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PubMed2002

The analysis of the fine specificity of celiac disease antibodies using tissue transglutaminase fragments.

Celiac disease is an intestinal malabsorption characterized by an intolerance to cereal proteins accompanied by immunological responses to dietary gliadins and an autoantigen located in the endomysium. The latter has been identified as the enzyme tissue transglutaminase which belongs to a family of enzymes that catalyze protein cross-linking reactions and is constitutively expressed in many tissues as well as being activated during apoptosis. In a recent paper, we described the selection and characterization of anti-transglutaminase Igs from phage antibody libraries created from intestinal lymphocytes from celiac disease patients. In this work, using transglutaminase gene fragments, we identify a region of tissue transglutaminase recognized by these antibodies as being conformational and located in the core domain of the enzyme. This is identical to the region recognized by anti-transglutaminase Igs found in the serum of celiac disease patients.

Antibody Specificity↗
PubMed2004

Celiac disease and lymphoma risk: a multicentric case--control study in Spain.

Celiac disease is a highly prevalent condition frequently misdiagnosed because of heterogeneity of the clinical symptoms. It is well recognized that enteropathy-associated T-cell lymphoma is an uncommon lymphoma type linked to celiac disease; it has also been suggested that other types of lymphomas may be associated with celiac disease. Our aim was to estimate the risk of all lymphoma associated with celiac disease. Serological markers and personal interviews were obtained from 298 consecutive lymphoma cases and 251 matched controls recruited in four Spanish hospitals. Celiac disease was detected in two cases (0.67%; n = 298) and in three controls (1.2%; n = 251). Treated celiac disease was observed in one patient with lymphoma and in two control subjects. In our series, there was no evidence that celiac disease was a risk factor for lymphoma (OR = 0.62, 95% CI = 0.10-3.79). Serological screening for CD is not recommended in people with lymphoma.

Case-Control Studies↗
PubMed1994

Insulin-like growth factor-I in celiac disease.

To contribute to the description of the physiopathological mechanisms of celiac disease, changes in insulin-like growth factor I (IGF-I) were followed-up in 21 children suspected of suffering from celiac disease. Thirteen children were suffering from celiac disease according to the original criteria of the European Society of Paediatric Gastroenterology and Nutrition. Ten celiac children changing from a gluten-containing to a gluten-free diet presented a significant rise in IGF-I (+1.54 mM per month). In a group of eight celiac children challenged with gluten, seven had a significant decrease in IGF-I (-1.11 mM per month), and five celiac children returning to the gluten-free diet after challenge with gluten had a marked but not significant increase in IGF-I (+1.7 mM per month). Eight children not suffering from celiac disease, but challenged with gluten, had a significant increase in IGF-I (+0.29 mM per month), corresponding to the expected age-dependent increase. The significant changes in IGF-I described under the diagnostic dietetic phases of celiac disease reflect the extent of growth retardation caused by the disease. IGF-I may be a supplementary aid in the diagnosis of celiac disease in describing individual changes under the dietetic phases.

Adolescent↗
PubMed2002

The use of a single serological marker underestimates the prevalence of celiac disease in Israel: a study of blood donors.

OBJECTIVES: Recent studies suggest that celiac disease was previously underdiagnosed. To find out whether antiendomysial antibodies underestimate the prevalence of celiac disease, we elected to use a strategy combining multiple serological markers to explore the prevalence of celiac disease in Israel and the usefulness of the various antibodies in screening for celiac disease. METHODS: Serum samples from 1571 healthy blood donors were tested. A small intestinal biopsy was offered to all patients who tested positive for either human tissue transglutaminase antibodies, an ELISA kit based on antiendomysium (EMA-ELISA), immunoglobulin A antigliadin verified by antiendomysial immunofluorescence antibodies, and to patients who were IgA deficient with elevated antigliadin IgG. RESULTS: A total of 59 subjects (3.8% of study population) were offered an intestinal biopsy based on serological findings, and 30 of 59 patients agreed to undergo intestinal biopsy (1.9% of study population). Celiac disease was diagnosed in 10 patients, establishing a prevalence of at least 1:157 in the general population (0.6%, CI = 0.3-1.1%). Using any serological marker alone would have underestimated the prevalence of celiac disease, as it was diagnosed in only two patients who tested positive for endomysial immunofluorescence antibodies (prevalence of 1:786, 0.1%, CI = 0.02-0.5%), six patients positive for tissue transglutaminase (prevalence of 1:262, 0.4%, CI = 0.1-0.9%), and seven patients positive for ELISA-EMA (prevalence of 1:224, 0.45%, CI = 0.2-0.9%). CONCLUSIONS: The prevalence of celiac disease in Israel is at least 1:157 in the general population, confirming its underdiagnosis in previous studies. The disparity between the various serological markers suggest that the use of one serological marker is insufficient for establishing the true prevalence of celiac disease.

