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Vitamin D deficiency is a major cause of hypocalcemic seizures in infants. Chronic enteropathy can cause both malnutrition and vitamin deficiency disorders, such as celiac disease, in Western Caucasians. However, gluten-related disorders are considered uncommon in most Asian countries, and there have been no reports of any infant being diagnosed with a gluten-related disorder in Japan. Here, we describe a case where a Japanese infant, with non-celiac gluten sensitivity, presented with hypocalcemic seizures resulting from a vitamin D deficiency. In this case, an eight-month-old boy had an afebrile seizure, and blood tests revealed both hypocalcemia and prolonged prothrombin time resulting in his transfer to our hospital. The presence of fatty stools and evidence of multiple vitamin deficiencies indicated some form of fat malabsorption. His laboratory and histological findings showed enteropathy, and he was thus diagnosed with non-celiac gluten sensitivity. Therefore, he was treated with a gluten-free diet supplemented with vitamins. This case suggests that infants with a vitamin D deficiency caused by celiac disease or non-celiac gluten sensitivity should be carefully monitored when they are given oral supplements of vitamin D, to prevent any adverse side-effects associated with the varied roles of vitamin D in the immune response.

Celiac disease (CD) represents A unique disorders in which consumption of a food ingredient namely gluten-containing grains (wheat, rye, barley) in combination with genetic susceptibility is fundamental for the development of an a guilefully evolving autoimmune reaction influence the gut and other organs. The present study determines the celiac disease among suspected children. From special the laboratory for Pathogenesis Analyses in Baghdad 100 blood children samples was collected during the period from 1st March 2018 till the 31 th of July 2018, analyzed by two serological test which were Anti-tissue transglutaminase (tGT) antibodies and Anti-gliadin antibodies for the presence of serum Immunoglobulin A (IgA tGT), Immunoglobulin G (IgG tGT), Immunoglobulin A (IgA AGA), Immunoglobulin G (IgG AGA) were measured by Enzyme-linked Immunosorbent Assay (ELISA). In result obtained positive serological test Trasglutaminase (tGT) for IgA tGT was 5 (16.7 %), IgG tGT was12 (40.0 %), more than Antiglidin Antibodies IgA AGA was 3 (10.0 %), IgG AGA was 10 (33.3 %). the males was 18 (32.1 %) more than female between (6 year - 9 year) age group which represent 10 (37.0 %). The symptoms of celiac disease found with weight loss 26 (86.7 %), chronic diarrhea 21 (70.0 %), vomiting 19 (63.3 %). In this study, obtained positive serological test Trasglutaminase for (IgA, IgG tGT) Antibodies in male between age group (6 year - 9 year) and with the symptoms more found with weight loss, chronic diarrhea, vomiting.

Immunological events that precede the development of villous atrophy in celiac disease (CeD) are still not completely understood. We aimed to explore CeD-associated antibody production (anti-native gliadin (AGA), anti-deamidated gliadin (DGP) and anti-tissue transglutaminase (anti-tTG)) in infants at genetic risk for CeD from the Italian cohorts of the PREVENT-CD and Neocel projects, as well as the relationship between antibody production and systemic inflammation. HLA DQ2 and/or DQ8 infants from families with a CeD case were followed from birth. Out of 220 at-risk children, 182 had not developed CeD by 6 years of age (CTRLs), and 38 developed celiac disease (CeD). The profiles of serum cytokines (INFγ, IL1β, IL2, IL4, IL6, IL10, IL12p70, IL17A and TNFα) and the expression of selected genes (FoxP3, IL10, TGFβ, INFγ, IL4 and IL2) were evaluated in 46 children (20 CeD and 26 CTRLs). Among the 182 healthy CTRLs, 28 (15.3%) produced high levels of AGA-IgA (AGA+CTRLs), and none developed anti-tTG-IgA or DGP-IgA, compared to 2/38 (5.3%) CeD infants (Chi Sq. 5.97, p = 0.0014). AGAs appeared earlier in CTRLs than in those who developed CeD (19 vs. 28 months). Additionally, the production of AGAs in CeD overlapped with the production of DGP and anti-tTG. In addition, gene expression as well as serum cytokine levels discriminated children who developed CeD from CTRLs. In conclusion, these findings suggest that the early and isolated production of AGA-IgA antibodies is a CeD-tolerogenic marker and that changes in gene expression and cytokine patterns precede the appearance of anti-tTG antibodies.

