Levels Of Antigliadin Antibodies Research Articles

Sieving out non-celiac gluten sensitivity amongst patients with irritable bowel syndrome

ObjectivesIt is challenging to make diagnosis of non-celiac gluten sensitivity/non-celiac wheat sensitivity (NCGS/NCWS) in clinical practice, since there is no biomarker and diagnosis is based on response to gluten-free-diet (GFD). We used anti-gliadin antibody (AGA) for screening patients with IBS for gluten-sensitivity. Methods492 Adult-patients with IBS underwent screening for celiac disease and gluten-sensitivity using IgA anti-tissue transglutaminase antibody and IgA-AGA and IgG-AGA, respectively. Patients with positive AGA (IgA and/or IgG) were invited to follow GFD, those willing were put on GFD for 6-weeks. Responsive patients were given gluten re-challenge. Diagnosis of NCGS was confirmed if they had recurrence of symptoms. ResultsOf 492 patients with IBS, AGA was positive in 61(12.4 %), hence suspected to have gluten-sensitivity. Of 31 who agreed to participate and followed GFD for 6-weeks, 17 (54.8 %) had complete (>30 % improvement) and 10(32.2 %) had partial (>20 % improvement) response. All 17 complete-responders were given gluten re-challenge for 6-weeks, symptoms recurred in all and hence were confirmed to have NCGS/NCWS. Significant decrease in AGA levels occurred almost in all GFD-responders. Conclusions12.4 % IBS patients have biological evidence of gluten/wheat-sensitivity. Almost 87 % patients with IBS having AGA responded to GFD. The value of AGA may further be explored as a biomarker for screening for the presence of NCGS, before recommending this test for the clinical practice.

Predictors of slow responsiveness and partial mucosal recovery in adult patients with celiac disease.

The present study aims to determine the rate of mucosal recovery and predictors of persistent mucosal damage after gluten free diet (GFD). Celiac disease (CD) is a complex multi-systemic autoimmune disease triggered by exposure to dietary gluten in genetically predisposed individuals. There is still little evidence on the best method for assessing GFD adherence and mucosal recovery during treatment. The retrospective study included only adult patients (age≥18 years old), with biopsy-proven CD evaluated at a tertiary referral centre between 2016 and 2021. We performed a logistic regression analysis to identify factors associated with partial mucosal recovery (MR) after GFD. We included in the multivariate analysis parameters available at the time of CD diagnosis. A total of 102 patients were enrolled, two thirds were females, median age of 39 years (yrs). The initial biopsy analysis showed different stages of villous atrophy (VA) in 79 (77.4%) cases, while in 23(22.5%) cases showed mild enteropathy (Marsh 1, 2). After at least 12 months of GFD, 26 (25.5%) patients had persistent VA despite good or excellent adherence to GFD. Younger patients (< 35yrs), who showed severe mucosal damage (Marsh 3c lesions) and who had increased anti-gliadin antibody (AGA) levels were at risk for failure to obtain mucosal recovery (MR). Logistic regression analysis demonstrated that complete mucosal atrophy (P=0.007) and high AGA antibody levels (cutoff 129 U/ml, P=0.001) were independent risk factors for lack of mucosal improvement after at least 12 months of GFD. Interestingly, genotype, tTG-IgA antibody levels, or duration of GFD levels did not influence the occurrence of MR. Although AGA seropositivity has lost much of their diagnostic significance in recent years due to the introduction of the more sensitive and specific antibody tests, our study reported that patients aged < 35 yrs, who showed severe mucosal damage (Marsh 3c lesions) and who had increased AGA antibody levels at diagnosis were at risk for failure to obtain MR. The elevated AGA levels at diagnosis could be used as a prognostic tool for assessing MR.

