Presence Of Antigliadin Antibodies Research Articles

Mo1653 Improvement of Gastrointestinal Symptoms After Gluten-Free Diet in Patients With Irritable Bowel Syndrome Is Dependent on the Presence of Anti-Gliadin Antibodies

Mo1653 Improvement of Gastrointestinal Symptoms After Gluten-Free Diet in Patients With Irritable Bowel Syndrome Is Dependent on the Presence of Anti-Gliadin Antibodies

Patients Who Avoid Wheat and Gluten: Is That Health or Lifestyle?

In a New York restaurant, a celiac patient requesting a gluten-free menu was asked by the server if the diet was for health or for lifestyle. This increasingly common exchange exemplifies the clinical conundrum clinicians face regarding the use of a gluten-free diet (GFD). Although humankind has likely existed in some form for 2.5 million years, it is only in the last 10,000 years that humans have been exposed to wheat, which was originally cultivated in the Fertile Crescent from *9000 BC to 4000 BC. Thus, wheat and therefore, gluten is a relatively novel component of the human diet. The globalization of wheat production, and subsequently its increased worldwide consumption, has increased the incidence and clinical recognition of gluten-related disorders [1]. The most notable gluten-related disorder is celiac disease (CD), a state of heightened immune response to ingested gluten in genetically susceptible individuals. Initial reports in the 1950s suggested this to be a rare condition affecting 1 in 8,000. Nevertheless, more recently, its prevalence in the United States and elsewhere is 0.71 % or 1 in 141 [2]. The sole effective treatment for CD is lifelong adherence to a strict GFD. More recently, a few case reports and series published in the 1980s described individuals intolerant to gluten, by way of experiencing irritable bowel syndrome (IBS) type symptoms, but in whom CD serologies and small intestinal biopsies were normal. Since the diagnosis or explanation for these symptoms was lacking and possibly dismissed, such patients were unclassifiable and untreatable [3]. Nonetheless, over the last few years, mounting media reports have speculated that the use of a GFD is rapidly growing to the point that it is now a big business, seemingly greatly exceeding the demand predicted from CD subjects alone. This media pressure finally prodded the scientific community into a response, led by an Australian group, who performed a landmark double-blind, randomised, placebo-controlled study reporting that gluten from two slices of bread and one muffin indeed induced gastrointestinal symptoms in subjects without CD [4]. Subsequently, a consensus of experts has introduced the term ‘‘non-celiac gluten sensitivity’’ (NCGS) to describe such subjects [5]. A subsequent flurry of research papers raised the ratio of publications for NCGS:CD from 1:438 to 1:10, to the point that NCGS is considered the new frontier of gluten-related disorders [6]. The pathophysiology of NCGS has not yet been fully elucidated. Whereas the innate and adaptive immune response to gluten is responsible for the manifestations seen in CD, only the innate immune system is seemingly triggered in NCGS. There have been promising reports of altered small bowel intestinal permeability, proliferation of peripheral blood monocytes, the presence of antigliadin antibodies, enhanced cytokine induction, and induction of basophil activation in NCGS, although these findings have not yet been confirmed [6]. Gluten is only one of the complex milieu of nutrients present in wheat, which also contains fructans, which are fermentable, poorly absorbed, short chain carbohydrates, also termed FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides and polyols). FODMAPS provoke gastrointestinal symptoms in IBS patients through mechanisms involving gut microbiota, gas production, and fermentation [7]. There is also emerging evidence that wheat-amylase trypsin inhibitors are also associated with intestinal symptoms [8]. Since it is unclear which component of wheat-based products is I. Aziz (&) D. S. Sanders Department of Gastroenterology, Room P39, Royal Hallamshire Hospital, Sheffield Teaching Hospitals, Sheffield S10 2JF, UK e-mail: imran.aziz@sth.nhs.uk

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.