A recent study suggested that digestion-resistant peptides derived from wheat gluten (mainly gliadin) could induce the secretion of anti-gliadin IgG antibodies in patients with schizophrenia. This research was then designed to replicate this initial finding in 134 drug-naïve patients with first-episode schizophrenia and 160 healthy controls. An enzyme-linked immunosorbent assay was developed in-house with 8 gliadin-derived peptide antigens to test anti-gliadin IgG antibodies in the circulation. The results showed that schizophrenia patients had significantly higher levels of plasma anti-AL2G2 IgG and anti-ABO3a IgG than healthy controls. Based on the specificity of 95%, anti-AL2G2 IgG assay had a sensitivity of 12.7% and anti-ABO3a IgG assay had a sensitivity of 17.2% for anti-ABO3a IgG assay. Increased levels of anti-AL2G2 and anti-ABC3a IgG antibodies were not correlated with total IgG levels in either the patient group or the control group. In conclusion, circulating IgG against AL2G2 and ABO3a may be useful biomarkers for identification of a gluten-sensitive subgroup of schizophrenia in the Chinese population although the present results are rather different from the work performed in a British population.

We have previously shown that 67% of patients with newly diagnosed coeliac disease (CD) presenting to gastroenterologists have evidence of neurological dysfunction. This manifested with headache and loss of co-ordination. Furthermore 60% of these patients had abnormal brain imaging. In this follow-up study, we re-examined and re-scanned 30 patients from the original cohort of 100, seven years later. There was significant reduction in the prevalence of headaches (47% to 20%) but an increase in the prevalence of incoordination (27% to 47%). Although those patients with coordination problems at baseline reported improvement on the gluten free diet (GFD), there were 7 patients reporting incoordination not present at baseline. All 7 patients had positive serology for one or more gluten-sensitivity related antibodies at follow-up. In total, 50% of the whole follow-up cohort were positive for one or more gluten-related antibodies. A comparison between the baseline and follow-up brain imaging showed a greater rate of cerebellar grey matter atrophy in the antibody positive group compared to the antibody negative group. Patients with CD who do not adhere to a strict GFD and are serological positive are at risk of developing ataxia, and have a significantly higher rate of cerebellar atrophy when compared to patients with negative serology. This highlights the importance of regular review and close monitoring.

Background Gluten sensitivity among psoriasis patients and its association with gender, age, disease duration and severity of psoriasis are under studied in Indians. Objective To examine association among serum levels of anti-tTG and anti-gliadin antibodies and clinical features including gender, age, duration and severity of psoriasis. Methods Serum levels of anti-transglutaminase and anti-gliadin antibodies were measured quantitatively in 80 (M:F 57:23) psoriasis patients aged 15 to 83 years and matched healthy subjects. Results 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. Conclusion 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.

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

To analyze the presence of total IgA and anti-gliadin antibodies (AGA) in BM from CD mothers who follow a gluten-free diet (GFD) and from mothers on a normal gluten-containing diet (ND). 218 samples of mature milk were obtained at different months of lactation (1–6) from 83 mothers (2 or more samples per mother) from Italy (Naples), The Netherlands (Leiden) and Spain (Madrid, Valencia and Reus): 42 CD mothers on GFD for more than 2 years and 41 non-CD mothers on a ND. Whey samples were analyzed for AGA-IgA by an indirect homemade ELISA and for total IgA (g/L) by a commercial ELISA kit. AGA-IgA was detected in BM, both in mothers on a GFD and mothers on a ND. AGA-IgA levels in both groups of mothers, CD and non-CD, show the same trend towards decreasing slightly along the months of lactation (p = 0.91). A different trend is observed for total IgA levels, decreasing markedly in CD mothers from the first month of lactation onwards but remaining stable in non-CD mothers (p = 0.048). A statistically significant association was found between the means of total IgA and AGA-IgA (p

