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Celiac Disease (celiac + disease)
Selected AbstractsPediatric and Adolescent Medicine Frontiers in Celiac DiseaseACTA PAEDIATRICA, Issue 1 2009Lars Stenhammar No abstract is available for this article. [source] The analysis of the fine specificity of celiac disease antibodies using tissue transglutaminase fragmentsFEBS JOURNAL, Issue 21 2002Daniele Sblattero 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. [source] Celiac disease and dermatitis herpetiformis: the spectrum of gluten-sensitive enteropathyINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 8 2003Amy S. Oxentenko No abstract is available for this article. [source] Celiac disease: India on the global mapJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2006Surender Kumar Yachha [source] Prevalence of celiac disease among school children in Punjab, North IndiaJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2006Ajit Sood Abstract Background:, Celiac disease, as of today, is said to exist in almost all parts of the world, although it is rare among people of purely African,Caribbean, Japanese and Chinese background. The disease has also been considered uncommon in India until recently. Hospital records have revealed an increasing trend of the disease in predominantly wheat-eating areas of North India. The aim of the present study was to determine the prevalence of celiac disease among school children in Punjab, North India. Methods:, The study was carried out in the Ludhiana district of Punjab, Northern India. A total of 4347 children aged 3,17 years attending different schools were enrolled. A structured questionnaire was used to collect sociodemographic data and symptoms and signs related to celiac disease and various sociodemographic factors. The screening for celiac disease for the suspected celiacs was done by testing for antitissue transglutaminase (anti-tTG) by indirect solid-phase immunometric assay (ELISA). All children with high anti-tTG whose parents consented underwent upper gastrointestinal endoscopy for small bowel biopsy from the second part of the duodenum. Histopathology was expressed according to the Marsh classification of 1992. Follow up was carried out among children who were put on a gluten-restricted diet, at monthly intervals for 3 months and every 3 months thereafter. The diagnosis of celiac disease was established on the basis of the revised European Society of Paediatric Gastroenterologists and Nutritionists (ESPGAN) criteria (confirmed cases). Results:, A total of 4347 school children (1967 girls, 2380 boys, age range 3,17 years) were screened for celiac disease. Out of these, 198 suspected children were identified for further evaluation. Twenty-one children tested positive for anti-tTG assay (10.6%, 95% confidence interval: 16.91,34.79). Seventeen of these 21 children agreed to undergo biopsy; of these, 14 had histological changes consistent with celiac disease and all these 14 children had clinical response to gluten restriction. Three children with high anti-tTG had normal mucosa on duodenal biopsy and were not labelled as being in the celiac disease group. In the final analysis the disease prevalence was one in 310 children. Conclusions:, This is the first study on celiac disease prevalence among school children from India. Although this disease frequency of one in 310 is thought to be an under-assessment, it clearly shows that celiac disease is not rare in wheat-eating areas of North India. [source] Chronic urticaria and associated coeliac disease in children: A case,control studyPEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 5 2005L. Caminiti Celiac disease (CD) and chronic urticaria (CU) are both sustained by immune mechanisms, but there are so far few data on their clinical association. We performed a case,control study to determine the occurrence of CD in urticaria and matched control children, and to assess the clinical relevance of this association. Children and adolescents were diagnosed to have severe chronic idiopathic urticaria in the presence of hives for more than 6 wk poorly or not responsive to oral antihistamines. Other known causes of urticaria had to be excluded. A matched control group without urticaria was enrolled. In both groups, the presence of CD was searched by assaying antitransglutaminase and antiedomysial antibodies, and confirmed with endoscopic intestinal biopsy. Results. CD was diagnosed and confirmed in 4/79 (5.0%) of children with CU and in 17/2545 (0.67%) of the controls (p = 0.0003). In the four children with urticaria and CD the gluten free diet (GFD) lead to complete remission of urticaria within 5,10 wk, whereas the disappearance of serological markers occurred in longer times (5,9 months). Conclusions. The presence of CD in children with CU was significantly more frequent than in controls. GFD resulted in urticaria remission. CD may be regarded in such subjects as a cause of CU. [source] Celiac disease and pulmonary hemosiderosis in a patient with chronic granulomatous diseasePEDIATRIC PULMONOLOGY, Issue 4 2004Dominik Hartl MD Abstract We report on a patient with the hitherto undescribed combination of chronic granulomatous disease, pulmonary hemosiderosis, and celiac disease. The hemosiderosis resolved with a gluten-free diet and glucocorticosteroid pulse therapy, but the restrictive lung function pattern remained unchanged. Lung function improved markedly by immunosuppression with daily glucocorticosteroid and azathioprine treatment. Pediatr Pulmonol. 