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PubMed2003

[Celiac disease and autoimmune diseases or systemic disease. Six cases and a review of the literature].

BACKGROUND: Celiac disease is an autoimmune disorder which may be associated with another autoimmune or systemic disease. OBJECTIVE: To determine the links between autoimmune diseases and celiac disease. PATIENTS AND METHODS: Among 31 patients with a celiac disease, we selected those who had another autoimmune or systemic disease. RESULTS: We report 6 patients with such disease association: 3 with autoimmune thyroiditis including one also with Grave's disease, 2 with systemic lupus erythematosus including one also with insulin-dependent diabetes mellitus, and 1 with temporal arteritis. CONCLUSION: The link between celiac disease and autoimmune thyroiditis or insulin-dependent diabetes mellitus seems to be real but many discrepancies are observed for the other autoimmune diseases. After a literature review, we suggest a summary of effective associations between celiac disease and autoimmune or systemic diseases.

Adolescent↗
PubMed1999

Helicobacter pylori infection in children with celiac disease: prevalence and clinicopathologic features.

BACKGROUND: Celiac disease is frequently associated with chronic gastritis. Helicobacter pylori is the main etiologic agent of chronic gastritis. The aim of this study was to assess the prevalence of H. pylori, the related symptoms, and the endoscopic and histologic gastric features in children with celiac disease. METHODS: Eight-one (24 boys, 57 girls; age range: 1.4-17.7 years, median 6.8) children with celiac disease were studied. All children had a blood sample taken. In a subgroup of 30 children who underwent endoscopy, three gastric biopsy specimens were taken for histology (hematoxylin and eosin, Giemsa, immunohistochemistry) and urease quick test. Symptom complaints were recorded. Age- and sex-matched (one case, one control) children without celiac disease were used for comparison. Serum H. pylori IgG were measured by means of a locally validated commercial enzyme-linked immunoassay. RESULTS: Overall, 15 of 81 (18.5%) children with celiac disease and 14 of 81 (17.3%) control children were positive for H. pylori. The percentage of H. pylori positivity was similar in children with untreated and treated celiac disease. Recurrent abdominal pain was the only symptom that helped to distinguish between H. pylori-positive and H. pylori-negative children. However, symptoms disappeared in patients with celiac disease after gluten withdrawal, irrespective of H. pylori status. All endoscopic (erythema, nodularity) and histologic (superficial-, interstitial-, lymphocytic-gastritis, activity, lymphoid follicles) findings did not differ between celiac and nonceliac H. pylori-positive children. CONCLUSIONS: Prevalence and clinical expressivity of H. pylori infection is not increased in children with celiac disease. The clinicopathologic pattern of the infection is not specifically influenced in this condition.

Abdominal Pain↗
PubMed1998

[Antigliadin antibodies in the absence of celiac disease].

Antigliadin antibodies (AGA) mark celiac disease, but AGA are also encountered in IgA-nephritis, psoriasis, sickle-cell anemia, hepatic disorders, juvenile rheumatoid arthritis, autoimmune thyroidism and in persons who occupationally contact great amounts of wheat. AGA IgA and/or IgG were registered in 19 of 60 subjects (51 adults and 9 children) with various immunomediated diseases without symptoms of celiac disease: in 4 cases of chronic active hepatitis, in 2 of 4 cases of chronic persistent hepatitis, in 4 of 16 cases of rheumatoid arthritis, in 3 of 19 cases of IgA-deficiency, in 1 of 8 cases of SLE, in 2 cases of postvaccine reaction, in all the single cases of juvenile rheumatoid arthritis, focal scleroderma, macroglobulinemia. IgA only occurred in in 6 patients, IgG- in 6 patients, both IgA and IgG in 7 patients. The most pronounced positive reaction to AGA was recorded in 8-year-old girl with juvenile rheumatoid arthritis. The emergence of AGA in immunomediated diseases may be attributed to the response to food protein in pathological conditions and is often unrelated closely with celiac disease.

