12 had increased levels to two or more fractions. Of the 17 patients with increased antibody titers, 16 had the G2m(n) immunoglobulin heavy chain allotype marker and 14 had the serologic HLA specificities-B8 or-DR3, or both. Definition of the wheat gliadin fractions and specific gliadin peptides that can activate celiac disease remains an open question. These data indicate that antigliadin antibody in the serum of asymptomatic patients with celiac disease who are maintained on a gluten-free diet can be directed against one or a multiple of gliadin fractions.

Antibodies↗

PubMed1999

Antibodies to human recombinant tissue transglutaminase measured by radioligand assay: evidence for high diagnostic sensitivity for celiac disease.

Celiac disease is associated with endomysial antibodies (EmA), which have recently been reported to be directed to tissue transglutaminase (tTG). To demonstrate binding of antibodies to recombinant tTG, human tTG was cloned, expressed by in vitro transcription/translation and used to develop novel radioligand assays for combined and single detection of immunoglobulin A (IgA) and G (IgG)-specific antibodies. IgA and IgG-tTGA were found in 43 (95.6%) of 45 patients with newly-diagnosed celiac disease verified by biopsy. In addition, all 30 sera from patients with gastrointestinal symptoms and positive EmA were positive for IgA-tTGA, and all but one serum (96.7%) had antibodies of the IgG class. Receiver-operating characteristic analysis including 574 sera from healthy controls revealed a specificity of 99.5%. By means of these new assays, we identified all patients with endomysial antibodies and achieved, at equal specificity, an even improved sensitivity (95.6%) as compared to EmA (91.1%) detected by the standard immunofluorescence test. Here, we have provided direct evidence that recombinant tTG is a major target of antibodies in celiac disease. Our data suggest that tTGA measured by radioligand assay have the power to overcome the limitations of the EmA-test. This new strategy may considerably facilitate large-scale screening for silent and latent celiac disease.

Adolescent↗

PubMed2002

Recent developments in celiac disease.

Celiac disease is a common disorder associated with a substantially increased standardized mortality ratio if it is left untreated or if the diagnosis is delayed. Diagnostic sensitivity of serologic testing is improved by the addition of IgG-based testing to standard IgA-based serologic testing for endomysial or transglutaminase autoantibodies. The role of intestinal permeability testing as an additional tool for screening and for monitoring the response to a gluten-free diet is discussed. The importance of diagnosing celiac disease in two clinical situations is considered: first, before immune-stimulating therapy with interferon for viral hepatitis is begun and second, in pregnancy when not only maternal but also paternal celiac disease may affect fetal outcome. The strong genetic component of the etiology of celiac disease is illustrated by a monozygotic twin concordance of nearly 90%, with susceptibility conveyed by human leukocyte antigen (HLA) genotypes DQ2 or DQ8 and one or more non-HLA genes. Progress toward identifying these genes from large linkage and association studies is reviewed.

Journal Article↗

PubMed2001

Celiac disease.

Celiac disease is more prevalent than it was previously thought to be, and screening of selected population groups may reveal many new cases. Tissue transglutaminase appears to have a significant role in the degradation of gliadin and antigen production. Specific gliadin epitopes have been defined using T-cell responses. Bone disease is a significant problem for patients with celiac disease but management guidelines are being developed. Refractory sprue (nonresponsive celiac disease) appears to be a manifestation of enteropathy-associated T-cell lymphoma in most cases.

Journal Article↗

PubMed2002

Mortality in patients with celiac disease.

Celiac disease is an autoimmune disorder triggered by ingestion of gluten-containing foods. Epidemiologic studies dating from the 1950s established its association with gastrointestinal malignancies, particularly small bowel lymphoma. Corrao et al. recently demonstrated that patients with celiac disease are at increased risk of mortality. Further, this risk is directly related to compliance with a gluten-free diet. Continued research is needed regarding the development of malignant complications related to celiac disease.

Adult↗

PubMed2005

Genetic testing: who should do the testing and what is the role of genetic testing in the setting of celiac disease?

Celiac disease is a remarkable and common immune-mediated disorder determined by both the presence of characteristic HLA alleles (DQ2 and DQ8) and one of the best characterized environmental factors (gliadin) for any common autoimmune disease. The discovery of transglutaminase autoantibodies and the development of assays for these antibodies has allowed the identification of a large number of asymptomatic individuals with autoimmunity and intestinal biopsy evidence of celiac lesions. Further understanding of the sequelae of asymptomatic celiac disease, and the interaction between genetic susceptibility and environmental factors, are likely to alter fundamentally both genetic screening for celiac disease and its therapy.

