Neurohormonal Factors in Functional Dyspepsia: Insights on Pathophysiological Mechanisms

Greydanus, Martin P.; Vassallo, Mario; Camilleri, Michael; Nelson, Daniel K.; Hanson, Russell B.; Thomforde, George M.

doi:10.1016/0016-5085(91)70018-s

Cited by 121 publications

(55 citation statements)

References 39 publications

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“…Vagal efferent dysfunction has also been documented in some patients with functional dyspepsia or IBS 1213 28 29 Camilleri and coworkers found impaired vagal function as assessed by a modified sham feeding test 12. Although these investigators also found lowered intestinal thresholds in subjects with dyspepsia and normal small bowel transit, they did not evaluate the association between sensory thresholds and pancreatic polypeptide responses,12 and they did not use a barostat with an infinitely compliant balloon in the experiment.…”

Section: Discussionmentioning

confidence: 99%

“…Recently we have shown impaired small intestinal motor responses to duodenal distension in patients with functional dyspepsia 1011 A reduced release of pancreatic polypeptide (PP) after sham feeding has been observed in some patients with functional dyspepsia, implicating impaired efferent cholinergic vagal function 12. In addition, there is evidence that vagal function may be impaired in patients with irritable bowel syndrome (IBS),13 a condition that frequently overlaps with functional dyspepsia 14.…”

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confidence: 99%

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Altered vagal and intestinal mechanosensory function in chronic unexplained dyspepsia

Holtmann

Goebell

Jockenhoevel

et al. 1998

Gut

123

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.05 versus all others). In healthy controls and patients with functional dyspepsia, insulin hypoglycaemia significantly (p<0.001) increased plasma PP levels. However, only two out of seven patients with functional dyspepsia had a more than twofold increase in PP values whereas all healthy controls had a more than twofold increase in PP levels after insulin hypoglycaemia (p<0.05). In contrast, there was no significant PP response in the gastrectomised patients (median 2%, range −10 to +23%). PP responses and visceral sensory thresholds were significantly correlated (r=0.65, p<0.002). Conclusions-The diminished PP response after insulin hypoglycaemia indicates disturbed eVerent vagal function in a subgroup of patients with functional dyspepsia. The data also suggest that the intact vagal nerve may exert an antinociceptive visceral eVect. (Gut 1998;42:501-506)

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Altered vagal and intestinal mechanosensory function in chronic unexplained dyspepsia

Holtmann

Goebell

Jockenhoevel

et al. 1998

Gut

123

View full text Add to dashboard Cite

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“…Plasma concentrations of pancreatic polypeptide were determined by a validated and specific radioimmunoassay 27. A change from baseline of greater than 25 pg/ml is considered normal26; failure of plasma pancreatic polypeptide levels to increase by more than 25 pg/ml after modified sham feeding suggests abdominal vagal dysfunction 429 …”

Section: Methodsmentioning

confidence: 99%

“…Gastric motor abnormalities such as delayed emptying,4 5impaired initial distribution of a meal within the stomach,6 antral hypomotility,7 reduced compliance,8 and altered myoelectric activity,9 10 have been identified in subgroups of patients with non-ulcer dyspepsia. These abnormalities do not always correlate temporally with symptoms.…”

mentioning

confidence: 99%

Gastric accommodation in non-ulcer dyspepsia and the roles ofHelicobacter pylori infection and vagal function

Thumshirn

Camilleri

Saslow

et al. 1999

Gut

147

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Background-The pathophysiological mechanisms in non-ulcer dyspepsia are incompletely understood. Aims-To compare gastric motor and sensory functions in Helicobacter pylori positive or negative patients with nonulcer dyspepsia. Patients-Seventeen patients with nonulcer dyspepsia and 16 asymptomatic controls. Methods-The following were evaluated: gastrointestinal symptoms; gastric emptying and orocaecal transit of solids; abdominal vagal function; gastric compliance; fasting and postprandial gastric tone and phasic contractions; symptoms during ingestion of cold water and during the distension of an intragastric bag; and somatic sensitivity and personality profile (Minnesota Multiphasic Personality Inventory, MMPI). Results-Gastric accommodation was reduced in H pylori negative dyspeptics relative to controls; the degree of accommodation was unrelated to H pylori status in dyspeptics. Increased postprandial gastric sensation was more frequent among H pylori positive patients (4/5 H pylori positive versus 4/12 H pylori negative patients). Intragastric meal distribution and orocaecal transit were normal; gastric emptying at four hours was abnormal in 4/17 patients. Vagal dysfunction was rare. Eight of 17 patients had somatisation or depression on MMPI. Conclusion-Impaired gastric accommodation is frequent in non-ulcer dyspepsia and seems to be unrelated to vagal efferent dysfunction. H pylori infection does not seem to influence gastric accommodation, but is associated with heightened sensitivity in dyspeptics. Therapeutic approaches that restore normal postprandial accommodation and gastric sensitivity should be tested in non-ulcer dyspepsia. (Gut 1999;44:55-64)

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“…Whether such sensory dysfunction extends beyond the stomach in patients with functional dyspepsia is controversial. For example, increased gastric but normal duodenal sensitivity was shown in a specific subset of patients with functional dyspepsia predominantly complaining of postcibal bloating,11 whereas other studies have reported an increased perception of small intestinal distension in these patients 1213 …”

Section: Digestive Tract Sensorimotor Physiology and Pathophysiologymentioning

confidence: 97%

Principles of applied neurogastroenterology: physiology/motility-sensation

Kellow

Delvaux

Azpiroz

et al. 1999

Gut

133

103

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Many of the symptoms characteristic of the functional gastrointestinal disorders (FGID) are consistent with dysfunction of the motor and/or sensory apparatus of the digestive tract. Those aspects of sensorimotor dysfunction most relevant to the FGID include alterations in: gut contractile activity; myoelectrical activity; tone and compliance; and transit, as well as an enhanced sensitivity to distension, in each region of the gastrointestinal tract. Assessment of these phenomena involves a number of techniques, some well established and others requiring further validation. Using such techniques, researchers have reported a wide range of alterations in sensory and in motor function in the FGID. Importantly, however, relationships between such dysfunction and symptoms have been relatively weak, and so the clinical relevance of the former remains unclear. Moreover, the proportions of patients in the various symptom subgroups who display dysfunction, and the extent and severity of their symptoms, require better characterization. On a positive note, progress is occurring on several fronts, especially in relation to functional dyspepsia and irritable bowel syndrome, and based on the data gathered to date, a number of areas where further advances are required can be highlighted. (Gut 1999;45(Suppl II):II17-II24)

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Neurohormonal Factors in Functional Dyspepsia: Insights on Pathophysiological Mechanisms

Cited by 121 publications

References 39 publications

Altered vagal and intestinal mechanosensory function in chronic unexplained dyspepsia

Altered vagal and intestinal mechanosensory function in chronic unexplained dyspepsia

Gastric accommodation in non-ulcer dyspepsia and the roles ofHelicobacter pylori infection and vagal function

Principles of applied neurogastroenterology: physiology/motility-sensation

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