Adolescent↗
PubMed1990

[Adenocarcinoma of the small intestine in celiac disease. Case report and literature review].

We describe three patients with celiac disease complicated by adenocarcinoma of the small intestine, and summarize the 36 cases of this association that have been reported. Retrospectively we found an increased risk (relative risk 25-250) of developing adenocarcinoma of the small intestine in patients with celiac disease in the region of Winterthur (north-east Switzerland). We therefore suggest that celiac disease be considered a premalignant condition not only for malignant lymphoma and gastrointestinal tumors, but also for adenocarcinoma of the small intestine. Synchronous or metachronous development of carcinoma in one of our patients and in two cases reported in the literature offer further evidence that celiac disease is a premalignant condition for adenocarcinoma of the small bowel. In several patients celiac disease was diagnosed only after diagnosis of the carcinoma. With regard to asymptomatic or subclinical celiac disease, it seems justifiable to search for possible underlying celiac disease in all patients with established diagnosis of adenocarcinoma of the small intestine.

Adenocarcinoma↗
PubMedDate not supplied

Celiac disease: a multisystem autoimmune disorder.

Just a few years ago, celiac disease was thought to be relatively rare in the United States, but recent data suggest celiac disease may affect 3 million Americans of all ages, many of whom have no diagnosis of the disease. With increased awareness of this disease among adult and pediatric primary care providers, there undoubtedly will be an increase in the number of persons being evaluated for celiac disease in outpatient diagnostic centers and gastroenterology practices. Gastroenterology nurses, therefore, need to have a thorough understanding of celiac disease to fully participate as members of the multidisciplinary team required to manage this challenging disease. This article discusses the pathogenesis, prevalence, diagnosis, clinical manifestations, management, and complications of celiac disease.

Autoimmune Diseases↗
PubMed2004

No allelic variation in genes with high gliadin homology in patients with celiac disease and type 1 diabetes.

Celiac disease (CD) is a complex inflammatory disorder of the small intestine, induced by dietary gluten in genetically susceptible individuals. CD is strongly associated with HLA-DQ2 and it has recently been established that gut-derived DQ2-restricted T cells from patients with CD predominantly recognize gluten-derived peptides in which specific glutamine residues are deamidated to glutamic acid by tissue transglutaminase. Recently, intestinally expressed human genes with high homology to DQ2-gliadin celiac T-cell epitopes have been identified. Single or double point mutations which would increase the celiac T-cell epitope homology, and mutation in these genes, leading to the expression of glutamic acid at particular positions, could hypothetically be involved in the initiation of CD in HLA-DQ2-positive children. Six gene regions with high celiac T-cell epitope homology were investigated for single-nucleotide polymorphisms using direct sequencing of DNA from 20 CD patients, 27 type 1 diabetes mellitus (T1DM) patients with associated CD, 24 patients with T1DM without CD and 110 healthy controls, all of Caucasian origin. No variants in any of these genes in any of the investigated groups were found. We conclude that gut-expressed human celiac epitope homologous peptides are unlikely to represent non-HLA risk factors in the development of celiac disease in Caucasians.

Celiac Disease↗
PubMed2005

Autoantibodies against soluble and immobilized human recombinant tissue transglutaminase in children with celiac disease.

