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논문 기본 정보

자료유형
학술저널
저자정보
Hye-Kyung Jung (Department of Internal Medicine Ewha Womans University College of Medicine Seoul Korea) Nicholas J. Talley (University of Newcastle and Hunter Medical Research Institute Newcastle)
저널정보
대한소화관운동학회(현 대한소화기능성질환.운동학회) Journal of Neurogastroenterology and Motility (JNM) Journal of Neurogastroenterology and Motility (JNM) Vol.24 No.3
발행연도
2018.1
수록면
345 - 354 (10page)

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Functional dyspepsia (FD) is a common disorder characterized by chronic epigastric pain or burning, or bothersome postprandial fullness or early satiation, without a definitive organic cause. The pathogenesis of FD is likely heterogeneous. Classically, motor disorders, visceral hypersensitivity, and brain-gut interactions have been implicated in the pathophysiology of FD, but recently an important role for chronic low-grade inflammation and infection in FD has been reported and confirmed. Duodenal low-grade inflammation is frequently observed in FD in those with and without documented previous gastroenteritis. Duodenal eosinophils and in some cases mast cells may together or separately play a key role, and immune activation (eg, circulating homing small intestinal T cells) has been observed in FD. Low-grade intestinal inflammation in patients with FD may provoke impairment in motor-sensory abnormalities along the gastrointestinal neural axis. Among FD patients, the risk of developing dyspeptic symptoms after a bout of gastroenteritis is 2.54 (95% CI, 1.76–3.65) at more than 6 months after acute gastroenteritis. Gut host and microbial interactions are likely important, and emerging data demonstrate both quantitative and qualitative changes of duodenal mucosal and fecal microbiota in FD. Food antigens (eg, wheat proteins) may also play a role in inducing duodenal inflammation and dyspepsia. While causation is not established, the hypothesis that FD is a disorder of microscopic small intestinal inflammation in a major subset is gaining acceptance, opening the possibility of novel treatment approaches that may be able to alter the natural history of the disorder.

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