Adult↗

PubMed2004

Structural basis for HLA-DQ2-mediated presentation of gluten epitopes in celiac disease.

Celiac disease, also known as celiac sprue, is a gluten-induced autoimmune-like disorder of the small intestine, which is strongly associated with HLA-DQ2. The structure of DQ2 complexed with an immunogenic epitope from gluten, QLQPFPQPELPY, has been determined to 2.2-A resolution by x-ray crystallography. The glutamate at P6, which is formed by tissue transglutaminase-catalyzed deamidation, is an important anchor residue as it participates in an extensive hydrogen-bonding network involving Lys-beta71 of DQ2. The gluten peptide-DQ2 complex retains critical hydrogen bonds between the MHC and the peptide backbone despite the presence of many proline residues in the peptide that are unable to participate in amide-mediated hydrogen bonds. Positioning of proline residues such that they do not interfere with backbone hydrogen bonding results in a reduction in the number of registers available for gluten peptides to bind to MHC class II molecules and presumably impairs the likelihood of establishing favorable side-chain interactions. The HLA association in celiac disease can be explained by a superior ability of DQ2 to bind the biased repertoire of proline-rich gluten peptides that have survived gastrointestinal digestion and that have been deamidated by tissue transglutaminase. Finally, surface-exposed proline residues in the proteolytically resistant ligand were replaced with functionalized analogs, thereby providing a starting point for the design of orally active agents for blocking gluten-induced toxicity.

Celiac Disease↗

PubMed1985

Copper deficiency in infants with active celiac disease.

Celiac disease was diagnosed in two unrelated infants aged 7 and 7.5 months with severe malnutrition. They showed typical clinical, biological, and histological signs of the disease. Moreover, accompanying copper deficiency was suggested by severe hypocupremia and persistent neutropenia; bone radiographs were also compatible with this diagnosis. Rapid and complete correction of these anomalies could only be obtained after addition of oral copper sulfate to the gluten-free diet. Mechanisms possibly involved in the development of copper deficiency in young infants with celiac disease are: chronic malabsorption; high copper needs in rapidly growing infants; and possibly increased biliary and digestive losses. It is therefore suggested that young children with severe celiac disease should be monitored for their copper status.

Celiac Disease↗

PubMed2001

Genes and environment in celiac disease.

Celiac disease is an intestinal disorder that develops as a result of interplay between genetic and environmental factors. HLA genes along with non-HLA genes predispose to the disease. Linkage studies have failed to identify chromosomal regions other than the HLA region which have major effects, indicating the existence of multiple non-HLA predisposing genes with modest effects. Association studies have shown that CTLA4 or a closely located gene is one of these genes. The primary HLA association in the majority of celiac disease patients is with DQ2 (DQA1*05/DQB1*02) and in the minority of patients with DQ8 (DQA1*0301/DQB1*0302). Gluten reactive CD4+ T cells can be isolated from small intestinal biopsies of celiac patients but not from controls. DQ2 or DQ8, but not other HLA molecules carried by patients, present peptides to these T cells. A number of distinct T cell gluten epitopes exist, most of them posttranslationally modified by deamidation. DQ2 and DQ8 bind the epitopes such that the glutamic acid residues created by deamidation are accommodated in pockets that have a preference for negatively charged side chains. There is evidence that deamidation in vivo is mediated by the enzyme tissue transglutaminase (tTG). Overall, the results point to control of the immune response to gluten by intestinal T cells restricted by the DQ2 or DQ8 molecules. This is likely to be a critical checkpoint for the development of celiac disease and could explain the dominant genetic role of HLA in this disorder. The products of the other predisposing genes may participate in pathway(s) that lead(s) to lesion formation. The minor genetic effects of the non-HLA genes could indicate a lack of critical checkpoints along these pathways, or that there are several pathways leading to the lesion formation.

Abatacept↗

PubMed2005

Clinical features and diagnosis of celiac disease.

