Serum Antigliadin Antibodies Research Articles

Gastrointestinal dysfunction in Parkinson's Disease: absence of anti-gliadin antibodies.

Parkinson disease (PD), which is a neurodegenerative disorder, includes several gastrointestinal symptoms that are similar to those of Celiac disease (CD). However, the presence of celiac antibodies in PD patients has not yet been studied. Our aim in this study is to compare anti-transglutaminase (ATA) and antigliadin antibodies (AGA) as well as gastrointestinal symptoms and nutrition habits between patients with Parkinson's disease (PD) and healthy controls. Serum AGA IgG and IgA and the ATA antibodies IgA and IgG were studied in 102 PD patients and 91 healthy controls. Gastrointestinal symptoms, specifically constipation, were investigated using the gastrointestinal system rating scale (GSRS) and the constipation rating scale (CRS). Dietary habits were also investigated and compared between the groups. No significant differences were found between the two groups in terms of celiac antibodies. As expected, the hypokinetic GSRS and CRS scores were significantly higher in the PD group (p<0.001). Dietary habits, especially carbohydrate-rich diets, had a negative impact on gastrointestinal symptoms in the PD patients. Studies have suggested a connection between PD and CD, which infers a probable non-celiac gluten intolerance and the need to offer PD patients an elimination diet. However, the results of our study did not support any link between celiac antibodies and PD. Notwithstanding, the negative impact of a carbohydrate-rich diet in PD patients still leaves a question regarding gluten sensitivity in these patients.

A gluten degrading probiotic Bacillus subtilis LZU-GM relieve adverse effect of gluten additive food and balances gut microbiota in mice

Gluten accumulation damages the proximal small intestine and causes celiac disease (CeD) which has not been effectively treated except by using a gluten-free diet. In this study, strain Bacillus subtilis LZU-GM was isolated from Pakistani traditional fermented sourdough and could degrade 73.7% of gluten in 24 h in vitro. Strain LZU-GM was employed for practical application to investigate gluten degradation in mice models. The results showed that strain LZU-GM was colonized in mice and the survival rate was around 0.95 % (P < 0.0001). The gluten degradation was 3-fold higher in the small intestine of the strain LZU-GM treated mice group remaining 1511.96 ng/mL of gluten peptides than the untreated mice group (6500.38 ng/mL). Immunochemical analysis showed that gluten-treated mice established positive antigliadin antibodies (AGA) in serum (IgA, IgG, and anti-TG2 antibodies) as compared to the strain LZU-GM treatment group. Furthermore, the number of IFN-γ, TNF-α, IL-10, and COX-2 cells decrease in the lamina propria of the strain LZU-GM treatment group (P < 0.0001). Microbial community bar plot analysis showed that Lactobacillus, Dubosiella, and Enterococcus genera were restored and stabilized in the LZU-GM treatment group while Blautia and Ruminococcus were found lower. The oral gavage of probiotic strain LZU-GM might be useful for gluten metabolism in the intestine during digestion and would be a long-term dietary treatment for CeD management.

The association of anti-gliadin and anti-transglutaminase antibodies and chronic plaque psoriasis in Indian patients: Preliminary results of a descriptive cross-sectional study.