2004; 38:344,348. © 2004 Wiley-Liss, Inc. [source] Celiac disease with Takayasu arteritisPEDIATRICS INTERNATIONAL, Issue 6 2005Nur Arslan No abstract is available for this article. [source] Current dilemmas in Down syndrome clinical care: Celiac disease, thyroid disorders, and atlanto-axial instability,AMERICAN JOURNAL OF MEDICAL GENETICS, Issue 3 2006William I. Cohen Abstract This study will discuss our current understanding of celiac disease (CD), thyroid disorders, and atlanto-axial instability, three important areas of medical management in individuals with Down syndrome (DS). In this study, we highlight our current knowledge, as well as what we need to study in order to gather the necessary data to refine the empirically based screening protocols which are now in place. © 2006 Wiley-Liss, Inc. [source] Celiac disease and epilepsy: favorable outcome in a child with difficult to control seizuresACTA NEUROLOGICA SCANDINAVICA, Issue 4 2003R. Pratesi We report the case of a child with difficulties to control epilepsy and celiac disease, diagnosed soon after the onset of the seizure disorder. Seizure frequency and pattern, in addition to electroencephalogram record were suggestive of Lennox,Gastaut syndrome. Diagnosis of celiac disease was determined by positive anti-endomysium and anti-transglutaminase tests, and abnormal jejunal biopsy. Gluten-free diet, started soon after the diagnosis, led to progressive seizure control, allowing significant decrease in dosage of anti-epileptic drugs. This case corroborates the importance of serological screening tests for celiac disease, at least in patients with difficult to control epilepsy. [source] The gluten connection: the association between schizophrenia and celiac diseaseACTA PSYCHIATRICA SCANDINAVICA, Issue 2 2006A. E. Kalaydjian Objective:, Schizophrenia affects roughly 1% of the population and is considered one of the top 10 causes of disability worldwide. Given the immense cost to society, successful treatment options are imperative. Based on initial findings, gluten withdrawal may serve as a safe and economical alternative for the reduction of symptoms in a subset of patients. Method:, A review of the literature relevant to the association between schizophrenia and celiac disease (gluten intolerance) was conducted. Results:, A drastic reduction, if not full remission, of schizophrenic symptoms after initiation of gluten withdrawal has been noted in a variety of studies. However, this occurs only in a subset of schizophrenic patients. Conclusion:, Large-scale epidemiological studies and clinical trials are needed to confirm the association between gluten and schizophrenia, and address the underlying mechanisms by which this association occurs. [source] Digestive peptidases in Tenebrio molitor and possibility of use to treat celiac diseaseENTOMOLOGICAL RESEARCH, Issue 3 2007Elena N. ELPIDINA Abstract Digestion in Tenebrio molitor larvae occurs in the midgut, where there is a sharp pH gradient from 5.6 in the anterior midgut (AM) to 7.9 in the posterior midgut (PM). Accordingly, digestive enzymes are compartmentalized to the AM or PM. Enzymes in the AM are soluble and have acidic or neutral pH optima, while PM enzymes have alkaline pH optima. The main peptidases in the AM are cysteine endopeptidases presented by two to six subfractions of anionic proteins. The major activity belongs to cathepsin L, which has been purified and characterized. Serine post-proline cleaving peptidase with pH optimum 5.3 was also found in the AM. Typical serine digestive endopeptidases, trypsin-like and chymotrypsin-like, are compartmentalized to the PM. Trypsin-like activity is due to one cationic and three anionic proteinases. Chymotrypsin-like activity consists of one cationic and four anionic proteinases, four with an extended binding site. The major cationic trypsin and chymotrypsin have been purified and thoroughly characterized. The predicted amino acid sequences are available for purified cathepsin L, trypsin and chymotrypsin. Additional sequences for putative digestive cathepsins L, trypsins and chymotrypsins are available, implying multigene families for these enzymes. Exopeptidases are found in the PM and are presented by a single membrane aminopeptidase N-like peptidase and carboxypeptidase A, although multiple cDNAs for carboxypeptidase A were found in the AM, but not in the PM. The possibility of the use of two endopeptidases from the AM , cathepsin L and post-proline cleaving peptidase , in the treatment of celiac disease is discussed. [source] Effect of intravenous immunoglobulin on cerebellar ataxia and neuropathic pain