Adolescent↗
PubMed2005

Follow-up of patients with celiac disease: achieving compliance with treatment.

Celiac disease is the only autoimmune condition for which we know the environmental trigger: gluten. Complete removal of gluten from the diet in a patient with celiac disease should result in symptomatic, serologic, and histologic remission. However, compliance with the gluten-free diet, especially in the United States, is extremely challenging. Compliance can be measured both noninvasively, by dietary history and measurement of serum antibodies, and invasively, by using endoscopic and histologic criteria. The advantages and disadvantages of these various modalities are discussed. The highest rates of compliance are reported in patients who are diagnosed as young children, whereas adolescents and those diagnosed via mass serologic screening have the most transgressions. Barriers to compliance include the poor palatability of gluten-free foods, confusing food-labeling practices, and common comorbid psychologic burdens such as anxiety and depression. Because celiac disease is a multisystemic disorder, physicians need to be aware of the potential autoimmune, nutritional, and malignant complications. An algorithm for the follow-up and management of the newly diagnosed celiac disease patient is presented, which includes regular follow-up; measurement of serum antibodies; eliciting a detailed dietary history; and examination for signs and symptoms of nutritional deficiencies, malignancy, and other autoimmune diseases. Ideally, a team approach to the follow-up of the newly diagnosed patient should include regular supervision by an interested physician, medical nutritional counseling by a registered dietician, and access to local and national support groups knowledgeable about this condition.

Adolescent↗
PubMed2004

[Celiac disease in adults: new aspects].

INTRODUCTION: Celiac disease also known as gluten-sensitive enteropathy is a complex disorder where genetically susceptible individuals develop in typical cases signs of malabsorption after ingestion of cereals. Malabsorption is due to total or subtotal atrophy of the small intestinal mucosa regressing after adherence to a gluten-free diet. The only effective therapy is life-long strict abstinence from wheat, rye and barley. CURRENT KNOWLEDGE AND KEY POINTS: During the last two decades spectrum of clinical features of adult celiac disease has been modified. About 60% of cases are now revealed by extraintestinal manifestations. Moreover, recent studies that used serological methods revealed existence of both latent and silent celiac sprue. The finding of the high frequency of atypical celiac sprue contributed to underestimation of the true prevalence of celiac disease until now, and explained that celiac disease could be unknown for a long time, with increased risk of nutritional deficiencies and malignancy. Concurrently, the finding that celiac disease is primarily associated to a few HLA class II molecules, and recent advent of tissue transglutaminase as the main auto-antigen eliciting anti-endomysial antibodies allowed to propose new pathogenesis hypothesis and efficient screening tests for celiac disease diagnosis. FUTURE PROSPECTS AND PROJECTS: New epidemiological data concerning adult celiac disease must incite to a more systematic screening in patients with atypical but evocative features, or in at-risk subjects. Introduction of enzyme linked immunosorbent assays (ELISA) for the detection for anti-tissue transglutaminase antibodies allows to make use of a new available and efficient diagnosis parameter, which could constitute the main screening test in the near future.

Adult↗
PubMed1999

Clinical features of celiac disease today.

The clinical spectrum of celiac disease has widened over the past decades. The condition is no longer a severe malabsorption syndrome. Instead, a typical celiac disease patient today has merely mild abdominal symptoms. Malabsorption can be subclinical or absent, and there is usually only moderate, if any, loss of weight. Simultaneously, the current prevalence has increased from 1:1,000 to 1:300 inhabitants, or even higher. Clinically silent celiac disease cases are being detected in increasing numbers since the introduction and widespread use of serologic screening tests. Symptoms of celiac disease can appear outside the intestine, a typical example being dermatitis herpetiformis. Gluten intolerance is no longer limited to overt villous atrophy. Inflammation without villous damage may be observed in genetically susceptible individuals. The term latent celiac disease is applied in situations where the patient has normal villous architecture while on a gluten-containing diet, but later develops small bowel villous atrophy compatible with celiac disease.

