https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:54300 Wed 28 Feb 2024 15:46:42 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:52496 Wed 06 Mar 2024 14:33:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:48579 Tue 21 Mar 2023 17:43:58 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33727 Helicobacter pylori (H. pylori) may explain a minority of cases of FD and in the Rome IV criteria H. pylori-associated dyspepsia (defined as symptom relief after eradication therapy) is considered a separate entity. Duodenal inflammation characterized by increased eosinophils and in some cases mast cells, may impair the intestinal barrier. Post-infectious gastroenteritis is now an established risk factor for FD. Other risk factors may include atopy, owning herbivore pets and exposure to antibiotics, together with gastroduodenal microbiome disturbances. Small bowel homing T cells and increased cytokines in the circulation occur in FD, correlating with slow gastric emptying, and a possible association with autoimmune rheumatological disease supports background immune system activation. A genetic predisposition is possible. FD has been linked to psychological disorders, but in some cases psychological distress may be driven by gut mechanisms. Therapeutic options are limited and, aside from responders to H. pylori eradication, provide only modest and temporary relief. Advances in understanding FD may alter clinical practice, and the treatment of duodenal inflammation or microbiome alterations may lead to a cure for a subset of these patients in the future.]]> Thu 13 Dec 2018 15:22:10 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50098 Mon 17 Jul 2023 11:05:36 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41982 Fri 19 Apr 2024 11:58:15 AEST ]]>