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PubMedDate not supplied

[Celiac disease and HLA in a hospital population of Uruguay].

Since the description of the association of HLA-B8 antigen with celiac disease, it has been confirmed by many authors. The incidence of HLA-B8 antigen is higher in adults and children when it is compared to apparently healthy controls. Some authors found a reduction on the incidence of HLA-B7 antigen and others suggested that a higher incidence of HLA-B12 antigen in patients HLA-B8 antigen negative, is associated with celiac disease. We studied 19 unrelated patients with celiac disease and 64 controls. Their ages range from 18 months to 18 years old, onset of the disease was during childhood. We determined twelve antigens of the HLA-A locus and thirteen antigens of the HLA-B locus. We used the NIH Microlymphocytotoxicity Technique. The degree of association was computed by the relative risk and the results were statistically evaluated by the X2. The statistically significant increase in frequency was shown only for HLA-A29 The results did not show neither the higher incidence for HLA-B8 found by other authors, nor the higher incidence for HLA-B12; however HLA-B7 was not detected in our patients. The final decision on the association of HLA-A29 antigen with celiac disease in our population will require examination of a broader panel of probands.

Adolescent↗
PubMed2005

Paterson Kelly syndrome in celiac disease.

The association of Paterson Brown Kelly Syndrome and celiac disease is not widely reported. Both the entities have iron deficiency anemia. This case report emphasizes the need of screening for celiac disease in patients with Paterson Kelly Syndrome.

Adult↗
PubMed2001

Serologic markers of untreated celiac disease in Libyan children: antigliadin, antitransglutaminase, antiendomysial, and anticalreticulin antibodies.

BACKGROUND: There are, as yet, no data available about the incidence of celiac disease in Libya. The aim of this study was to test the occurrence of serologic markers in a group of Libyan children with positive clinical and histologic findings indicative of celiac disease diagnosis. METHODS: Thirty-nine children with untreated celiac disease and 50 healthy school children, all younger than 14 years, were included in the study. Enzyme-linked immunosorbent assay for immunoglobulin G and immunoglobulin A (IgA) antigliadin, antitissue transglutaminase, and anticalreticulin antibodies was used to evaluate the serologic markers of the celiac patients. Immunoglobulin A antiendomysial antibodies were detected by indirect immunofluorescence using human umbilical cord tissue. RESULTS: Clinical symptoms at presentation were weight loss (82%), abdominal distension (61.5%), diarrhea or steatorrhea (59%), pallor (41%), abdominal pain (20.5%), constipation (15%), vomiting (10%), and short stature (7.7%). Most of these symptoms disappeared after introduction of a gluten-free diet. Of 39 patients, only 23 (59%) were endomysium positive and positive also in all other serologic markers. The second group of patients with positive clinical and biopsy findings but antiendomysial antibody-negative findings was subdivided into two subgroups according to the IgA antigliadin antibody results. Individuals in the IgA gliadin-negative subgroup also lacked IgA autoantibodies. CONCLUSIONS: The authors' findings stress the importance of serologic testing not only for screening but also for confirmation of celiac disease.

Adolescent↗
PubMed1986

An HLA-D region restriction fragment length polymorphism associated with celiac disease.

This study is the first to describe a molecular marker that distinguishes the celiac disease HLA-D region haplotype from a serologically identical haplotype in unaffected controls. Using a DQ beta chain cDNA probe and the restriction endonuclease Rsa I, we have detected a polymorphic 4.0 kb fragment which, in DQw2 individuals, is associated with a 40-fold increased relative risk of developing celiac disease. This finding should permit the identification of the celiac disease susceptibility gene(s) in the HLA-D region and facilitate a more precise dissection of the molecular and immunogenetic mechanisms involved in the pathogenesis of that disease.

Celiac Disease↗
PubMed2003

[The neurological manifestations of celiac disease in children].

Neurological manifestations are occasionally associated with celiac disease in both adults and children. In the past these manifestations were related to nutritional deficiencies. However, since neurological manifestations can be demonstrated in patients without nutritional deficiencies, the etiology may be immune or toxic mediated. We present an update on the neurological manifestations of celiac disease, particularly in children.

Adolescent↗
PubMed1990

Celiac disease: parental knowledge and attitudes of dietary compliance.

