Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CELIAC DISEASE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources
PubMed2002

Fracture risk in patients with celiac Disease, Crohn's disease, and ulcerative colitis: a nationwide follow-up study of 16,416 patients in Denmark.

The authors studied fracture risk among 16,416 Danish patients with bowel disease. All patients diagnosed with celiac disease (n = 1,021), Crohn's disease (n = 7,072), or ulcerative colitis (n = 8,323) in Denmark between January 1, 1983, and December 31, 1996, were included. Each patient was compared with three age- and gender-matched controls randomly drawn from the background population. No increase in fracture risk could be demonstrated for celiac disease before or after diagnosis. In patients with Crohn's disease, overall fracture risk was increased both before diagnosis (incidence rate ratio = 1.15, 95% confidence interval (CI): 1.00, 1.32) and after diagnosis (incidence rate ratio = 1.19, 95% CI: 1.06, 1.33). Bowel surgery was associated with a decreased risk of sustaining a fracture before diagnosis (odds ratio = 0.70, 95% CI: 0.54, 0.90) and after diagnosis (hazard ratio = 0.81, 95% CI: 0.67, 0.99). Overall fracture risk was not increased in patients with ulcerative colitis, except for a small increase around the time of diagnosis. Increasing age and having a fracture before diagnosis increased the risk of sustaining a new fracture after diagnosis. Crohn's disease was associated with a minor increase in overall fracture risk in contrast to ulcerative colitis and celiac disease. The severity of the inflammatory process and the amount of corticosteroids given may explain the difference in fracture risk.

Adult↗
PubMed2001

Immunologic evidence of no harmful effect of oats in celiac disease.

BACKGROUND: It was recently shown that antiendomysial antibodies (EMAs), which are highly sensitive and specific for celiac disease, are produced by intestinal mucosa. Furthermore, EMAs were detected previously in supernatant fluid from cultured duodenal mucosa specimens collected from untreated celiac disease patients and in culture media of biopsy specimens collected from treated celiac disease patients after an in vitro challenge with gliadin. Moreover, it was recently shown in vivo that oats are not toxic to celiac disease patients, suggesting the safety of oats in a gluten free-diet. OBJECTIVE: The objective was to better define the controversial role of oats in celiac disease to determine whether oats can be safely included in a gluten-free diet. DESIGN: We used an in vitro model to test whether oats induce EMA production in supernatant fluid from cultured duodenal mucosa specimens collected from 13 treated celiac disease patients. The biopsy specimens were cultured with and without peptic-tryptic digest (PT) of gliadin and avenin (from oats) and in medium alone. Samples from 5 of the 13 patients were cultured with the C fraction of PT-avenin. Indirect immunofluorescence was used to detect EMAs. RESULTS: EMAs were detected in specimens from all 13 patients after the challenge with gliadin but not after culture in medium alone. By contrast, no EMAs were detected in any of the specimens cultured with PT-avenin and its C fraction. CONCLUSIONS: Because the in vitro challenge with PT-avenin and its C fraction did not induce EMA production in treated celiac disease patients, it appears that oats have no harmful effect on celiac disease. Therefore, oats can be safely included in a gluten-free diet.

Adolescent↗
PubMedDate not supplied

The incidence of childhood celiac disease in Sweden.

Within a defined population in southeast Sweden, celiac disease was diagnosed in 167 children born between 1970 and 1982. The diagnosis was based on the criteria of the European Society for Paediatric Gastroenterology and Nutrition. Another six children had an initial flat small intestinal mucosa but do not yet fulfill the criteria for the diagnosis of celiac disease. The incidence of celiac disease was 1.27/1,000 live births for the years 1970-1976 and 1.43/1,000 for 1977-1982. In contrast to our findings, a decline in the disorder during the late 1970s was reported from other countries. We discuss the observation that the incidences of celiac disease in children are moving discrepantly in different populations.

Adolescent↗
PubMed2004

Development of clinical celiac disease after pancreatoduodenectomy: a potential complication of major upper abdominal surgery.

BACKGROUND: Celiac disease is a gluten-induced disease of global malabsorption. There is a subset of patients with celiac disease who are free of major symptoms but who have typical damage to the intestinal mucosa (silent disease). We present the case of a 50-year-old white woman with no clinical symptoms of celiac disease who developed diarrhea and weight loss 12 weeks after a pancreatoduodenectomy for ampullary cancer. METHODS: Microbiological and biochemical examination of the feces did not provide clues useful to diagnosis, and diarrhea was not affected by pancreatic enzyme replacement or administration of antiperistaltic drugs. RESULTS: Review of the pathologic specimen and blood tests were compatible with celiac disease. CONCLUSION: This clinical scenario illustrates that subclinical celiac disease may be an underdiagnosed cause of malabsorption after major upper gastrointestinal surgery and should be considered in the differential diagnosis of diarrhea after pancreatoduodenectomy.