Rare Complications of Celiac Disease: Clinicopathologic Features

Celiac disease (CD) is an immune mediated disorder characterised by intolerance to glutens in certain grains like whet, barley, and rye. The exposure to gliadin protein component in the susceptible individuals leads to an inflammatory reaction damaging small bowel mucosa with progressive disappearance of intestinal villi. The damaged intestinal mucosa leads to malabsorption. The usual symptoms of celiac disease include diarrhea, steatorrhea, weight loss, fatigue, and abdominal pain. Diagnosis is based on clinical features, duodenal biopsy, elevated levels of anti-gliadin antibodies and response to gluten free diet. Contrary to common belief, celiac disease is a protein systemic disease rather than merely a pure digestive alteration. Celiac disease is closely associated with genes that code HLA -II antigens mainly of DQ2 and DQ8 classes, production of disease specific antibodies (i.e., endomysial antibodies), multiorgan involvement, comorbidity with other autoimmune diseases (shared autoimmunity), familial aggregation, and immune system dysregulation. The clinical presentation of celiac disease can be variable. In mild form, patients can be almost asymptomatic whereas in the most severe form, the patients are at increased risk of life-threatening complications. Celiac disease has a well-known association with other autoimmune diseases such as autoimmune liver diseases (autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis), diabetes mellitus, autoimmune thyroid diseases, skin diseases such as dermatitis herpetiformis, rheumatoid arthritis, systemic lupus erythematosus, Sjogren’s syndrome, psoriasis, sarcoidosis, immune thrombocytopenic purpura, and pancreatitis. In addition, celiac disease may be associated with rare but potentially serious complications such as, collagenous sprue, ulcerative jejunoileitis, refractory celiac disease (RCD), enteropathy associated T-cell lymphoma, small bowel adenocarcinoma (SBA), hyposplenism, and cavitating mesenteric lymph node syndrome (CMLNS). The present article describes clinicopathologic features of these rare but serious complications of celiac disease.

Maternal antibodies to gliadin and autism spectrum disorders in offspring-A population-based case-control study in Sweden.

While individuals diagnosed with autism spectrum disorders (ASD) have higher levels of antibodies directed towards gliadin, a component of wheat gluten, no study has examined anti-gliadin antibodies (AGA) in etiologically relevant periods before diagnosis. The objective of this study was to investigate if maternal levels of AGA, during pregnancy and at the time of birth, are associated with ASD in offspring. We analyzed AGA in archived neonatal dried blood spots (NDBS) for 921 ASD cases and 1090 controls, and in paired maternal sera collected earlier in pregnancy for a subset of 547 cases and 428 controls. We examined associations with ASD diagnoses as a group and considering common comorbidities (intellectual disability [ID] and attention-deficit/hyperactivity disorder). We compared 206 cases to their unaffected siblings to examine the potential for confounding by shared familial factors. Odds of ASD tended to be lower among those with the highest levels (≥90th percentile) of AGA compared to those with low levels (<80th percentile; OR 0.78, 95% CI 0.56-1.09, measured in NDBS). This pattern was more apparent for ASD with comorbid ID when measured in NDBS (0.51, 0.30-0.87), with a similar trend in maternal sera (0.55, 0.24-1.29). High levels of AGA were similarly associated with lower odds of ASD in the sibling comparison. In summary, we found little association between maternal antibodies raised against components of gluten and risk of ASD in general. Exposure to high levels of AGA in the pre- and perinatal periods may be protective in terms of risk for ASD with ID. LAY SUMMARY: There is a debate among both scientists and community members as to whether an immune reaction to gluten exposure could be considered a cause of autism. We examined antibodies that are directed against gliadin, a part of gluten, in samples collected from pregnant mothers and their newborn babies. We did not see any major differences in the antibody level among those children diagnosed with ASD or their mothers compared to children who were not diagnosed with ASD. High levels of the antibodies were in fact associated with a somewhat lower risk of ASD with co-occurring intellectual disabilities, though we cannot tell from this study why that might be the case.

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.

Проницаемость кишечника и непереносимость глютена и казеина у детей с расстройствами аутистического спектра