Parents of 43 children with celiac disease, 28% of whom were classified as noncompliant, were interviewed. The knowledge, attitudes, and dietary behavior of parents of compliant patients were compared with those of noncompliant patients. Parents of compliant patients are better educated and from a higher social class. Although objective knowledge of the disease is similar in both groups, parents of compliant patients consider themselves adequately informed about the disease and are better able to choose gluten-free items from a menu. Parents of compliant patients are less worried about health in general but are more concerned with possible adverse effects celiac disease might have on the future of their children. Parents of both groups are not significantly different with regard to their understanding of the diet, the tendency to use medical care, and the perception of barriers to compliance or social support. It was concluded that to increase dietary compliance in celiac patients, parents should be guided mainly by the following three purposes: (1) enhancing their subjective evaluation of their own knowledge of celiac disease; (2) improving their practical ability to handle a menu; (3) increasing their anxiety regarding possible long-term adverse effects.

Adolescent↗
PubMed1999

In vitro production of endomysial antibodies in cultured duodenal mucosa from patients with celiac disease.

OBJECTIVE: Endomysial antibodies (EMAs) had been found recently after in vitro gluten challenge of duodenal mucosa from treated celiac patients. This was a promising result for diagnosis of potential/latent celiac disease. Therefore, we tested the usefulness of the production of EMAs of in vitro-challenged mucosa for diagnosis of celiac disease and determined the location of EMA production. METHODS: We investigated EMAs in the serum, in the supernatants of in vitro gliadin-challenged duodenal mucosa specimens in 68 patients, and in homogenized native duodenal and gastric specimens in seven patients. Twenty-one of the 68 patients served as nonceliac controls, 11 as candidates for potential celiac disease, 23 celiac patients were on glutenfree diet, and 13 were newly diagnosed. RESULTS: EMAs were just found in the supernatants of duodenal biopsies of those celiac patients who had demonstrable EMAs in serum, independent of gliadin challenge. In these patients EMAs were also found in homogenized native duodenal biopsies, but not in gastric biopsies. CONCLUSIONS: EMAs seem to be produced in the small bowel mucosa of celiac patients, but not in other tissues such as gastric mucosa. The production of EMAs could not be initiated under standard in vitro conditions and therefore, such as in vitro challenge cannot be used for diagnostic purposes.

Adult↗
PubMedDate not supplied

What is the role of celiac disease in enteropathy-type intestinal lymphoma? A retrospective study of nine cases.

BACKGROUND AND AIMS: It is generally accepted that enteropathy-type intestinal lymphoma (EATL) arises against a background of gluten enteropathy. We investigate whether patients with this diagnosis had celiac disease or pre-existing celiac disease, based on gliadin and endomysium antibodies, as well as duodenal biopsies, HLA typing and response to gluten-free diet. METHODS AND RESULTS: Retrospective study of patients with the diagnosis of peripheral T cell lymphoma of the intestine between January 1990 and January 2002 at the university hospital Gasthuisberg Leuven (n = 14). Patients in whom serologic testing was performed or patients known with pre-existing celiac disease (CD) were included (n = 9). Six of these nine patients were tested for endomysium antibodies (AEM), none of them were positive. Of the six patients with biopsies of mucosa uninvolved by lymphoma, all of them had villous atrophy; five had increased intraepithelial lymphocytes (IEL). In the four patients were HLA typing was performed, the results were compatible with CD. The three patients with initially diagnosed celiac disease all improved on gluten free diet (control biopsies improved as well, but failed to normalise). Of the six other patients, one patient never started GFD, two didn't get better, one initially went better after GFD, and one went better with the concomitantly started chemotherapy. CONCLUSION: There are two possible explanations: Either these patients with EATL have indeed gluten intolerance but the sensitivity of AEM is overestimated in this patient population; or these patients don't have gluten intolerance and EATL itself can mimic CD or other factors mimicking CD are at risk for developing EATL.

Autoantibodies↗
PubMed2006

Usefulness of duodenal biopsy during routine upper gastrointestinal endoscopy for diagnosis of celiac disease.