OBJECTIVES: The conformation of tissue transglutaminase might influence the performance of immunoassays to detect autoantibodies from patients with celiac disease. The present study investigated how the exposure of tissue transglutaminase kept in a liquid phase and fixed to a solid support affected the binding of immunoglobulin (Ig)A and IgG autoantibodies in children with untreated and treated celiac disease. METHODS: Included were 73 untreated celiac disease children, 50 controls and 80 children with treated celiac disease. IgA and IgG antitissue transglutaminase were measured with solid phase enzyme-linked immunoassay (ELISA) and liquid phase radioligand binding assays. For IgG antitissue transglutaminase detection with radioligand binding assays antihuman IgG and protein A were used. IgA endomysial autoantibodies were measured by indirect immunofluorescence. RESULTS: Both ELISA and radioligand binding assays detected IgA antitissue transglutaminase in 65 of 73 untreated celiac disease children and in 2 of 50 controls. One additional control child was detected with radioligand binding assays. Endomysial autoantibodies were present in 62 of 73 celiac disease children and in 2 of 50 controls. IgG antitissue transglutaminase was detected with both ELISA and radioligand binding assays in 40 of 73 untreated celiac disease children and in 2 of 50 controls. Radioligand binding assays using protein A detected 20 of 73 additional untreated celiac disease children and one control child with increased IgG antitissue transglutaminase. In treated celiac disease children, 21 of 80 were IgA antitissue transglutaminase positive with radioligand binding assays, 3 of 80 with ELISA, whereas none had endomysial autoantibodies. CONCLUSIONS: No qualitative differences between radioligand binding assays and ELISA in IgA or IgG antitissue transglutaminase binding from untreated celiac disease children was demonstrated. However, discrepancies in the binding of IgA antitissue transglutaminase from a subgroup of treated celiac disease children indicated that alterations of tissue transglutaminase might occur on fixation of the antigen. Protein A used for radioligand binding assays seemed not to assess IgG autoantibodies exclusively. IgA antitissue transglutaminase detection in screening of childhood celiac disease can be performed either by ELISA or radioligand binding assays because the two assays are interchangeable.

Adolescent↗
PubMed1999

Gallbladder emptying and somatostatin and cholecystokinin plasma levels in celiac disease.

OBJECTIVE: Gallbladder hypomotility in celiac disease has been attributed to decreased cholecystokinin secretion. The possible influence of somatostatin, which inhibits gallbladder motility, however, has never been evaluated. In this study gallbladder emptying and cholecystokinin and somatostatin plasma levels were evaluated in response to a fatty meal in patients with celiac disease at diagnosis and after long-term gluten-free diet and in controls. METHODS: Gallbladder volume and plasma levels of cholecystokinin and somatostatin were measured by ultrasonography and radioimmunoassay, respectively, at 0 time and 30, 60, 75, and 90 min after an oral fatty meal (227 kcal, 45% fat) in 10 celiac patients at diagnosis and after 18 months of successful gluten-free diet and in 10 healthy subjects. The pattern of gallbladder emptying was evaluated by mixed factorial analysis of variance and the curve fitting by multiple regression analysis. RESULTS: Patients at diagnosis had significantly greater fasting gallbladder volume and higher somatostatin plasma levels than controls (25.7 +/- SD 9.7 ml vs 16.8 +/- 7.0 ml, p = 0.021 and 9.3 +/- 4.6 vs 4.8 +/- 3.4 pmol/L, p = 0.023, respectively), significantly lower fatty meal-induced gallbladder ejection fraction (55 +/- 11.2% vs 76 +/- 7.2%, p = 0.005), and cholecystokinin peak and smaller area under the cholecystokinin secretion curve (3.1 +/- 2.3 pmol/L vs 10.5 +/- 6.9 pmol/L, p = 0.028 and 157 +/- 142 pmol/L/90 min vs 453 +/- 229 pmol/L/90 min, p = 0.028, respectively). The two groups had a similar emptying pattern (p = 0.8913) expressed by a significant quadratic term of the emptying function (p = 0.0001). The mean overall emptying volume was significantly greater in patients than in controls (p = 0.0007). Gluten-free diet normalized these findings. CONCLUSIONS: In patients at diagnosis, elevated somatostatin levels were associated with increased gallbladder fasting volume, whereas decreased cholecystokinin secretion was responsible for the reduced gallbladder emptying. Gluten-free diet reversed these abnormalities.

Adult↗
PubMed2004

Severe malabsorption due to refractory celiac disease complicated by extensive gastric heterotopia of the jejunum.

