Nutrient-specific modulation of gastric mechanosensitivity in patients with functional dyspepsia

Barbera, Roberta; Feinle, Christine; Read, N W

doi:10.1007/bf02212683

Cited by 126 publications

(91 citation statements)

References 17 publications

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“…As a consequence, acute capsaicin application evokes a feeling of warmth and pain, which can be desensitized during prolonged application. The finding that intraduodenal lipid (but not glucose) infusion sensitizes the stomach to distension in patients with functional dyspepsia, but not in controls 77 , suggests a cross-sensitization between mechanosensors and chemosensors and could explain why fatty meals can exaggerate symptoms related to gastric filling. Lipids in the duodenum can provoke symptoms through different possible mechanisms: direct neuronal stimulation, higher lipid sensitivity of enteroendocrine cells or nerves, increased levels of systemic or local cholecystokinin (which is secreted by lipid-activated enteroendocrine cells, stimulates the release of digestive enzymes and bile and induces satiety) and/or increased sensitivity to cholecystokinin involving type A cholecystokinin receptors 78 .…”

Section: Gastroduodenal Sensitivitymentioning

confidence: 94%

Functional dyspepsia

Enck¹,

Azpiroz

Boeckxstaens

et al. 2017

Nat Rev Dis Primers

260

247

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| Functional dyspepsia is one of the most prevalent functional gastrointestinal disorders. Functional dyspepsia comprises three subtypes with presumed different pathophysiology and aetiology: postprandial distress syndrome (PDS), epigastric pain syndrome (EPS) and a subtype with overlapping PDS and EPS features. Functional dyspepsia symptoms can be caused by disturbed gastric motility (for example, inadequate fundic accommodation or delayed gastric emptying), gastric sensation (for example, sensations associated with hypersensitivity to gas and bloating) or gastric and duodenal inflammation. A genetic predisposition is probable but less evident than in other functional gastrointestinal disorders, such as irritable bowel syndrome (IBS). Psychiatric comorbidity and psychopathological state and trait characteristics could also play a part, although they are not specific to functional dyspepsia and are less pronounced than in IBS. Possible differential diagnoses include Helicobacter pylori infection and peptic ulceration. Pharmacological therapy is mostly based on the subtype of functional dyspepsia, such as prokinetic and fundus-relaxing drugs for PDS and acid-suppressive drugs for EPS, whereas centrally active neuromodulators and herbal drugs play a minor part. Psychotherapy is effective only in a small subset of patients, whereas quality of life can be severely affected in nearly all patients. Future therapies might include novel compounds that attempt to treat the underlying gastric and duodenal inflammation. NATURE REVIEWS | DISEASE PRIMERS VOLUME 3 | ARTICLE NUMBER 17081 | 1 PRIMER © 2 0 1 7 M a c m i l l a n P u b l i s h e r s L i m i t e d , p a r t o f S p r i n g e r N a t u r e . A l l r i g h t s r e s e r v e d .standard therapy for gastro -oesophageal reflux disease. Paediatric dyspeptic symptoms are being addressed in a separate classification effort 10 . This Primer covers functional dyspepsia in adults only, although we sporadically refer to paediatric functional dyspepsia when similarities exist. EpidemiologyThe population prevalence of functional dyspepsia is quite variable across the globe, with overall high numbers (10-40%) in Western countries and low numbers (5-30%) in Asia, independent of the respective functional dyspepsia definitions 11 . A large-scale health and nutrition survey from France 12 (which involved >35,000 people) identified that 15% of individuals had suspected functional dyspepsia, 28% had irritable bowel syndrome (IBS) and 6% had both. The population of patients who are affected by both IBS and functional dyspepsia has been reported to range between 10% and 27% in previous studies 13 and to approach 30% in popu lation samples; it could be even higher in specific populations 14,15 . This observation has given rise to the term 'overlap syndrome' (REF. 13), which calls into question the sensitivity and specificity of the Rome criteria, at least for IBS and functional dyspepsia. This argument is also supported by the observation that patients with functional dyspepsia m...

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Section: Gastroduodenal Sensitivitymentioning

confidence: 94%

Functional dyspepsia

Enck¹,

Azpiroz

Boeckxstaens

et al. 2017

Nat Rev Dis Primers

260

247

View full text Add to dashboard Cite

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“…These include delayed gastric emptying, hypersensitivity to gastric distension, impaired gastric accommodation to a meal, abnormal duodenojejunal motility, or central nervous system dysfunction (1)(2)(3)(4)(5)(6)(7). In addition, recent studies have suggested the importance of duodenal motor and sensory dysfunction in the genesis of dyspeptic symptoms (8)(9)(10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

A Pilot Study on Duodenal Acid Exposure and Its Relationship to Symptoms in Functional Dyspepsia with Prominent Nausea

et al. 2004

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BACKGROUND: Duodenal hypersensitivity to acid and decreased duodenal clearance of exogenous acid have been reported in functional dyspepsia (FD). However, the relevance of these abnormalities to spontaneous duodenal acid exposure and dyspeptic symptoms in FD is unknown. AIMS:To determine spontaneous duodenal acid exposure and its relationship with symptoms, duodenal sensitivity to acid, and the effects of a 5-HT 3 receptor antagonist on duodenal responses to acid in FD. METHODS:Eleven FD patients with prominent nausea and 11 healthy controls underwent 24-h ambulatory duodenal pH monitoring with assessment of dyspeptic symptoms. On the next day, duodenal bolus infusions of 5 ml of acid and normal saline were given in a randomized double-blind manner and repeated after ondansetron or a placebo. RESULTS:Nighttime duodenal acid exposure was similar, but FD patients had lower duodenal pH and higher duodenal % time (pH < 4) than controls during the daytime and in the second postprandial 2 h (p < 0.05). Seven patients (64%) with duodenal acid exposure above the normal range had higher severity scores for several dyspeptic symptoms including nausea. However, the symptom severity was poorly or weakly correlated to duodenal pH, and brief duodenal acid infusion did not affect any symptoms. Duodenal responses to exogenous acid were unaffected by 5-HT 3 receptor antagonism.CONCLUSIONS: Spontaneous duodenal acid exposure is increased in a subset of FD patients with prominent nausea, and this is associated with more severe dyspeptic symptoms. However, a direct relationship between duodenal acid exposure and symptom severity is lacking.

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“…Different factors such as delayed gastric emptying (Stanghellini V et al, 1996;Sarnelli G et al, 2003), hypersensitivity to gastric distension (Bradette M et al, 1991;Mearin F et al, 1991;Barbera R et al, 1995;Tack J et al, 2001), impaired gastric accommodation to a meal (Tach J et al, 1998), abnormal duodenojejunal motility (Holtmann G et al, 1996;Wilmer A et al, 1998), duodenal motor and sensory dysfunction Schwarz MP et al, 2001), duodenal hypersensitivity (Schwartz MP et al, 2001), Helicobacter pylori infection, and psychosocial factors have been implicated in the pathogenesis of FD. Among these factors, acid is thought to be more important because proton pump inhibitors (PPIs) and histamine 2 (H2)-receptor antagonists have been proposed to be effective therapies for a subset of patients with FD.…”

Section: Pathogenesis and Evaluationmentioning

confidence: 99%