AIM: To describe the trend in duodenal biopsy performance during routine upper gastrointestinal endoscopy in an adult Spanish population, and to analyze its value for the diagnosis of celiac disease in clinical practice. METHODS: A 15 year-trend (1990 to 2004) in duodenal biopsy performed when undertaking upper gastrointestinal endoscopy was studied. We analysed the prevalence of celiac disease in the overall group, and in the subgroups with anaemia and/or chronic diarrhoea. RESULTS: Duodenal biopsy was performed in 1033 of 13 678 upper gastrointestinal endoscopies (7.6%); an increase in the use of such was observed over the study period (1.9% in 1990-1994, 5% in 1995-1999 and 12.8% in 2000-2004). Celiac disease was diagnosed in 22 patients (2.2%), this being more frequent in women than in men (3% and 1% respectively). Fourteen out of 514 (2.7%) patients with anaemia, 12 out of 141 (8.5%) with chronic diarrhoea and 8 out of 42 (19%) with anaemia plus chronic diarrhoea had celiac disease. A classical clinical presentation was observed in 55% of the cases, 23% of the patients had associated dermatitis herpetiformis and 64% presented anaemia; 9% were diagnosed by familial screening and 5% by cryptogenetic hypertransaminasaemia. CONCLUSION: Duodenal biopsy undertaken during routine upper gastrointestinal endoscopy in adults, has been gradually incorporated into clinical practice, and is a useful tool for the diagnosis of celiac disease in high risk groups such as those with anaemia and/or chronic diarrhoea.

Adult↗
PubMedDate not supplied

[Prevalence of serologic markers in celiac disease in trisomy 21 in Tunisia].

PURPOSE: This study was aimed to investigate the prevalence of serologic markers of celiac disease in Tunisian patients with trisomy 21. METHODS: Twenty seven patients with trisomy 21 were prospectively screened by indirect immunofluorescence for anti-reticulin and anti-endomysium antibodies, and by an ELISA method for anti-gliadin and anti-transglutaminase antibodies. None of the 27 patients had known celiac disease at the time of the study. RESULTS: Anti-reticulin, anti-endomysium, anti-gliadin and anti-transglutaminase antibodies were found in respectively 11%, 11%, 18.5%, and 14.8% of cases. Only one patient with all serologic markers of celiac disease underwent biopsy which shows a villous atrophy. CONCLUSION: Anti-endomysium and anti-transglutaminase antibodies are good immunologic markers for the screening for celiac disease, a screening which is justified in patient with trisomy 21.

Adolescent↗
PubMed1991

Gastrointestinal endocrine cell hyperplasia in celiac disease: a selective proliferative process of serotonergic cells.

Untreated celiac disease is characterized by gastrointestinal endocrine cell hyperplasia (ECH). This study investigated the constitutive nature of the ECH. Ten duodenal biopsies showing villous atrophy from adult celiacs were evaluated against ten sex- and age-matched controls. The mean number of endocrine cells per unit length of mucosa in the celiacs was compared with the control group using the Student t test. These values, respectively, were as follows: Churukian-Schenk method, 52.4 versus 29.6 (P = 0.001); Fontana-Masson, 32.5 versus 18.4 (P = 0.016); chromogranin, 33.4 versus 23.6 (P = 0.017); serotonin, 44.7 versus 26.7 (P = 0.006); somatostatin, 5.0 versus 5.4 (P = 0.631); and gastrin, 0.37 versus 0.37 (P = 1.000). There was thus ECH as shown by the first four stains with, in some areas, the endocrine cells continuously abutting against each other to form linear profiles. With respect to specific hormonal products, only serotonin showed ECH. These results suggest that the ECH in celiac disease is not a haphazard process but, instead, a selective proliferation of certain endocrine cell types.

Adult↗
PubMed2006

Epilepsy and celiac disease: favorable outcome with a gluten-free diet in a patient refractory to antiepileptic drugs.

BACKGROUND: There is a well-documented relationship between epilepsy and celiac disease, including a syndrome characterized by epilepsy, occipital calcifications, and celiac disease. REVIEW SUMMARY: We report the case of a 23-year-old woman with an 11-year history of refractory epileptic seizures and newly diagnosed biopsy-proven celiac disease with increased antiendomysium immunoglobulin A antibodies. The patient showed a dramatic improvement after starting a gluten-free diet. CONCLUSION: This case emphasizes the need to include celiac disease in the differential diagnosis when investigating the etiology of epilepsy in refractory patients.

Adult↗
PubMedDate not supplied

[Assessment of gliadin in pharmaceutical products - important information to the orientation of celiac disease patients].