Gluten sensitivity among psoriasis patients and its association with gender, age, disease duration and severity of psoriasis are under studied in Indians. To examine association among serum levels of anti-tTG and anti-gliadin antibodies and clinical features including gender, age, duration and severity of psoriasis. Serum levels of anti-transglutaminase and anti-gliadin antibodies were measured quantitatively in 80 (M:F 57:23) psoriasis patients aged 15 to 83years and matched healthy subjects. Forty-five (56.3%) patients were aged ≥41years, duration of disease was >5years in 43(53.8%) patients, and 22 (27.5%) patients had moderate-to-severe psoriasis. Two (2.5%) patients had arthritis and elevated serum anti-gliadin antibody. Significantly more patients than controls had elevated serum anti-gliadin antibody (67.5% vs. 2.5%) and anti-transglutaminase antibody levels (62.5% vs. 0%). Two patients, each with mild and moderate-to-severe psoriasis, had highly elevated serum anti-gliadin antibody and symptoms akin to coeliac disease. Except for a longer duration of psoriasis in patients with elevated anti-gliadin antibodies, there was no statistically significant difference in gender, age, and severity of psoriasis when compared with patients having normal levels. Significant elevation of serum anti-transglutaminase and anti-gliadin antibodies levels is noted in psoriasis patients reflecting a possible link. However, results need careful interpretation for any significance of gluten sensitivity in pathogenesis of psoriasis/arthritis or as a stand-alone risk factor for chronicity/severity of psoriasis or whether gluten-free diet will be ameliorating. Small number of subjects, cross-sectional study design, lack of pathological/endoscopic diagnosis and follow-up are study limitations.

Gut antibody deficiency in CD19−/− mice results in a spontaneous Celiac-Like sprue

Abstract Primary immunodeficiencies are heritable disorders of the immune response that most commonly manifest as an inability to generate immunoglobulin A (IgA). Despite its prevalence, IgA deficiency is considered a benign form of antibody deficiency due to a lack of easily observed clinical symptoms. CD19 is an important co-receptor that facilitates B cell receptor signaling and B cell development into antibody-secreting plasma cells. CD19 deficiency is a known genetic risk factor for the development of common variable immunodeficiency (CVID). Here, we utilize the CD19−/− mouse model to quantify the role of IgA deficiency on gut homeostasis. Our results indicate that CD19−/− mice develop a severe gut IgA deficiency associated with aberrant anti-commensal IgA responses that result in the outgrowth of anaerobic bacteria in the gut. More importantly, anaerobic expansion results in intestinal malabsorption under steady-state conditions. Intestinal malabsorption is associated with defects in normal hepatobiliary circulation, vitamin deficiency, and dyslipidemia. Additionally, results from histological analysis and RNAseq experiments indicate that CD19−/− mice develop intestinal epithelial cell (IEL) lymphocytosis mediated by CD8aa+TCRgd lymphocytes. Finally, CD19−/− mice, while deficient in anti-gliadin antibody (AGA) production compared to WT mice, demonstrate a significantly stronger relationship between serum AGA titers and total serum IgG and IgA production compared to WT animals and have significantly elevated ileal expression of tissue transglutaminase 2. Collectively, we believe that we have identified a novel mouse model of sero-negative celiac disease that will be of great value to the celiac research community.

The Significance of Low Titre Antigliadin Antibodies in the Diagnosis of Gluten Ataxia.

Background: Patients with gluten ataxia (GA) without enteropathy have lower levels of antigliadin antibodies (AGA) compared to patients with coeliac disease (CD). Magnetic Resonance Spectroscopy (NAA/Cr area ratio) of the cerebellum improves in patients with GA following a strict gluten-free diet (GFD). This is associated with clinical improvement. We present our experience of the effect of a GFD in patients with ataxia and low levels of AGA antibodies measured by a commercial assay. Methods: Consecutive patients with ataxia and serum AGA levels below the positive cut-off for CD but above a re-defined cut-off in the context of GA underwent MR spectroscopy at baseline and after a GFD. Results: Twenty-one consecutive patients with GA were included. Ten were on a strict GFD with elimination of AGA, 5 were on a GFD but continued to have AGA, and 6 patients did not go on a GFD. The NAA/Cr area ratio from the cerebellar vermis increased in all patients on a strict GFD, increased in only 1 out of 5 (20%) patients on a GFD with persisting circulating AGA, and decreased in all patients not on a GFD. Conclusion: Patients with ataxia and low titres of AGA benefit from a strict GFD. The results suggest an urgent need to redefine the serological cut-off for circulating AGA in diagnosing GA.

