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PubMed2005

Intestinal involvement is not sufficient to explain hypertransaminasemia in celiac disease?

Chronic unexplained hypertransaminasemia is an isolated clinical manifestation of celiac disease (CD) and lacks of a clear physiopathological explanation. Since CD and tropical sprue (TS) have similar intestinal functional and histological pattern of injury and that an increased inflammatory response has been reported to occur in patients with irritable bowel syndrome (IBS), liver involvement might be expected to occur either in TS or IBS. However, according to author's prior observations, the frequency of hypertransaminasemia is significantly higher in CD than in TS and IBS-diarrhea predominant patients (IBS-D). Thus, based on current knowledge, intestinal mucosal damage, increased intestinal permeability and/or an active intestinal inflammatory response do not completely explain liver damage in CD. We hypothesize that other factors, unique to CD not present in TS or IBS-D, like gluten toxicity and the presence of tissular transglutaminase (tTG) an auto-antigen with pro-inflammatory and remodeling properties, act in addition to intestinal mucosal injury and account to hypertransaminasemia in CD. Further research focusing on the mechanisms of gluten and tTG hepatic toxicity, and/or the characterization of the expression, secretion and enteral-hepatic transport of certain pro-inflammatory cytokines is needed, to understand the possible links between intestinal and liver disorders seen in CD.

Animals↗
PubMedDate not supplied

Antibodies to 90 kilodalton glycoprotein in childhood and adolescent celiac disease: relationship to reticulin antibodies.

Antibodies to 90 kilodalton (kDa) glycoprotein, a mannose-rich protein of skin and intestinal mucosa, were determined in 31 children or adolescents with untreated celiac disease, in 30 of these patients during gluten withdrawal, and in 17 patients on gluten challenge. Highly elevated antibody levels to 90 kDa glycoprotein were found in patients with untreated celiac disease. Close, positive correlation (r = 0.74, p less than 0.0005) was found between the age of these patients and the level of 90 kDa glycoprotein antibodies. The antibodies to 90 kDa glycoprotein behaved, compared with the reticulin antibodies, in a different manner kinetically. During gluten challenge antibodies to 90 kDa glycoprotein increased on an average 2.6 months later than the antibodies to reticulin. On the other hand, in patients undergoing gluten withdrawal the antibodies to reticulin markedly decreased or disappeared during the first 3 months on the diet, whereas the level of 90 kDa glycoprotein antibodies did not decrease until the 5th to 11th months on the diet. These results suggest that the antibodies reacting with the 90 kDa glycoprotein differ from those reacting with reticulin and that in celiac patients undergoing gluten challenge the synthesis of reticulin antibodies is an earlier event than the production of 90 kDa glycoprotein antibodies. The level of 90 kDa glycoprotein antibodies may reflect the extent of tissue damage.

Adolescent↗
PubMedDate not supplied

Catch-up growth after the introduction of a gluten-free diet in children with celiac disease.

The rhythm of nutritional recovery in 11 children with celiac disease after the introduction of a gluten-free diet was studied. The mean age of the patients at the moment of the diagnosis was 2.8 +/- 1.2 years and they were followed up for a period of 3.4 +/- 1.9 years. The nutritional status was evaluated by the utilization of the following parameters: the weight-for-age, height-for-age and weight-for-height. It was verified that none child was well nourished at the moment of the diagnosis and during the evolution 9 of them reached a complete recovery of their nutritional status for the weight in a mean period of time of 5.8 +/- 2.7 months; 5 of these children remained well nourished during the follow-up, 3 for 33 months and 1 for just a month. The other 2 children were initially classified as PCM II and turned to PCM I. The height-for-age index revealed that only 6 children had recovered from malnutrition and only 4 remained like this during all the follow-up. The other 2 children suffered nutritional aggravation and turned to be PCM I, but after a mean time of 18.4 months both resumed the rhythm of growth. Nutritional dwarfsism in 45.45% and chronic evoluted malnutrition in 54.55% were the patterns of malnutrition observed in this group of patients.

Body Height↗
PubMed2006

Characterizing the circulating, gliadin-specific CD4+ memory T cells in patients with celiac disease: linkage between memory function, gut homing and Th1 polarization.