BACKGROUND: Some drugs might contain gliadin which can be dangerous for celiac disease patients. OBJECTIVE: Detect gliadin in pharmaceutical products commonly used in Brazil. METHODS: We analyzed 78 pharmaceutical products selected aleatory from a list of 180 products most frequently sold at Brazilian community pharmacies. The analyzed samples were analgesics (n = 9), anthelmintics (n = 3), antacids (n = 8), antibiotics (n = 13), anticholesteremics (n = 1), anticonvulsants (n = 2), antidepressants (n = 2), antiemetics (n = 3), antihypertensives (n = 3), antihistaminics (n = 3), anti-inflammatories (n = 7), antipyretics (n = 2), bronchodilators (n = 1), laxatives (n = 1), oral contraceptives (n = 5) and vitamins (n = 10). The samples were analyzed by enzyme immunoassay based on monoclonal antibodies omega-gliadins, the elected technique according to the Codex Alimentarius Commission WHO/FAO. All samples were analyzed in duplicate. The sensitivity of this test is 4 mg of gliadin/100 g of product. RESULTS: Only one (1.3%) out of 78 pharmaceutical products contained detectable amounts of gliadin (5.5 mg/100 g). The active ingredient of this drug is ranitidine. According to the Codex Alimentarius Commission WHO/FAO the intake of 10 mg of gliadin/day should not be exceeded by celiac disease patients. Considering the amount of gliadin in each capsule of ranitidine, the ingested quantity would be lower than the maximum allowed for celiac patients. CONCLUSIONS: In this study gliadin was not detected in pharmaceutical products in harmful amount for celiac disease patients.

Brazil↗
PubMedDate not supplied

[Some clinical aspects of celiac disease (author's transl)].

220 jejunal biopsies have been performed in 146 children. Out of these, thirteen have been recognized as suffering from celiac disease. Furthermore, the possibility of celiac disease being associated with other gastrointestinal disorders, either of the stomach or of the sigma and rectum has been considered. Any explanation for this association can only be hypothetical, because the pathogenesis of celiac disease needs further study.

Biopsy↗
PubMed2002

Immunohistochemical analysis of ZO-1 in the duodenal mucosa of patients with untreated and treated celiac disease.

BACKGROUND/AIM: ZO-1 is a good marker for tight junction integrity which may be damaged in many intestinal diseases. ZO-1 can also accumulate in the cellular nucleus in addition to sites of cell-cell contact, suggesting a potential role in cellular proliferation and differentiation. We evaluated the expression and distribution of ZO-1 in patients with celiac disease before and after a gluten-free diet. METHODS: The ZO-1 expression was evaluated semiquantitatively by means of immunohistochemical analysis in duodenal bioptic specimens of 10 consecutive patients with celiac disease before and after a gluten-free diet and in 10 controls. Furthermore, the nuclear staining was analyzed quantitatively, evaluating 3,000 cells for each count, and it was expressed as a percentage of labeled nuclei over the total of analyzed cells. RESULTS: The intestinal mucosa of untreated celiac disease patients shows a globally lower ZO-1 labeling than that of controls. The expression of ZO-1 in the treated celiac mucosa did not differ significantly from normal intestinal mucosa of healthy subjects. At the crypt level of untreated celiac mucosa, a low intensity of nuclear labeling (1.75 +/- 0.32%) was found, while in both treated celiac disease patients and in normal subjects we observed a statistically significant higher percentage of strongly labeled nuclei (53.72 +/- 6.30% and 56.79 +/- 5.45%, respectively; p = 0.0002). CONCLUSIONS: Our data show a global underexpression of ZO-1 in the duodenal mucosa of active celiac disease patients. Gluten withdrawal allows a normalization of the ZO-1 expression in treated celiac disease patients. Furthermore, the particular pattern of ZO-1 resembles the cellular distribution in undifferentiated cells and may be the result of immaturity of the enterocytes in untreated celiac sprue.

Adult↗
PubMed2006

In celiac disease, a subset of autoantibodies against transglutaminase binds toll-like receptor 4 and induces activation of monocytes.

