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PubMed1999

Influence of jejunal morphology changes on exocrine pancreatic function in celiac disease.

BACKGROUND: Concurrent exocrine pancreatic dysfunction may be one of the factors implicated in malabsorption in untreated celiac disease, as shown by studies on bicarbonate and pancreatic enzyme secretion. The purpose of this study was to evaluate exocrine pancreatic function in relation to jejunal morphology in celiac disease. METHODS: Thirty-six patients fulfilling the ESPGHAN criteria for celiac disease, aged 3 to 18 years and 36 control subjects matched for age and sex were investigated. The design of the study included measurement of serum pancreatic isoamylase by a chromogenic method after selective inhibition of sialic isoamylase in the untreated phase in patients consuming a gluten-containing diet and after gluten elimination for a period of 1 year; fecal human elastase activity determined by enzyme-linked immunosorbent assay in patients consuming a gluten-free diet and again after gluten challenge for 6 months; correlation of serum pancreatic isoamylase and fecal elastase to the jejunal morphology, classified by criteria described by Marsch; the enzymes in the control group; and ultrasonography of the pancreas in both groups. RESULTS: Enzyme values obtained from celiac disease patients with normal mucosa were significantly higher than those obtained from patients with villous atrophy (p < 0.001) and comparable to those obtained from the control group. Serum pancreatic isoamylase activity increased to normal after gluten elimination, and human elastase activity decreased to values below 200 microg/g of stool after gluten challenge. Enzyme activity was related inversely to the degree of intestinal damage. The echogenicity of the pancreas was normal, regardless of enzyme activity or gut morphology. CONCLUSIONS: Exocrine pancreatic function is abnormal in celiac disease when mucosal atrophy is present. Exocrine pancreatic function parameters are associated with the changes of intestinal mucosal morphology in three consecutive phases of the disease.

Adolescent↗
PubMed2002

Gluten-sensitive enteropathy (celiac disease): more common than you think.

Gluten-sensitive enteropathy or, as it is more commonly called, celiac disease, is an autoimmune inflammatory disease of the small intestine that is precipitated by the ingestion of gluten, a component of wheat protein, in genetically susceptible persons. Exclusion of dietary gluten results in healing of the mucosa, resolution of the malabsorptive state, and reversal of most, if not all, effects of celiac disease. Recent studies in the United States suggest that the prevalence of celiac disease is approximately one case per 250 persons. Gluten-sensitive enteropathy commonly manifests as "silent" celiac disease (i.e., minimal or no symptoms). Serologic tests for antibodies against endomysium, transglutaminase, and gliadin identify most patients with the disease. Serologic testing should be considered in patients who are at increased genetic risk for gluten-sensitive enteropathy (i.e., family history of celiac disease or personal history of type I diabetes) and in patients who have chronic diarrhea, unexplained anemia, chronic fatigue, or unexplained weight loss. Early diagnosis and management are important to forestall serious consequences of malabsorption, such as osteoporosis and anemia.

Celiac Disease↗
PubMedDate not supplied

Celiac disease: strongly heritable, oligogenic, but genetically complex.

Celiac disease, or gluten-sensitive enteropathy, is a small intestinal disorder which affects up to 1:250 people in the United States. Disease development has a strong genetic component, with a sibling relative risk (lambda(s)) of 30. One susceptibility locus is the MHC region, with a particular association with the HLA-DQ alleles DQA1*0501 and DQB1*0201. However, haplotype sharing studies suggest that genes within the MHC complex contribute no more than 40% to the sibling familial risk of disease. This means that the stronger genetic risk is likely to be conferred by a small number of non-HLA-linked genes. Genome-wide linkage studies, plus linkage and association studies of candidate loci have been used to try to identify these genes. However, these studies have either failed to detect loci, or produced inconsistent results. Such difficulties in identifying susceptibility genes are encountered when investigating any complex genetic disorder. Information from the Human Genome Project, coupled with new technology for high throughput single nucleotide polymorphism typing may help to identify the non-HLA determinants of celiac disease in the future.

Celiac Disease↗
PubMed2001

Celiac disease without villous atrophy: revision of criteria called for.