Celiac disease is a chronic enteropathy caused by intolerance to gluten. The true prevalence of this condition is much greater than previously recognized, with increasing numbers of silent cases being diagnosed. Population-based studies, using serologic screening, have indicated that the prevalence of celiac disease in Caucasian populations is .5%-1%. The pattern of incidence is changing, with a greater proportion of cases diagnosed later in adulthood. The pathologic lesion is characterized by a flattened small intestinal mucosa with a lymphocytic infiltrate, crypt hyperplasia, and villous atrophy. Absorptive function may be impaired and patients can experience gastrointestinal symptoms and malabsorption leading to development of anemia, osteoporosis, or other complications. Untreated celiac disease is associated with significant morbidity and increased mortality, largely owing to the development of enteropathy-associated intestinal lymphoma. The pathologic changes and symptoms resolve when gluten is excluded from the diet for a sustained period.

Age of Onset↗

PubMed2003

Familial occurrence of inflammatory bowel disease in celiac disease.

BACKGROUND: The authors have previously reported a possible increased risk of the familial occurrence of Crohn's disease in patients with celiac disease. AIM: The aim of the current study was to evaluate in a case-control study the familial occurrence of inflammatory bowel disease (IBD) in first-degree relatives of patients with celiac disease. METHODS: One hundred eleven consecutive patients with biopsy-proven celiac disease were interviewed to ascertain whether IBD was present in first-degree relatives. The number of relatives, their ages, and possible IBD status were collected in a questionnaire. When a diagnosis of familial IBD was reported, the diagnosis was checked in the hospital records. Two hundred twenty-two controls matched for age and sex (111 from the general population and 111 from orthopedic wards) were also interviewed regarding the possible occurrence of IBD in first-degree relatives. The chi2 test was used to evaluate the difference in proportion of familial occurrence of IBD among individuals with celiac disease and controls. RESULTS: Among 600 first-degree relatives of patients with celiac disease, 10 cases of IBD were identified among first-degree relatives (7 cases of ulcerative colitis and 3 cases of Crohn's disease), whereas only 1 case of IBD was identified among the 1,196 first-degree relatives of control patients (p < 0.01). When ulcerative colitis and Crohn's disease were analyzed separately, only the prevalence of ulcerative colitis was statistically significant (p </= 0.02). CONCLUSIONS: This case-control study shows that there is a significantly increased prevalence of familial ulcerative colitis in patients with celiac disease. There was no significant increase in the prevalence of Crohn's disease in patients with celiac disease. The possible role of this association is discussed.

Adult↗

PubMed2005

Evidence of a correlation between mannose binding lectin and celiac disease: a model for other autoimmune diseases.

Celiac disease is a multifactorial disorder caused, in genetically susceptible patients, by the ingestion of dietary gluten. Very little is known about the genetic factors, but there is a strong association of two HLA haplotypes (DQ2 or alpha1*05, beta1*02 and DQ8 or alpha1*0301, beta1*0302) with the disease. We investigated the relationship between polymorphisms in the first exon of the MBL2 gene, which encodes for mannose binding lectin (MBL) and celiac disease. Moreover we studied the MBL role by immunohistochemistry and TUNEL. Results were confirmed by clinical findings. We enrolled 149 Italian celiac patients; 116 were characterized by the presence of DQ2 or DQ8. The HLA haplotype was established by allelic specific PCR while the MBL2 genotype was resolved by melting temperature assay. Immunohistochemistry and TUNEL assays were performed on serial sections of biopsy specimens from celiac patients and healthy controls. MBL2 allele and genotype frequencies varied significantly between celiac patients and healthy controls. The frequencies of the 0 allele were 28% in DQ2 or DQ8 celiac patients, 36% in HLA atypical celiac patients, and 22% in healthy controls. Interestingly, the MBL2 0/0 genotype was present in 7 of 33 HLA atypical celiac patients (21%) and in 13 of 116 HLA typical celiac patients (13%) but in only 7 of 147 healthy controls (5%). Furthermore, we found that MBL2 genotype is strongly associated with the occurrence of secondary autoimmune diseases. Immunohistochemistry and TUNEL findings support a role of MBL2 in the clearance of apoptotic cells. In conclusion, MBL2 variants, responsible for lower MBL levels, are associated with celiac disease and higher risk of developing autoimmune diseases. Here we propose a role for MBL in the disease which could be easily applied to other autoimmune disorders.

Adolescent↗

PubMed2005

Innate and adaptive immunity: the yin and yang of celiac disease.

Celiac disease is a multigenetic complex inflammatory disorder with an autoimmune component, induced by gluten, a protein found in wheat. It is a unique human disease model to dissect the innate and adaptive immune mechanisms underlying T-cell-mediated tissue destruction and the development of T-cell lymphoma in conditions of chronic T-cell activation.

Autoimmune Diseases↗