associated with celiac diseaseEUROPEAN JOURNAL OF NEUROLOGY, Issue 12 2008N. Souayah Background:, Cerebellar syndrome and small fiber neuropathy may complicate celiac disease (CD) and may be resistant to a strict gluten-free diet. Methods:, Case series. Results:, We report three patients with biopsy-proven CD who developed cerebellar ataxia and neuropathic pain despite strict adherence to a gluten-free diet. A small fiber neuropathy was suggested by skin biopsy findings in two patients. All patients' symptoms, including small fiber neuropathy symptoms, responded to treatment with intravenous immunoglobulin (IVIG). Discontinuation of IVIG in two patients resulted in worsened ataxia that reversed after resumption of IVIG. Conclusion:, Intravenous immunoglobulin may be effective in treating cerebellar ataxia and small fiber neuropathy associated with CD, suggesting an immune pathogenesis. Further prospective, controlled studies are necessary to determine the long-term response to IVIG or other immunomodulation therapy. [source] Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease,HEPATOLOGY, Issue 6 2009Luca Miele The role played by the gut in nonalcoholic fatty liver disease (NAFLD) is still a matter of debate, although animal and human studies suggest that gut-derived endotoxin may be important. We investigated intestinal permeability in patients with NAFLD and evaluated the correlations between this phenomenon and the stage of the disease, the integrity of tight junctions within the small intestine, and prevalence of small intestinal bacterial overgrowth (SIBO). We examined 35 consecutive patients with biopsy-proven NAFLD, 27 with untreated celiac disease (as a model of intestinal hyperpermeability) and 24 healthy volunteers. We assessed the presence of SIBO by glucose breath testing (GBT), intestinal permeability by means of urinary excretion of 51Cr-ethylene diamine tetraacetate (51Cr-EDTA) test, and the integrity of tight junctions within the gut by immunohistochemical analysis of zona occludens-1 (ZO-1) expression in duodenal biopsy specimens. Patients with NAFLD had significantly increased gut permeability (compared with healthy subjects; P < 0.001) and a higher prevalence of SIBO, although both were lower than in the untreated celiac patients. In patients with NAFLD, both gut permeability and the prevalence of SIBO correlated with the severity of steatosis but not with presence of NASH. Conclusions: Our results provide the first evidence that NAFLD in humans is associated with increased gut permeability and that this abnormality is related to the increased prevalence of SIBO in these patients. The increased permeability appears to be caused by disruption of intercellular tight junctions in the intestine, and it may play an important role in the pathogenesis of hepatic fat deposition. (HEPATOLOGY 2009.) [source] Acute experimental colitis and human chronic inflammatory diseases share expression of inflammation-related genes with conserved Ets2 binding sitesINFLAMMATORY BOWEL DISEASES, Issue 2 2009Tineke C.T.M. van der Pouw Kraan PhD Abstract Background: Ulcerative colitis (UC) and Crohn's disease (CD) are characterized by chronic inflammation of the gastrointestinal tract, with overlapping clinical characteristics and unknown etiology. We reasoned that in intestinal inflammation the initial activation of the innate immune response fails to resolve, finally resulting in uncontrolled chronic inflammatory bowel disease. Methods: To identify the early inflammatory events in colitis that remain active in human chronic colitis, we analyzed the changes of the colonic transcriptome during acute experimental colitis and compared the outcome with previously published profiles of affected tissues from patients with UC and CD, and as a control for intestinal inflammation in general, tissues from celiac disease patients. Rheumatoid arthritis synovial tissues were included as a nonintestinal inflammatory disease. The expression profiles of each disease were analyzed separately, in which diseased tissues were compared to unaffected tissues from the same anatomical location. Results: Gene ontology analysis of significantly regulated genes revealed a marked activation of immunity and defense processes in all diseases, except celiac disease, where immune activation is less prominent. The control region of upregulated genes contained an increase in Ets2 binding sites in experimental colitis, UC, and rheumatoid arthritis, and were associated with upregulated immune activity. In contrast, upregulated genes in celiac disease harbored the transcription factor binding site GLI, which binds to the Gli family of transcription factors involved in hedgehog signaling, affecting development and morphogenesis. Conclusion: Ets2 may be an important transcription factor driving inflammation in acute as well as chronic inflammatory disease. (Inflamm Bowel Dis 2008) [source] Common biostructure of the fecal flora in celiac disease, Crohn's disease, and carcinoid tumorsINFLAMMATORY BOWEL DISEASES, Issue 11 2008Yvonne Döerffel No abstract is