Current diagnostic criteria of celiac disease require small bowel villous atrophy, although the damage develops gradually. We therefore searched for evidence of disease in 10 adults suspected to have celiac disease, but evincing only minor mucosal inflammation and increase in gammadelta+ cells without villous atrophy. Twenty untreated celiac and 27 nonceliac patients served as biopsy controls. CD3+, alphabeta+, and gammadelta+ cells were increased in patients with only minor mucosal lesions, but less than in celiac patients. The inflammation resolved on gluten-free diet, and abdominal symptoms were alleviated. Eight of 10 had positive endomysial, seven gliadin, and nine tissue transglutaminase antibodies; all normalized on diet. Eight patients had osteopenia; HLA DQ2 was found in all. Minor mucosal lesions with an increase in gammadelta+ intraepithelial lymphocytes were suggestive of celiac disease. Our patients showed a clinical, histological, and serological recovery on diet; risk of osteopenia speaks in favor of dietary treatment.

Adult↗
PubMed2005

Association of adult celiac disease with surgical abdominal pain: a case-control study in patients referred to secondary care.

BACKGROUND: Acute abdominal pain is the most common indication for surgical admission. Nonspecific abdominal pain (NSAP) may account for up to 40% of cases. There has been no published prospective study in which adult patients presenting with acute abdominal pain are investigated for celiac disease. AIMS: We aimed to assess the association of celiac disease with surgical abdominal pain. PATIENTS AND METHODS: A case-control study was undertaken involving 300 consecutive new unselected patients presenting with acute abdominal pain (in a university hospital) and healthy controls (age and sex matched) without abdominal pain (n = 300). Initial investigations for celiac disease were immunoglobulins, IgA/IgG anti-gliadin (AGA), and endomysial antibodies (EMA). Any patient with a positive IgA AGA, EMA, or only IgG AGA in the presence of IgA deficiency was offered a small bowel biopsy to confirm the diagnosis. RESULTS: : There were 33 patients with abdominal pain who had positive antibodies, of whom 9 had histologically confirmed celiac disease (6 EMA positive; 3 EMA negative). One antibody positive patient (EMA in isolation) declined duodenal biopsy and the remaining 23 had normal duodenal mucosa. Within the control group, there were 2 cases of celiac disease. Compared with matched controls the association of acute abdominal pain with celiac disease gave an odds ratio 4.6. (P = 0.068, 95% confidence interval, 1.11-19.05). When only considering NSAP the prevalence of celiac disease was highly significant at 10.5% (9 of 86, P = 0.006). Patients' symptoms improved on a gluten-free diet at 12- to 18-month follow-up. CONCLUSION: Celiac disease was diagnosed in 3% of patients who presented with unselected acute abdominal pain to secondary care. Targeting patients who have NSAP or celiac associated symptoms/diseases may improve the diagnostic yield.

Abdomen, Acute↗
PubMed2002

Etiology of nonresponsive celiac disease: results of a systematic approach.

OBJECTIVES: Nonresponse or relapse of symptoms is common in patients with celiac disease treated with gluten free diet. Refractory sprue (RS) is defined as initial or subsequent failure of a strict gluten-free diet to restore normal intestinal architecture and function in patients who have celiac-like enteropathy. The aims of this study were: 1) to identify causes of persistent symptoms in patients referred with presumed diagnosis of nonresponsive celiac disease (NCD); and 2) to characterize patients with true RS. METHODS: Patients were identified who had been systematically evaluated for NCD between January 1997, and May 2001. Patient records and small bowel biopsy results were reviewed. RESULTS: A total of 55 patients were referred with a presumed diagnosis of NCD. Six did not have celiac disease and had other diseases responsible for their symptoms. Diarrhea, abdominal pain, and weight loss were the most common reasons for evaluation in cases of NCD, whereas weight loss, steatorrhea, and diarrhea were the most common presenting features of RS (nine patients). Of the 49 patients with celiac disease, 25 were identified as having gluten contamination. Additional diagnoses accounting for persistent symptoms included: pancreatic insufficiency, irritable bowel syndrome, bacterial overgrowth, lymphocytic colitis, collagenous colitis, ulcerative jejunitis, T-cell lymphoma, pancreatic cancer, fructose intolerance, protein losing enteropathy, cavitating lymphadenopathy syndrome, and tropical sprue. CONCLUSIONS: Based on this study, we conclude the following: 1) gluten contamination is the leading reason for NCD; 2) of NCD cases, 18% are due to RS; and 3) alternative diseases or those coexistent with celiac disease and gluten contamination should be ruled out before a diagnosis of RS is made.

Adult↗
PubMed2002

Tissue transglutaminase antibody determination in celiac disease. Analysis of diagnostic specificity of anti-human IgA-type assays.