Celiac disease (CD) is a chronic, immune-mediated disorder of the gut, driven by T cells reacting locally to a distinct antigen, gliadin. Thus, CD offers the opportunity to study the T cell memory response to gliadin and whether gut tropism and T helper cell type 1 (Th1) polarization, which characterize the effector phase, are preserved in the memory progeny. It is notable that previous studies yielded conflicting results as to the presence of gliadin-specific memory CD4+ T cells in the peripheral blood of CD patients. However, we used a different and highly sensitive approach based on fluorescein-derived label dilution, whereby the memory cells are identified operationally by their greater capacity to proliferate upon re-encounter with antigen. Thus, using flow cytometry, we could resolve multiple successive generations as well as immunophenotype the dividing cells. Here, we show that the peripheral blood lymphocyte of some CD patients on a gliadin-free diet, but not healthy donors, contains a detectable population of CD4+ memory T cells specific for deamidated gliadin. Moreover, these gliadin-specific memory T cells are marked by a distinctive phenotype: They express high levels of the gut-homing beta7 integrins and primarily produce interferon-gamma and tumor necrosis factor alpha. We conclude that memory for gliadin-derived antigens within the circulating CD4+ T cells is linked with gut tropism as well as Th1 polarization.

Adolescent↗
PubMed2004

Fermentation of endogenous substrates is responsible for increased fasting breath hydrogen levels in celiac disease.

Fasting breath hydrogen (FBH) levels are frequently increased in celiac disease (CD). In this study we sought to determine whether the unknown source of the fermented substrates is endogenous glycoproteins shed or exuded through the damaged mucosa. To test the role of nonabsorbable exogenous substrates, we subjected 39 untreated and 23 treated CD patients and 37 healthy volunteers to the H(2) breath test after administration of lactulose after both an unrestricted and a restricted pretest meal. To test the relevance of endogenous substrates, we measured breath H(2) excretion during a 9-hour fast and after the administration of lactulose solution. To determine whether the luminal content of CD patients contains an increased amount of fermentable substrates, we incubated samples of jejunal juice from 7 untreated CD patients, 6 healthy volunteers, and 6 dyspeptic patients in vitro with a fecal homogenate obtained from a healthy H(2)-producer volunteer and measured the cumulative H(2) production. Untreated CD patients showed higher FBH levels than did treated patients and healthy volunteers. Only in untreated CD did FBH levels show no difference if a restricted or an unrestricted dinner was eaten the evening before the test. Nine-hour FBH levels were significantly higher in untreated CD than in healthy volunteers, whereas no difference was found after administration of lactulose. In vitro H(2) production was significantly higher in untreated CD patients than in controls. Increased FBH levels in CD do not depend on fermentation of malabsorbed exogenous substrates; endogenous substrates are increased in the lumens of CD patients and may be responsible for increased FBH levels.

Adult↗
PubMed2003

Tissue transglutaminase immunoglobulin isotypes in children with untreated and treated celiac disease.

OBJECTIVES: Tissue transglutaminase (tTG) autoantibodies are serologic markers for celiac disease (CD). The aim was to determine the diagnostic sensitivity and specificity of different immunoglobulin isotypes against tTG. METHODS: Immunoglobulin A (IgA)-tTG, IgG-tTG, and IgG1-tTG were measured in radioligand binding assays in 67 children with untreated and 89 children with treated CD and compared with 48 biopsy controls. IgM-tTG was measured in children with untreated CD and in biopsy controls. IgA endomysial autoantibodies (EMA) were analyzed in all children using an immunofluorescence method. RESULTS: The sensitivity of IgA-tTG and IgG-tTG was 85.1% (57 of 67) and 83.6% (56 of 67), respectively, which both increased to 93.8% (45 of 48) in children diagnosed at age 2 years or older. Both had a specificity of 93.8% (45 of 48). IgA-EMA had a sensitivity of 80.6% (54 of 67) and a specificity of 91.7% (44 of 48). In treated CD, IgA-tTG and IgG-tTG were detected in 21.3% (19 of 89) and in 14.6% (13 of 89), respectively, despite negative EMA titers. IgG1-tTG was correlated to age (r = -0.47, P = 0.0005) and detected in 50.7% (34 of 67) with untreated CD compared with 11.2% (10 of 89) with treated CD and with 4.2% (2 of 48) of biopsy controls ( P < 0.0001, respectively). IgM-tTG was detected in 1.5% (1 of 67) with untreated CD and in none of biopsy controls. CONCLUSION: IgA-tTG and IgG-tTG analyzed in radioligand binding assays are equivalent to IgA-EMA as screening tests for CD during childhood, but an intestinal biopsy is still the method of choice to establish the diagnosis. Although IgG1-tTG was more common at young age of diagnosis, both IgG1-tTG and IgM-tTG had low specificity and sensitivity and may not be useful as screening tests for CD.