available for this article. [source] Active Crohn's disease and ulcerative colitis can be specifically diagnosed and monitored based on the biostructure of the fecal floraINFLAMMATORY BOWEL DISEASES, Issue 2 2008Alexander Swidsinski MD Abstract Background: The intestinal microflora is important in the pathogenesis of inflammatory bowel disease (IBD). The impact of its spatial organization on health and disease is unknown. Methods: We investigated sections of paraffin-embedded punched fecal cylinders. Fluctuations in spatial distribution of 11 bacterial groups were monitored in healthy subjects (n = 32), patients with IBD (n = 204), and other gastrointestinal diseases (n = 186) using fluorescence in situ hybridization (FISH). Results: The microbial structure differed in patients with Crohn's disease (CD), ulcerative colitis (UC), and healthy and disease controls. The profiles of CD and UC were distinctly opposite in 6 of 11 FISH probes used. Most prominent were a depletion of Faecalibacterium prausnitzii (Fprau<1 × 109/mL) with a normal leukocyte count in CD and a massive increase of leukocytes in the fecal-mucus transition zone (>30 leukocytes/104,m2) with high Fprau in patients with UC. These 2 features alone enabled the recognition of active CD (Crohn's Disease Activity Index [CDAI] >150) or UC (Clinical Activity Index [CAI] >3) with 79%/80% sensitivity and 98%/100% specificity. The mismatch in the sensitivity was mainly due to overlap between single IBD entities, and the specificity was exclusively due to the similarity of Crohn's and celiac disease. When inflammatory bowel disease (IBD) patients were pooled the sensitivity was 100% for severe disease, 84% for moderate activity, 72% for IBD with ,12 months remission, and 24% for IBD with >12 months remission. Conclusions: The fecal flora is highly structured and spatially organized. Diagnosing IBD and monitoring disease activity can be performed based on analysis of punched fecal cylinders independent from the patient's complaints. (Inflamm Bowel Dis 2007) [source] Local and systemic interleukin-18 and interleukin-18-binding protein in children with inflammatory bowel diseaseINFLAMMATORY BOWEL DISEASES, Issue 1 2008Steven T. Leach Abstract Background: Interleukin-18 (IL-18) is increased in the inflamed mucosa of patients with Crohn's disease (CD). The balance between this pleiotropic proinflammatory cytokine and its natural inhibitor, IL-18-binding protein (IL-18BP), may contribute to the pathogenesis of inflammatory bowel disease (IBD). Methods: Serum and mucosal biopsies were collected from children with IBD, from children with celiac disease, and from controls. Biopsies were maintained in culture for 24 hours, and supernatant was collected. Serum and supernatant IL-18 and IL-18BPa concentrations were measured by immunoassay. Disease activity score (PCDAI) and standard serum inflammatory markers (albumin, platelets, ESR, and CRP) were recorded. Results: Serum IL-18 was greater in children with CD (537 pg/mL) than in controls (335 pg/mL; P < 0.05) but not in children with ulcerative colitis (UC) or IBD type unclassified (IBDU). Mucosal IL-18 was greater in children with CD and UC/IBDU than in controls (P < 0.01). Serum IL-18BPa was increased in children with CD compared with that in controls (3.9 versus 2.6 ng/mL; P < 0.05), but was not elevated in children with UC/IBDU. Furthermore, calculated free-serum IL-18 was elevated in CD, but not UC/IBDU, compared with that in controls (P = 0.001). Total and free-serum IL-18 were elevated in severe CD relative to in mild/moderate disease. Conclusions: IL-18, produced in the colons of children with IBD, may contribute to local inflammatory changes. Systemic IL-18 level may be a useful indicator of gut inflammation. Furthermore, free IL-18 is greatly elevated in children with CD, suggesting that compensatory increases in IL-18BPa are insufficient. Further exploration of the role of this cytokine in the pathogenesis of IBD is now required. (Inflamm Bowel Dis 2007) [source] Inflammatory bowel disease in patients with celiac diseaseINFLAMMATORY BOWEL DISEASES, Issue 6 2005Alice Yang MD Abstract Background: Several case reports and series report an association between celiac disease and inflammatory bowel disease (IBD); however, there is no current data assessing this association. We therefore studied the occurrence of these conditions in a cohort of patients with celiac disease seen at a referral center. Methods: A database of patients with celiac disease seen between 1981 and 2002 was analyzed. Only biopsy-proven adults were included. Patients who had endoscopic and pathologic evidence of IBD were identified, and their pathology was reviewed. Age- and sex-adjusted prevalence rate ratios were determined by comparing results with population-based prevalence data. Results: Among 455 patients with celiac disease, IBD was identified in 10 (5 had ulcerative colitis and 5 had Crohn's disease). This represented an age- and sex-adjusted prevalence rate ratio for ulcerative colitis of 3.56 (95% confidence interval, 1.48-8.56) and