Serum antigliadin antibodies in cerebellar ataxias: a systematic review and meta-analysis

BackgroundGluten sensitivity refers to prominent immunological responses to gluten, usually in conjunction with elevated levels of serum antigliadin antibody (AGA). The association between AGA and cerebellar ataxias has been inconsistently...

Serum Anti-Gliadin Antibodies and The Risk of Cerebellar Ataxias: A Systematic Review and Meta-analysis (P1.071)

Serum Anti-Gliadin Antibodies and The Risk of Cerebellar Ataxias: A Systematic Review and Meta-analysis (P1.071)

SERUM ANTIGLIADIN ANTIBODIES IN EGYPTIAN CHILDREN WITH AUTISM SPECTRUM DISORDER: RELATIONSHIP TO GASTROINTESTINAL SYMPTOMS, BEHAVIORAL AND SOCIAL COMMUNICATIONS

Objectives: Gastrointestinal symptoms are major characteristic in children with autism spectrum disorder (ASD), drawing attention to a potent association with gluten sensitivity. The goal of this study was to evaluate anti-gliadin antibodies serum levels in a group of Egyptian children with ASDs and to address the potential link to gastrointestinal (GI) symptoms, behavioral, and social communications.Patients and Methods: This descriptive case–control study included 45 children diagnosed as ASD according to Diagnostic and Statistical Manual of Mental Disorders 5th Edition and a history of GI symptoms, compared with 45 apparently healthy children of matched age and sex. Serum anti-gliadin antibodies were measured using enzyme-linked immunosorbent assay kits.Results: Serum levels of IgM, IgA, and IgG class antibodies to gliadin showed a significant increase compared to healthy controls (p&lt;0.000). Multiple logistic regression analysis showed a significant association between the high serum levels of IgA and IgM class antibodies to gliadin in the studied patients and GI symptoms (p&lt;0.05). A significant association was detected between the high serum levels of IgG antibodies to gliadin and the behavior symptoms (p&lt;0.05).Conclusions: The anti-gliadin antibody response and its association with GI symptoms indicated the involvement of abnormal immunologic intestinal permeability in affected children. Immune system of some autistic patients could be abnormally triggered by gluten assumption.

Gluten Sensitivity among Egyptian Infants with Congenital Heart Disease.

BACKGROUND:Gastrointestinal symptoms are a common feature in infants with congenital heart disease.AIM:This study was designed to evaluate age-dependent serum levels of antigliadin antibodies among malnourished Egyptian infants with congenital heart disease (CHD) and gastrointestinal symptoms.SUBJECTS AND METHODS:This case-control study conducted on 60 infants with established congenital heart disease. They were subdivided into cyanotic and acyanotic groups, and each group includes 30 patients compared with thirty apparently healthy infants of matched age, sex, and social class. Serum antigliadin antibodies levels were measured using ELISA.RESULTS:The mean age of introduction of cereals in the diet and appearance of gastrointestinal symptoms were six months. On comparison with controls, patients showed highly significant higher serum levels of antigliadin antibodies (P < 0.000). On analysing risk factors using odds ratio, the age at onset of GIT symptoms, diarrhoea, abdominal pain, and distension had been found to be significantly associated with high serum antigliadin antibodies among malnourished CHD infants with a prediction of 95%.CONCLUSION:Serum IgA, IgM, and IgG class antibodies to gliadin play a significant role in the pathogenesis of malnutrition in infants with CHD. Gluten containing foods should never be introduced before the end of the six months.