Autoimmune Diseases↗
PubMed2005

Mapping of gluten T-cell epitopes in the bread wheat ancestors: implications for celiac disease.

BACKGROUND AND AIMS: Celiac disease is a prevalent disorder characterized by a chronic intestinal inflammation driven by HLA-DQ2 or -DQ8-restricted T cells specific for ingested wheat gluten peptides. The dominant T-cell responses are to epitopes that cluster within a stable 33mer fragment formed by physiologic digestion of distinct alpha-gliadins. Celiac disease is treated by excluding all gluten proteins from the diet. Conceivably, a diet based on baking-quality gluten from a wheat species that expresses no or few T-cell stimulatory gluten peptides should be equally well tolerated by the celiac patients and, importantly, also be beneficial for disease prevention. METHODS: To identify baking quality, harmless wheat, we followed the evolution of the wheat back to the species that most likely have contributed the AA, BB, and DD genomes to the bread wheat. Gluten were extracted from a large collection of these ancient wheat species and screened for T-cell stimulatory gluten peptides. RESULTS: Distinct differences in the intestinal T-cell responses to the diploid species were identified. Interestingly, we found that the fragments identical or equivalent to the immunodominant 33mer fragment are encoded by alpha-gliadin genes on the wheat chromosome 6D and thus absent from gluten of diploid einkorn (AA) and even certain cultivars of the tetraploid (AABB) pasta wheat. CONCLUSIONS: These findings have implications for celiac disease because they raise the prospect of identifying or producing by breeding wheat species with low or absent levels of harmful gluten proteins.

Amino Acid Sequence↗
PubMedDate not supplied

Changes in gastrointestinal permeability in celiac disease.

Increased gastrointestinal permeability was found in celiac disease already 20 years ago. Originally a genetical defect was supposed leading to elevated permeability and later to celiac disease. However, patients under long-term gluten-free diet normalized their permeability tests. On the other side, unaffected relatives of patients with celiac disease showed high permeability but not different from patients with irritable bowel syndrome and with a tendency for normalization during follow-up. In active symptomatic celiac disease, permeability is elevated in the gastroduodenum - measured by sucrose test - as well as in the small intestine - measured by lactulose/mannitol ratio. The sensitivity in active celiac disease is high (near 100%), the specificity is low due to high permeability in many intestinal diseases as in acute infectious gastroenteritis, Crohn's disease, nonsteroidal anti-inflammatory drug treatment, etc. In contrast, lactulose/mannitol test permeability is much less sensitive in silent celiac disease without diarrhea (74%). The real importance of permeability disease is established by its use for follow-up of celiac patients under gluten-free diet whereas it is correlated to the degree of mucosal atrophy. In vitro tests also show increased lactulose mucosal to serosal flux in celiac disease, but not correlated to oral permeability test. In conclusion, lactulose/mannitol test is the only noninvasive functional test in celiac disease which has essential importance in active celiac disease and in follow-up under diet.

Celiac Disease↗
PubMed1993

Celiac disease among Ashkenazi Jews from Israel. A study of the HLA class II alleles and their associations with disease susceptibility.

The immunogenetics of celiac disease demonstrates a highly significant association with the HLA class II alleles DQA1*0501 DQB1*0201 encoded in either a cis- or trans-configuration. In Northern Europe, these alleles are found in linkage disequilibrium with DRB1*0301 while in Southern Europe an additional secondary association through linkage disequilibrium is seen with the combination DRB1*1101/0701. This study examines 34 Ashkenazi Jews with celiac disease and 36 ethnically matched controls to determine alleles at the DRB, DQA1, DQB1, and DPB1 loci using SSO probes in conjunction with gene amplification by the PCR. The results confirm a highly significant association with the DQA1*0501 DQB1*0201 allelic combination (71% celiac vs 8% control individuals; p = 0.00005; chi 2 = 21.4). Of celiac subjects, 29% were negative for the proposed DQ susceptibility alleles, the majority of whom were DRB1*0402 positive (20% overall celiac group). No additional susceptibility was associated at the DRB3 and DPB loci. This study confirms that the MHC-linked celiac disease susceptibility among Ashkenazi Jews is closely associated with the presence of the combination of alleles DQA1*0501 DQB1*0201. However, within this population of relatively high-prevalence celiac disease, 30% of celiac patients do not carry these alleles and are therefore not covered by a single "unifying" hypothesis.