Celiac Disease↗
PubMed1984

Determination of enteroglucagon in plasma for detection of celiac disease in children.

To evaluate the plasma enteroglucagon assay as a test for the detection of celiac disease, we have determined basal and postprandial concentrations of enteroglucagon in plasma of children who underwent small-intestinal biopsy because of suspected celiac disease. In the 14 children with untreated celiac disease both basal [81 (SD 33) pmol/L] and postprandial [129 (SD 26) pmol/L] concentrations of enteroglucagon were significantly higher (p less than 0.001) than in the 45 children with other gastrointestinal disorders [24 (SD 9) pmol/L, and 50 (SD 22) pmol/L, respectively] and in the 15 children without gastrointestinal disorders [14 (SD 10) pmol/L, and 35 (SD 8) pmol/L, respectively]. All children with celiac disease had either basal or postprandial plasma enteroglucagon concentrations exceeding the mean + 2 SD of the results for the children with other gastrointestinal disorders. Eight of 10 children with celiac disease in whom both concentrations were measured had increased values for both. In our study the sensitivity for detection of celiac disease was 100% and the specificity 97%. Evidently determination of plasma enteroglucagon concentration is effective in diagnosing celiac disease, thereby improving the selection of patients for small-intestinal biopsy.

Adolescent↗
PubMed1993

T-cell receptor variable genes and genetic susceptibility to celiac disease: an association and linkage study.

BACKGROUND: Genetic susceptibility of celiac disease is primarily associated with a particular combination of and HLA-DQA1/DQB1 gene; however, this does not fully account for the genetic predisposition. Therefore, the aim of this study was to examine whether T-cell receptor (TCR) genes may be susceptibility genes in celiac disease. METHODS: HLA class II typing was performed by polymerase chain reaction amplification in combination with sequence-specific oligonucleotide hybridization. TCR alpha (TCRA), TCR gamma (TCRG), and TCR beta (TCRB) loci were investigated by restriction fragment length polymorphism analysis. RESULTS: Allelic frequencies of TCRA, TCRG, and TCRB variable genes were compared between patients with celiac disease (n = 53) and control patients (n = 67), and relative risk (RR) estimates were calculated. The RR was 1.67 for allele C1 at TCRA1, 3.35 for allele D2 at TCRA2, 1.66 for allele B2 at TCRG, and 1.35 for allele B at TCRB, showing no significant association. Additionally, linkage analysis was performed in 23 families. The logarithm of odd scores for celiac disease vs. the TCR variable genes at TCRA, TCRG, and TCRB showed no significant linkage. CONCLUSIONS: These data suggest that the analyzed TCR variable gene segments V alpha 1.2, V gamma 11, and V beta 8 do not play a major role in susceptibility to celiac disease.

Adolescent↗
PubMed2005

[Screening for celiac disease in high risk groups].

Several epidemiological studies show that celiac disease with extraintestinal manifestations is 15 times more frequent than celiac disease with intestinal symptoms. Fifteen years ago the iceberg model was proposed to explain the epidemiology of this disease. On the one hand, there are a quantifiable number of patients who are correctly diagnosed since they have symptoms suggestive of this disease and who form the visible part of the iceberg. However, several studies using screening serology demonstrate that for each patient diagnosed, there is a mean of 5-10 patients without a diagnosis. These patients form the submerged part of the iceberg (monosymptomatic or silent celiac disease). The most widely accepted strategy to investigate the submerged part of the "celiac iceberg" is screening of known risk groups through a systematic search for celiac disease in these groups.

Celiac Disease↗
PubMed2004

Celiac disease. CME update for family physicians.