for Crohn's disease of 8.49 (95% confidence interval, 3.53-20.42). Conclusion: Within our cohort of patients with celiac disease, IBD was significantly more common than in the general population. [source] Signal transducers and activators of transcription 3 signaling pathway.INFLAMMATORY BOWEL DISEASES, Issue 2 2005An Essential Mediator of Inflammatory Bowel Disease, Other Forms of Intestinal Inflammation Abstract Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of chronic inflammatory bowel disease (IBD), are characterized by mucosal immune cell activation that is driven by a cytokine imbalance. Several cytokines involved in IBD act through the activation of the signal transducers and activators of transcription (STAT) family. We investigated the activation of STAT3 in the mucosa of CD and UC patients, and evaluated whether this event is specific for IBD patients. Using immunofluorescence and immunoblotting, total and phosphorylated STAT3 levels were assessed in biopsy specimens, isolated lamina propria mononuclear cells, and peripheral blood mononuclear cells from patients with CD, UC, other forms of intestinal inflammation, and control subjects. Immunoblotting revealed phosphorylated STAT3 in mucosal biopsy specimens from patients with CD, UC, celiac disease, and acute self-limited colitis, but not in the normal mucosa of control subjects. In IBD patients, STAT3 activation was confined to actively inflamed areas. Accordingly, activated STAT3 was detected in isolated lamina propria mononuclear cells from inflamed IBD tissues, but not in peripheral blood mononuclear cells from control subjects or IBD patients. Immunofluorescence demonstrated that the sources of activated STAT3 were macrophages and T lymphocytes, but not neutrophils. STAT3 activation also was detected in T cells infiltrating the duodenal mucosa of celiac disease patients. We conclude that STAT3 signaling occurs in both CD and UC, where it is strictly confined to areas of active inflammation and is limited to infiltrating macrophages and T cells. The occurrence of STAT3 signaling in other acute and chronic intestinal inflammatory conditions suggests that, rather than a specific feature of IBD, it represents a fundamental signaling pathway that is shared by multiple forms of gut inflammation. [source] Mechanisms and modulation of intestinal epithelial repairINFLAMMATORY BOWEL DISEASES, Issue 1 2001Dr. Axel U. Dignass Abstract The mucosal epithelium of the alimentary tract represents a crucial barrier to a broad spectrum of noxious and immunogenic substances within the intestinal lumen. An impairment of the integrity of the mucosal epithelial barrier is observed in the course of various intestinal disorders including inflammatory bowel diseases (IBD), celiac disease, intestinal infections, and various other diseases. Furthermore, even under physiologic conditions temporary damage of the epithelial surface mucosa may be caused by proteases, residential flora, dietary compounds, or other factors. Generally, the integrity of the intestinal mucosal surface barrier is rapidly reestablished even after extensive destruction because of an enormous regenerative capability of the mucosal surface epithelium. Rapid resealing of the surface epithelium is accomplished by epithelial cell migration, also termed epithelial restitution, epithelial cell proliferation, and differentiation. Healing of the intestinal surface epithelium is regulated by a complex network of highly divergent factors, among them a broad spectrum of structurally distinct regulatory peptides that have been identified within the mucosa of the intestinal tract. These regulatory peptides, conventionally designated as growth factors and cytokines, play an essential role in regulating differential epithelial cell functions to preserve normal homeostasis and integrity of the intestinal mucosa. In addition, a number of other peptide molecules such as extracellular matrix factors and blood clotting factors, and also nonpeptide molecules including phospholipids, short-chain fatty acids, adenine nucleotides, trace elements, and pharmacological agents, have been demonstrated to modulate intestinal epithelial repair mechanisms. Some of these molecules may be released by platelets, adjacent stromal cells, inflammatory cells, or injured epithelial and nonepithelial cells and may play an important role in the modulation of intestinal injury. Repeated damage and injury of the intestinal surface are key features of various intestinal disorders including IBD and require constant repair of the epithelium. Enhancement of intestinal repair mechanisms by regulatory peptides or other modulatory factors may provide future approaches for the treatment of diseases that are characterized by injuries of the epithelial surface. [source] Mucosal tissue transglutaminase expression in celiac diseaseJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 2 2009Vincenzo Villanacci Abstract Tissue transglutaminase (tTG) plays an important role in celiac disease pathogenesis and antibodies to tTG are a diagnostic marker of