Levels Of Antigliadin Antibodies Research Articles

Adherence to Gluten-Free Diet and Serum Antigliadin Antibodies in Celiac Disease

In 134 patients with celiac disease the compliance with a gluten-free diet (GFD) and the presence of antigliadin antibodies (AGA) were evaluated. Compliance with the GFD was good in 71%, moderate in 11% and poor in 18%. High levels of AGA (IgA and IgG) were found in 24.2% of patients with good GFD, in 40% of those with moderate GFD and in 75% of those with poor GFD compliance. Our data suggest that the presence of AGA is correlated with the degree of adherence to the GFD, and that AGA measurement may be of some value in the monitoring of GFD in patients with celiac disease.

Antigliadin antibody levels in symptomless celiac disease

Antigliadin antibody levels in symptomless celiac disease

ADENOVIRUS ANTIBODIES IN CHILDHOOD COELIAC DISEASE, ANTI-GLIADIN ANTIBODIES IN ADENOVIRUS DISEASED CHILDREN - WHAT IS THE CHAIN OF EVENTS?

We have analysed serum antibodies by ELISA to evaluate the possible relationship between adenovirus infections and coeliac disease (CD). Sera were collected from 24 children with CD (mean age 9.6 yrs, range 2-16.5 yrs) and 24 age- and sex-matched healthy controls. The sera were taken at the time of the initial diagnosis of CD. During autumn -88 an outbreak of adenovirus epidemic took place in our community. Paired sera from 62 children hospitalized for adenovirus infection were available. The ELISA analysis revealed an excess of adenovirus IgA-antibodies in the children with CD. When antibodies to other viral antigens (rubella, mumps, herpes simplex virus) were measured increased IgA-antibody levels to rubella and mumps viruses were also found. Anti-gliadin antibodies were determined in the 62 adenovirus diseased children. In 9 cases the anti-gliadin antibody levels were found to be increased. When anti-reticulin antibodies were analysed 3 out of the 9 cases showed increased antibody levels. Our results indicate that children with CD show enhanced IgA responses to viral infections, adenovirus included. CD may also predispose to adenovirus infections. We conclude that both the phenomena are most likely due to the genetic constitution and phenotype of the children with CD. The role of adenoviruses in the pathogenesis of CD remains open.

The Urinary Excretion of Polyethylene Glycol as a Test for Mucosal Integrity in Children with Celiac Disease

Summary:We compared the results of various noninvasive tests with small bowel histology in 61 children with celiac disease. The most sensitive predictors of small bowel histology were serum levels of anti‐gliadin antibodies (AGAs) (90%) and the urinary excretion of polyethylene glycol (PEG) (69%). The sensitivity for the fecal fat analysis was 61% and for the d‐xylose test 34%. The specificity was 96% for both the PEG and the d‐xylose tests, 92% for the fecal fat, and 68% for AGAs. The predictive value of the PEG test was significantly better than that of d‐xylose (p < 0.05). The best combination of tests for the prediction of small bowel histology was the PEG test and the measurement of serum levels of AGAs. Agreement in the results of these two tests helps to time appropriately the second and third small bowel biopsies.

Antigliadin antibodies detected by enzyme-linked immunosorbent assay as a marker of childhood celiac disease

Using an enzyme-linked immunosorbent assay (ELISA) assay, we studied the sera of 17 patients with celiac disease and 114 control subjects for the levels of IgG and IgA antigliadin antibodies. As a group, the patients with celiac disease had significantly higher levels of antigliadin antibodies of both IgG and IgA classes (p less than or equal to 0.001). However, there was a significant overlap of values, resulting in respective sensitivities and specificities of 88% and 90% for IgG antigliadin antibodies, and 73% and 65% for IgA antigliadin antibodies. The combined use of both IgG and IgA antigliadin antibody levels produced a sensitivity of 86% and a specificity of 90%. A gluten-free diet in celiac patients did not seem to affect these results. We conclude that the antigliadin antibody ELISA assay cannot be used as a definitive diagnostic test for celiac disease. The small-bowel biopsy remains the principal diagnostic method; the ELISA assay should, at best, be considered a screening test for this disease.