OBJECTIVE: To review current understanding of the epidemiology, pathophysiology, diagnosis, and management of celiac disease. QUALITY OF EVIDENCE: Few recent randomized controlled trials (level I evidence) have studied treatments for celiac disease. There are recent comparative studies (level II evidence) and there is well established consensus (level III evidence) on diagnosis and treatment of celiac disease. MAIN MESSAGE: Celiac disease is an immune-mediated small bowel enteropathy caused by exposure to wheat gluten protein. The disease can be insidious and often presents with only subtle extraintestinal manifestations in a variety of organ systems. Recent epidemiologic surveys suggest celiac disease is much more common in North America than previously thought. Advances in immunology and screening have made diagnosis more reliable than in the past. Removing gluten from the diet is effective in most cases. CONCLUSION: Celiac disease manifests subtly and is an easy diagnosis to miss. Good laboratory screening tests and effective treatment are available. Family practitioners should consider celiac disease in patients who present with confounding symptoms.

Algorithms↗
PubMed1997

IgA endomysium antibodies on human umbilical cord: an excellent diagnostic tool for celiac disease in childhood.

BACKGROUND: An improvement in screening for celiac disease has recently been described that uses human umbilical cord as a substitute for monkey esophagus to determine IgA endomysium antibodies in adults. As using monkey esophagus is ethically questionable for large-scale screening, we studied whether substitution of umbilical cord would be suitable for pediatric patients as well. METHODS: Serum from 53 children with untreated celiac disease, 22 in remission and 13 on challenge, were screened for antigliadin IgA, antigliadin IgG, and IgA reticulin antibodies, in addition to IgA endomysium antibodies tested both on monkey esophagus and on human umbilical cord. Controls included 20 patients with cow-milk-sensitive enteropathy, 23 with inflammatory bowel disease, and 23 with diabetes mellitus, and 48 patients who were biopsied to exclude celiac disease either because of positive gliadin antibody test or disturbed growth. RESULTS: Sensitivity (0.94) and specificity (1.0) were similar for umbilical cord and esophageal determinations in active celiac disease. Both substrates detected identical positive cases and neither gave false-positive results. In celiac patients on a gluten-free diet, endomysium antibodies with either substrate were positive in seven identical cases and negative in 15 of 22 cases. Correlations with reticulin antibodies were comparable with human umbilical cord and monkey esophagus (0.83 and 0.85, respectively; Spearman Correlation Section Pair-Wise deletion). CONCLUSIONS: Human umbilical cord is an excellent substitute for monkey esophagus to determine endomysium antibodies in celiac diagnosis in children and adolescents.

Adolescent↗
PubMed1995

T cell receptor gamma gene polymorphisms and class II human lymphocyte antigen genotypes in patients with celiac disease from the west of Ireland.

Although celiac disease has one of the strongest human lymphocyte antigen (HLA) class II associations of any human illness, it is clear that at least one gene that is not linked to the HLA region also is required for its pathogenesis. The occurrence of large numbers of gamma delta T cells in the bowel mucosa of patients and the recent description of T cell receptor (TCR) gamma chain polymorphic variants identified by restriction fragment length polymorphism analysis led the authors to examine TCR gamma genotypes in relation to HLA-DR, DQ genotypes in 89 patients with celiac disease and 55 control subjects from the West of Ireland. The overall frequency of TCR gamma genotypes in patients and control subjects was comparable. However, most of the patients had 1 of 3 HLA-DR3 genotypes (DR3/15, 3/7, or 3/3), and there was a significant alteration of the expected frequency of TCR gamma genotypes among patients with these three genotypes. The major differences were an increased association of HLA-DR3 homozygosity, with TCR gamma genotypes having a 16.0 kb fragment and an increased frequency of DR3/7 heterozygosity and decreased frequency of DR3/15 heterozygosity, respectively, in association with the TCR gamma 13.0/11.3 kb genotype. Based on their results, there is the possibility that an interaction between the products of two polymorphic and unlinked gene regions contributes to the pathogenesis of celiac disease.

Celiac Disease↗
PubMed1998

[Celiac disease in insulin-dependent diabetes mellitus].

A coincidence of celiac disease and insulin-dependent diabetes mellitus has been described in several studies. Celiac disease appears to be more common among patients with IDDM than in general population. The diagnosis of celiac disease requires histologic evidence of villous atrophy and a positive antibody test result. Typical gastrointestinal complaints of celiac disease are rare in IDDM patients, while atypical isolated symptoms of celiac are more common. It is recommended that all young diabetic patients, even those asymptomatic, should be screened for celiac. Routine screening is recommended repeatedly during first years after the diagnosis of IDDM.

Celiac Disease↗
PubMed2004

Celiac disease as a cause of growth retardation in childhood.