Background & Aims There is controversy over the association between celiac disease (CeD) and inflammatory bowel diseases (IBD). We performed a systematic review and meta-analysis to assess evidence for an association between CeD and IBD. Methods We searched databases including MEDLINE, EMBASE, CENTRAL, Web of Science, CINAHL, DARE, and SIGLE through June 25, 2019 for studies assessing the risk of CeD in patients with IBD, and IBD in patients with CeD, compared with controls of any type. We used the Newcastle-Ottawa Scale to evaluate the risk of bias and GRADE to assess the certainty of the evidence. Results We identified 9791 studies and included 65 studies in our analysis. Moderate certainty evidence found an increased risk of CeD in patients with IBD vs controls (risk ratio [RR] 3.96; 95% confidence interval [CI] 2.23–7.02) and increased risk of IBD in patients with CeD vs controls (RR 9.88; 95% CI 4.03–24.21). There was low-certainty evidence for the risk of anti-Saccharomyces antibodies, a serologic marker of IBD, in patients with CeD vs controls (RR 6.22; 95% CI 2.44–15.84). There was low-certainty evidence for no difference in risk of HLA-DQ2 or DQ8 in patients with IBD vs controls (RR 1.04; 95% CI 0.42–2.56), and very low-certainty evidence for an increased risk of anti-tissue transglutaminase in patients with IBD vs controls (RR 1.52; 95% CI 0.52–4.40). Patients with IBD had a slight decrease in risk of anti-endomysial antibodies vs controls (RR 0.70; 95% CI 0.18–2.74), but these results are uncertain. Conclusions In a systematic review and meta-analysis, we found an increased risk of IBD in patients with CeD and increased risk of CeD in patients with IBD, compared with other patient populations. High-quality prospective cohort studies are needed to assess the risk of CeD-specific and IBD-specific biomarkers in patients with IBD and CeD.

Altered immune function and inflammation are seen in schizophrenia, however, peripheral inflammatory markers are not consistently elevated in all people, suggesting inflammation may be present only in a subgroup. We measured TNF-α and IL-Iβ in 100 people with schizophrenia or schizoaffective disorder and correlated these with antibodies to gliadin, a protein found in wheat, barley and rye that has been found to be elevated in some people with schizophrenia. We hypothesized that higher peripheral antigliadin antibodies (AGA IgG) would be associated with higher peripheral inflammation as measured by TNF-α and IL-1β. Mean log transformed values of TNF-α, (p = .029) and IL-1β (p = .016) were over twofold higher in people with schizophrenia who had high levels of AGA IgG (≥7 U) compared to those who did not have positivity to AGA IgG. We found a significant positive correlation between AGA IgG and the log transformed TNF-α (r = 0.42, p < .0001) as well as IL-Iβ (r = 0.51, p < .0001). The relationship was independent of cigarette smoking, body mass index and antipsychotic medications. People with schizophrenia having higher levels of AGA IgG show higher levels of peripheral inflammation and may define a subgroup with distinct pathophysiology and potentially novel treatment targets.

BACKGROUND: Hashimoto’s thyroiditis is in coexistence with many autoimmune disorders, especially celiac disease. There are a limited number of studies evaluating the prevalence of celiac-related antibodies in patients with Hashimoto’s thyroiditis. OBJECTIVE: This study aimed to further investigate the prevalence of undiagnosed celiac disease in patients with Hashimoto’s thyroiditis and the relationship between these two autoimmune disorders in these patients SUBJECTS AND METHODS: This study was performed on 82 women aged 20-50 years including 40 patients with Hashimoto’s thyroiditis and 42 healthy age-matched individuals. Anthropometric assessments were performed and biochemical parameters including thyroid hormones (TSH, T3 and T4), antithyroid antibodies, anti-tissue transglutaminase and anti-gliadin antibodies were measured by enzyme linked immunosorbent assay (ELISA). RESULTS: The prevalence of IgG and IgA anti-tissue transglutaminase antibodies and IgA anti-gliadin antibody was higher in Hashimoto’s thyroiditis patients compared with control group (15% vs. 7%, 22.5% vs. 17% and 15% vs. 12% respectively). In ordinal regression model, serum IgG anti-tissue transglutaminase and IgA anti-gliadin antibodies were significant predictors of antithyroid antibodies in patients with Hashimoto’s thyroiditis (P < 0.05). A significant relationship between serum TSH and IgG anti-gliadin antibody were also found (P = 0.003). CONCLUSION: To our findings, a high prevalence of anti-tissue transglutaminase and IgA anti-gliadin antibodies and their positive relationship with antithyroid antibodies in patients with Hashimoto’s thyroiditis were reported. These findings further warrant the need for interventions to reduce the prevalence of these antibodies in Hashimoto’s thyroiditis for preventing the occurrence of celiac disease in these patients.