Objective. To analyze correlation between the level of intestinal fatty-acid binding protein (I-FABP) and concentration of serological markers of gluten and casein intolerance in children with autism spectrum disorder (ASD). Patients and methods. This study included 55 children aged between 3 and 15 years diagnosed with ASD. Twenty of them followed a gluten-free diet (GFD). All patients were tested for their serum levels of anti-gliadin IgG, anti-deamidated gliadin peptide IgA, anti-casein IgG, and anti-I-FABP IgG using enzyme-linked immunosorbent assay (ELISA). To exclude selective immunodeficiency, we also measured total IgA level. Statistical analysis was performed using the Statistica 10.0 software. We have constructed a three-dimensional surface using paired samples correlations. Results. The level of I-FABP varied between 1.63 and 209 pg/mL (mean 63.54 ± 48.5 pg/mL); its concentration decreased with age (r = -0,786). Increased levels of anti-gliadin antibodies were observed in 17.1% of children with ASD; 73.5% of patients had elevated levels of anti-casein antibodies; none of participants had anti-I-FABP antibodies. Conclusion. After constructing a multidimensional surface for three parameters, we have found certain correlations between the parameters examined, which reflects the existing relationships between them. We suggest using multidimensional descriptive statistics as the basis for constructing relationship functions in further research. Key words: autism, diet therapy, serological markers, leaky gut syndrome, gluten intolerance

Randomized controlled trial of a gluten-free diet in patients with schizophrenia positive for antigliadin antibodies (AGA IgG): a pilot feasibility study

Approximately one-third of people with schizophrenia have elevated levels of anti-gliadin antibodies of the immunoglobulin G type (AGA IgG) — a higher rate than seen in healthy controls. We performed the first double-blind clinical trial of gluten-free versus gluten-containing diets in a subset of patients with schizophrenia who were positive for AGA IgG. In this pilot feasibility study, 16 participants with schizophrenia or schizoaffective disorder who had elevated AGA IgG (≥ 20 U) but were negative for celiac disease were admitted to an inpatient unit for a 5-week trial. All participants received standardized gluten-free meals and were randomized in a double-blind fashion to receive a shake containing 10 g of gluten flour or 10 g of rice flour each day. Participants were rated for psychiatric, cognitive and gastrointestinal symptoms at baseline and endpoint. Of the 16 participants, 14 completed the 5-week trial (2 discontinued early for administrative reasons). Compared with participants on the gluten-containing diet, participants on the gluten-free diet showed improvement on the Clinical Global Impressions scale (Cohen d = –0.75) and in negative symptoms (Cohen d = –0.53). We noted no improvement in positive or global cognitive symptoms, but did observe an improvement in attention favouring the gluten-free diet (Cohen d = 0.60). Robust improvements in gastrointestinal adverse effects occurred in the gluten-free group relative to the glutencontaining group. Adverse effects were similar between groups. This study was limited by its small sample size; larger studies are needed. This feasibility study suggests that removal of gluten from the diet is associated with improvement in psychiatric and gastrointestinal symptoms in people with schizophrenia or schizoaffective disorder.

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.

Serological Update on Celiac Disease Diagnostics in Adults

Celiac disease (CD) is an inflammatory disorder of the small intestines which serological diagnosis has come to the forefront with the development of the immunological testing. We aimed to explore the performance characteristics of a panel of serological tests in patients with CD. We assessed the serum levels of anti-tissue transglutaminase (anti-tTG), anti-deamidated gliadin peptides (anti-DGP), anti-actin (AAA), anti-gliadin antibodies (AGA) and cytokine IL-17A by performing ELISA; and anti-tTG, AGA and anti-Saccharomyces cerevisiae antibodies (ASCA) by immunoblot in 35 newly diagnosed adult patients with biopsy-proven CD and 25 age- and sex-matched healthy persons. The average serum levels of anti-tTG, anti-DGP, AGA, AAA, and ASCA were at significantly higher levels in patients with CD compared to healthy persons (p<0.001). We also observed that the serum level of IL-17A was about 70 times higher in CD patients than in the healthy persons (p=0.027). Anti-DGP antibodies showed highest diagnostic sensitivity (100%), followed by AGA and anti-tTG antibodies within the CD group. ROC curve analysis revealed the excellent performance of anti-DGP, anti-tTG, and AGA in the diagnosis of CD patients (AUC 1.000, 0.994, 0.992 respectively, p<0.001). Although the diagnosis of CD relays on biopsy, immunological serological testing could be employed with advantages in diagnosis and monitoring of CD patients.

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.