Adolescent↗
PubMed2004

Bone quantitative ultrasound and bone mineral density in children with celiac disease.

OBJECTIVES: Osteoporosis is the most common manifestation of untreated celiac disease (CD). Bone quantitative ultrasound (QUS) has recently emerged as a new modality for bone status assessment. We evaluated bone status in children with CD using dual-energy x-ray absorptiometry and quantitative ultrasound. METHODS: This cross-sectional study included 41 children (13 girls, 28 boys) aged 11.2 +/- 3.6 years with CD. All children had been diagnosed with CD for at least 1 year (mean, 5.7 +/- 4.3 years). The results of lumbar spine bone mineral density assessed by dual-energy x-ray absorptiometry and the measurements of the velocity of ultrasound wave (at distal radius and midshaft tibia sites), expressed as speed of sound in m/s, were compared between children adherent to gluten-free diet (GFD) and non-compliant children. RESULTS: Speed of sound z-scores at tibia were below -2 SD in 20 of 41 children (49%), whereas lumbar spine bone mineral density z-scores were below -2 SD in 4 of 41 (10%) children with CD (P = 0.0002). Only 19 of 41 children were strictly compliant to GFD. The prevalence of tibia speed of sound z-scores <-2 SD was significantly higher in non-compliant children (15 of 22, 68%) compared with children on GFD (5 of 19, 26%), (P = 0.01). Children non-compliant with GFD had significantly worse tibia speed of sound z-scores (-2.3 +/- 1.8, mean +/- SD) compared with children on GFD (-1.2 +/- 1.5, mean +/- SD) (P = 0.04). CONCLUSIONS: Children with CD on a gluten-containing diet had higher prevalence of abnormal tibia bone SOS and lower z-scores compared with children on a GFD. These differences were not detected by spinal dual-energy x-ray absorptiometry or radius speed of sound. The value of quantitative ultrasound for screening and follow-up of children with CD should be further evaluated.

Absorptiometry, Photon↗
PubMed2001

Basal and fat-stimulated plasma peptide YY levels in celiac disease.

The distal gut hormone peptide YY (PYY) mediates feedback inhibition of gastric acid secretion, gastrointestinal motility, and pancreatic enzyme output. To investigate the influence of maldigestion on PYY, we determined plasma PYY levels in patients with celiac disease under basal conditions and in response to intraduodenal fat. Basal PYY was increased in untreated celiac patients (N = 13) compared to patients on a gluten free diet (N = 9) [15.6 (11.8-27.0) pM vs 12.2 (10.1-13.1) pM; P < 0.05] and compared to control subjects (N = 15) [9.5 (8.3-10.4) pM; P < 0.001]. Integrated PYY in response to intraduodenally infused predigested fat (1071+/-293 pM 80 min) was significantly (P < 0.05) greater than in response to undigested fat (322+/-223 pM 80 min) in six untreated celiacs. Plasma concentrations of PYY and cholecystokinin were strongly correlated (r = 0.79; P < 0.001). We conclude that basal PYY levels in untreated celiac disease are elevated, that predigestion of fat enhances PYY release in these patients, and that PYY secretion is correlated with CCK release.

Case-Control Studies↗
PubMed1990

A new laboratory kit for anti-gliadin IgA at diagnosis and follow-up of childhood celiac disease.

A new laboratory kit measuring anti-gliadin IgA level by enzyme immunoassay has been evaluated to assess the test's potential for screening children with suspected celiac disease for small intestinal biopsy and predicting mucosal relapse after gluten challenge. One hundred thirty children were tested, and the results were related to the histopathologic findings of the intestinal mucosa and the final diagnosis. The sensitivity of the test was 97% and the specificity was 92% in the studied population. Forty-five children with celiac disease on different diets were observed. All had reduced anti-gliadin IgA levels on a gluten-free diet, and 91% had normal levels after 1 year. Two of four patients with increased values had an insufficient diet. During gluten challenge, 38 of 45 children showed increased anti-gliadin IgA levels. Of the remaining seven, five reacted either with immediate and strong symptoms or had spontaneously reduced gluten intake, or had an acquired IgA deficiency. In two cases, there was no explanation. In five children without relapse on gluten challenge, the anti-gliadin IgA level remained normal. Provided that IgA deficiency is ruled out and the gluten intake is sufficient, the test is reliable for screening and has a potential to replace the third biopsy.