Gluten-Sensitive Enteropathy in Childhood

Genetic and environmental factors (breast feeding, probably viral infections) play a role in the expression of the disease. Prevalence of GSE in childhood did not substantially decrease in the last 15 years in all European countries, where GSE is still more common in infantile age and presents frequently gastrointestinal symptoms. A decrease has been reported in childhood in several United Kingdom areas and in Finland, where the clinical presentation is changing, shifting upward with age and coming closer to the adult type of the disease. The following clinical problems have been reported in the recent literature: enamel hypoplasia; monosymptomatic short stature; arthritis and other immunologic diseases; association with diabetes, atopy, Iga deficiency, and probably Down's syndrome. Delay in puberty and other peculiar problems of the disease have been described in adolescents. Tests assessing the permeability of the small intestine and the blood levels of antigliadin antibodies have recently gained success as noninvasive tools for the diagnosis of the GSE. The gluten should be withdrawn from the diet and the challenge with gluten should be performed not before 12 months of gluten-free diet with an accurate timing of the biopsy on the basis of the antigliadin and antireticulin antibodies, to avoid clinical and growth damage. Celiac children do require a permanent gluten-free (and not poor) diet. In reality, too many celiac adolescents are off-diet.

IgA anti-endomysial antibodies in dermatitis herpetiformis: correlation with jejunal morphology, gluten-free diet and anti-gliadin antibodies.

Circulating IgA-class anti-endomysium antibodies (EmA) can be detected by indirect immunofluorescence on monkey oesophagus sections. We found EmA in 22 (76%) of 29 patients with dermatitis herpetiformis (DH) on a normal, gluten-containing diet. The highest frequency (100%) of EmA was observed in patients with sub-total villous atrophy. IgA-class antigliadin antibodies (AGA) were found using an ELISA method in 59% of 29 DH patients and in 86% of those with sub-total villous atrophy. There was a significant correlation between EmA titres and AGA levels in individual patients. Gluten-free diet (GFD) treatment caused a rapid decrease in EmA titres; only three of the 12 patients still showed raised EmA after 6-12 months on a GFD and two of these three had failed to adhere to a strict diet. In contrast, no decrease in EmA titres occurred in four patients maintained on a normal diet, and two of the three patients with initially negative EmA developed positive titres when continuing on a normal diet. These results show that both IgA-class EmA and AGA are good indicators of jejunal damage in DH. The rapid fall of EmA titres after gluten withdrawal indicates that this test is also useful for monitoring a patient's adherence to a GFD.

Antibodies to Gliadin by ELISA as a Screening Test for Childhood Celiac Disease

SummaryThe sera of 309 children who were subjected to jejunal biopsy were tested for antigliadin antibodies (AGA) with enzyme‐linked immunosorbent assay (ELISA) in order to evaluate the usefulness of this test as a screening test for childhood celiac disease (CD). Thirty‐one children had flat intestinal mucosa later confirmed to be due to CD. Ninety percent of these children had significantly elevated levels of IgA class AGA and 94% had significantly elevated levels of IgG class AGA as compared to standard references. Two hundred and seventy‐eight children had normal villous structure. In this group, 37 children out of 271 (seven excluded because of selective IgA deficiency) had elevated levels of IgA class AGA, and 93 children out of 278 had elevated levels of IgG class AGA. We conclude that ELISA‐AGA is suitable as a screening test for childhood CD.

Antibodies to gliadin by ELISA as a screening test for childhood celiac disease.

The sera of 309 children who were subjected to jejunal biopsy were tested for antigliadin antibodies (AGA) with enzyme-linked immunosorbent assay (ELISA) in order to evaluate the usefulness of this test as a screening test for childhood celiac disease (CD). Thirty-one children had flat intestinal mucosa later confirmed to be due to CD. Ninety percent of these children had significantly elevated levels of IgA class AGA and 94% had significantly elevated levels of IgG class AGA as compared to standard references. Two hundred and seventy-eight children had normal villous structure. In this group, 37 children out of 271 (seven excluded because of selective IgA deficiency) had elevated levels of IgA class AGA, and 93 children out of 278 had elevated levels of IgG class AGA. We conclude that ELISA-AGA is suitable as a screening test for childhood CD.