Molecular Identification of Giardia intestinalis in Patients with Dyspepsia

Background/Aims:Giardia intestinalis triggers symptoms of functional dyspepsia. The aim of this study was to distinguish genotypes of G. intestinalis isolated from dyspeptic patients to evaluate their correlation with dyspeptic symptoms. Methods: In total, 120 dyspeptic subjects were investigated by upper endoscopy, including gastric and duodenal biopsies for histopathological examination, and parasitological examination of their stools and duodenal aspirates was performed. The patients were classified into five groups: group I (G. intestinalis) included 19 patients, group II (Helicobacter pylori) included 36 patients, group III (coeliac disease) included 3 patients, group IV (mixed G. intestinalis and H. pylori infection) included 4 patients, and group V (unexplained aetiology) included 58 patients. Genotyping of G. intestinalis was performed for groups I and IV using PCR-RFLP. The urease test was performed for H. pylori. Serum anti-gliadin, anti-endomysial and anti-transglutaminase antibody estimation was performed for the diagnosis of coeliac disease. Results: Genotype A of G. intestinalis was detected in the stool samples of 68.42% (13/19) and the duodenal aspirates of 42.1% (8/19) of dyspeptic patients harbouring the parasite. Genotype B was detected in 31.58% (6/19) of cases in stool samples and in 3 cases in duodenal aspirates. Conclusions:H. pylori, G. intestinalis and coeliac disease are common causes of dyspepsia. G. intestinalis genotype A demonstrated a greater association with dyspeptic symptoms.

Coeliac Disease-Associated Antibodies in Psoriasis

BackgroundThe possible relationship between psoriasis and coeliac disease (CD) has been attributed to the common pathogenic mechanisms of the two diseases and the presence of antigliadin antibodies in patients has been reported to increase the incidence of CD.ObjectiveThe aim of this report was to study CD-associated antibodies serum antigliadin antibody immunoglobulin (Ig)A, IgG, anti-endomysial antibody IgA and anti-transglutaminase antibody IgA and to demonstrate whether there is an increase in the frequency of those markers of CD in patients with psoriasis.MethodsSerum antigliadin antibody IgG and IgA, antiendomysial antibody IgA and anti-transglutaminase antibody IgA were studied in 37 (19 males) patients with psoriasis and 50 (23 males) healthy controls. Upper gastrointestinal endoscopy and duodenal biopsies were performed in patients with at least one positive marker.ResultsAntigliadin IgA was statistically higher in the psoriasis group than in the controls (p<0.05). Serological markers were found positive in 6 patients with psoriasis and 1 person from the control group. Upper gastrointestinal endoscopy was performed in all these persons, with biopsies collected from the duodenum. The diagnosis of CD was reported in only one patient with psoriasis following the pathological examination of the biopsies. Whereas one person of the control group was found to be positive for antigliadin antibody IgA, pathological examination of the duodenal biopsies obtain from this patient were found to be normal.ConclusionAntigliadin IgA prominently increases in patients diagnosed with psoriasis. Patients with psoriasis should be investigated for latent CD and should be followed up.

Increased Risk of Coeliac Disease in Patients with Congenital Hypothyroidism

Background: In patients with congenital hypothyroidism (CH), the presence of coeliac disease (CD) has been sporadically described. Methods: Seventy-nine consecutive children (58 females and 21 males; age range 3.1–12.1 years) with permanent CH were studied. For all patients, a family history of autoimmune diseases as far as second-degree relatives was collected, and total serum IgA, antigliadin, anti-endomysium and anti-transglutaminase antibodies were evaluated. In the subjects positive for CD antibodies, the CD diagnosis was confirmed by jejunal biopsy. One hundred and eighty-two Italian children from the same geographical area, matched for age and sex, acted as controls. Results: In CH patients, a statistically significant difference was found in the familial occurrence of autoimmune diseases compared to controls (22 vs. 7.9%; p < 0.001). A total of 6 patients (4 girls, 2 boys; 7.6 vs. 1%; p < 0.005) were positive for CD antibodies. In 5 of these patients (6.3%), the diagnosis of CD was confirmed histologically. Conclusion: Our data show a higher prevalence of CD in children with permanent CH and suggest that these patients should be monitored carefully for CD. Other studies are needed to confirm our results and to explain the causes of this possible relationship.