Adolescent↗
PubMedDate not supplied

Spectrum of gastritis in celiac disease in childhood.

Celiac disease (CD) may cause changes throughout the gastrointestinal tract. The pathology is best described in the distal duodenum and jejunum. It is also associated with lymphocytic gastritis (LG) and varioliform gastritis in adults and children, but the histologic spectrum in the gastric biopsy and the clinical implications are undefined. In this report we relate our experience with the clinical, endoscopic, and histologic changes in gastric biopsies in CD in childhood. Slides (hematoxylin and eosin stained) were reviewed from 33 celiac children, 5 having had more than 1 gastric biopsy during a 7-year period. Gastric intraepithelial lymphocyte (IEL) counts were compared with those of 10 histologically normal controls (normal range, 1-7 IEL/100 antral or body epithelial cells) and 10 nonceliac chronic gastritis (CG) biopsies without H. pylori (normal range, 1-19 IEL/100 antral cells), noting changes in the epithelium and lamina propria (LP). LG was present in 29/33 initial biopsy sets. Fifteen of 29 showed LG/CG. The IEL number was greater in LG/CG than in LG only (27.2 +/- 9.3, n = 14 vs. 18.6 +/- 13.4, n = 15 in the antrum; 23.5 +/- 2.8, n = 4 vs. 13.0 +/- 8.4 in the body). In CD the difference between these mean values and those of normal and nonceliac CG controls was statistically significant. In CG/LG the inflammatory infiltrate was predominantly diffuse/superficial in the LP; mucin depletion was noted in 11/15. The IELs were in the LG/CG range in two CG controls. The IELs were normal at follow-up in five cases. There were no statistically significant differences between the groups with respect to clinical parameters or gastric endoscopic findings. No child had varioliform gastritis. We conclude that in CD children, the stomach is endoscopically unremarkable but may show LG, or LG/CG with or without mucin depletion, or occasionally appear normal. Gastric histology returned to normal with gluten withdrawal. Normal gastric histology is not typical, but does not exclude CD.

Biopsy↗
PubMed1997

[Primary non-Hodgkin's lymphoma of the intestine associated with asymptomatic celiac disease in adults].

Celiac disease (CD), a gluten-induced enteropathy, is characterized by typical intestinal involvement with classical clinic features in childhood and less frequent features in adult patients. Recognizing pauci- and asymptomatic patients is a critical point in the clinical management of CD because of the high mortality associated with the onset of complications. Among these, malignant diseases are the most severe, particularly squamous cell carcinoma and lymphoma, the latter accounting for 50% of all malignancies occurring in CD patients. The authors describe a 57 years old patient with CD and Enteropathy-Associated-T-Cell Lymphoma, who had no intestinal symptoms but only severe pruritus and hypereosinophilia.

Celiac Disease↗
PubMed1991

[Incidence of celiac disease in Vizcaya].

Celiac disease (CD) is a permanent gluten-sensitive enteropathy appearing in individuals genetcally predisposed. Its incidence varies according to the authors, but is situated about 1/1.500 alive newborn infants (ANI). Recently, a decreased in the incidence of the disease as well as a delay in the onset of symptoms have been reported in several countries. The incidence of the disease in Spain is unknown so we have studied it in our population. In the period 1976-1987, 117 patients were suspected to have CD in the different centers performing intestinal biopsies in Vizcaya. Diagnosis was confirmed in 87 cases, thus implying an incidence of 1/2.151 ANI. Age onset has been stable along the years, and most cases continue to be diagnosed during the first 2 years of life.