CHANGES IN INTESTINAL PERMEABILITY RELATED TO GLUTEN (G) INGESTION IN CHILDREN WITH CELIAC DISEASE (CD)

Intestinal permeability to polyethylene glycol (PEG) (MW 238-590) and serum antigliadin antibody levels (AGA) were studied in children with CD, diagnosed according to ESPGAN criteria. Results of intestinal permeability to PEG (obtained as described previously, NASPG/ESPGAN, 1985:80) were expressed as N1/2, the theoretical polymer length whose recovery is 50% of the maximally recovered polymer (normal > 12). At diagnosis, 0/9 children had normal N1/2 and AGA. Twenty-four/28 children on a G-free diet had normal N1/2. Two children with abnormal N1/2 admitted ingesting G; one had abnormal N1/2 at 56 d but normal after 180 d. Only 5 had normal AGA. After 30 d on a G-free diet, 7/8 children had normal N1/2; but none had normal AGA. After 77 d on the diet, 12/14 had normal N1/2; only 3 had normal AGA. Upon reintroduction of G, N1/2 were abnormal in 17/36 with a tendency towards normal levels with longer re-exposure, although small bowel biopsies were abnormal. Regression analysis between N1/2 and duration of re-exposure to G indicated a significant association (r=0.5, P < 0.05); for every day of re-exposure, N1/2 improved by 0.006 units. Conclusion: Intestinal permeability rapidly improves with elimination of G from the diet and PEG serves as a good indicator to detect children who are noncompliant. In addition, an apparent adaptation of the bowel occurs with prolonged re-exposure to G, and while histological changes persist and AGA remain elevated, intestinal permeability tends to improve.

Antigliadin antibodies and gluten-free diet in dermatitis herpetiformis

IgA and IgG class antigliadin antibodies (AGA) were analysed with ELISA technique from serum samples of 30 dermatitis herpetiformis patients. Jejunal biopsies were performed to all patients before any treatment and high levels of IgA class AGA were found to be associated with subtotal villous atrophy. Fourteen patients started gluten-free diet (GFD) which caused a significant decrease in both IgA and IgG class AGA. The decrease of IgA AGA was faster than that of IgG AGA and IgA antibody levels fell to normal range during the GFD treatment in all but one patient. In contrast, 5 out of 8 patients followed on normal died showed increasing IgA AGA levels and all of them had a rise in IgG AGA. IgA and IgG class antibodies to cow´s milk were also measured in these patients but in contrast to AGA the diets had no clearcut effect on these antibodies.

Specificity of antigliadin antibody in celiac disease

Celiac disease is activated in genetically susceptible individuals by the dietary ingestion of wheat gluten and similar proteins in other grains. Gliadins are a complex mixture of proteins that contain at least 40 different components in a single variety of wheat. We have purified the four major electrophoretic fractions of wheat gliadin and examined the specificity of antigliadin antibody for those fractions by radioimmunoassay in 30 patients with celiac disease and 30 matched controls. All patients had been on a gluten-free diet for more than 18 mo and were clinically asymptomatic at the time of study. Seventeen of 30 patients had increased antibody levels to one or more of the gliadin fractions. Twelve of 17 patients had elevated antibody to A or 6Dα-gliadin, 9 of 17 to β-gliadin, 10 of 17 to γ-gliadin, and 8 of 17 to ω-gliadin. Of the 17 subjects, 5 had increased antigliadin antibody levels to one gliadin fraction only, whereas 12 had increased levels to two or more fractions. Of the 17 patients with increased antibody titers, 16 had the G2m(n) immunoglobulin heavy chain allotype marker and 14 had the serologic HLA specificities -B8 or -DR3, or both. Definition of the wheat gliadin fractions and specific gliadin peptides that can activate celiac disease remains an open question. These data indicate that antigliadin antibody in the serum of asymptomatic patients with celiac disease who are maintained on a gluten-free diet can be directed against one or a multiple of gliadin fractions.

Coeliac disease: genetic, immunological and environmental factors in disease pathogenesis.