Incidences of food allergies are on the rise, which can greatly affect the well-being of children as well as adults. Intolerance to gluten, a protein composite of gliadin and glutenin, present in wheat, barley, and rye and several cereals, can be the causative agent of celiac disease (CD) and other allergic reactions. A gluten-free diet has become essential for people affected by CD, and consequently, the amount of gluten in food products needs to be strictly controlled. In this paper, we report an electrochemical label-free immunosensor for ultrasensitive and specific detection of gliadin. The sensor takes advantage of the specific properties of porous reduced graphene oxide (prGO) covalently functionalized with anti-gliadin antibodies using 1-pyrenecarboxylic acid as linker molecule. Using differential pulse voltammetry (DPV) and [Fe(CN)6]3-/4- as a redox probe, a decrease of current is linked to the presence of gliadin. The sensor achieved a detection limit of 1.2 ng mL–1 over a 1.2–34 ng mL–1 linear r...

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%.Цель исследования. Определить частоту выявления целиакии у больных с патологией органов пищеварения. Материалы и методы. Обследовали 318 больных с гастроэнтерологической патологией, поступивших на стационарное лечение в Центральный научно-исследовательский институт гастроэнтерологии с сентября по октябрь 2012 г. Возраст больных составил от 18 до 74 лет (средний 51,5±16,4 года). Определяли антитела к глиадину (АГА) иммуноглобулина А (АГА IgA) и иммуноглобулина G (АГА IgG), антитела к тканевой трансглутаминазе IgA (АтТГ IgA) и IgG (АтТГ IgG). При повышенных уровнях антител выполняли эзофагогастродуоденоскопию с биопсией слизистой оболочки двенадцатиперстной кишки. Результаты. У 41 из 318 больных выявлено повышение АГА (12,9%), из них АГА IgA у 17 (5,35%) и АГА IgG также у 17 (5,35%). У 7 (2,2%) пациентов отмечено повышение уровня обоих антител (АГА IgA и АГА IgG). Чаще антитела были повышены у больных с заболеваниями печени (21,8%) и воспалительными заболеваниями кишечника (21,6%). У 6 (1,9%) из 318 больных выявлены как АтТГ IgA и АтТГ IgG, так и АГА IgA и АГА IgG. У 3 (0,94%) из 318 пациентов диагноз целиакии подтвержден результатами гистологического исследования слизистой оболочки двенадцатиперстной кишки. Заключение. Частота выявления целиакии у больных гастроэнтерологического профиля составляет 0,94%.

Background There is an increasing interest in diet as a modifying factor in multiple sclerosis (MS), and gluten has been suggested to affect MS. Objective The aim of this systematic review is to qualitatively evaluate the evidence on the role of gluten in MS. Methods A review protocol was submitted to PROSPERO. A systematic literature search was conducted in PubMed, Web of Science, Scopus, Embase, Cab Abstracts, and Google Scholar. Studies on patients with MS, clinically isolated syndrome, or celiac disease presenting with MS-related markers were included, if they investigated effects of diets containing specified amounts of gluten or associations between gluten sensitivities and MS. Results Forty-nine publications presenting 50 studies/cases met the inclusion criteria. Study designs, methods, and outcomes varied broadly across studies. Two intervention studies found a positive effect of a gluten-free diet on disease-related markers in patients with MS. One prospective cohort study also found a positive effect of a gluten-free diet, while a survey found intake of cereal/bread to be protective against MS. Four observational studies did not find increased comorbidity of MS and celiac disease. Seventeen studies investigated the level of different gluten-sensitivity markers in patients with MS with inconsistent results. Finally, 12 cases and 13 posters/abstracts/master's theses contributed to shed light on the topic. Conclusions There is still not sufficient evidence to state whether gluten plays a role in MS, but limitations of current evidence have been identified and directions of future research have been suggested.