In vitro digestive stability of complexes between gliadin and synthetic blocking peptides

Celiac disease is caused by an inappropriate immune response to incompletely digested gluten proteins. We investigated whether synthetic peptides with high affinity to wheat gliadin could be selected with a phage display technique and whether complexes between such peptides and gliadin could sustain gastric and pancreatic digestion. Two synthetic peptides, P61 and P64, were selected because of their high affinity to immobilized gliadin. They were allowed to form complexes with gliadin, whereafter the complexes were subjected to in vitro digestion with gastric and pancreatic enzymes. The digestion products were analyzed with Western blot and RP HPLC. The results showed that both peptides formed stable complexes with intact gliadin and that complexes between gliadin and peptide P64 partly resisted gastrointestinal digestion. The two peptides reduced the binding of serum anti-gliadin IgA antibodies by 12%, and 11.5%, respectively, and the binding of anti-gliadin antibodies of the IgG isotype by 13% and 10%. Thus peptides produced by a phage display technique could interact stably with gliadin partly masking epitopes for antibody binding. A combination of peptides of this kind may be used to block gliadin-immune system interactions.

Detection of Antigliadin Autoantibodies in Celiac Patient Samples Using a Cyclodextrin-Based Supramolecular Biosensor

Celiac disease is a condition associated with the ingestion of gluten by genetically susceptible individuals. Measurement of serum antigliadin antibodies is a diagnostic tool also used as a means of monitoring a patient's compliance to a gluten-free diet. In this work, we demonstrate the applicability of an electrochemical supramolecular platform based on cyclodextrin-modified gold surfaces to detect antigliadin antibodies in real serum samples. Several support layer-biorecognition element combinations were tested in order to maximize the electrochemical response, and the assay was optimized in terms of incubation times and resistance to nonspecific interactions. The developed supramolecular biosensor was then applied to the amperometric detection of antigliadin IgA and IgG autoantibodies in real samples of celiac disease patients under follow-up treatment; the results were compared with a commercial enzyme linked immunosorbent assay (ELISA) test, and an excellent correlation was observed between both methods.

Identification of gliadin-binding peptides by phage display

BackgroundCoeliac disease (CD) is a common and complex disorder of the small intestine caused by intolerance to wheat gluten and related edible cereals like barley and rye. Peptides originating from incomplete gliadin digestion activate the lamina propria infiltrating T cells to release proinflammatory cytokines, which in turn cause profound tissue remodelling of the small intestinal wall. There is no cure for CD except refraining from consuming gluten-containing products.ResultsPhage from a random oligomer display library were enriched by repeated pannings against immobilised gliadin proteins. Phage from the final panning round were plated, individual plaques picked, incubated with host bacteria, amplified to a population size of 1011 to 1012 and purified. DNA was isolated from 1000 purified phage populations and the region covering the 36 bp oligonucleotide insert from which the displayed peptides were translated, was sequenced. Altogether more than 150 different peptide-encoding sequences were identified, many of which were repeatedly isolated under various experimental conditions. Amplified phage populations, each expressing a single peptide, were tested first in pools and then one by one for their ability to inhibit binding of human anti-gliadin antibodies in ELISA assays. These experiments showed that several of the different peptide-expressing phage tested inhibited the interaction between gliadin and anti-gliadin antibodies. Finally, four different peptide-encoding sequences were selected for further analysis, and the corresponding 12-mer peptides were synthesised in vitro. By ELISA assays it was demonstrated that several of the peptides inhibited the interaction between gliadin molecules and serum anti-gliadin antibodies. Moreover, ELISA competition experiments as well as dot-blot and western blot revealed that the different peptides interacted with different molecular sites of gliadin.ConclusionsWe believe that several of the isolated and characterised gliadin-binding peptides described here could provide valuable tools for researchers in the field of CD by facilitating studies on localisation and uptake of various gliadin peptides in the small intestine. In future work, the potential of these peptides to detoxify gluten will be investigated.

Positive serum antigliadin antibodies without celiac disease in the elderly population: does it matter?