gluten-sensitive enteropathy. The aim of this study was to investigate the localization of tTG in the duodenal mucosa in control tissues and in different histological stages of celiac disease by using a commercial and a novel set of anti-tTG monoclonal antibodies, to see whether this assessment can be useful for diagnostic purpose. The distribution of tTG was firstly evaluated in 18 untreated celiac patients by using a commercial monoclonal antibody (CUB7402) against tissue transglutaminase enzyme and directed against the loop-core region of the enzyme. Thereafter, in further 30 untreated celiac patients we employed three newly characterized anti-tTG monoclonal antibodies produced against recombinant human-tTG. The epitopes recognized are located in three distinct domains of the protein corresponding to the core, C1 and C2 protein structure. Eleven age- and sex-matched patients with chronic duodenitis acted as controls. All subjects underwent upper endoscopy to obtain biopsy samples from the duodenum. Overall, we found that (i) tTG is equally expressed in CD at different stages of disease; (ii) tTG is expressed, at similar level, in CD and controls with duodenitis. Assessment of tTG level in biopsy samples by immunohistochemical methods is not useful in the clinical diagnostic work-up of CD. [source] Low specificity of anti-tissue transglutaminase antibodies in patients with primary biliary cirrhosisJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 5 2006N. Bizzaro Abstract The association between celiac disease (CD) and primary biliary cirrhosis (PBC) is well documented in medical literature; however, a high frequency of false positive results of the anti-transglutaminase (anti-tTG) test has been reported in patients with PBC. To verify if the positive results for anti-tTG autoantibody are false positives due to cross reactivity with mitochondrial antigens, we studied 105 adult patients affected with PBC, positive for anti-mitochondrial M2 antibodies. Anti-tTG IgA antibodies were studied by using six different immunoenzymatic assays that employ the tTG antigen obtained from different sources (human recombinant, placenta, red blood cells, and guinea pig liver). On the whole, 28 out of 105 PBC subjects tested positive for anti-tTG IgA antibodies, but only two were eventually found to be affected by CD; the other 26 were shown to be false positive. The specificity of the various antigenic substrates ranged from 88.5% of the human erythrocytes tTG to 97.1% of the human recombinant tTG. The results of this study showed that a true association between PBC and CD was present in only 2% of the patients and that, in most cases, the false positive results were attributable to the type of substrate utilized in the assay. J. Clin. Lab. Anal. 20:184,189, 2006. © 2006 Wiley-Liss, Inc. [source] Role of anti-transglutaminase (anti-tTG), anti-gliadin, and anti-endomysium serum antibodies in diagnosing celiac disease: A comparison of four different commercial kits for anti-tTG determinationJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 3 2001D. Basso Abstract The aims of this study were: (1) to compare the diagnostic efficacy for celiac disease (CD) diagnosis of serum determination of anti-gliadin (AG) (IgA and IgG) and anti-endomysium (AE) with that of anti-transglutaminase (AtTG); and (2) to compare the accuracy of four different assays to measure AtTG. We studied 72 children: the histological diagnosis of CD was made in 38 cases and excluded in the remaining 34 children. In fasting sera we measured AE, AG-IgA and IgG, and AtTG, the latter with four different commercial kits (Eurospital, Medipan, Inova, Arnika). Moreover AtTG was measured in a group of 58 CD children after a gluten-free diet. AE was positive in all but 1 case of CD patients (sensitivity = 97%); false positive results were found in 1/34 controls (specificity = 97%). When a specificity of 95% was fixed, the sensitivities were 97% for AE, 83% for AG-IgA, and 63% for AG-IgG; the sensitivities of anti-tTG were 90, 84, 84, and 75% when measured with Eurospital, Medipan, Inova, and Arnika kits respectively. The new AtTG seems to be accurate enough to be proposed as a noninvasive diagnostic tool for CD diagnosis; the 4 kits analyzed showed similar diagnostic efficacy. J. Clin. Lab. Anal. 15:112,115, 2001. © 2001 Wiley-Liss, Inc. [source] Prevalence, human leukocyte antigen typing and strategy for screening among Asian first-degree relatives of children with celiac diseaseJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2 2010Anshu Srivastava Abstract Background and Aim:, Data on prevalence, human leukocyte antigen (HLA) typing and small bowel histology among first-degree relatives of subjects with celiac disease (CD) is scarce. This prospective study evaluated the prevalence and role of HLA DQ2/8 testing in screening of first-degree relatives of children with CD. Methods:, Thirty confirmed children with CD and 91/94 first-degree relatives (parents and siblings) were enrolled. HLA DQ2/8 testing was carried out in all index CD cases. Clinical evaluation with