Coeliac disease in humans is activated by the dietary ingestion of wheat gliadins and similar proteins in other grains. We have studied genetic, immunological and environmental factors that may play a role in the pathogenesis of disease. In mice, two genetic regions, the major histocompatibility complex (H-2) and the immunoglobulin heavy chain constant region, were shown to regulate the production of anti-gliadin antibody. In coeliac disease patients on a gluten-free diet, elevated levels of antigliadin antibody were associated with the immunoglobulin heavy chain allotype marker G2m(n). Studies of additional environmental factors involved in coeliac disease revealed a region of amino acid sequence homology and immunological crossreactivity between A-gliadin, a wheat gliadin component known to activate coeliac disease and the Elb early region protein of human adenovirus 12, an adenovirus serotype usually isolated from the human intestinal tract. Specific HLA markers may be associated with coeliac disease because they reflect the host's response to virus.

Influence of Genetic Factors on the Serum Levels of Antigliadin Antibodies in Celiac Disease

SummaryThe relationship between titers of antigliadin antibodies (IgA class and total immunoglobulins IgA, IgG, and IgM) and HLA‐DR antigens was studied in two random samples of unrelated Spanish children with celiac disease. One of these groups had been on a gluten‐free diet for at least 6 months and the other had been given a similar regimen followed by at least 6 months on a gluten‐containing diet. Children with celiac disease who had the DR7 antigen but not DR3 showed significantly higher antigliadin antibody titers on a gluten‐containing than on a gluten‐free diet, whereas those with DR3 but not DR7 did not show this difference. With respect to DR phenotypes, the children with DR3/DR7 and DR7/DR5 phenotypes had significantly higher antibody titers while consuming gluten than when on a gluten‐free diet. However, children with celiac disease with the DR31DR3 phenotype showed similar antigliadin antibody titers on both diets. The present results suggest that genetic factors in the DR region influence the humoral immune response to gliadin in celiac disease.

Serum IgG Antibodies to Gliadin in Children with Celiac Disease as Measured by an Immunofluorescence Method

Serum IgG Antibodies to Gliadin in Children with Celiac Disease as Measured by an Immunofluorescence Method

Gluten-sensitive enteropathy. Immunoglobulin G heavy-chain (Gm) allotypes and the immune response to wheat gliadin.

Anti-gliadin antibody was measured by radioimmunoassay in 30 Caucasians with gluten-sensitive enteropathy (GSE). 22 GSE patients maintained on a gluten-free diet for 1.5 to 20 yr (mean duration 76 mo) had elevated serum concentrations of IgG antigliadin antibody. Among GSE patients on a gluten-free diet, antigliadin antibody was seen only in those having the chromosome 14-encoded IgG immunoglobulin heavy chain allotype marker G2m(n). IgG antigliadin antibody was found in GSE patients with G2m(n) regardless of whether the HLA-B8 and/or -DR3 major histocompatibility complex antigens that occur frequently in GSE were present. No patient lacking G2m(n) had significant levels of antigliadin antibody. The association between antigliadin antibody and the immunoglobulin heavy chain allotype marker G2m(n) in GSE patients likely reflects the presence of Gmn-linked variable region genes or Gmn-linked genes that regulate variable region gene expression.

IgA ANTIGLIADIN ANTIBODIES: A MARKER OF MUCOSAL DAMAGE IN CHILDHOOD COELIAC DISEASE

Antigliadin antibodies in serum samples of 31 children with coeliac disease were measured by an enzyme-linked immunosorbent technique. In young patients (<2 years) tested before gluten withdrawal IgA antigliadin antibody levels were invariably above the levels of 36 controls. The titres fell rapidly when gluten was eliminated from the diet and rose on its reintroduction. The titres were not always greater than the control level in older untreated patients. IgA antigliadin antibodies seem to be a good marker of the immune reaction in the jejunum triggered by gluten. In 2 IgA-deficient patients gluten challenge caused an increase in IgM antigliadin antibodies, and at the same time the number of IgM-containing cells increased in the jejunal mucosa. Rising IgG antigliadin antibody levels after gluten elimination were seen in 6 patients, 5 of whom had very low complement C3 levels before gluten elimination.