Biopsy↗
PubMed2004

Transglutaminase 2 in celiac disease: minireview article.

Celiac disease (CD) is an autoimmune pathology of the small intestine triggered, in genetically predisposed patients, by the exposition to gliadin, a flour protein, thus evoking local immune reactions and mucosal atrophy. The discovery that type 2 transglutaminase (TG2) is the main, if not the sole, target of the endomysium CD-specific autoantibodies assigned to this enzyme a master regulator role of CD. Two separated events, both based on the finding that gliadin is able to act as a TG2 substrate, have been described to indicate that TG2 is involved in both the humoral and cellular immune responses. In this paper we review the novel insights on the localization and enzymatic activity of TG2 in the small intestinal mucosa. Moreover, we report on the capability of gliadin and its peptides to act as TG2 substrates.

Celiac Disease↗
PubMed1985

The effect of early feeding on the onset of symptoms in celiac disease.

The appearance of celiac disease in infancy has often been related to the time when gluten is introduced into the diet, and more recently, to the kind of milk received in the early months. This retrospective study attempts to clarify the relation between breast-feeding and gluten introduction to the onset of symptoms of the disease. One hundred forty-six children with celiac disease, aged from 4 months to 11 years, were studied. The timing and types of feeds were recorded as well as the presenting symptoms of the disease. Data were analyzed by nonparametric statistical methods, as well as by parametric analysis after appropriate transformation. Children breast-fed for 3 months or more showed a marked delay in the onset of the disease and a longer latency time from gluten introduction to onset of disease, when compared with bottle-fed children. This relationship was present for both statistical analyses and was unrelated to the age at gluten introduction into the diet. Onset of disease was positively correlated to the duration of breast-feeding and not related to the age at gluten introduction.

Breast Feeding↗
PubMed2004

Allele and haplotype frequencies for HLA class II (DQA1 and DQB1) loci in patients with celiac disease from Spain.

Celiac disease (CD) is a complex and multifactorial disease, defined as a malabsorptive disorder of the small intestine resulting from ingestion of gluten. Genetic susceptibility to CD has been associated with human leukocyte antigen (HLA)-DQ2 heterodimer, encoded by the DQA1*0501 and DQB1*02 genes. However, HLA risk factors do not explain the whole genetic predisposition: not all DQ2-encoding haplotypes confer equal susceptibility to CD. The aim of the present work was to confirm the aforementioned findings in a southern European population. With this purpose, 136 unrelated children diagnosed with CD were typed at the DNA level for HLA-DQA1 and -DQB1 loci. Patients are currently attended at the Donostia Hospital (province of Guipúzcoa, Spain). HLA class II typing was performed by polymerase chain reaction-sequence specific primer procedures. Conspicuous frequencies of the alleles associated with susceptibility to CD were observed (DQA1*0501: 0.592, DQB1*0201: 0.471). Accordingly, the haplotypes DQA1*0501-DQB1*0201 and DQA1*0201-DQB1*0202 revealed a strong linkage disequilibrium (18.84% and 18.75%, respectively) when compared with the Spanish general population. Of the total sample, 93.4% (127 individuals) were carriers of DQ2 heterodimer, either in homozygosis or in heterozygosis. This percentage coincides with figures reported in previous studies, implying the effect of other genes in the development of CD.

Adolescent↗
PubMed2006

18F-FDG PET versus CT for the detection of enteropathy-associated T-cell lymphoma in refractory celiac disease.