Biopsy is onerous and, for this reason, immunodiagnostics in sera of celiac disease patients are an "additional diagnostic standard." The objective of the study was to investigate the variability in diagnostic specificity of ELISAs for the detection of IgA anti-tissue transglutaminase antibodies in serum of celiac disease patients who underwent biopsy. All patients were included in the study on the basis that they had a small intestinal biopsy. We studied 18 patients with histological proven celiac disease (7 male, 11 female, mean age +/- SD: 35+/-19 years) from Graz, Austria. Healthy control subjects were also entered into the study. The determinations of the anti-tissue transglutaminase antibodies were simultaneously performed together with the endomysium and gliadin antibody markers. We analysed the 216 serum values according to Cochran's non-parametric Q-test. The complexity to the analysis reflects the complexity of the diagnostic situation with the patients. No real differences were found in the reactions of the anti-human IgA-type anti-tissue transglutaminase ELISAs. Based on these results, an association was established between the outcomes of anti-human IgA-type ELISAs for the specific antigen and patients with histologically proven celiac disease, treated for celiac disease after histology was carried out and the diagnosis was made, and healthy controls. The detection of IgA anti-tissue transglutaminase antibodies in serum is a promising alternative to the indirect immunofluorescence determination of IgA-type endomysium antibodies. One ELISA for the specific antigen showed some advantage with respect to its extended scale of detection. Immunopathology of celiac disease can be based on the results of the appropriate IgA anti-tissue transglutaminase ELISAs under uncomplicated gastrointestinal conditions.

Antibodies, Monoclonal↗
PubMed2001

Prevalence and clinical picture of celiac disease in italian down syndrome patients: a multicenter study.

BACKGROUND: A multicenter research study of Down syndrome patients was carried out to estimate the prevalence of celiac disease in patients with Down syndrome and to show clinical characteristics and laboratory data of Down syndrome patients. METHODS: The authors studied 1,202 Down syndrome patients. Fifty-five celiac disease patients (group 1) were compared with 55 immunoglobulin A antigliadin-positive antiendomysium antibodies-negative patients (group 2) and with 57 immunoglobulin A antigliadin-negative antiendomysium antibodies-negative patients (group 3). RESULTS: Celiac disease was diagnosed in 55 of 1,202 Down syndrome patients (4.6%). In group 1, weight and height percentiles were shifted to the left, whereas these parameters were normally distributed in groups 2 and 3. In celiac patients, diarrhea, vomiting, failure to thrive, anorexia, constipation, and abdominal distension were higher than in the other two groups. Low levels of hemoglobinemia, serum iron, and calcium were observed more frequently in group 1. The diagnosis of celiac disease was made after a mean period of 3.8 years from the initiation of symptoms. Sixty-nine percent of patients showed a classic presentation, 11% had atypical symptoms, and 20% had silent celiac disease. Autoimmune disorders were more frequent (30.9%) in group 1 than in the other two groups examined (15%; P < 0.05). CONCLUSIONS: This study reconfirms a high prevalence of celiac disease in Down syndrome. However, the diagnostic delay, the detection of atypical symptoms or silent form in one third of the cases, and the increased incidence of autoimmune disorders suggest the need for the screening of celiac disease in all Down syndrome patients.

Adolescent↗
PubMedDate not supplied

A 70-year-old man with isolated weight loss and a pellagra-like syndrome due to celiac disease.

An elderly man was diagnosed with celiac disease, which presented with three notable features: first, presentation at the age of 70 with no prior gastrointestinal symptomatology or positive family history; second, triggering of all symptoms following recent myocardial infarction and infective endocarditis; third, presentation with marked (more than 20 percent) weight loss and pellagra-like skin lesions despite nearly normal examination and laboratory tests. Thus, celiac disease may present as a pellagra-like syndrome in the elderly with predominant weight loss that is enhanced by the related taste disturbances.

Age of Onset↗
PubMed2006

[Diagnostic validity of anti-tissue transglutaminase and anti-endomysium antibodies in children with celiac disease].