Objective. Antigliadin antibodies (AGA) show good sensitivity but low specificity for celiac disease and can also be found in healthy individuals. However, data suggest that AGA positivity might be related to distinct disease entities such as allergy and gluten ataxia. Our aim here is to explore the clinical relevance of positive AGA in the elderly population. Material and methods. Serum IgA- and IgG-class AGA and IgA-class tissue transglutaminase antibodies (tTGA) were determined in 2815 individuals aged 52–74 years. Equal numbers of AGA- and tTGA-negative participants of similar age and gender, but without known celiac disease, were randomly selected as controls. Information on clinical history was obtained from hospital records in all groups. Results. Altogether 381 persons were positive for IgA/IgG-class AGA; 38 (14%) of them were also positive for tTGA. Out of the biopsied subjects, 34 (100%) in the AGA+ tTGA+ group and five (9%) in AGA+ tTGA− group had celiac disease. Rheumatoid arthritis and depression were found significantly more often in AGA-positives than controls. The significance remained even when tTGA-positive and known celiac disease cases were excluded. No statistical differences were found in the occurrence of neurological diseases, diabetes, allergic and cardiovascular diseases or malignancies. Conclusions. Although AGA positivity is of clinical relevance only in a subset of elderly people, it seems to be related to rheumatoid arthritis and depression, both conditions linked to celiac disease. Further studies are needed to reveal the mechanisms underlying this. The poor specificity of AGA for celiac disease was here once more in evidence.

381 Conventional AGA Positivity in Children Under Two Years of Age: Celiac Disease or Food Allergy? the Role of Anti-Deamidated Gliadin Peptide Antibodies

Background: Chronic gastrointestinal symptoms in children aged less than two years often represent a clinical challenge for paediatricians, since discriminating between coeliac disease (CD) and food allergy (FA) in this age group might be quite tricky, as classical serum markers for CD, except anti-gliadin antibodies (AGA), are not uncommonly negative. Objective: The aim of our study was to assess the role of aDGP as diagnostic tool differentiating between CD and FA in children aging less than 24 months with high levels of serum AGA, when EmA and anti-tTG are negative. Methods: We investigated 40 children (median age: 16,8 months; age range: 4-24 months), with chronic gastrointestinal symptoms suggesting either CD or FA and with high serum levels of conventional AGA, with normal values of serum IgA, anti-transglutaminase (anti-tTG) and anti-endomysial (EmA) antibodies and without sensitization to the most common food antigens. All of them underwent measurement of serum levels of aDGP (IgA and IgG) and upper gastrointestinal endoscopy with duodenal biopsies; 40 controls were ageand sex-matched to these patients in order to clarify the aDGP specificity. Results: 29 patients (group A) had normal levels of aDGP; their histological features were compatible with Marsh I to III lesions and mimicked CD. However, all of them markedly improved on a cow's milk, soy and egg free diet containing gluten. After three months, these food antigens were reintroduced; subsequently, the vast majority of children (93,1%) belonging to group A experienced a clinical relapse and the return to the previous oligoantigenic diet was once more beneficial. On the other hand, 11 patients (group B) had high serum levels of aDGP (IgG positivity in all of them; IgA positivity in 9), whereas histology showed the same lesions of group A. HLA typing was obtained; haplotypes carried by children of group B were consistent with CD genetic pattern. Moreover, they significantly improved on a gluten free diet containing cow's milk, soy and egg. None of the control group (group C) was aDGP positive. Conclusions: Our data indicate that serum IgG aDGP may be of pivotal usefulness in identifying celiac patients under two years of age with chronic gastrointestinal symptoms and only conventional AGA positivity, distinguishing them from FA. Although the great clinical improvement with GFD in group B, gluten challenge will be permorfed to confirm CD diagnosis.