Celiac disease detection rate in gastroenterological patients

To determine celiac disease detection rate in patients with digestive disease. A total of 318 gastroenterological patients admitted to be treated at the Central Research Institute of Gastroenterology in September to October 2012 were examined. The patients' age was 18 to 74 years (mean 51.5±16.4 years). Immunoglobulin A (IgA) and immunoglobulin G (IgG) anti-gliadin antibodies (AGA), IgA anti-tissue transglutaminase (anti-tTG) antibodies and IgG anti-tTG antibodies were determined. When the antibodies were elevated, esophagogastroduodenoscopy with duodenal biopsy was performed. Forty-one of the 318 patients were found to have higher AGA (12.9%); out of them IgA AGA were in 17 (5.35%) patients and IgG AGA were also in 17 (5.35%). Elevated levels of both antibodies (IgA AGA and IgG AGA) were seen in 7 (2.2%) patients. Overall, the detection rate of increased AGA levels was 12.9%. The antibodies were more commonly higher in patients with liver diseases (21.8%) and in those with inflammatory bowel diseases (21.6%). Both IgA anti-tTG, IgG anti-tTG and IgA AGA, IgG AGA were detected in 6 (1.9%) of the 318 patients. The diagnosis of celiac disease was verified by duodenal histological examination in 3 (0.94%) of the 318 patients. The celiac disease detection rate in gastroenterological patients was 0.94%.

ABSTRACT 496

Background and aims: Idiopathic pulmonary hemosiderosis (IPH) may occasionally be associated with coeliac disease (CD); this association is known as the Lane-Hamilton syndrome, first reported in 1971 in a young adult. Aims: Since then a few cases have been reported in literature. Methods: Case presentation. Results: A four year old boy presented to us with history of respiratory distres and an episode of hemoptysis. Anamnestic there were no medical problems, despite pallor and prolonged fatique. On auscultation, end inspiratory rales are heard. Investigation showed a hemoglobin level of 2.2 g/dl. Chest radiograph showed bilateral diffuse alveolar infiltrates over middle and lower zones. On fallow up he got respiratory failure and he was ventilated with low tidal volume ventilation. The lung biopsy showed haemosiderin laden macrophages in the alveolar spaces. Since an assosiation between CD and IPH has been previously described a workup for CD was also performed. Positive IgA endomysial antibody (1/320 titer) and IgA antigliadin antibody levels were detected. Duodenal biopsy showed partial villous atrophy and increased numbers of intra-epithelial lymphocytes, confirming the diagnosis of CD. Immunosuppressive therapy and gluten free diet was started. The patient was extubated after 26 days of invasive ventilation and he was put on non invasive ventilation. He was discharged after a hospital day of 48 days. During 1 years of fallow -up he had no occurance episodes of intrapulmonary hemorrhage. Conclusions: In conclusion, IPH and CD may have a common pathogenetic link and patients with IPH should be screened for CD even in the absence of gastrointestinal symptoms.

Non-selective betablocker therapy decreases intestinal permeability and serum levels of LBP and IL-6 in patients with cirrhosis

We evaluated the gastrointestinal permeability and bacterial translocation in cirrhotic patients with portal hypertension (PHT) prior to and after non-selective betablocker (NSBB) treatment. Hepatic venous pressure gradient (HVPG) was measured prior to and under NSBB treatment. Gastroduodenal and intestinal permeability was assessed by the sucrose-lactulose-mannitol (SLM) test. Anti-gliadin and anti-endomysial antibodies were measured. Levels of LPS-binding protein (LBP) and interleukin-6 (IL-6) were quantified by ELISA, and NOD2 and toll-like receptor 2 (TLR2) polymorphisms were genotyped. Fifty cirrhotics were included (72% male, 18% ascites, 60% alcoholic etiology). Abnormal gastroduodenal and intestinal permeability was found in 72% and 59% of patients, respectively. Patients with severe portal hypertension (HVPG ≥20 mm Hg; n=35) had increased markers of gastroduodenal/intestinal permeability (urine sucrose levels p=0.049; sucrose/mannitol ratios p=0.007; intestinal permeability indices p=0.002), and bacterial translocation (LBP p=0.002; IL-6 p=0.025) than patients with HVPG <20 mm Hg. A substantial portion of patients showed elevated levels of anti-gliadin antibodies (IgA: 60%, IgG: 34%) whereas no anti-endomysial antibodies were detected. A significant correlation of portal pressure (i.e., HVPG) with all markers of gastroduodenal/intestinal permeability and with LBP and IL-6 levels was observed. NOD2 and TLR2 risk variants were associated with abnormal intestinal permeability and elevated markers of bacterial translocation. At follow-up HVPG measurements under NSBB, we found an amelioration of gastroduodenal/intestinal permeability and a decrease of bacterial translocation (LBP - 16% p=0.018; IL-6 - 41% p<0.0001) levels, which was not limited to hemodynamic responders. Abnormal SLM test results and higher LBP/IL-6 levels were associated with a higher risk of variceal bleeding during follow-up but not with mortality. Abnormal gastroduodenal/intestinal permeability, anti-gliadin antibodies, and bacterial translocation are common findings in cirrhotic patients and are correlated with the degree of portal hypertension. NSBB treatment ameliorates gastroduodenal/intestinal permeability and reduces bacterial translocation partially independent of their hemodynamic effects on portal pressure, which may contribute to a reduced risk of variceal bleeding.