Antibodies↗
PubMed2003

Celiac disease association with CD8+ T cell responses: identification of a novel gliadin-derived HLA-A2-restricted epitope.

One of the diagnostic hallmarks of the histological lesions associated with celiac disease is the extensive infiltration of the small intestinal epithelium by CD8(+) T cells of unknown Ag specificity. In this study, we report recognition of the gliadin-derived peptide (A-gliadin 123-132) by CD8(+) T lymphocytes from celiac patients. A-gliadin 123-132-specific IFN-gamma production and cytotoxic activity were detected in PBMCs derived from patients on gluten-free diet, but not from either celiac patients on gluten-containing diet or healthy controls. In contrast, A-gliadin 123-132-specific cells were isolated from small intestine biopsies of patients on either gluten-free or gluten-containing diets. Short-term T cell lines derived from the small intestinal mucosa and specific for the 123-132 epitope recognized human APC pulsed with either whole recombinant alpha-gliadin or a partial pepsin-trypsin gliadin digest. Finally, we speculate on a possible mechanism leading to processing and presentation of class I-restricted gliadin-derived epitopes in celiac disease patients.

Adolescent↗
PubMed1987

Massive hepatic steatosis complicating adult celiac disease: report of a case and review of the literature.

Hepatomegaly, chronic diarrhea, and weight loss in a middle-aged woman were found to be due to massive hepatic steatosis and adult celiac disease. After she was on a gluten-free diet for 1 yr, improvement in clinical, laboratory, and pathological parameters was witnessed. Massive hepatic steatosis complicating adult celiac disease is an uncommon occurrence, differing from other, more frequently encountered hepatopathies in this disease, insofar as pathogenetic and prognostic aspects are concerned.

Adult↗
PubMed1997

Autism and celiac disease: failure to validate the hypothesis that a link might exist.

Autism is a heterogeneous condition and the possible pathogenic role of several different factors has been postulated. Association between celiac disease and neurological manifestations such as drug resistant epilepsy and cerebral calcifications is well known. Some authors in the past also reported the existence of a linkage with autism. On the basis of these observations, we have evaluated 120 patients with celiac disease diagnosed at the Pediatric Clinic of the University of Catania, Italy, in order to identify behavioral problems and autistic features: there were 20 controls for this part of the study. At the same time, AGA and AEMAb were assayed in 11 patients with infantile autism and 11 age- and sex-matched controls. No celiac case was detected among the group of autistic patients and, although two of them had slightly increased levels of AGA IgG and AEMAb, subsequent antibodies determinations and jejunal biopsies gave normal results. Moreover none of the celiac patients had a positive DSM-III-R test for infantile autism.

Autistic Disorder↗
PubMed2002

Diagnosis of celiac disease in pregnancy and puerperium: think about it.

We report 10 cases of celiac disease (CD) diagnosed after a pregnancy. During late pregnancy and/or puerperium a latent CD may be unmasked, so patients with mild gastrointestinal symptoms or anemia in pregnancy should be investigated to detect the disease before it might seriously affect maternofetal health.

Adult↗
PubMed1991

A family study confirms that the HLA-DP associations with celiac disease are the result of an extended HLA-DR3 haplotype.

Genotyping for HLA-DR, -DQ, and -DP antigens by restriction fragment length polymorphism (RFLP) analysis along with identification of restriction fragments associated with celiac disease (CD) were undertaken in 13 families in which more than one member had CD. Major histocompatibility complex class II haplotypes for the family members were constructed which included both genotypes and RFLP markers. In 12 of the families all the affected members shared an HLA haplotype which included HLA-DR3a, DQw2 and a BglII 4.0-kb DQA fragment. Eight of these 12 haplotypes also included HLA-DPw1 and both a RsaI 4.0-kb DPB fragment and an XbaI 16.0-kb DPA fragment. In one family, the two affected members shared an HLA-DR7, DQw2 haplotype, although both their second haplotypes included HLA-DR3a and -DQw2. The results suggest that HLA-DP genes do not play an independent predisposing role in the etiology of CD but do mark a disease-associated extended haplotype. This haplotype contains genes coding for specific HLA products which may be necessary for the disease to develop. The findings support the hypothesis that the presence of a specific DQ alpha/DQ beta heterodimer, encoded in a cis arrangement on HLA-DR3a haplotypes, predisposes to celiac disease.

