Increased perception of physiological or minor noxious stimuli has been demonstrated in patients with functional dyspepsia in both the fasting and postprandial states.
FUNCTIONAL DYSPEPSIA FREE
In some circumstances motor abnormalities can be demonstrated in symptom free patients, and on other occasions symptomatic patients are found to have normal motor function.
5 Furthermore, although altered motility is frequent in functional dyspepsia, a relationship between these disorders and dyspeptic symptoms has not been established. 13 However, our data failed to find confirmatory evidence of a role for vagal dysfunction in patients with functional dyspepsia. Studies suggest abnormal gastrointestinal parasympathetic or sympathetic function in a small number of patients with gastroparesis, as well as in some patients with normal emptying, 2 or antral hypomotility. The underlying mechanism for impaired gastric motor function is uncertain. Impaired accommodation, which is a disturbance of “diastolic” function of the stomach, has recently been shown to be a frequent finding in patients with functional dyspepsia. 12 Normally, the proximal stomach relaxes in response to meal ingestion in order to act as a reservoir and to enable an increase in gastric volume without a significant increase in gastric pressure. The suggestion that patients with functional dyspepsia may have abnormal motor function of the proximal stomach was initially made by Coffin et al who documented hyporeactivity or reduced reflex fundic relaxation in response to duodenal distension. 11 Even though antral hypomotility and delayed gastric emptying are frequent in patients with functional dyspepsia, the clinical importance of these findings remains uncertain as they do not always correlate with symptoms. The presence of antral hypomotility has been shown by manometric techniques, 8 and is sometimes accompanied by disordered intestinal motility. The onset of dyspeptic symptoms after food digestion suggests a disturbance of postprandial gastric motility leading to slowed gastric emptying accompanied by feelings of prolonged gastric distension, bloating, and nausea.ĭelayed gastric emptying has been reported to occur in between 30% and 70% of patients with functional dyspepsia. Gastrointestinal motor abnormalities such as delayed emptying, 2, 3 impaired initial distribution of a meal within the stomach, 4 impaired accommodation to a meal, 5– 7 antral hypomotility, 8 gastric dysrhythmias (tachygastrias, bradygastrias, and mixed dysrhythmias), 9, 10 and altered duodenojejunal motility have all been identified in subgroups of patients with functional dyspepsia. Future therapeutic strategies should be aimed at reducing nociception as well as enhancing the accommodation response. Patients with delayed gastric emptying generally complain of predominant discomfort. In terms of symptoms, impaired accommodation is significantly correlated with early satiety, and hypersensitivity is significantly correlated with pain and belching.
Impaired accommodation is a frequent pathophysiological disturbance among patients with and without H pylori infection. Meta-analysis of seven controlled studies reported a non-significant odds ratio in favour of H pylori therapy in patients with functional dyspepsia. The role of Helicobacter pylori in functional dyspepsia is difficult to define. Patients typically present with gastric hypersensitivity resulting from abnormal afferent function. Approximately 50% of patients with functional dyspepsia have motor disorders, such as impaired fundic relaxation, antral dilation and/or hypomotility, gastroparesis, small bowel dysmotility, or abnormal duodenogastric reflexes.
The major pathophysiological mechanisms responsible for functional dyspepsia include psychosocial factors and alterations in motility and visceral sensation.
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