Small-intestinal TG2-specific plasma cells at different stages of coeliac disease.

Background: In coeliac disease, ingestion of gluten induces the production of transglutaminase 2 (TG2)-targeted autoantibodies by TG2-specific plasma cells present at high frequency in the small intestinal mucosa in untreated disease. During treatment with a gluten-free diet (GFD), the number of these cells decreases considerably. It has not been previously investigated whether the cells are also present prior to development of villous atrophy, or in non-responsive patients and those with dietary lapses.

Injection of celiac disease patient sera or immunoglobulins to mice reproduces a condition mimicking early developing celiac disease.

Unlabelled: Typical features of celiac disease are small-bowel villus atrophy, crypt hyperplasia, and inflammation which develop gradually concomitant with ingestion of gluten. In addition, patients have anti-transglutaminase 2 (TG2) autoantibodies in their serum and tissues. The aim of this study was to establish whether celiac disease can be passively transferred to mice by serum or immunoglobulins.

Impaired epithelial integrity in the duodenal mucosa in early stages of celiac disease.

The small-bowel mucosal damage characteristic of celiac disease (CD) develops from normal villus morphology to inflammation and finally to villus atrophy with crypt hyperplasia. Patients with early stage CD may already suffer from abdominal symptoms before the development of villus atrophy. Although epithelial junctional integrity is compromised in overt disease, the appearance of such changes in early phases of the disorder is not known.

Small bowel transglutaminase 2-specific IgA deposits in dermatitis herpetiformis.

Dermatitis herpetiformis (DH) is an extraintestinal manifestation of coeliac disease. Untreated coeliac disease patients are known to have transglutaminase 2 (TG2)-targeted IgA deposits in the small bowel mucosa. To evaluate whether similar intestinal IgA deposits are also present in DH and whether the deposits disappear with gluten-free diet, 47 untreated and 27 treated DH patients were studied.

Validation of morphometric analyses of small-intestinal biopsy readouts in celiac disease.

Background: Assessment of the gluten-induced small-intestinal mucosal injury remains the cornerstone of celiac disease diagnosis. Usually the injury is evaluated using grouped classifications (e.g.

An update on the diagnostics of celiac disease.

In celiac disease, highly sensitive and specific serum endomysial and transglutaminase 2 antibody tests are widely used in identifying patients for diagnostic endoscopy and small-bowel biopsy. In addition, the recently developed deamidated gliadin peptide antibody tests show promise in celiac disease diagnostics. In view of these apparent problems attending the diagnostic gold standard, gluten-induced small-bowel mucosal villous atrophy with crypt hyperplasia, other diagnostic approaches beyond conventional histology have been introduced.

IgA-class autoantibodies against neuronal transglutaminase, TG6 in celiac disease: no evidence for gluten dependency.

Background: It has been suggested that antibodies against transglutaminase (TG) 6 could serve as a biomarker to identify a subgroup of gluten-sensitive patients who may be at risk of developing neurological disease. We here investigated whether TG6-targeted autoantibodies are a characteristic feature of celiac patients, especially those with neurological symptoms, and further, whether such antibodies are gluten-dependent.

Methods: Serum IgA-class TG6 autoantibodies were measured in untreated and treated celiac patients with and without neurological manifestions and in non-celiac controls.

Serodiagnostic assays for celiac disease based on the open or closed conformation of the autoantigen, transglutaminase 2.

The autoantigen of celiac disease, transglutaminase 2 (TG2), adopts an open conformation during enzymatic activation. We studied diagnostic accuracy of serodiagnostic assays using TG2 in its open and closed conformation as antigens in patients with diagnostic difficulties. The open TG2 antibody (TG2ab) test identified 93% of untreated celiac patients in contrast to 44%, 27%, and 68% detected by closed and conventional TG2ab and endomysial antibody (EmA) tests, respectively.

Coeliac disease--a diagnostic and therapeutic challenge.

During the past 20 years the diagnosis of coeliac disease has improved significantly. However, at the same time the true prevalence of the condition has doubled, involving more than 2% of the population in some countries. Due to mild or atypical symptoms, the diagnosis remains a challenge for the health care system.

Intestinal transglutaminase 2 specific antibody deposits in non-responsive coeliac disease.

Background And Aims: The diagnosis of coeliac disease is problematic in individuals not responding to a gluten-free diet. Small-bowel villous atrophy occurs in other enteropathies and non-responsive patients are often seronegative. We investigated whether small-bowel mucosal transglutaminase-2 specific autoantibody deposits distinguish non-responsive coeliac disease from other enteropathies.

Celiac disease without villous atrophy in children: a prospective study.

Objective: To establish whether children who are endomysial antibody (EmA) positive and have normal small-bowel mucosal villous morphology are truly gluten-sensitive and may benefit from early treatment with a gluten-free diet.

Study Design: Children who were EmA positive with normal small-bowel mucosal villi were compared with children who were seropositive with villous atrophy by using several markers of untreated celiac disease. Thereafter, children with normal villous structure either continued on a normal diet or were placed on a gluten-free diet and re-investigated after 1 year.

Usefulness of small-bowel mucosal transglutaminase-2 specific autoantibody deposits in the diagnosis and follow-up of celiac disease.

Background: Diagnosis of celiac disease may be problematic in that small-bowel villous atrophy sometimes occurs in conjunction with other enteropathies, develops gradually and may be patchy. Furthermore, as the often compromised quality of biopsy specimens renders diagnosis difficult, new diagnostic tools are warranted.

Goals: As the celiac disease-specific autoantibodies are found deposited at their production site, in the small-bowel mucosa, they may be useful in diagnostics, especially in problematic cases.

Oats do not induce systemic or mucosal autoantibody response in children with coeliac disease.

Objectives: A gluten-free diet omitting wheat, rye, and barley is the only effective treatment for coeliac disease. The necessity of excluding oats from the diet has remained controversial. We studied the toxicity of oats in children with coeliac disease during a 2-year follow-up by investigating jejunal transglutaminase 2 (TG2)-targeted IgA-class autoantibody deposits, a potentially more sensitive disease marker than serum antibodies or conventional histology.

Gluten-dependent small bowel mucosal transglutaminase 2-specific IgA deposits in overt and mild enteropathy coeliac disease.

Objectives: In coeliac disease, immunoglobulin (Ig)A-class autoantibodies against transglutaminase-2 are produced in the small intestinal mucosa, where they are deposited extracellularly. It remains unclear whether positive intestinal transglutaminase-2-targeted IgA deposits in subjects having normal small bowel mucosal morphology are signs of early-stage coeliac disease. We evaluated the gluten dependency of these deposits in overt and mild enteropathy coeliac disease.

Family type and criminal behaviour of male offspring: the Northern Finland 1966 Birth Cohort Study.

Background: Unstable family environment during childhood is known to predispose to juvenile delinquency.

Aims: This study explored whether childhood family structure is associated with violent behaviour of adult offspring.

Methods: We used a large, unselected general population birth cohort (n = 5589 males) linked with the national crime registers (up to the age of 32 years).