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Background In the past decade, a number of population-based studies have examined the prevalence of coeliac disease in individuals with type 1 diabetes but prevalences have differed considerably. Aim To examine the prevalence of coeliac disease in individuals with type 1 diabetes. Methods A systematic review of English-language articles published in PubMed Medline between 2000 and May 2014. Search terms included 'celiac disease' or 'coeliac disease' and 'diabetes mellitus'. Studies were selected with at least 100 individuals with type 1 diabetes being screened for coeliac disease where the coeliac diagnosis was later confirmed through small intestinal biopsy. Data synthesis used random-effects inverse variance-weighted models, and metaregression was used to examine heterogeneity in subgroups. Results A pooled analysis, based on 26,605 patients with type 1 diabetes, found a prevalence of biopsy-confirmed coeliac disease of 6.0% (95% CI = 5.0-6.9%). Heterogeneity was large ( I2 = 93.2%). The prevalence was lower in adults with type 1 diabetes (2.7%), and in mixed populations with both children and adults with type 1 diabetes (4.7%) than in children (6.2%) with type 1 diabetes ( P < 0.001). Additional subgroup analyses could not explain the large variation in coeliac disease prevalence between studies. Conclusion More than one in twenty patients with type 1 diabetes have biopsy-verified coeliac disease. This prevalence is high enough to motivate screening for coeliac disease among patients with type 1 diabetes. [ABSTRACT FROM AUTHOR]

Summary: Background: Treatment for coeliac disease is a lifelong strict gluten‐free diet. Although guidelines recommend regular follow‐up with dietary interviews and coeliac serology, these methods may be inaccurate. Aim: To evaluate the usefulness of faecal gluten immunogenic peptides to support the diagnosis and to determine the adherence to the gluten‐free diet in coeliac children. Methods: Multicentre prospective observational study including 64 coeliac children. Faecal gluten peptides, and tissue transglutaminase and deamidated gliadin peptide antibodies were analyzed at diagnosis, and 6, 12 and 24 months thereafter. Gluten consumption was estimated from gluten peptide levels. Results: Most children (97%) had detectable gluten peptides at diagnosis. On a gluten‐free diet, the rate of gluten peptides increased from 13% at 6 months to 25% at 24 months. Mean estimated gluten exposure dropped from 5543 mg/d at diagnosis to 144 mg/d at 6 months, then increased to 606 mg/d by 24 months. In contrast, deamidated gliadin peptide antibodies normalised and only 20% had elevated tissue transglutaminase antibody by 24 months. The elevation of tissue transglutaminase antibody was more prolonged in patients with detectable gluten peptides (P < 0.05). Nevertheless, absolute levels of tissue transglutaminase antibody had low sensitivity to identify patients with detectable gluten peptides (P > 0.1). Dietitian assessment was only moderately correlated with gluten peptide detection (κ = 0.5). Conclusions: Faecal gluten peptides testing may guide treatment of coeliac disease prior to diagnosis and during the assessment diet adherence. Further studies could determine if early identification of gluten exposure reduces the need for expensive/invasive investigations for non‐responsive coeliac disease. ClinicalTrials.gov Number: NCT02711397. [ABSTRACT FROM AUTHOR]

Background A gluten-free diet is currently the only reliable therapeutic strategy that is approved for coeliac disease ( CD). For many patients, however, compliance remains inadequate. Aim To investigate the immunogenicity of wheat flour that was pre-treated with selected lactobacilli and fungal proteases (hydrolysed wheat gluten) in coeliac patients. Methods The immunogenicity of hydrolysed wheat gluten was evaluated both in vitro in intestinal T cell lines ( TCLs) and in vivo in treated CD patients after a short-term gluten challenge. Twenty treated CD patients were enrolled and equally randomised into two groups. The patients ate bread that was prepared with hydrolysed wheat flour or natural wheat flour (10 g of gluten/d for 3 days). The interferon ( INF)-γ responses to natural gliadin and a 33-mer peptide were assessed by the enzyme-linked immunospot ( ELISPOT) assay on peripheral blood mononuclear cells ( PBMCs) both before and 6 days after the start of the challenge. Results Hydrolysed wheat was not able to activate the TCLs from the coeliac intestinal mucosa. Consistent with the in vitro results, no significant increase in INF-γ secretion was observed in patients who consumed hydrolysed wheat flour. Conversely, the consumption of natural wheat gluten mobilised INF-γ secreting cells in the blood ( P<.05). Conclusions We confirm that fermentation of wheat flour with sourdough lactobacilli and fungal proteases is capable of abolishing the T cell immunogenicity of gluten in coeliac patients. Our data also validate the short-term oral challenge as a useful tool for testing the efficacy of novel therapeutic approaches. [ABSTRACT FROM AUTHOR]