a questionnaire, total serum immunoglobulin A (IgA), human IgA-tissue transglutaminase (IgA-tTGA) and HLA DQ2/8 testing was carried out in all first-degree relatives. Subjects who were positive for IgA-tTGA were recommended endoscopic duodenal biopsy to document histological changes of CD. Results:, Nine first-degree relatives were positive for IgA-tTGA, seven underwent duodenal biopsy and four subjects had Marsh IIIa changes suggestive of CD. The prevalence of histologically confirmed CD in first-degree relatives was 4.4%. The prevalence of potential CD was 9.8%. IgA-tTGA-positive subjects (4/9) were significantly more often symptomatic than IgA-tTGA-negative first-degree relatives (2/82). Twenty-nine (96.6%) index cases of CD and all IgA-tTGA-positive first-degree relatives were positive for HLA DQ2. None of the index CD cases or first-degree relatives were HLA DQ8-positive. A total of 85% of the first-degree relatives were positive for HLA DQ2 and thus at risk of developing CD. Conclusions:, In this first Asian study on a limited number of families of children with CD, 4.4% of the first-degree relatives had CD. Only 15% of the first-degree relatives were negative for HLA DQ2/DQ8. Initial evaluation with HLA and serology followed by only serial serology in HLA-positive relatives is recommended. [source] Fifty years of Australian pediatric gastroenterologyJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2009Don Cameron Abstract When the Gastroenterological Society of Australia (GESA) began 50 years ago there were very few pediatric gastroenterologists in the world. The ,Mother' of Paediatric Gastroenterology was Australian Charlotte (,Charlo') Anderson who established one of the world's first pediatric gastroenterology units in Melbourne in the early 1960s. Her earlier work in Birmingham had identified gluten as the component of wheat responsible for celiac disease and helped separate maldigestion (cystic fibrosis) and mucosal malabsorption. The first comprehensive textbook of Paediatric Gastroenterology was edited by Charlotte Anderson and Valerie Burke in 1975. Rudge Townley succeeded Charlotte Anderson in Melbourne and went on to further develop small bowel biopsy techniques making it a safe, simple, and quick procedure that led to much greater understanding of small bowel disease and ultimately the discovery of Rotavirus by Ruth Bishop et al. and subsequently to Rotavirus immunization. Australian Paediatric Gastroenterology subsequently developed rapidly with units being established in all mainland capital cities by the end of the 1970s. The Australian Society of Paediatric Gastroenterology Hepatology and Nutrition (AuSPGHAN) was established in the 1980s. Australians have contributed significantly in many areas of gastroenterology in infants, children, and adolescents including celiac disease, cystic fibrosis, liver disease, transplantation, gastrointestinal infection, allergy, indigenous health, inflammatory bowel disease, gastrointestinal motility, and the development of novel tests of gastrointestinal function and basic science. There have also been major contributions to nutrition in cystic fibrosis, end-stage liver disease, and intestinal failure. The future of Australian Paediatric Gastroenterology is in good hands. [source] Effect of a gluten-free diet on growth and small-bowel histology in children with celiac disease in IndiaJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 8 2007Surender K Yachha Abstract Background and Aim:, Follow-up studies on growth and histological recovery of children with celiac disease (CD) while on a gluten-free diet (GFD) are lacking from Asia. We therefore assessed the effects of this diet. Methods:, Forty-two children with CD were enrolled. Weight and height were expressed as weight for height (WfH) and height standard deviation scores (HSDS), respectively. Twenty-five children had repeated duodenal biopsies after 1,2 years and 14 had a third biopsy after 3,7 years of GFD. Compliance was checked by regular interview and IgA antiendomysial antibody estimation (EMA). Results:, At diagnosis (n = 25), mean HSDS was ,3.3 ± 1.6 with 76% having a HSDS of <,2; 60% were undernourished (WfH mean 81.6 ± 5.7). Over a mean follow up of 3.7 years, HSDS improved to ,1.3 ± 1.7 and 84% cases achieved normal nutrition. Mean height velocity was 13.9 cm during first year and 5.6 cm in subsequent years. Small-bowel biopsies at diagnosis showed subtotal villous atrophy (Marsh IIIb) in 18 (72%) and partial villous atrophy (Marsh IIIa) in seven (28%) patients. Repeat biopsy at 1,2 years showed shift from subtotal to partial villous atrophy in 94% (n = 17/18) and normalization in one patient. In patients with Marsh IIIa improvement of partial villous atrophy was observed in all. Immunoglobulin A endomysial antibody was negative in 81%. Repeat biopsies at 5 years of GFD showed improvement to Marsh I,II, but none normalized. Conclusion:, The majority of children with CD show normalization of nutrition and growth after GFD. Small-bowel histology improves markedly but does not normalize