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Functional dyspepsia is a clinical syndrome defined by chronic or recurrent symptoms of pain or discomfort centred upon the upper abdomen without a cause being identified by conventional diagnostic means.1 The pathophysiology of functional dyspepsia is unknown but a number of mechanisms have been proposed, such as delayed gastric emptying, hypersensitivity to gastric distension, impaired accommodation to a meal, Helicobacter pylorigastritis, or central nervous system dysfunction.
Dyspeptic symptoms occur in approximately 25% of the general population and only about one quarter of these seek medical attention.2 The reasons underlying health care seeking behaviour in functional dyspepsia are unknown, and may relate both to symptom severity and psychological factors.2 Except for the possible involvement of H pylori, the symptom pattern and underlying mechanisms in non-consulters with dyspepsia have received little attention. Recent developments of less invasive techniques, such as gastric emptying breath tests or a caloric satiety test,3 may facilitate studies in non-consulting subjects in the general population.
Because of its presumed pivotal role in the occurrence of functional gastrointestinal disorders, visceral sensitivity and its modulation is a topic of intense ongoing research. In this issue ofGut, Holtmann and colleagues used a gastric barostat procedure to study the sensitivity to repeated gastric distension in eight currently asymptomatic dyspeptic subjects who were non-consulters compared with eight asymptomatic age and sex matched controls, all of whom were H pylorinegative (see page 332).4 The selection of non-consulting dyspeptic subjects was careful and thoughtful, adequately eliminating other causes of upper gastrointestinal discomfort. Assessment of visceral sensitivity using intragastric balloon distension in non-consulting dyspeptic subjects is an extremely challenging task, and the authors are to be commended for their endeavour.
In subjects with a history of dyspeptic symptoms, baseline thresholds for first perception were significantly lower than in asymptomatic controls. All subjects had a normal psychological profile. Although this observation might suggest that hypersensitivity to gastric distension is a mechanism underlying dyspeptic symptoms in non-consulters, several issues must be taken into consideration.
In the past, differences in mechanosensory function have been reported for patients with functional dyspepsia as a group compared with normal controls. This approach has not allowed the emergence of a consistent correlation between symptoms and observed impaired function. More recently, it has become clear that functional dyspepsia should be considered a heterogeneous disorder where distinct pathophysiological abnormalities are present in subgroups of patients linked to specific symptom patterns. Thus delayed gastric emptying is present in one third of patients who are more likely to be female and to suffer from postprandial fullness and vomiting.5 Impaired accommodation is present in 40% of patients and is associated with symptoms of early satiety and weight loss.3Hypersensitivity to gastric distension was estimated to be present in about 50% of dyspeptic patients.6 7 Extrapolating from patients with functional dyspepsia who seek medical attention, it seems likely that non-consulting subjects with dyspeptic symptoms are a heterogeneous group also. Unfortunately, the paper by Holtmannet al provides only group means, and does not reveal the proportion of symptomatic subjects that were outside the range of normal, nor does it detail the type of symptoms they experienced.
Assuming a 50% prevalence of hypersensitivity to gastric distension, it seems surprising that a significant difference was found at baseline. This may be partly explained by the method used to quantify perception thresholds. Although most barostat protocols use pressure increments as a driving stimulus, it is now clear that activation of gastric tension receptors is required to generate perception.8 Only intraballoon pressures higher than the intra-abdominal pressure (termed the minimal distending pressure, MDP) can distend the stomach, and hence activate tension receptors. Consequently, thresholds are preferably expressed as pressure increments above MDP.3 6 Moreover, patients with functional dyspepsia are likely to have a lower intra-abdominal pressure as they often have a lower body mass index.5 It is unclear in the present paper, where MDP was 1.5 mm Hg lower in subjects with a history of dyspepsia, whether expressing baseline threshold perception pressures relative to MDP would still have generated a significant difference in baseline threshold.
Regardless of baseline perception thresholds, the response to repeated distensions was strikingly different in dyspeptic versus control subjects. In control subjects, sensory thresholds increased in response to repeated distensions while this tendency was absent in dyspeptic subjects. In patients with irritable bowel syndrome (IBS), it has been reported that repetitive stimulation demonstrates sensory abnormalities more consistently than measurements of perception thresholds.9 An abnormal response to repeated distensions in both dyspepsia and IBS may well indicate dysfunction of descending inhibitory pathways. However, before considering absence of this sensory adaptation as a valid marker for functional dyspepsia, additional studies are required on larger numbers of consulting and symptomatic subjects.
Although altered visceral sensitivity is believed to play a key role in the development of symptoms in patients with functional gastrointestinal disorders, proving that symptoms are really attributable to altered sensitivity has remained problematic.9 In the present paper, hypersensitivity and abnormal adaptation to repeated mechanical stimuli were reported in non-consulters with dyspeptic symptoms. However, as all subjects were asymptomatic in the period preceding the barostat studies, it seems at least debatable that these disorders are directly involved in symptom generation. Moreover, if visceral hypersensitivity is responsible for induction of symptoms, lowering of discomfort or pain thresholds rather than of thresholds for first perception would seem to be more relevant. The thresholds for discomfort or pain, obtained during “ramp” distensions (that is, 2 mm Hg increments, duration of each pressure step 30 seconds, maximum pressure 35 mm Hg (or occurrence of pain)), did not seem to differ between non-consulting dyspeptic subjects and controls.
In view of the heterogeneity of functional dyspepsia in consulters, eight subjects seems a very small group to draw firm conclusions on the characteristics of non-consulting dyspeptics. However, further characterisation of this population will help us to understand why dyspeptic subjects come to medical attention. In addition, the absence of sensory adaptation to repeated distension has the potential to be a relevant pathophysiological feature of functional dyspepsia and similar studies in symptomatic dyspeptic subjects are warranted.
See article on page 332
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