BACKGROUND: Celiac disease is a small intestine inflammatory disorder with multiple organ involvement, sustained by an inappropriate immune response to dietary gluten. Anti-transglutaminase antibodies are a typical serological marker in patients with active disease, and may disappear during a gluten-free diet treatment. Involvement of infectious agents and innate immunity has been suggested but never proven. Molecular mimicry is one of the mechanisms that links infection and autoimmunity. METHODS AND FINDINGS: In our attempt to clarify the pathogenesis of celiac disease, we screened a random peptide library with pooled sera of patients affected by active disease after a pre-screening with the sera of the same patients on a gluten-free diet. We identified a peptide recognized by serum immunoglobulins of patients with active disease, but not by those of patients on a gluten-free diet. This peptide shares homology with the rotavirus major neutralizing protein VP-7 and with the self-antigens tissue transglutaminase, human heat shock protein 60, desmoglein 1, and Toll-like receptor 4. We show that antibodies against the peptide affinity-purified from the sera of patients with active disease recognize the viral product and self-antigens in ELISA and Western blot. These antibodies were able to induce increased epithelial cell permeability evaluated by transepithelial flux of [(3)H] mannitol in the T84 human intestinal epithelial cell line. Finally, the purified antibodies induced monocyte activation upon binding Toll-like receptor 4, evaluated both by surface expression of activation markers and by production of pro-inflammatory cytokines. CONCLUSIONS: Our findings show that in active celiac disease, a subset of anti-transglutaminase IgA antibodies recognize the viral protein VP-7, suggesting a possible involvement of rotavirus infection in the pathogenesis of the disease, through a mechanism of molecular mimicry. Moreover, such antibodies recognize self-antigens and are functionally active, able to increase intestinal permeability and induce monocyte activation. We therefore provide evidence for the involvement of innate immunity in the pathogenesis of celiac disease through a previously unknown mechanism of engagement of Toll-like receptor 4.

Adolescent↗
PubMed2001

A prospective, longitudinal study of the long-term effect of treatment on bone density in children with celiac disease.

OBJECTIVE: Because osteopenia is a frequent complication of celiac disease, we evaluated the impact of a long-term gluten-free diet (GFD), initiated during childhood, on bone density. study design: Patients with celiac disease (n = 19; mean age, 14.2 +/- 2.6 years) were studied after 4.3 +/- 0.6 years of GFD. Bone density had been measured at diagnosis and after 1 year of GFD. We also studied 211 healthy children as a control group. Bone mineral density was measured by dual-energy x-ray absorptiometry. Intact parathyroid hormone (PTH) and bone-specific alkaline phosphatase (BALP) levels were measured in serum, and N-terminal telopeptide of type I collagen (NTx) was measured in urine. RESULTS: Although at diagnosis bone mineral content, bone area, and bone mineral density were significantly lower than in control subjects, the 3 measurements were normal after GFD. None of the patients on a GFD showed elevated values of PTH. Patients on a GFD had BALP (110.2 +/- 67.2 U/L) and NTx levels (261.9 +/- 187.8 nmol bone collagen equivalents/mmol creatinine) that were significantly higher than those of control subjects. The levels of BALP and NTx were significantly higher in patients with good compliance with the GFD, compared with patients with poorer compliance. CONCLUSIONS: This study shows that bone mineral content, bone area, and bone mineral density improve significantly with a GFD.

Absorptiometry, Photon↗
PubMed2002

Bone-specific antibodies in sera from patients with celiac disease: characterization and implications in osteoporosis.

Osteopenia and osteoporosis are well-known complications detected in celiac disease patients with still obscure pathogenesis. In the present study we investigated the presence of circulating anti-bone autoantibodies in patients with celiac disease and explored their role in the associated bone disease. We evaluated serum samples from 33 patients at the time of diagnosis and from 20 of them after treatment. Sera from patients with inflammatory bowel disease (n = 9), nonceliac osteoporotic (n = 18), and healthy individuals (n = 10) were used as controls. The presence of IgA specific anti-bone antibodies was first investigated using indirect immunofluorescence on cryosections of fetal rat tibia (20-day pregnancy). Furthermore, samples were homogenized and total tissue extracts were subjected to Western blot analysis to confirm immunoreactivity. At diagnosis, sera from 51.5% (17/33) of celiac patients had antibodies that recognized antigenic structures in chondrocytes and the extracellular matrix along mature cartilage, bone interface, and perichondrium of fetal rat bone. Among controls, only two osteoporotic patients showed very low titles of anti-bone autoantibodies. The immunostaining was localized in areas where an active mineralization process occurred and was similar to the distribution of the native bone tissue transglutaminase. The frequency of patients with positive baseline titers of anti-bone antibodies diminished significantly after treatment (P = 0.048). Western blot assays confirmed the presence of autoantibodies in sera from patients with a positive immunofluorescence staining. Autoantibodies recognized a major protein band on tissue extracts with a molecular weight of 77-80 kDa, which could be displaced when sera were preadsorbed with human recombinant tissue transglutaminase. We provide original evidence that patients with celiac disease have IgA-type circulating autoantibodies against intra- and extracellular structures of fetal rat tibia. Our findings suggest that these antibodies recognize bone tissue transglutaminase as the autoantigen, and based on the localization of the immunoreactivity we speculate that they might have an active role in the pathophysiology of celiac disease-associated bone complications.

Adult↗