IgA subclass antibodies to gliadin in serum and intestinal juice of patients with coeliac disease

Serum IgA anti-gliadin antibodies (AGA) were positive in 25 (68%) of 37 untreated adults with coeliac disease belonging mostly to IgA1 subclass (88%) and only in a few cases to IgA2 (12%). Antisecretory component IgA AGA were present in serum of seven patients (28%) by immunofluorescence and in nine (36%) by ELISA. The search for IgA AGA in jejunal juice of eight untreated children with coeliac disease was positive in seven cases (88%), with consistent finding of antisecretory component IgA AGA. These antibodies belonged with equal proportion to IgA1 and IgA2 subclasses. This study shows that in intestinal secretions of untreated coeliac disease cases the IgA immune response to gliadin is confined to polymeric anti-secretory component IgA with the same prevalence of IgA1 and IgA2 subclasses, while in serum IgA AGA are largely monomeric, more frequently of IgA1 than of IgA2 subclass, and with a lower proportion of polymeric anti-secretory component IgA (20-36%). The finding of secretory IgA AGA in serum of patients with coeliac disease could result from a spill-over from the intestinal mucosal synthesis into the circulation.

Low Prevalence of Neurologic and Psychiatric Manifestations in Children with Gluten Sensitivity

To determine the frequency of neurologic manifestations in children with gluten sensitivity (GS) and the frequency of GS in children with neurologic disease. A total of 835 children with GS (based on positive titers for serum anti-gliadin antibody [AGA], anti-endomysial antibody [EMA], and anti-tissue transglutamine [tTG] antibody and a positive gut biopsy), representing the local childhood GS population in the town of Catania, Italy, were recruited, prospectively followed up, and screened for neurologic and psychiatric disturbances between 1991 and 2004. Serum AGA, EMA, and anti-tTG antibody titers were estimated in a prevalence sample of 630 consecutive children with neurologic disorders of unknown cause despite full investigation, 300 children with known neurologic syndromes, and 300 healthy children who served as controls. Statistical significance was assessed by the chi(2) test and Yates' chi(2) test. Neurologic or psychiatric problems were noted in 15 of 835 children with GS (1.79%) with previously diagnosed GS enteropathy (GSE). In 7 of 630 children (1.1%) with a cryptogenic neurologic disorder, GS was identified based on GS autoantibody screening. These 22 children had febrile seizures, epilepsy, headache, mental retardation, neuropathy, and bipolar disorder; no children had ataxia or cerebellar disturbances. The HLAs were DQ2 (n = 16), DQ8 (n = 4), and DQ2/DQ8 (n = 2). Two of the 300 healthy controls (0.66%) had GS. Based on our findings, the prevalence of neurologic/psychiatric manifestations in this group of children with GS was low but slightly higher than that in the controls (P = .041). Children with known (P = .772) and cryptogenic (P = 1.0) neurologic disorders did not exhibit a higher prevalence of GS.

Longitudinal follow-up examination of antigliadin antibody positive children and adults

We previously investigated the prevalence of asymptomatic celiac disease in 3004 healthy children and 4313 adult blood donors by screening for IgA and IgG class antigliadin antibodies (AGA) and IgA class anti-endomysial antibodies (EmA). In none of the 162 exclusive AGA-positive adults and in only one of the 117 exclusive AGA-positive children could celiac disease be diagnosed. We followed up AGA-positive individuals in respect of the significance of the AGA. All AGA-positive children and adults were invited for a follow-up clinical examination and laboratory investigations including AGA-IgA, AGA-IgG and EmA. Celiac disease-specific antibodies were also determined in stool samples. Sixty-nine adults and 47 children returned for follow-up. In 26 (37.7%) cases of the 69 adults formerly tested AGA-positive, AGA were still detectable after an average period of 3.7 years. In 21 (44.7%) cases of 47 formerly AGA-positive children, AGA were still detectable after an average period of 4.3 years. None of the 69 adults and 47 children showed seroconversion to EmA. There were no significant abnormalities in the laboratory results or any clinical signs of enteropathy. The appearance of fecal and serum antibodies was compared in 112 subjects but no correlation between fecal and serum antigliadin antibodies was found. In both studied populations of adults and children, AGA disappeared in more than 50% of the cases. The appearance of AGA has to be interpreted as a non-specific immunomodulation phenomenon, confirming the low specificity of AGA as a serologic marker for celiac disease.