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Symptoms and gastric functions in dyspepsia – goodbye to gastroparesis or to inadequate studies?

Sir, we read with interest Dr Quigley's recent editorial `Symptoms and gastric function in dyspepsia ± goodbye to gastroparesis? By commenting upon the paper by Ahluwalia et al., this editorial stressed three main concepts: (a) the relationship between dyspeptic symptoms and gastrointestinal motor disorders is a complex one; (b) gastric emptying is the result of a series of integrated motor events, and techniques capable of measuring these specific events may help to identify the motor disorders more directly associated with perception of dyspeptic symptoms; (c) factors other than these motor disorders (including gastroduodenal hypersensitivity) may also be involved in the pathogenesis of dyspepsia. We agree with all these statements that basically summarize the most updated view on the pathogenesis of functional dyspepsia, but we believe that some aspects of this editorial reflect a somewhat oldfashioned approach to the problem and require further discussion. As stated by Dr Quigley, `our problems begin with the very definition of this disorder' and lack of clearness and consistency in the included criteria may undermine any effort to increase our knowledge. The term dyspepsia should incorporate pain as well non-painful sensations (i.e. postprandial fullness, early satiety, anorexia, epigastric bloating, nausea and vomiting), but many tend to forget it. For instance, the disappointing attempts to isolate various subgroups of dyspepsia mentioned in Dr Quigley's editorial are often represented by studies including exclusively patients with epigastric pain (with or without other complaints), or, on the contrary, patients with symptoms suggestive of motor disorders. Both approaches are obviously inadequate to detect subgroups with different underlying pathophysiological features among dyspeptic patients. Inadequacy of the instruments used for measuring symptoms is also an important confounding factor in the current literature. The diagnosis of functional digestive syndromes is, by definition, based on nothing but the words of the patients and the relative interpretations given by doctors. An international agreement has been achieved on definitions of individual dyspeptic symptoms which helps to differentiate dyspepsia from gastro-oesophageal reflux disease and irritable bowel syndrome. Overlaps among different clinical conditions are frequent in medicine, but this should not discourage investigators and doctors from identifying and managing appropriately distinct nosologic entities with different pathophysiological features. As demonstrated by several studies, the mere presence of digestive symptoms or of clusters of symptoms is of negligible clinical utility. In fact these symptoms, in their milder form, are present in many healthy subjects and in individuals not seeking medical help. Analysis of severity of symptoms (and not of their mere presence) has proven to be of diagnostic value in gastro-oesophageal reflux disease and can also help to identify subgroups with distinctive features in the `big bag' of dyspepsia. Dr Quigley acknowledges that the `more detailed evaluation of symptoms, which includes not only a definition of their presence or absence, but also an assessment of severity, may allow one to better identify those with gastroparesis'. However, he inexplicably seems to disregard these findings obtained with a detailed analysis of symptoms, and to keep in greater consideration other studies which have obvious limitations. Specifically: Hausken et al. evaluated patients with focal lesions of the gastric mucosa and compared their antral areas to those of a gender-not-matched group of controls, as well as a global symptom score which turned out to be only partially related to antral motor events; Scott et al. only included patients complaining of pain; Troncon et al. did not provide any analysis of dyspeptic symptoms. Also the paper of Ahluwalia et