Assessment of the response to gluten-free diet in an Iraqi population with coeliac disease. A histological and serological follow-up study.

IntroductionCoeliac disease (CD) is a common diagnosis among children and adults in Iraq; however, removal of gluten from the diet is essential for patients with CD. The aim of this study, the first such study in Iraq, was to assess the serological and histological recovery profiles of coeliac patients, in both children and adults groups after commencing a gluten-free diet (GFD) for at least 1 year ± 1 month.Material and methodsThe study group comprised 78 proved coeliac patients (46 children and 32 adults, median age: 15 years, range: 1–66 years) who all agreed to undergo endoscopy in addition to serological assessment before and after treatment. The duodenal biopsies were interpreted histologically according to modified Marsh criteria and the sera were tested for anti-gliadin antibody (AGA), endomysium antibody (EMA) and anti-tissue transglutaminase antibody (tTG).ResultsComplete histological remission was seen in 29 (63.1%) of 46 treated children CD patients, while only 5 (10.9%) showed Marsh IIIa changes compared with 11 (24%) before GFD. Similarly none of the 32 adults after GFD showed Marsh IIIb and Marsh IIIc compared with 46.9% and 28.1% before treatment respectively (p = 001). Meanwhile, there was strongly significant reduction in AGA, EMA, and tTG antibodies levels (p = 0.00001) following GFD.ConclusionsRepeating the duodenal biopsy 1 year ±1 month after diagnosis and starting a GFD supports the routine measurement of using histological findings as a gold standard test to confirm recovery of Iraqi CD patients along with using known coeliac serology antibodies.

Autism spectrum disorder and celiac disease: no evidence for a link

To evaluate the possible association between celiac disease (CD) and/or gluten sensitivity (GS) and autism spectrum disorder (ASD). Occurrences of CD were determined in a group of children and adolescents affected by ASD and, conversely, occurrences of ASD were assessed in a group of biopsy-proven celiac patients. To detect the possible existence of GS, the levels of antigliadin antibodies in ASD patients were assessed and compared with the levels in a group of non-celiac children. The prevalence of CD or GS in ASD patients was not greater than in groups originating from the same geographical area. Similarly the prevalence of ASD was not greater than in a group of biopsy-proven CD patients. No statistically demonstrable association was found between CD or GS and ASD. Consequently, routine screening for CD or GS in all patients with ASD is, at this moment, neither justified nor cost-effective.

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.

Intestinal barrier gene variants may not explain the increased levels of antigliadin antibodies, suggesting other mechanisms than altered permeability