Refractory celiac disease denotes that patients considered to have celiac disease fail to respond histologically to treatment with a gluten-free diet. Among several causes of nonresponsiveness, enteropathy-type T-cell lymphoma is most important because of its almost invariably rapid lethal outcome. We present the case of a 44-year-old patient with refractory celiac disease complicated by unusually severe malabsorption. Repeated duodenal biopsies disclosed normal and slightly shortened villi, focal crypt hypertrophy, and a moderate increase of intraepithelial lymphocytes consistent with celiac disease, but unable to explain the severe malabsorption. To rule out cryptic lymphoma, push enteroscopy was done providing 21 biopsies taken along the entire jejunum. Surprisingly, about 70% of the biopsies were composed of gastric glands covered by nonabsorptive-type, strongly periodic acid-Schiff-positive surface epithelium and showed a villous architecture. Alternating with the gastric mucosa, there were areas of flat mucosa with elongated crypts and occasional erosions. Irrespective of the type of surface epithelium, intraepithelial lymphocytes were increased with counts up to 80/100 epithelial cells. Despite harboring an aberrant immunophenotype, overt T-cell lymphoma was ruled out histologically and by lack of monoclonality, as tested by polymerase chain reaction. To the best of our knowledge, this is the first case of refractory celiac disease complicated by extensive jejunal gastric heterotopia, which might have contributed to the severe malabsorption.

Adult↗
PubMed2003

Fracture risk in people with celiac disease: a population-based cohort study.

BACKGROUND & AIMS: People with celiac disease are at risk of developing osteoporosis, but the extent of any increased fracture risk is unclear. We performed a population-based cohort study by using the General Practice Research Database to quantify the fracture risk in people with celiac disease compared with the general population. METHODS: We identified 4732 people with celiac disease, of whom 1589 were "incident" cases, and 23,620 age- and sex-matched control subjects. We used Cox regression to estimate the hazard ratios for any fracture, hip fracture, and ulna or radius fracture in the celiac disease cohort compared with the general population. RESULTS: In the incident subjects with celiac disease, the mean age at diagnosis was 44 years, and 67% were women. The overall hazard ratio for any fracture was 1.30 (95% confidence interval, 1.16-1.46), for hip fracture was 1.90 (95% confidence interval, 1.20-3.02), and for ulna or radius fracture was 1.77 (95% confidence interval, 1.35-2.34). The absolute difference in the overall fracture rate was 3.20 per 1000 person-years and for hip fracture it was 0.97 per 1000 person-years in those older than 45 years. In 1589 incident subjects, the excess fracture risk was slightly lower compared with the "prevalent" subjects (hazard ratio for any fracture, 1.19 vs. 1.40, respectively). CONCLUSIONS: There were small increases in both the absolute and relative fracture risks in people with celiac disease; the excess risks were slightly lower in those with a more recent diagnosis. Our data indicate that concerns regarding a markedly increased fracture risk in celiac disease are unwarranted.

Adolescent↗
PubMed2001

Linkage analysis of HLA and candidate genes for celiac disease in a North American family-based study.

BACKGROUND: Celiac disease has a strong genetic association with HLA. However, this association only explains approximately half of the sibling risk for celiac disease. Therefore, other genes must be involved in susceptibility to celiac disease. We tested for linkage to genes or loci that could play a role in pathogenesis of celiac disease. METHODS: DNA samples, from members of 62 families with a minimum of two cases of celiac disease, were genotyped at HLA and at 13 candidate gene regions, including CD4, CTLA4, four T-cell receptor regions, and 7 insulin-dependent diabetes regions. Two-point and multipoint heterogeneity LOD (HLOD) scores were examined. RESULTS: The highest two-point and multipoint HLOD scores were obtained in the HLA region, with a two-point HLOD of 3.1 and a multipoint HLOD of 5.0. For the candidate genes, we found no evidence for linkage. CONCLUSIONS: Our significant evidence of linkage to HLA replicates the known linkage and association of HLA with CD. In our families, likely candidate genes did not explain the susceptibility to celiac disease.

Journal Article↗
PubMed1996

TNF2, a polymorphism of the tumour necrosis-alpha gene promoter, is a component of the celiac disease major histocompatibility complex haplotype.