Serological markers of coeliac disease in the children and adolescents with type 1 diabetes mellitus

We have studied the frequency of antibodies, markers of coeliac disease, in the children presenting with type 1 diabetes mellitus and obtained clinical and metabolic characteristics of seropositive and seronegative groups. The study included 499 diabetic children and adolescents admitted to the Pediatric Department of the Endocinological Research Centre. They were examined for the presence of anti-gliadin antibodies (anti-GL) and antibodies against tissue transglutaminase (anti-TG). These serological markers of coeliac disease were detected in 7.4% of the patients. More specific anti-TG occurred in 3.2% of the cases. As many as 29.7% of the seropositive patients with DM1 had gastrointestinal symptoms, such as stool disturbances, abdominal distension and pain, vomiting, and reduced appetite. Similar symptoms were documented in 11.7% of the seronegative children. Iron deficiency anemia was diagnosed in 24.3 and 8.6% of the seropositive and seronegative patients respectively (p&lt;0.05). There was no significant difference between the children with type 1 diabetes mellitus having serological markers of coeliac disease and the seronegative patients in terms of anthropometric characteristics, plasma levels of glycated hemoglobin and vitamin D. It is concluded that the presence of serological markers of coeliac disease is association with a number of clinical manifestations confirms the necessity of immunological screening for coeliac disease among patients with DM1.

Hippocampal sclerosis in refractory temporal lobe epilepsy is associated with gluten sensitivity

Background:Previous studies have associated coeliac disease (CD) and gluten sensitivity (defined as the presence of anti-gliadin antibodies and positive immunogenetics) with cerebellar degeneration and epilepsy with occipital calcifications. Hippocampal sclerosis...

The Significance of Coeliac Disease Antibodies in Patients with Ankylosing Spondylitis: A Case-Controlled Study

The presence of anti-gliadin antibodies (AGA) and their relationship with intestinal permeability and prevalence of undiagnosed coeliac disease (CD) in ankylosing spondylitis (AS) were investigated. Blood samples from 30 AS patients and 19 age- and sex-matched controls were analysed for human leucocyte antigen (HLA)-B27, AGA and endomysial antibodies (EMA). Immunoglobulin (Ig) A-type AGA and IgG-type EMA were determined by enzyme-linked immunosorbent assay. AGA-positive patients were examined by gastroduodenoscope and proximal small bowel mucosa biopsies were performed. Eleven (36.7%) AS patients were AGA positive (compared with none of the control subjects) and three (10.0%) of these AS patients were also EMA-positive. The presence of AGA was not associated with more severe AS. Mild-to-severe villous atrophy and hyperplasia of crypts with increased chronic inflammatory cells in the lamina propria, which is typical of CD, was only observed in one AGA/EMA positive AS patient; CD was subsequently diagnosed by histology. Although AGA positivity might contribute to the pathogenesis of AS by increasing intestinal permeability to micro-organisms or by modifying intestinal immune mechanisms, further work is required to clarify its role in AS.

Celiac disease associated antibodies in persons with latent autoimmune diabetes of adult and type 2 diabetes

Background: Celiac Disease (CD) is present in 1–16.4% of patients with type 1 diabetes mellitus. The most important serological markers of CD are anti-endomysial (EMA), anti-tissue transglutaminase (tTGA) and antigliadin antibodies (AGA).Aim/hypothesis: The objective of this work is to determine the frequency of tTGA and/or AGA in latent autoimmune diabetes of adult (LADA) and subjects with type 2 diabetes (T2DM), as well as to evaluate their relation with several clinical and biochemical characteristics.Subjects and Methods: Forty three subjects with LADA and 99 with T2DM were studied. The presence of AGA, tTGA was determined in the sera of these patients. The variables: sex, age, duration of diabetes, treatment, body mass index (BMI) and fasting blood glucose concentration were also recorded.Results: No differences were found in the frequency of celiac disease associated antibodies between LADA and T2DM subjects. The presence of celiac disease related antibodies was more frequent in patients with a normal or low BMI.Conclusions: Celiac disease does not seem to be related with pancreatic autoimmunity in type 2 diabetes. Celiac disease causes a decrease of body mass index in type 2 diabetes while pancreatic islet autoimmunity in this entity masks this effect.

Pemphigus Improving with Gluten-free Diet

Sir, Serum IgA class anti-endomysial antibodies (EMA) are markers of coeliac disease and dermatitis herpetiformis (DH) and are useful in monitoring compliance to diet. Their overall sensitivity for the diagnosis of DH is about 80% and their specificity around 96% (1). As anti-gliadin antibodies (AGA) have already been reported in pemphigus (2, 3), the presence of AGA in another patient with pemphigus may not surprise, but the finding of IgA-EMA in yet another, and the response of both patients to a gluten-free diet treatment are worthy of attention.

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

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

Diagnosis of coeliac disease: time for a change?

