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Background Severity of villous atrophy in celiac disease (CeD) is the cumulative effect of enterocyte loss and cell regeneration. Gluten-free diet has been shown to benefit even in patients having a positive anti-tissue transglutaminase (tTG) antibody titre and mild enteropathy. Aim We explored the balance between mucosal apoptotic enterocyte loss and cell regeneration in mild and advanced enteropathies. Methods Duodenal biopsies from patients with mild enteropathy (Marsh grade 0 and 1) ( n = 26), advanced enteropathy (Marsh grade ≥2) ( n = 41) and control biopsies ( n = 12) were subjected to immunohistochemical staining for end-apoptotic markers (M30, H2AX); markers of cell death (perforin, annexin V); and cell proliferation (Ki67). Composite H -scores based on the intensity and distribution of markers were compared. Results End-apoptotic markers and marker of cell death (perforin) were significantly up-regulated in both mild and advanced enteropathies, in comparison to controls; without any difference between mild and advanced enteropathies. Ki67 labelling index was significantly higher in crypts of mild enteropathy, in comparison to controls, suggesting maintained regenerative activity in the former. Conclusions Even in patients with mild enteropathy, the rate of apoptosis is similar to those with advanced enteropathy. These findings suggest the necessity of reviewing the existing practice of not treating patients with mild enteropathy. [ABSTRACT FROM AUTHOR]

Objective. Abnormally high number of duodenal intraepithelial lymphocytes is frequently found in many conditions including mild enteropathy celiac disease (CD) and functional gastrointestinal syndromes, but is unclear whether lymphocytosis affects the clinical phenotype particularly in functional syndromes. Materials and methods. We compared clinical characteristics of celiac patients with lymphocytic duodenosis and normal villous structure with those of patients with functional gastrointestinal syndromes with and without lymphocytic duodenosis. We retrospectively identified 3 cohorts among patients referred for suspected CD: (1) 'CoelD', 135 patients (age 36 ± 14 years) with mild enteropathy CD; (2) 'LymD', 245 patients (38 ± 12 years) with functional gastrointestinal syndromes and lymphocytic duodenosis; and (3) 'NorD', 147 patients (37 ± 15 years) with functional syndromes and normal duodenal histology. Results. Prevalence of gastrointestinal symptoms was similar in the three cohorts, but prevalence of extra-intestinal manifestations (42% vs. 27% vs. 18%, p < 0.003) and of associated diseases (35% vs. 15% vs. 14%, p < 0.0001) was higher in 'CoelD' than in 'LymD' and 'NorD', respectively. Prevalence of Helicobacter pylori infection was similar in the three cohorts. The proportion of patients with final diagnosis of irritable bowel syndrome-diarrhea (38% vs. 37%), dyspepsia (31% vs. 27%), functional pain (14% vs. 19%), and functional diarrhoea (14% vs. 11%) was virtually the same in the cohorts with (LymD) and without (NorD) lymphocytic duodenosis. Conclusions. Lymphocytic duodenosis has different clinical presentation in patients with mild enteropathy CD than those with functional gastrointestinal syndromes, and is not specific for any particular functional syndrome. [ABSTRACT FROM AUTHOR]

Abstract: Background and aims: We assessed whether mild enteropathy with negative coeliac serology may be gluten-dependent, and a cause of iron-deficiency anaemia. In cases not responding to gluten-free diet, the role of Helicobacter pylori infection was evaluated. Methods: 55 consecutive unexplained iron-deficiency anaemia patients were included. In all of them we performed: HLA-DQ2/DQ8 coeliac genetic study, distal duodenum biopsies, and tests to assess H. pylori infection. A gluten-free diet or H. pylori eradication was used as indicated. Final diagnosis was established based on response to specific therapy after a 12-month follow-up period. Results: Histological findings were: (1) group A (positive genetics): 21 Marsh I, 2 Marsh IIIA, 12 normal; (2) group B (negative genetics): 16 Marsh I, 4 normal. Final diagnosis of anaemia in patients with enteropathy were: group A, gluten-sensitive enteropathy, 45%; H. pylori infection, 20%; gluten-sensitive enteropathy plus H. pylori, 10%; other, 10%; unknown, 15%; group B, gluten-sensitive enteropathy, 10%; H. pylori infection, 0% (1 non-eradicated case, 10%); non-steroidal anti-inflammatory drug intake, 20%; other, 20%; unknown, 40% (p =0.033). Conclusions: Mild enteropathy is frequent in patients with unexplained iron-deficiency anaemia and negative coeliac serology. Most cases are secondary to either gluten-sensitive enteropathy or H. pylori infection, or both; however, there is also a substantial number of patients without a definitive diagnosis. [Copyright &y& Elsevier]

Celiac disease patients may suffer from a number of extra-intestinal diseases related to long-term gluten ingestion. The diagnosis of celiac disease is based on the presence of a manifest small intestinal mucosal lesion. Individuals with a normal biopsy but an increased risk of developing celiac disease are referred to as potential celiac disease patients. However, these patients are not treated. This review highlights that patients with normal biopsies may suffer from the same extra-intestinal gluten-induced complications before the disease manifests at the intestinal level. We discuss diagnostic markers revealing true potential celiac disease. The evidence-based medical literature shows that these potential patients, who are "excluded" for celiac disease would in fact benefit from gluten-free diets. The question is why wait for an end-stage disease to occur when it can be prevented? We utilize research on dermatitis herpetiformis, which is a model disease in which a gluten-induced entity erupts in the skin irrespective of the state of the small intestinal mucosal morphology. Furthermore, gluten ataxia can be categorized as its own entity. The other extra-intestinal manifestations occurring in celiac disease are also found at the latent disease stage. Consequently, patients with celiac traits should be identified and treated. [ABSTRACT FROM AUTHOR]