Celiac disease (CD) is an immune disease triggered by the cereal antigen gliadin, resulting in villous atrophy in the small intestine. Susceptibility to the development of CD is strongly influenced by genes in the major histocompatibility complex, in particular alleles of the DQ genes in the class II region. However recent evidence has suggested that the major histocompatibility complex (MHC) class III region may be linked to celiac disease independently of the class II region. Among the genes located in this area is TNF-alpha, which encodes the cytokine tumor necrosis factor-alpha which has a broad range of pro-inflammatory, immunomodulatory and catabolic activities. Therefore, aberrant expression of TNF-alpha could be important in the pathogenesis of MHC-associated immune disorders. A TNF-alpha variant with a polymorphism in its promoter region has been described and designated TNF2. TNF2 has been associated with a variety of MHC-linked diseases, including systemic lupus erythematosus, dermatitis herpetiformis and insulin-dependent diabetes mellitus (IDDM), as well as parasitic infections. TNF2 has previously been shown to be associated with the MHC haplotype HLA A1-B8-DR3-DQ2, which confers susceptibility to CD. We have analyzed the distribution of TNF2 alleles in a group of celiac patients (n = 52) compared to controls (n = 52) in an effort to evaluate its role, if any, in susceptibility to the condition. TNF2 has a frequency of 0.5000 (SE +/- 0.0490) in CD, compared to 0.1635 (+/- 0.0362) in a control sample (p < 10(-6)). Of 52 patients, 44 carried one or more TNF2 alleles. Analysis indicates that the distribution of TNF2 is best explained by assuming 100% allelic association between it and HLA-DQB1*0201 (frequency = 0.7791 +/- 0.0447). However, the number of TNF2 heterozygotes significantly exceeds expectations and measurements of linkage disequilibrium confirm that allelic associations spanning the DQ and TNF regions are strongly maintained in CD. Taken together, these results indicate that TNF2 may have a role in the pathogenesis of CD; however, since it is not an independent association, the possibility that TNF2 constitutes a passive component of the CD haplotype cannot be excluded.

Alleles↗
PubMed2000

Usefulness of screening program for celiac disease in autoimmune thyroiditis.

We determined the prevalence of celiac disease in subjects with autoimmune thyroiditis compared with sick and healthy subjects. The screening was performed with IgA-class endomysium antibody, by indirect immunofluorescence using human umbilical cord as the antigenic substrate. Six of the 172 patients with autoimmune thyroiditis were found to be anti-endomysium positive (3.4%) and five of these underwent intestinal biopsy, which showed total villous atrophy. By contrast, 3 (0.75%) of 396 patients with nongastroenterologic malignancies and 10 (0.25%) of 4000 blood donors were found to have celiac disease. The prevalence of autoimmune diseases was significantly higher in patients with both celiac disease and autoimmune thyroiditis than in patients with autoimmune thyroiditis alone (P = 0.01). This study confirms that celiac disease is increased among patients with autoimmune thyroiditis. We suggest that these patients may benefit from screening for celiac disease so as to eliminate symptoms and limit the risk of developing other autoimmune disorders.

Adolescent↗
PubMed2002

Celiac disease and HLA DQ in patients with IgA nephropathy.

OBJECTIVES: Despite some reports on an association between celiac disease and IgA nephropathy, the evidence is still sparse. Celiac disease is strongly associated with the HLA DQ2 and DQ8 haplotypes, which might explain the potential risk of patients to contract various autoimmune conditions. In this study, we sought to establish how common celiac disease is in patients with IgA nephropathy, and whether the possible association can be explained by similar HLA DQ status. METHODS: A total of 223 consecutive adult patients with IgA nephropathy were studied; 95 cadaver organ transplant donors served as controls for HLA DQ analysis. The diagnosis of celiac disease was based on small bowel mucosal biopsy. All known celiac cases were recorded, and eligible patients (n = 168) underwent serological screening for celiac disease as well as HLA DQ2 and DQ8 analysis. Screening methods were serum endomysium and tissue transglutaminase antibodies; patients who tested positive underwent mucosal biopsy. RESULTS: Eight patients (3.6%, 95% CI = 1.6-7.0%) with IgA nephropathy were found to have celiac disease; three of them were identified by serological screening. All celiac cases had the HLA DQ2 or DQ8 haplotype, but these were not more common in patients with IgA nephropathy than in controls. As many as 14% of HLA DQ2 positive patients with IgA nephropathy had celiac disease. Gluten-free diet had no apparent influence on the course of nephropathy. CONCLUSIONS: Although there is no increase in celiac-type HLA DQ, patients with IgA nephropathy carry a risk of contracting celiac disease. It can be hypothesized that the increased intestinal permeability in IgA nephropathy may predispose genetically susceptible patients to celiac disease.