UNLABELLED: Tissue transglutaminase (tTG) plays a decisive role in the pathomechanism of celiac disease. Unchanged gliadin peptides bind to HLA-DQ2 with a week affinity, after that they are recognized by gliadin specific T-lymphocytes and the whole immune reaction is started which damages intestine mucous and causes the release of tTG. Tissue transglutaminase deaminates gliadin peptides enhancing the whole process. The aim of this study was determination of correlation between antiendomysial antibodies and anti-tissue transglutaminase antibodies in children with celiac disease, and the assessment of their usefulness in the diagnosis of celiac disease. MATERIAL AND METHODS: 109 children, aged 6 moths to 16 years (average 8.8 years) were included into the study. In all children an intestine biopsy was performed and/or antiendomysial antibodies were determined. In all children tissue transglutaminase antibodies were measured. Antibodies against tissue transglutaminase were determined using ELISA method. Antiendomysial antibodies were determined using the immunofluorescence method. RESULTS: In patients with normal mucous with lack of lymphocyte infiltration no IgAEmA were present in the blood. In the groups with subtotal and total villous atrophy all IgAEmA titres were positive. A positive titre of IgAEmA was observed only in childrerl with villous atrophy, which yields specificity of the test of 100%, sensitivity was 81%. Sensitivity of the anti-tTG antibodies test for detecting villous atrophy was 83% for IgA and 52% for IgG. There is a positive correlation between IgAEmA and anti-tTG antibodies. CONCLUSIONS: High sensitivity and specificity of determination of antibodies against tTG in IgA class causes that these tests may serve as a screening test in diagnosis and monitoring of celiac disease in children.

Adolescent↗
PubMed1994

Celiac disease and other nutrient related injuries to the gastrointestinal tract.

Celiac disease is the major nutrient-induced disease of the small intestine. The disease is traditionally characterized by villous atrophy responsive to gliadin. Recent data suggest that there is an extended spectrum of gluten sensitivity that includes first-degree relatives and patients with latent celiac disease. Genetic studies have identified HLA DQ A1 *0501 B1 *0201 as the predominant HLA gene most tightly linked to this condition. Gliadin-specific T cell clones restricted by DQ have now been identified in the small intestine lamina propria. Such T cells may be important in mediating many of the features of the disease. This review discusses the interrelationship of genetics, cereal chemistry, environmental factors, and immunology involved in the pathogenesis of celiac disease and explores its relationship with other nutrient-induced enteropathies.

Amino Acid Sequence↗
PubMed1995

Primary T cell CD30-positive anaplastic large-cell lymphoma associated with adult-onset celiac disease and presenting with skin lesions.

We report the case of a 52-year-old woman with primary CD30+ anaplastic large-cell lymphoma of T cell phenotype with skin involvement, stage IVB, fulfilling almost all the clinical, histopathologic and immunophenotypic criteria for this disease, associated with adult-onset celiac disease. The diagnoses of malignancy and celiac disease were made during the same clinical episode. The clinical course of the patient has been extremely favorable and she is in complete remission, 15 months after finishing consolidation therapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1982

Foods for patients with celiac disease.

As a general rule patients with celiac disease must avoid five cereals--wheat rye, triticale, barley and oats. Very sensitive individuals must also avoid two products of these cereals--malt and hydrolyzed vegetable protein. Some less sensitive individuals may be able to tolerate barley and oats in small quantities. All other foods are acceptable, including the cereals corn, rice, buckwheat, millet and sorghum, as well as malt-flavored breakfast cereals. Wine, spirits, beer and ale are also acceptable unless otherwise contraindicated. Monosodium glutamate, other food additives and pharmaceutical preparations are also acceptable. The ingredients of prepackaged processed foods are listed on the labels. Patients with celiac disease must examine labels to ensure that they avoid the harmful cereals. With appropriate precautions they need not be concerned about eating away from home.

Adult↗
PubMed1992

Celiac disease. A gastrointestinal disease with environmental, genetic, and immunologic components.

In summary, research in immunogenetics, protein chemistry, and molecular biology is leading to a greater understanding of the contribution of genetic, environmental, and immunologic factors to the etiopathogenesis of celiac disease. Taken together, the findings discussed in this article suggest that understanding of the contribution of a major genetic factor to celiac disease susceptibility is closer at hand. Thus, the pathogenesis of celiac disease appears to involve an interaction between the gene products of the HLA class II D region on chromosome 6 and the gliadin proteins, possibly because of their homology with an intestinal viral protein. A logical extension of these findings would predict that T cells, particularly CD4 T cells, play a key role in the pathogenesis of celiac disease by virtue of their recognition of a gliadin or viral peptide in conjunction with the HLA class II D-region gene products. Nonetheless, the precise mechanisms by which the HLA class II genes and their products contribute to celiac disease is not known. Further, the precise peptide sequence in gliadin that interacts with the relevant HLA class II D-region molecule is not known. Finally, the role of CD4 T cells in the pathogenesis of celiac disease, either directly or indirectly by their ability to regulate other T-cell subsets and antibody-producing B cells, remains to be defined. The lessons learned and to be learned from celiac disease will substantially increase our understanding of the mechanisms that are important in this disease as well as in other intestinal and HLA-associated autoimmune diseases.