Introduction : Pustular palmoplantar psoriasis (PPP) is a rare type of psoriasis affecting mainly distal parts of the limbs. Despite numerous theories about etiology of PPP, the pathogenesis still remains unclear. Recent data indicate that interleukin (IL)-15, IL-17 and IL-22 enhance a proinflammatory response in certain skin inflammatory diseases such as psoriasis and atopic dermatitis. There is also evidence that anti-endomysial (anti-EMA) and anti-gliadin (AGA) antibodies are engaged in PPP development. Aim : To assess IL-15, IL-17, IL-22 serum levels and evaluate the presence of anti-endomysial and anti-gliadin antibodies in patients with PPP. Material and methods : The study group consisted of 20 females of the mean age of 51.8 suffering from PPP. Additionally 29 healthy individuals, age and sex matched, served as controls. ELISA was performed to evaluate serum IL-15, IL-17, IL-22 concentrations while an indirect immunofluorescence test (IIF) was used to determine anti-EMA and AGA presence. Results: The mean value of IL-15 and IL-22 serum concentrations was significantly higher in the study group than in the control group (IL-15: 6.48 vs. 4.88 pg/ml; IL-22: 81.47 vs. 4.90 pg/ml, respectively; p < 0.05 for all comparisons). The IL-17 serum level in the study group was higher when compared to the control group (2.0 vs. 0.75 pg/ml), however the results were not statistically significant (p = 0.26). There were no anti-EMA and AGA antibodies detected, both in the control and study group. Conclusions : The results obtained may suggest involvement of IL-15 and IL-22 in the pathogenesis of PPP.

Background Gluten is the target of several diseases such as wheat allergy (WA), celiac disease (CD) and non-celiac gluten sensitivity (NCGS). NCGS is a new clinical entity characterized by gastrointestinal and extraintestinal symptoms comparable to those of CD patients but to date still lacking of specific biomarkers so that NCGS diagnosis can be reached only by excluding CD and WA, and based on the direct association between gluten ingestion and symptoms onset. Previous studies showed that antigliadin antibodies (AGA) IgG are the most prevalent positive antibodies in NCGS population. Aim The first aim of the study was to estimate AGA distribution and prevalence in a NCGS population. The second aim was to identify a serological pattern to help the diagnosis and/or to mark the NCGS disease. Methods Sera from 59 patients with suspected NCGS, 90 CD patients and 70 healthy individuals were assessed for AGA IgG/IgA, IgG/IgA deamidated gliadin peptide antibodies (DGP-AGA), tissue transglutaminase antibodies IgA (tTGA), endomysial antibodies IgA (EmA) and HLA typing (Eurospital, Trieste, Italy). Results We evaluated data by a dual statistical approach: logistic regression and receiver operating characteristic (ROC) analysis; therefore, we showed a poor diagnostic accuracy of AGA IgG in NCGS condition. Conclusion Our preliminary data showed that AGA IgG didn't seem to be a strongly sensitive marker, even if it has been recently proposed as promising marker for NCGS condition, together with negativity for other celiac disease related antibodies. It can partially help the NCGS diagnosis, if it is integrated in the overall management of the patient. More in-depth clinical and laboratory researches are mandatory.

Celiac disease (CD) is now considered, more than a just gluten sensitivity enteropathy, a multiple and systemic immune-mediate disorder triggered by the ingestion of wheat gluten and related proteins. Following the discovery of a link between gluten and CD, it was demonstrated that gliadin, one of the two principal protein groups comprising gluten, plays a key role in CD. It has since become clear that the different and crucial roles of gliadin in CD result from its ability to activate multiple signaling pathways that modulate CD pathology. Most of these pathways involve the host innate and adaptive immune responses, but some pathways are activated when gliadin interacts with the intestinal cellular compartment. The long pentraxin (PTX3), a marker of the acute-phase inflammatory response, plays an important role in innate immunity and in modulation of the adaptive immune response. We investigated whether CD patients, considered as a model of gluten-sensitivity condition, have increased PTX3 levels. Our data showed that PTX3 serum levels were high in active CD patients and serum levels of PTX3 correlated with DGP IgA levels. We provide evidences that the bad compliance of GFD in patients 2 concurred with a pathological PTX3 concentration that could follow the improvement of both gastrointestinal and extraintestinal symptoms. We hypothesized that PTX3 is able to modulate the innate response to gliadin in CD and it could regulate the adaptive immune response. It is also evidenced that a common "wooden horse" of CD and Non Celiac Gluten Sensitivity (NCGS) is the ingestion of gluten and related toxic peptides. At the moment we don't have adequate elements to suggest the use of PTX3 in diagnosis of NCGS, but we are obliged to speculate about the possible role of PTX3 molecules in NCGS pathogenesis. The identified new strategies and uses of PTX3 could improve the management of gluten sensitivity conditions in the next future.