UNLABELLED: Refractory celiac disease (RCD) can evolve into enteropathy-associated T-cell lymphoma (EATL). 18F-FDG PET has been reported to discriminate between RCD and EATL. Because prospective data are lacking, we designed a prospective study to evaluate the potential of 18F-FDG PET for detection of EATL in patients with RCD and compared the results with those obtained using abdominal CT in a referral center. METHODS: Between April 2003 and April 2005, 8 consecutive patients (median age, 66 y; range, 52-89 y) with EATL and 30 patients (median age, 61 y; range, 44-71 y) with RCD were included. CT and 18F-FDG PET were performed on all patients. Histologic evidence of EATL was identified in tissue samples obtained during upper gastrointestinal endoscopy or surgical resection. RESULTS: Villous atrophy was found in all patients with RCD and all (except 1) patients with EATL in nontumoral mucosa. Histologic examination of 1 patient with EATL localized in the duodenum showed intraepithelial lymphocytosis only. 18F-FDG PET could reveal sites histologically proven to be EATL in all 8 patients, whereas CT showed normal findings in 1 patient with EATL. 18F-FDG PET detected unsuspected extraintestinal sites affected by EATL in 2 patients. CT showed abnormalities such as a thickened small-bowel wall or lymphadenopathy in 14 patients with RCD lacking evidence of EATL at follow-up. 18F-FDG PET findings were positive in 3 and equivocal in another 3 patients with RCD. 18F-FDG PET was more sensitive and specific than CT (100% vs. 87% and 90% vs. 53%, respectively). CONCLUSION: Our data show that 18F-FDG PET is more sensitive in detecting EATL in patients with RCD than is CT. 18F-FDG PET, in addition to conventional CT, is recommended for evaluating patients with RCD.

Adult↗
PubMed1996

An autosomal screen for genes that predispose to celiac disease in the western counties of Ireland.

Celiac disease is a strongly heritable gastrointestinal illness that is an especially important model of the genetically complex multifactorial immune mediated diseases. The HLA component of celiac disease (a specific HLA-DQ heterodimer)is largely established and is relatively uncomplicated, and the environmental component (gluten and related grain storage proteins in the diet) is remarkably well understood. Previous family studies of celiac disease suggested that there is at least one important non-HLA locus. This locus may be a stronger genetic factor than HLA, and it apparently has a recessive mode of inheritance. We used a three step genome screening protocol to identify loci that contribute to celiac disease in the western counties of ireland, a region with the highest prevalence of celiac disease in the world. The most significant of several possible non-HLA loci that we found was on chromosome 6p about 30 cM telomeric from HLA. It has a multipoint maximum lod score of 4.66 (compared with 4.44 for HLA-DQ) and appears to have a recessive mode of inheritance. Our study localizes and provides strong evidence for linkage of at least one non-HLA locus to celiac disease and may serve as a prototype for an efficient approach to screening the human genome for loci that contribute to complex diseases.

Adolescent↗
PubMed2004

Collagenous colitis as the presenting feature of biopsy-defined celiac disease.

BACKGROUND: Prior case reports have linked celiac disease with collagenous colitis, but serological and retrospective pathologic survey studies of small intestinal biopsies have produced conflicting results. METHODS: In this report, consecutive patients with chronic diarrhea and the initial finding of collagenous colitis were evaluated to determine if occult celiac disease was also present. All 36 patients with no exclusions were offered upper endoscopy and biopsies. If the changes of untreated celiac disease were detected in the small intestinal biopsies, then a gluten-free diet was instituted. Diet response was based on resolution of diarrhea and normalization of repeated small intestinal biopsies. RESULTS: Eight patients, or over 20%, had severely abnormal small bowel biopsy changes characteristic of untreated celiac disease. In some, lymphocytic or collagenous gastritis were also detected with or without celiac disease. All 8 patients were treated with a gluten-free diet alone and, in all, diarrhea improved and small intestinal biopsies normalized. In 5, however, repeated colonic biopsies showed persistent collagen deposits. Autoimmune thyroid disease or neoplastic diseases, like lymphoma known to be associated with celiac disease were also noted in this cohort with collagenous colitis, often in the absence of celiac disease. CONCLUSIONS: This study indicates that collagenous colitis may be the presenting clinical and pathologic feature of celiac disease. Diagnosis of collagenous colitis should lead the clinician to consider exclusion of underlying occult celiac disease.

Adult↗