Antibody Formation↗
PubMed1998

Use of immunoglobulin A-antiendomysial antibody to screen for celiac disease in North American children with type 1 diabetes.

OBJECTIVE: Our objective was to determine if a serological marker, the immunoglobulin A antiendomysial antibody (IgA-EMA), can be used to screen for celiac disease in North American children with type 1 diabetes. RESEARCH DESIGN AND METHODS: Subjects included 236 diabetes clinic patients and 56 gastrointestinal clinic patients who underwent intestinal biopsy for suspected malabsorption. Total IgA and IgA-EMA assays were performed. Diabetic patients who were positive for IgA-EMA were asked to undergo biopsy. RESULTS: Of 236 diabetic patients tested, none were IgA deficient and 19 were positive for IgA-EMA (8%). Of 17 patients biopsied, 12 had celiac disease and 3 were symptomatic. The estimated prevalence of celiac disease was 5.1%, consistent with data from European diabetic clinics. Of the 56 gastrointestinal clinic patients, the 3 who were IgA-EMA positive had biopsies diagnostic of celiac disease. Three were found to be IgA deficient, one of whom had celiac disease. Of the 50 IgA-sufficient and IgA-EMA-negative patients, 1 had celiac disease and 49 did not. The IgA-EMA test had a sensitivity of 94% and a specificity of 91% for IgA-sufficient biopsied patients. CONCLUSIONS: IgA-EMA is an appropriate tool for demonstrating an increased prevalence of celiac disease in a North American pediatric diabetic population. Positive testing should be confirmed by intestinal biopsy, and false-positive results require serial follow-up. Symptomatic children require biopsy regardless of their IgA-EMA status.

Adolescent↗
PubMed2004

Relationship of HLA-DQ8 and severity of celiac disease: comparison of New York and Parisian cohorts.

BACKGROUND & AIMS: Celiac disease is a polygenic disorder associated with HLA-DQ2 or HLA-DQ8, which are present in greater than 90% of patients. The disease is considered milder in the United States compared with Europe. We assessed whether differences in the frequency of HLA type may account for differences in severity of the disease by using cohorts of patients from New York and Paris. METHODS: HLA-DQ typing was performed on patients with celiac disease in New York and Paris. Clinical and pathologic data were compared between the New York and Parisian cohorts and also correlated with the different HLA types (HLA-DQ2, HLA-DQ2/-DQ8, HLA-DQ8). RESULTS: Among these patients, the disease was milder in the New York cohort compared with the Parisian cohort. There were fewer patients with a classical presentation (45% and 89%, respectively; P < 0.001) and less severe pathology (total villous atrophy, 64% and 89%, respectively; P < 0.05), and less marked intraepithelial lymphocytosis (intraepithelial leukocytes [IELs]/100 enterocytes, 48.1 and 82.5, respectively; P < 0.0001). HLA-DQ2 homozygotes were less prevalent in the New York cohort compared with the Parisian cohort (59% and 79%, respectively; P = 0.08). HLA-DQ8 alleles were more prevalent in the New York cohort compared with the Parisian cohort (41% and 21%, respectively; P = 0.026). There was, however, no difference in the clinical or pathologic parameters of severity when we compared the groups based on HLA type. CONCLUSIONS: HLA-DQ8 alleles were increased in the New York cohort of patients with celiac disease; however, this did not account for less severe manifestations of the disease.

Adult↗
PubMed2004

The prevalence of epilepsy in patients with celiac disease.

PURPOSE: The relation between celiac disease and epilepsy is uncertain. Previous studies have suggested an association, whereas others have not. METHODS: We ascertained the prevalence of active epilepsy in a cohort of 801 celiac patients by patient interviews and retrospective case note review. All the celiac patients had diagnostic confirmation by small bowel biopsy. RESULTS: Twenty-one patients had a history of epileptic seizures, but only nine (1.1%) had active epilepsy. No specific epileptic syndrome was identified. CONCLUSIONS: This study suggests that a causal relation between gluten sensitivity and active epilepsy is unlikely.

Adolescent↗
PubMed1991

[Celiac disease in the adult--a case report].

The diagnosis of celiac disease is often missed particularly in cases of adult onset. We report the case of a man in his seventh decade who had been treated for many years for endocrine symptoms and signs of malabsorption. The first biopsy diagnosis of celiac disease was ignored. After a second jejunal biopsy, adequate treatment with a gluten-free diet was initiated. This resulted in recovery. The fact that celiac disease may often present for the first time in adults and that symptoms are not always clear are stressed as well as screening for the disease with the aid of endoscopic techniques.

Biopsy↗