Background Patients with coeliac disease are considered as individuals for whom pneumococcal vaccination is advocated. Aim To quantify the risk of community-acquired pneumonia among patients with coeliac disease, assessing whether vaccination against streptococcal pneumonia modified this risk. Methods We identified all patients with coeliac disease within the Clinical Practice Research Datalink linked with English Hospital Episodes Statistics between April 1997 and March 2011 and up to 10 controls per patient with coeliac disease frequency matched in 10-year age bands. Absolute rates of community-acquired pneumonia were calculated for patients with coeliac disease compared to controls stratified by vaccination status and time of diagnosis using Cox regression in terms of adjusted hazard ratios ( HR). Results Among 9803 patients with coeliac disease and 101 755 controls, respectively, there were 179 and 1864 first community-acquired pneumonia events. Overall absolute rate of pneumonia was similar in patients with coeliac disease and controls: 3.42 and 3.12 per 1000 person-years respectively ( HR 1.07, 95% CI 0.91-1.24). However, we found a 28% increased risk of pneumonia in coeliac disease unvaccinated subjects compared to unvaccinated controls ( HR 1.28, 95% CI 1.02-1.60). This increased risk was limited to those younger than 65, was highest around the time of diagnosis and was maintained for more than 5 years after diagnosis. Only 26.6% underwent vaccination after their coeliac disease diagnosis. Conclusions Unvaccinated patients with coeliac disease under the age of 65 have an excess risk of community-acquired pneumonia that was not found in vaccinated patients with coeliac disease. As only a minority of patients with coeliac disease are being vaccinated there is a missed opportunity to intervene to protect these patients from pneumonia. [ABSTRACT FROM AUTHOR]

Background The majority of deleterious health consequences of coeliac disease ( CD) are most likely to be secondary to intestinal inflammation; hence, mucosal recovery is a desirable goal of therapy. Follow-up in CD is controversial and serological response is often used as a surrogate for histological recovery. Aims To inform the clinical management of CD using comparative serological and histological data from a biopsy-driven pathway of care. Methods A retrospective analysis of the Cambridge Coeliac Clinic database of 595 patients routinely followed up by biopsy and serology. Results Paired biopsy results were available for 391 patients (15% seronegative). Persisting villous atrophy ( VA) occurred in 182 patients (47%). The sensitivity of anti-tissue transglutaminase ( TTG) antibody for ongoing VA was only 43.6%. Information on dietetic management and further biopsy to assess response was available for 94 initially unresponsive patients, in whom targeted dietetic intervention by removal of identified gluten sources or avoidance of trace amounts of gluten led to resolution of persistent VA in 50%. The effects of institution of a formal care pathway are analysed in 298 patients. Discharge to primary care and clinical management was facilitated by the information derived from repeat biopsy. Conclusions Serology appears to be a poor surrogate marker for mucosal recovery on a gluten-free diet; dietary assessment fails to identify a potential gluten source in many patients with ongoing villous atrophy. The benefits of re-biopsy on diet include stratification of patients with coeliac disease suitable for early discharge from secondary care or those requiring more intensive clinical management. [ABSTRACT FROM AUTHOR]

Background Accelerated progression of atherosclerosis and increased cardiovascular risk have been described in immune-mediated disorders, but few data are available in coeliac disease. Aim To evaluate instrumental and biochemical signs of atherosclerosis risk in 20 adults at first diagnosis of coeliac disease and after 6-8 months of gluten-free diet with mucosal recovery. Methods We analysed total, high-density lipoprotein ( HDL) and low-density lipoprotein ( LDL) cholesterol, triglycerides, homocysteine, C-reactive protein, folate and vitamin B12; ultrasound measurement of carotid intima-media thickness (IMT) and endothelium-dependent dilatation were both carried on at diagnosis and after gluten withdrawal. Twenty-two healthy members of the hospital staff served as matched controls for vascular examinations. Results At baseline, mean total and HDL-cholesterol (HDL-C) were both within normal range, while mean LDL-cholesterol concentration was slightly increased; diet was associated with an increment in total and HDL-C (68.2 ± 17.4 vs. 51.4 ± 18.6 mg/dL; P < 0.001) and a significant improvement in total/ HDL-C ratio (3.05 ± 0.71 vs. 3.77 ± 0.92; P < 0.02). Mean plasma homocysteine was elevated and not influenced by diet. C-reactive protein significantly decreased with diet (1.073 ± 0.51 vs. 1.92 ± 1.38 mg/dL; P < 0.05). At baseline, in coeliacs, IMT was increased (0.082 ± 0.011 vs. 0.058 ± 0.012 cm; P < 0.005), while endothelium-dependent dilatation was decreased (9.3 ± 1.3 vs. 11.2 ± 1.2%; P < 0.05). Both parameters improved after gluten abstinence. Conclusions Adults with coeliac disease seem to be at potentially increased risk of early atherosclerosis as suggested by vascular impairment and unfavourable biochemical risk pattern. Chronic inflammation might play a determining role. Gluten abstinence with mucosal normalisation reverts to normal the observed alterations. [ABSTRACT FROM AUTHOR]