Diagnosing coeliac disease is not easy. Current recommendations stem from a 1970 statement of the European Society for Paediatric Gastroenterology and Nutrition (ESPGAN)l and call for: histological evidence of the lesion; evidence of its disappearance after an adequate period on a gluten free diet; and evidence of its recurrence after the reintroduction of gluten into the diet. Such a procedure, which seems to be widely accepted in Europe,2 is probably optimal for a firm diagnosis, but has several drawbacks, particularly in the light of new developments that have since taken place. Firstly, the time required for the final diagnosis is unduly long (three years on average); secondly, it does not take into account the variability in clinical expression of the disease; thirdly, it does not take into account the fact that after the age of 2 years it is highly unusual for subtotal villous atroph! to be caused by diseases other than coeliac disease ; and, fourthly, it means re-exposing a child to the offending agent in order to reproduce the mucosal damage. Furthermore, even this challenge (which is now known to be potentially harmful to the child's growing potential3 4) might be inconclusive, as evidence is now mounting that relapse may take longer than two years.2 5 6 It is therefore not surprising that several workers have started to adopt a somewhat more flexible attitude to the diagnosis that takes into account some new laboratory investigations (particularly the presence of antigliadin antibodies) and improved knowledge of the clinical range of the disease that has been acquired since the diagnostic protocol was introduced almost 20 years ago. For these reasons, the Italian Working Group for Paediatric Gastroenterology (which was formed in 1976 and has 250 members) undertook an evaluation of the current approach to the diagnosis of coeliac disease in Italy to verify whether a simplified, more flexible approach was possible. The following points were retrospectively assessed, in a total of 3138 patients with coeliac disease from 33 different centres: (i) the importance of human leucocyte antigen (HLA) typing and the presence of antigliadin antibodies; (ii) the need for repeated intestinal biopsy in so called 'atypical' cases or in cases presenting in older children; (iii) the predictive value of the presence of 'flat mucosa' in a child with clinical or laboratory evidence, or both, suggesting coeliac disease; and (iv) the feasibility and evaluation of gluten challenge. The collected data were analysed and presented by invited experts in a two day meeting in Trieste in May 1987. During the meeting each point was discussed and a final consensus was reached, in a session chaired by A Rubino. The most important points are summarised below.

Detection of antigliadin antibodies in bullous diseases and their recognition of similar antigenic polypeptides.

The presence of antigliadin antibodies (AGA) in dermatitis herpetiformis (DH) has been associated with gluten-sensitive enteropathy. Because of the discrepancies in the specificity of AGA, we examined the sera of patients with DH, pemphigus and pemphigoid for AGA both by enzyme immunoassay and by immunofluorescence. Approximately 80-90% of sera of patients with DH had AGA. AGA were not disease-specific, they also occurred in about 40-80% of patients with pemphigus and pemphigoid depending on the method employed. In addition, AGA were also present in normal subjects. The incidence of AGA increased with age. AGA from patients with various bullous diseases recognized the same polypeptides thus suggesting that the presence of AGA cannot be regarded as a serological marker of DH.

Vesicular pemphigoid vs dermatitis herpetifomis

We describe a patient with clinical features of dermatitis herpetiformis (DH) and histopathologic features suggestive of both DH and bullous pemphigoid (BP). Immunofluorescent (IF) studies of skin biopsy revealed IgG and C3 deposits along the basement membrane zone (BMZ) in a linear pattern and circulating BMZ antibodies in the serum consistent with BP. The patient's condition evolved over 5 years into a typical case of DH characterized by histologic findings of papillary edema and neutrophilic infiltrates and evidence by IF findings of granular IgA deposits in the dermal papillae and the presence of antigliadin antibodies in the serum.

Anti-gliadin antibodies and small intestinal mucosal damage in dermatitis herpetiformis.

Sera from forty-six patients with dermatitis herpetiformis (DH) were examined for anti-gliadin antibodies (AGA) by the enzyme linked immunosorbent assay (ELISA) test and by a simple new immunofluorescent (IF) test. AGA were present in fifteen out of thirty-two patients taking a normal diet, but in none of the fourteen taking a gluten-free diet (GFD). The presence of circulating AGA was related to the severity of the enteropathy. AGA were present in all ten patients with a flat mucosa and in four of six with a convoluted mucosa, but in only one out of thirty patients with normal morphology of the small intestine. However, in those patients taking a normal diet and with a normal morphology of the intestine there was evidence of gluten sensitivity compared to those taking a GFD, as the intraepithelial lymphocyte count (IELC) was significantly raised in the peri-nuclear and supra-nuclear positions. The study shows that the presence of AGA in the serum is a good indication of the degree of gluten sensitivity as expressed by severe mucosal damage in patients with DH.