OBJECTIVE: To study the effect of non-steroidal anti-inflammatory drugs (NSAID) and of Helicobacter pylori infection on the gastric mucosa in children with upper GI bleeding (UGIB). METHODS: Eighty-four children, 41 males (mean age 92.6 months, 4-168 months) underwent an upper GI endoscopy with gastric biopsies for UGIB. Biopsies were analysed for histological assessment according to the updated Sydney classification and bacterial culture. The presence of H. pylori infection was retained when histology and/or culture were positive. A negative result was retained when both tests were concomitantly negative. Children were divided into two groups according to the severity of mucosal endoscopic injury. The risk factors, i.e. NSAIDs intake, laboratory haemostatic disorders, were reported. RESULTS: Helicobacter pylori infection was detected in 41 children (48.8%) out of the 84 presented with UGIB. Severe endoscopic damage (SED) group (n = 38, 45.2%), exhibited frank gastric lumen haemorrhage (n = 12), petechia (n = 12), erosions (n = 8), ulcerations (n = 4) in the gastric antrum and corpus. Mild endoscopic damage (MED) group (n = 46, 54.8%), exhibited; congestive mucosa (n = 16), nodular mucosa (n = 15) and pale mucosa (n = 4); 25 children out of 84 (29.8%) received NSAID. According to the severity of endoscopic injuries, none of the following risk factors exhibited significant results; gender, GI endoscopy <24 h, H. pylori infection. H. pylori-positive patients exhibited the same NSAIDs intake level between both groups, SED group; 9 NSAIDs intake (41%) versus 13 without NSAIDs intake (59%), n.s. and MED group; 5 NSAID intake (26%) versus 14 without NSAID intake (74%), n.s. CONCLUSION: In children presenting with UGIB, gut mucosal damage severity is significantly correlated to NSAIDs level intake especially in children younger than 24 months. The presence of H. pylori infection in children receiving NSAID seems not to increase gut mucosal injury severity.
OBJECTIVE: To study the effect of non-steroidal anti-inflammatory drugs (NSAID) and of Helicobacter pyloriinfection on the gastric mucosa in children with upper GI bleeding (UGIB). METHODS: Eighty-four children, 41 males (mean age 92.6 months, 4-168 months) underwent an upper GI endoscopy with gastric biopsies for UGIB. Biopsies were analysed for histological assessment according to the updated Sydney classification and bacterial culture. The presence of H. pyloriinfection was retained when histology and/or culture were positive. A negative result was retained when both tests were concomitantly negative. Children were divided into two groups according to the severity of mucosal endoscopic injury. The risk factors, i.e. NSAIDs intake, laboratory haemostatic disorders, were reported. RESULTS:Helicobacter pyloriinfection was detected in 41 children (48.8%) out of the 84 presented with UGIB. Severe endoscopic damage (SED) group (n = 38, 45.2%), exhibited frank gastric lumen haemorrhage (n = 12), petechia (n = 12), erosions (n = 8), ulcerations (n = 4) in the gastric antrum and corpus. Mild endoscopic damage (MED) group (n = 46, 54.8%), exhibited; congestive mucosa (n = 16), nodular mucosa (n = 15) and pale mucosa (n = 4); 25 children out of 84 (29.8%) received NSAID. According to the severity of endoscopic injuries, none of the following risk factors exhibited significant results; gender, GI endoscopy <24 h, H. pyloriinfection. H. pylori-positive patients exhibited the same NSAIDs intake level between both groups, SED group; 9 NSAIDs intake (41%) versus 13 without NSAIDs intake (59%), n.s. and MED group; 5 NSAID intake (26%) versus 14 without NSAID intake (74%), n.s. CONCLUSION: In children presenting with UGIB, gut mucosal damage severity is significantly correlated to NSAIDs level intake especially in children younger than 24 months. The presence of H. pyloriinfection in children receiving NSAID seems not to increase gut mucosal injury severity.
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