Adolescent↗
PubMed2006

Change in lipid profile in celiac disease: beneficial effect of gluten-free diet.

PURPOSE: Celiac disease is associated with hypocholesterolemia, which is thought to contribute to a favorable cardiovascular risk profile. This led to suggestions that the diagnosis of celiac disease and its treatment with a gluten-free diet may result in elevation of the serum cholesterol level and worsen this risk profile. However, no study proves this in adults. We therefore examined the effect of a gluten-free diet on the lipid profile in patients with celiac disease. SUBJECTS AND METHODS: We identified 132 patients with celiac disease who adhered to a gluten-free diet and had lipid profiles performed before and after a median of 20.5 months on the diet. The patients lacked diseases that may affect serum lipids. RESULTS: There were significant increases in total cholesterol and high-density lipoprotein (HDL) cholesterol (P < .0001) but not low-density lipoprotein (LDL) cholesterol (P=.06). The LDL/HDL ratio decreased by 0.36+/-0.7 (P < .0001). Both men and women had a significant increase in total cholesterol and HDL and a significant decrease in the LDL/HDL ratio. Only men had increases in LDL (P=.02). The greatest increase in lipid values was seen in those with the lowest initial values. The largest increase in HDL was seen in subjects with more severe disease as indicated by low albumin level and presence of total villous atrophy. CONCLUSIONS: Diagnosis of celiac disease and its treatment with a gluten-free diet resulted in improvement in the lipoprotein profile, which included an increase in HDL and a decrease in the LDL/HDL ratio.

Adult↗
PubMed2000

Significance of unsuspected celiac disease detected at endoscopy.

BACKGROUND: Endoscopy provides an opportunity to diagnose unsuspected celiac disease. METHODS: We prospectively identified patients undergoing endoscopy for reasons other than the evaluation of diarrhea or suspected malabsorption, who had endoscopic signs in the duodenum suggestive of celiac disease and in whom villous atrophy was confirmed. Patients were assessed for nutritional deficiencies, reduced bone density, parameters of calcium metabolism, and malignancies. RESULTS: Nine patients (3 women and 6 men) were identified among 1749 patients undergoing endoscopy between January 1990 and May 1998, representing a rate of unsuspected celiac disease of 1 per 194 endoscopies. The duodenal abnormalities were as follows: reduced or absent folds in 6, scalloped folds in 5, mosaic appearance in 3, and mucosal fissures in 2. Assessment revealed iron deficiency in 5, folate deficiency in 1, osteopenia in 4, osteoporosis in 1, and hypocalciuria in 4. Three had malignancies associated with celiac disease, 2 esophageal squamous carcinomas, and 1 jejunal adenocarcinoma. CONCLUSIONS: Unsuspected celiac disease can be diagnosed at endoscopy by recognition of changes in the duodenum. When detected, patients have one or more manifestations of the disease. Celiac disease is more common in the United States than previously considered and endoscopy provides an opportunity to establish the diagnosis.

Adult↗
PubMed2002

Ganglioside reactive antibodies in the neuropathy associated with celiac disease.

We tested patients with celiac disease (CD) for the presence of serum anti-ganglioside antibodies. Six of twenty-seven patient sera were reactive against brain gangliosides by an agglutination immunoassay. Neurological examination in all six revealed the presence of distal sensory loss, consistent with the diagnosis of peripheral neuropathy. When tested by ELISA for antibodies to isolated GM1, GM2, GD1a, GD1b, GT1b, and GQ1b gangliosides, all six were positive for IgG antibodies to at least one. The neuropathy of celiac disease may be autoimmune and associated with anti-ganglioside antibodies. The presence of IgG reactivity furthermore implicates a T cell-mediated response to ganglioside antigens.

Adult↗