There is evidence that children with autism spectrum disorders (ASDs) display an increased immune reactivity against gluten, which is supposed to be the effect of intestinal barrier abnormalities. The aim of study was to evaluate the relation of antibody induced by gluten to zonulin and intestinal fatty acid binding proteins (I-FABP), that is, serological markers of an impaired gut barrier. The study included 77 patients with ASDs. Zonulin, I-FABP, celiac-specific antibodies, anti-gliadin antibodies (AGA), and antibodies against neural transglutaminase 6 (TG6) of immunoglobulin (Ig) A and IgG classes were detected in sera. Celiac-specific antibodies were negative in all ASD children, four children (5.2%) had positive anti-TG6 antibodies, and increased AGA-IgG production was found in 21 patients (27.3%). Mean levels of zonulin and I-FABP in ASD patients were similar to those found in healthy controls and revealed a negative correlation with age, whereas regression analysis revealed a significant positive relationship between antibody production and the age. Serum concentrations of zonulin and I-FABP showed no statistically significant association with antibody positivity. An increased production of antibodies related to gliadin and neural TG6 in ASD children is not related to serological markers of an impaired intestinal barrier.

Although no biomarker has been identified to date, previous studies have reported that about 50% of patients with suspected non-celiac gluten sensitivity (NCGS) had positive first generation anti-gliadin antibodies (AGAs), especially of the IgG class. These antibodies are not specific for NCGS, being also found in CD (80-90%), autoimmune liver disorders (21.5%), connective tissue disease (9%) and IBS (20%), as well as in healthy controls (2-8%), but their finding in patients with a clinical phenotype consistent with NCGS has been regarded as an element supporting this diagnosis. Even though the correlation between AGA IgG and NCGS condition turned out to be statistically significant in most studies, AGA IgG does not seem to be an adequately strong marker for its lacking diagnostic accuracy. However it can partly help the NCGS diagnosis, integrated in the overall management of the patient. Therefore, in the presence of clinical symptoms that suggest NCGS, IgG AGA positivity, together with negative anti-tTG, EMA, and anti-deamidated-gliadin-peptides (DGP) antibodies, NCGS diagnosis might be suspected. Future researches are necessary to identify reliable biomarkers for NGCS diagnosis and to better define clinically and serologically NCGS patients.

AIM To assess the prevalence of a panel of serologic markers that reflect gut barrier dysfunction in a mixed cohort of pediatric and adult primary sclerosing cholangitis (PSC) patients. METHODS Sera of 67 PSC patients [median age (range): 32 (5-79) years, concomitant IBD: 67% and cirrhosis: 20%] were assayed for the presence of antibodies against to F-actin (AAA IgA/IgG) and gliadin (AGA IgA/IgG)] and for serum level of intestinal fatty acid-binding protein (I-FABP) by ELISA. Markers of lipopolysaccharide (LPS) exposure [LPS binding protein (LBP)] and various anti-microbial antibodies [anti-OMP Plus IgA and endotoxin core IgA antibody (EndoCAb)] were also determined. Poor disease outcome was defined as orthotopic liver transplantation and/or liver-related death during the follow-up [median: 99 (14-106) mo]. One hundred and fifty-three healthy subjects (HCONT) and 172 ulcerative colitis (UC) patients were the controls. RESULTS A total of 28.4%, 28.0%, 9% and 20.9% of PSC patients were positive for AAA IgA, AAA IgG, AGA IgA and AGA IgG, respectively. Frequencies of AAA IgA and AAA IgG (P < 0.001, for both) and AGA IgG (P = 0.01, for both) but not AGA IgA were significantly higher compared to both of the HCONT and the UC groups. In survival analysis, AAA IgA-positivity was revealed as an independent predictor of poor disease outcome after adjusting either for the presence of cirrhosis [HR = 5.15 (1.27-20.86), P = 0.022 or for the Mayo risk score (HR = 4.24 (0.99-18.21), P = 0.052]. AAA IgA-positivity was significantly associated with higher frequency of anti-microbial antibodies (P < 0.001 for EndoCab IgA and P = 0.012 for anti-OMP Plus IgA) and higher level of the enterocyte damage marker (median I-FABPAAA IgA pos vs neg: 365 vs 166 pg/mL, P = 0.011), but not with serum LBP level. CONCLUSION Presence of IgA type AAA identified PSC patients with progressive disease. Moreover, it is associated with enhanced mucosal immune response to various microbial antigens and enterocyte damage further highlighting the importance of the gut-liver interaction in PSC.