PURPOSE OF REVIEW: Celiac disease is a syndrome characterized by damage of the small intestinal mucosa caused by the gluten fraction of wheat proteins and similar alcohol-soluble proteins (prolamines) of barley and rye in genetically susceptible subjects. The presence of gluten in these subjects leads to a self- perpetuating mucosal damage, and the elimination of gluten results in full mucosal recovery. The clinical manifestations of celiac disease are protean in nature and vary markedly with the age of the patient, the duration and extent of disease, and the presence of extraintestinal pathologic changes. In addition to the classic gastrointestinal form, a variety of other clinical manifestations of the disease have been described, including atypical and asymptomatic forms. Although the typical form of celiac disease, characterized by failure to thrive, is still the most frequent presentation in the pediatric age group, severe growth delay is less commonly seen in developed countries. RECENT FINDINGS: Recent epidemiologic studies suggest that celiac disease-associated growth retardation is becoming a tangible health problem in developing countries, where the problem has been historically overlooked. Given the protean nature of the clinical presentation of celiac disease, the diagnosis is extremely challenging and relies on a sensitive and specific algorithm that allows the identification of different manifestations of the disease. Serologic tests developed in the past decade provide a noninvasive tool for screening individuals at risk for the disease as well as the general population. SUMMARY: The current gold standard for the diagnosis of celiac disease remains histologic confirmation of the intestinal damage in serologically positive individuals. The keystone treatment of celiac disease patients is a lifelong elimination diet in which food products containing gluten are avoided.

Autoimmune Diseases↗
PubMedDate not supplied

[Liver abnormalities in adult celiac disease. Clinicopathologic characterization and outcome after therapy].

BACKGROUND AND AIM: The clinical manifestations of adult celiac disease are highly varied and may include liver disease. The present study aimed to characterize liver abnormalities and outcome after a gluten-free diet in patients with celiac disease diagnosed in a hepatology clinic. MATERIAL AND METHOD: The clinical records of patients diagnosed with celiac disease during a 7-year period were reviewed. RESULTS: Of 1916 patients attending a first consultation at the clinic, 10 were finally diagnosed with celiac disease. All patients had been referred for evaluation of persistent elevation of liver enzyme levels. All patients were young (mean age 30 years, range 21-39 years) and there were more women than men (eight women, 80%). Six patients (60%) had additional manifestations attributable to undiagnosed celiac disease, sometimes since childhood. In all patients, elevation of liver enzyme levels was moderate and overall liver function was preserved. Liver biopsy was performed in five patients and all showed chronic periportal infiltrate. Immunohistochemical studies revealed that the infiltrate was mainly composed of CD8-positive T lymphocytes. In all patients, a gluten-free diet was followed by normalization of liver enzyme levels. CONCLUSIONS: Although celiac disease is not highly frequent, it should be considered in the differential diagnosis of patients with persistent abnormalities of liver markers. The most conspicuous histopathological change is periportal T-cell infiltrate. Liver abnormalities in celiac disease are generally mild and improve after a gluten-free diet.

Adult↗
PubMedDate not supplied

Perinuclear antineutrophil cytoplasmic antibodies in collagenous or lymphocytic colitis with or without celiac disease.

Microscopic forms of colitis, including lymphocytic and collagenous colitis, have been observed in both those with and without celiac disease. Although perinuclear antineutrophil cytoplasmic antibodies (p-ANCA) occur in most patients with ulcerative colitis, investigations in microscopic, particularly lymphocytic, colitis are still needed. In this study atypical p-ANCA was evaluated in 55 patients, including 27 with celiac disease alone, 13 with celiac disease and concomitant lymphocytic colitis, and 15 with microscopic forms of colitis, including lymphocytic and collagenous colitis. Nine patients (16.3%) had atypical p-ANCA, including six with celiac disease and three with a microscopic form of colitis alone. Although five of the six positive celiac disease patients had lymphocytic colitis, all three celiac disease patients with associated primary sclerosing cholangitis--a separate risk factor for a positive assay result--were serologically positive for atypical p-ANCA. These results indicate for the first time that this serological marker may occur in histologically defined celiac disease with or without concomitant lymphocytic colitis. Furthermore, these results suggest that the pathogenesis of ulcerative colitis differs from that of lymphocytic colitis and further emphasizes the heterogeneous nature of these newly recognized types of colonic inflammatory mucosal disorders.

Adolescent↗
PubMed2004

Gastrointestinal motility disturbances in celiac disease.