even after 5 years of GFD. [source] Prevalence of celiac disease among school children in Punjab, North IndiaJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2006Ajit Sood Abstract Background:, Celiac disease, as of today, is said to exist in almost all parts of the world, although it is rare among people of purely African,Caribbean, Japanese and Chinese background. The disease has also been considered uncommon in India until recently. Hospital records have revealed an increasing trend of the disease in predominantly wheat-eating areas of North India. The aim of the present study was to determine the prevalence of celiac disease among school children in Punjab, North India. Methods:, The study was carried out in the Ludhiana district of Punjab, Northern India. A total of 4347 children aged 3,17 years attending different schools were enrolled. A structured questionnaire was used to collect sociodemographic data and symptoms and signs related to celiac disease and various sociodemographic factors. The screening for celiac disease for the suspected celiacs was done by testing for antitissue transglutaminase (anti-tTG) by indirect solid-phase immunometric assay (ELISA). All children with high anti-tTG whose parents consented underwent upper gastrointestinal endoscopy for small bowel biopsy from the second part of the duodenum. Histopathology was expressed according to the Marsh classification of 1992. Follow up was carried out among children who were put on a gluten-restricted diet, at monthly intervals for 3 months and every 3 months thereafter. The diagnosis of celiac disease was established on the basis of the revised European Society of Paediatric Gastroenterologists and Nutritionists (ESPGAN) criteria (confirmed cases). Results:, A total of 4347 school children (1967 girls, 2380 boys, age range 3,17 years) were screened for celiac disease. Out of these, 198 suspected children were identified for further evaluation. Twenty-one children tested positive for anti-tTG assay (10.6%, 95% confidence interval: 16.91,34.79). Seventeen of these 21 children agreed to undergo biopsy; of these, 14 had histological changes consistent with celiac disease and all these 14 children had clinical response to gluten restriction. Three children with high anti-tTG had normal mucosa on duodenal biopsy and were not labelled as being in the celiac disease group. In the final analysis the disease prevalence was one in 310 children. Conclusions:, This is the first study on celiac disease prevalence among school children from India. Although this disease frequency of one in 310 is thought to be an under-assessment, it clearly shows that celiac disease is not rare in wheat-eating areas of North India. [source] Gastrointestinal: Sonographic features of celiac diseaseJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2004S RICKES No abstract is available for this article. [source] Prevalence of undiagnosed coeliac syndrome in osteoporotic womenJOURNAL OF INTERNAL MEDICINE, Issue 4 2001R. Nuti Abstract.,Nuti R, Martini G, Valenti R, Giovani S, Salvadori S, Avanzati A (Institute of Internal Medicine, Metabolic Disease Unit, University of Siena, Siena, Italy). Prevalence of undiagnosed coeliac syndrome in osteoporotic women. J Intern Med 2001; 250: 361,366. Objectives.,The aims of the study were to quantify the prevalence of asymptomatic coeliac disease (CD) in a cohort of osteoporotic females, and to investigate the features of bone loss. Design and subjects.,We studied 255 women (mean age 66.6 ± 8.5 SD) with primary osteoporosis (WHO diagnostic criteria). After the first CD screening with the measure of serum IgG antigliadin antibodies (IgG-AGA), 53 women showed a positive test: antibodies to tissue transglutaminase (TG-ab) were subsequently determined to confirm the diagnosis of CD. Bone metabolism was evaluated by: serum and urinary calcium, serum and urinary phosphate, serum alkaline phosphatase, urinary crosslaps, serum 25(OH)D and serum parathyroid hormone. Results.,High levels of IgG-AGA and TG-ab were observed in 24 patients with a prevalence of serological disease of 9.4%. These women were characterized, in comparison with the other patients, by a statistically significant reduction in serum 25(OH)D (17.8 ± 7.2 vs. 55.1 ± 20.3 nmol L,1, P < 0.01) together with a significant increase of iPTH (65.1 ± 29.7 vs. 35.1 ± 20.0 pg mL,1; P < 0.01). Patients with high TG-ab levels showed also slightly raised values of urinary crosslaps (288 ± 88 vs. 270 ± 90 ,m mol,1 Cr). In IgG-AG positive patients a statistically significant inverse correlation was found between 25(OH)D serum levels and log-transformed TG-ab values (r: ,0.95, P < 0.001). Intestinal biopsies were obtained in 10 TG-ab positive women and verified CD in six patients. Conclusions.,These data support the hypothesis that patients with undiagnosed celiac disease develop high remodelling processes related to calcium malabsorption, secondary hyperparathyroidism and unavailability of vitamin D with a consequent more marked bone loss. [source] | |||||||||||||||||||||||||||||||||||||