AIM: To elaborate recommendations for rehabilitation of patients with gluten-sensitivity celiac disease (GCD) on the basis of a long-term follow-up/MATERIAL AND METHODS: Eighty-seven patients with GCD were followed up for as long as 31 years. Of those, 72.4% of the patients kept strictly to their gluten-free diet (GFD) throughout the follow-up; 9.2% did not follow the diet periodically; and 18.4% did not at all. The sera from 71 patients were tested for IgA and IgG anti-gliadin antibodies (AGAb) and anti-tissue transglutaminase antibodies (AтTGAb) at as long as 19-year follow-up. AGAb and AтTGAb were estimated by enzyme immunoassay (IMMCO Diagnostics). All the patients underwent endoscopic and histological examinations of the small bowel mucosa (SBM)/RESULTS: To support the validity of keeping to the GFD, the time course of clinical, laboratory, and morphological changes were analyzed in 63 and 24 GFD followers and non-followers, respectively. The GFD non-followers were more frequently found to have diarrheic syndrome, symptoms of malabsorption syndrome, lower serum concentrations of hemoglobin, total protein, iron, and calcium; no SBM structural recovery was seen in any patient. When the GFD was long adhered to, there was also a reduction in detection rates and AGAb and AтTGAb concentrations/CONCLUSION: The adherence to the GFD was ascertained to contribute to fuller rehabilitation in the patients. However, even the patients who had strictly kept to their GFD showed periods of an exacerbation and incomplete SBM structural recovery. Therefore, the rehabilitation system for patients with GCD must involve diagnostic, therapeutic, and organizational measures that promote not only rapid clinical recovery, but also better quality of life in these patients.

Celiac disease (CD) is a gluten-triggered autoimmune disorder of the small intestine. A lifelong gluten-free diet (GFD) is the only approved treatment; however, strict adherence is difficult and many suffer from inadvertent gluten exposure. Oral egg yolk anti-gliadin antibody (AGY) is a novel treatment to neutralize gluten and may improve the efficacy of the GFD. To determine the safety, tolerability, and potential efficacy of AGY in patients with CD. This 6-week, open-label, single-arm study was conducted in adults with biopsy-proven CD on a GFD. Safety measures included adverse events, physical examination, and clinical laboratory tests. Additional measures included a daily Celiac Symptom Index, Health-Related Quality of life, anti-tissue transglutaminase and anti-gliadin IgA/IgG, and lactulose/mannitol excretion ratio (LMER). A 2-week run-in period to assess questionnaire compliance and acceptability of baseline safety laboratory results was followed by a 4-week treatment period with two AGY capsules taken before meals. Ten patients completed the study (mean age 43.4 years, nine female). All followed a GFD for at least 6 months (mean 5 years). No safety concerns were identified. Most patients had fewer celiac symptoms (especially tiredness, headache, and bloating), improved quality of life, lowered antibodies, and lowered LMER when taking AGY compared to the run-in period. In our cohort, AGY was safe and potentially associated with improved CD-related outcome measures in patients on a GFD. A larger study powered for further safety and efficacy evaluation is planned.