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Objectives: Lymphocytic gastritis (LG) has been described in coeliac disease (CD) patients and in patients with Helicobacter pylori (Hp) infection but the pathogenetic mechanism remains unknown. Aims: The aim of our study was to evaluate the characteristics of the gastric mucosa and the prevalence of lymphocytic gastritis in a large series of CD children and adolescents. Methods: 167 CD children at the diagnosis (F 108; range 11 months–18 years), consecutive performing the upper-intestinal endoscopy at our Department over the period Jan 2008-Dec 2009, were enrolled. Duodenal (2 bulb and 4 distal duodenum samples) together with gastric antral biopsies, were performed. CD diagnosis was performed according to the NASPGHAN criteria. Hp infection was diagnosed by histology and the rapid urease test. Gastric lesions and duodenal biopsies were classified according to the modified Updated Sydney System and to the modified Marsh classification, respectively. Anthropometric and clinical data of each patient were registered at the diagnosis. Moreover, gastric parietal cells antibodies (APCA) were determined with an ELISA. Results: Gastric alterations was found in 38/167 CD children (23%). Particularly, lymphocytic gastritis was found in 13 CD patients (7.8%); superficial chronic gastritis (SCG) was detected in 24 celiacs (14.4%); and one child (0.6%) showed severe interstitial chronic gastritis (ICG). 3/38 children (one with LG, one with SCG and one with ICG) presented Hp infection. Ten patients with LG were symptomatic (7 typical and 3 atypical) while four were silent. Among patients with SCG, 16 children were typical, 5 atypical and 3 silent, and the prevalent symptoms were diarrhoea, abdominal pain and low weight growth. In the table are shown histological grading of the gastric mucosa in LG and SCG patients. The most frequent duodenal lesion, total villous atrophy (Marsh 3C), was detected in 100% and 92% of LG and SCG CD patients. Among CD children, no APCA were found in patients without gastritis, while 3/22 with gastric lesions were positive for APCA (one with mild LG and the other two with mild SCG).

Objectives: Lymphocytic gastritis (LG) has been described in coeliac disease (CD) patients and in patients with Helicobacter pylori (Hp) infection but the pathogenetic mechanism remains unknown. Aims: The aim of our study was to evaluate the characteristics of the gastric mucosa and the prevalence of lymphocytic gastritis in a large series of CD children and adolescents. Methods: 167 CD children at the diagnosis (F 108; range 11 months–18 years), consecutive performing the upper-intestinal endoscopy at our Department over the period Jan 2008-Dec 2009, were enrolled. Duodenal (2 bulb and 4 distal duodenum samples) together with gastric antral biopsies, were performed. CD diagnosis was performed according to the NASPGHAN criteria. Hp infection was diagnosed by histology and the rapid urease test. Gastric lesions and duodenal biopsies were classified according to the modified Updated Sydney System and to the modified Marsh classification, respectively. Anthropometric and clinical data of each patient were registered at the diagnosis. Moreover, gastric parietal cells antibodies (APCA) were determined with an ELISA. Results: Gastric alterations was found in 38/167 CD children (23%). Particularly, lymphocytic gastritis was found in 13 CD patients (7.8%); superficial chronic gastritis (SCG) was detected in 24 celiacs (14.4%); and one child (0.6%) showed severe interstitial chronic gastritis (ICG). 3/38 children (one with LG, one with SCG and one with ICG) presented Hp infection. Ten patients with LG were symptomatic (7 typical and 3 atypical) while four were silent. Among patients with SCG, 16 children were typical, 5 atypical and 3 silent, and the prevalent symptoms were diarrhoea, abdominal pain and low weight growth. In the table are shown histological grading of the gastric mucosa in LG and SCG patients. The most frequent duodenal lesion, total villous atrophy (Marsh 3C), was detected in 100% and 92% of LG and SCG CD patients. Among CD children, no APCA were found in patients without gastritis, while 3/22 with gastric lesions were positive for APCA (one with mild LG and the other two with mild SCG).