It is quite frequent to recognize celiac patients who show gastrointestinal motor abnormalities in clinical practice. In fact, in 30 to 60% of patients, physical examination and dyspeptic symptoms (epigastric discomfort, early satiety) suggest a gastrointestinal motility disorder. Consistent data are now available on the presence of a disturbed motility of the esophagus, stomach, small intestine, gallbladder, and colon of untreated celiac patients. Gastrointestinal abnormalities differ in different gastrointestinal districts. In fact, esophageal transit, gastric and gallbladder emptying, and orocecal transit time are delayed, while colonic transit is faster. These findings are related to the complex interactions among reduced absorption of food constituent (in particular, fat), neurologic alteration, and hormonal derangement. Motility disorders of the gut are also a predisposing factor in the development of small intestinal bacterial overgrowth and may contribute both to development of symptoms in some untreated celiacs and to the persistence of symptoms after gluten-free diet in some of them. All these alterations fortunately disappear after gluten-free diet, and patients return to well being status. Whatever the initial event in the pathogenesis of the celiac lesions may be, we know for certain at this time that gastrointestinal disturbances play an important role in the genesis of gastrointestinal symptoms in celiac disease and that surveillance for celiac disease in patients complaining of dysmotility-like dyspeptic symptoms should be increased.

Celiac Disease↗
PubMed1990

Small intestinal villous adenoma and celiac disease.

We describe the first patient with presumed celiac disease to present with a jejunal villous adenoma. Small bowel adenocarcinoma complicating celiac disease probably arises from adenoma, although this has not been previously addressed. The literature concerning factors in celiac disease predisposing to small intestinal epithelial neoplasia is reviewed.

Adenoma↗
PubMedDate not supplied

[Celiac disease under treatment: evaluation of bone mineral density].

OBJECTIVE: The present study was designed to compare the bone mineral density of children and adolescents with celiac disease to the bone mineral density of controls, and to evaluate laboratory analysis of calcium metabolism of celiac disease patients. METHODS: Thirty celiac disease patients (17 children, 13 adolescents), on a gluten-free diet, and 23 healthy subjects were studied. Tests of bone mineral density of the lumbar spine (DEXA, Lunar) were performed in all patients and controls. Laboratory analysis of calcium metabolism was performed in all patients. RESULTS: Mean weight and height of adolescents with celiac disease were lower than mean weight and height of controls (p<0.05). Bone mineral density in adolescents with celiac disease was significantly reduced if compared to controls (p=0.015), whereas no significant difference was found among children with celiac disease and controls. The number of adolescents who had started a gluten-free diet after the age of 2 years was higher than in children (p=0.003). Serum levels of ionized calcium, total calcium and parathormone were normal. CONCLUSION: The bone mineral density of adolescents with celiac disease was lower than controls; whereas, no difference was found between the bone mineral density of children with celiac disease and controls.

Adolescent↗
PubMed2006

IL-10 polymorphisms are associated with early-onset celiac disease and severe mucosal damage in patients of Caucasian origin.

PURPOSE: Polymorphisms in cytokine genes can determine their level of expression and affect the phenotypic expression of immunomediated diseases, such as celiac disease (CD). We thus evaluated cytokine polymorphism prevalence in CD patients and population controls, and assessed the correlation between specific polymorphisms and celiacs' clinical characteristics. METHODS: 155 CD patients and 202 population controls were enrolled in the study. Cytokine polymorphisms (TNFalpha -308 and -238, IL-1beta -511 and +3954, IL-1b RN + 2018, IL-6 -174, IL-10 -1082, -819 and -592, TGFbeta1 + 29 and +74, IFN-gamma + 874) and HLA class II alleles were determined by sequence-specific primer polymerase chain reaction or restriction fragment length polymorphism analysis. Duodenal histology was classified using Marsh's criteria. Variables significantly associated with CD patients' characteristics were identified by multivariate logistic regression analysis. RESULTS: A significantly higher frequency of -308 TNFalpha polymorphism was observed in CD patients compared to the entire population control group, although no difference was detected when population controls were stratified according to HLA class II. Among celiacs, early onset of the disease (< or =2 year old) and the presence of a severe intestinal lesion (Marsh 3C) were significantly associated with the -1082 A/A IL-10 genotype which corresponds to a low producer phenotype (OR 3.28, 95% CI 1.49-7.19 and OR 2.60, 95% CI 1.04-6.49, respectively). CONCLUSION: The association between IL-10 genotypes and both histological severity at diagnosis and age of onset could be related to an alteration in cytokine balance, and supports the idea that the various clinical manifestations of the disease could be determined by a different genetic background.

Age of Onset↗