Various genes may influence intestinal barrier function, including MAGI2, MYO9B, and PARD3, which are associated with celiac disease. Because direct measurement of intestinal permeability is difficult, antibodies against gliadin (AGA) and Baker's yeast (anti- Saccharomyces cerevisiae antibodies [ASCA]) can be used as an indirect test. The objective of this study was to investigate whether intestinal permeability, represented by AGA, was correlated with MAGI2, MYO9B, and PARD3. Analyses were performed in patients with Down syndrome, a population with suspected increased intestinal permeability. Correlations between AGA and ASCA were investigated. Patients with Down syndrome ( n = 126) were genotyped for six single-nucleotide polymorphisms in MAGI2 (rs1496770, rs6962966, rs9640699), MYO9B (rs1457092, rs2305764), and PARD3 (rs10763976). An allele dosage association of these risk genes and AGA levels was performed. The correlation between AGA and ASCA was studied. A strong correlation was found between AGA and ASCA ( p < 0.01). The patient group with one or more risk genotypes had lower mean AGA levels (trend test p = 0.007) and consisted of a larger number of patients with normal AGA levels ( p = 9.3 × 10 −5). Celiac-associated risk genotypes are associated with lower AGA values instead of elevated ones. Thus, other immunologic phenomena play a role in the increased prevalence of elevated AGA in patients with Down syndrome, possibly involving altered induction and/or maintenance of tolerance.

Antigliadin antibodies in Cuban patients with spinocerebellar ataxia type 2

Objective:To evaluate the significance of antigliadin antibodies (AGA) levels for spinocerebellar ataxia type 2.Methods:We determined AGA levels in 64 patients with spinocerebellar ataxia type 2 and in 65 healthy matched...

Celiac disease and antibodies associated with celiac disease in patients with inflammatory myopathy

Celiac disease is usually associated with autoimmune disorders and has occasionally been reported in patients with inflammatory myopathies. Our aim was to determine the presence of celiac disease and antibodies associated with celiac disease in patients with inflammatory myopathies and to investigate their relationship. Serum antigliadin, anti-tissue transglutaminase, and antiendomysial antibodies were determined in 51 patients with inflammatory myopathies. HLA-DQ2 and -DQ8 alleles were studied to assess their complementary diagnostic value. Jejunal biopsy was performed in patients with moderate to high levels of antigliadin antibodies. Patients with jejunal histology consistent with celiac disease initiated a gluten-free diet. Seventeen patients (31%) were positive for antigliadin antibodies, which were significantly more frequent in patients with inclusion-body myositis than dermatomyositis (P < 0.001). Positive status to HLA-DQ2 and/or -DQ8 did not differ between antigliadin-positive (75% and 12.5%) or -negative (60% and 15%) patients. Three of five jejunal biopsies were diagnostic for celiac disease with histological normalization after a gluten-free diet. Thus, celiac disease is more prevalent in patients with inflammatory myopathies than in the general population. Positive status to HLA-DQ2 allele, which is known to be more frequent in patients with inflammatory myopathies, could explain the high prevalence of antigliadin antibodies in this population. The diagnostic value of HLA-DQ2 or -DQ8 haplotypes to detect celiac disease in patients with inflammatory myopathy is limited.

IS THERE A CONNECTION BETWEEN CEREBRAL PALSY AND CELIAC DISEASE?

Objectives: Malnourishment can often be seen in children with severe neurological diseases including cerebral palsy (CP). Weight and height were sparsely measured and followed in these children even though it is well known that long periods of starvation can affect the neurodevelopment. Due to the spasticity in children with severe CP this group of children also have an increased need of nutrients. Apart from the spasticity several additional causes can worsen the nutritional status in these children, for instance disturbed swallowing, vomiting, gastro-oesophageal reflux with or without aspiration, delayed stomach emptying. The problem of not getting enough calories in these children have been increasingly recognised in the 1990s and more active efforts to meet this need have been done. Much is still unknown about nutritional status in these children. We don't know how the enteral uptake is working and what metabolic effects long periods of starvation might have. One observation we have seen in some children with severe CP and slow growth is an increased level of antibodies against gliadin. What this means is not clear. Does all children with cerebral palsy have a high risk of increased levels of celiac markers? Is it due to malnourishment? Do they have celiac disease? Our aims were therefore, to study laboratory markers for celiac disease in children with cerebral palsy. Methods: 100 children with cerebral palsy, from two countys were screened for IgG and IgA antigliadin-antibodies, endomysial antibodies (EMA) and anti-tissue transglutaminase (tTG). The age range was from 1.5–23 years. Results: 42% of the children had increased levels of antigliadin-antibodies (IgG and IgA) and anti-tTG. All were negative for EMA. Conclusion: High levels of antigliadin-antibodies are seen in children with cerebral palsy. Small bowel biopsies will be done in all of these patients.