Adolescent↗
PubMedDate not supplied

Common variable immunodeficiency, insulin-dependent diabetes mellitus and celiac disease.

Common variable immunodeficiency is a disorder characterised by hypogammaglobulinemia with B-lymphocytes in peripheral blood and repeated infections. We report a child with a diagnosis of diabetes mellitus and celiac disease during lactation, and in whom common variable immunodeficiency was diagnosed at the age of 5. During evolution of the disease he presented multiple respiratory infections in spite of substitution therapy with gamma globulins. He presented pulmonary fibrosis with a pulmonary volume reduced, and a spirometric restrictive patron. Immunologically, he presents reduction in CD4 lymphoid population. He expresses the alleles DQ2 A1 0501 and B1 which are strongly associated with susceptibility to insulin-dependent diabetes mellitus and celiac disease, but don't express antigens HLA class II DR3 and DR4 that are more frequent in these entities. The main disease and all the complications had affected his curve pondostatural.

Adolescent↗
PubMed2002

Assessment of correlation between the presence of antiendomysial antibodies and small intestine mucosal villous atrophy in the diagnostics of celiac disease.

BACKGROUND: The aim of the study was to analyze the degree of correlation between the presence of serum antiendomysial antibodies and villous atrophy in small intestine mucosa in patients with celiac disease. MATERIAL/METHODS: Retrospective analysis carried out in a group of 88 children and young adults (28 males, 60 females aged from 2 to 23) hospitalized in the Clinic from 1990 to the present with positive results of serum antiendomysial antibody test performed because of suspected celiac disease. The IgA - EmA test was performed after determination of whole IgA level in the serum using indirect immunofluorescence technique with monkey esophagus as an antigen. All patients underwent endoscopic small intestine biopsy with histopathological assessment of mucosal bioptates using standard hematoxylin and eosin staining. RESULTS: The serum levels of IgA in all investigated patients were normal. The levels of antiendomysial antibodies expressed in IF units ranged from 10 to 40960. Histopathological assessment of small intestine mucosal bioptates revealed partial (in 13.6% of patients) or total (in 86.4% of patients) villous atrophy. CONCLUSIONS: The study demonstrated complete correlation between the presence of serum antiendomysial antibodies and villous atrophy in the small intestine mucosa.

Adolescent↗
PubMed2003

A collaborative European search for non-DQA1*05-DQB1*02 celiac disease loci on HLA-DR3 haplotypes: analysis of transmission from homozygous parents.

The HLA-DQA1*05 with DQB1*02 alleles are a major risk factor for celiac disease (CD). To search for additional human leukocyte antigen (HLA) risk factors, we looked on the DR3-DQ2 risk haplotype, selected because it carries both DQ risk alleles in cis and is the more represented among CD patients. In a European consortium, we identified 109 families with a parent homozygous for DQA1*05-DQB1*02. We typed ten microsatellites in the extended HLA complex, and applied the homozygous-parent transmission disequilibrium test (HPTDT) and extended-TDT to transmissions from homozygous parents. These methods eliminate confounding due to linkage disequilibrium between candidate disease loci and the known risk factor DQA1*05-DQB1*02, and are favorable when sufficient families are available. We did not find evidence of association with any single marker or allele, although weak evidence for additional risk was observed, represented by preferential transmission of six adjacent markers. We tested the largest ever reported HPTDT population in CD, providing unprecedented power. We did not find significant evidence of additional risk-modifying factors on the DR3 haplotype, independent of DQA1*05-DQB1*02, although a weak tendency was observed for the B8-DR3 haplotype. This effect should be tested in large populations with significant representations of both B8-DR3 and non-B8 DR3 haplotypes.

Celiac Disease↗
PubMedDate not supplied

[Demonstration of celiac disease in Cuba].

A study performed in 50 children carriers of celiac disease with ages between 8 months and 14 years of age, is presented; diagnosis was proved based on clinical picture, histological changes of jejunal mucosa, intestinal absorption tests and response to the suppression of gluten from the diet, with clinical, histological and biochemical control according to international criteria. It has been insisted on the familial study and the gluten overload test and its incidency in the black race. The development of public health has made it possible to demostrate the existence of this disease in our country.

Adolescent↗