Functional dyspepsia is one of the most relevant functional gastrointestinal disorders (FGIDs) among general population. Rome III criteria defined functional dyspepsia as the presence of symptoms from the gastroduodenal region (early satiation, postprandial fullness, epigastric pain or burning) in the absence of any organic, systemic or metabolic disease that is likely to explain the symptoms. Etiological causes are still unclear, and the pathophysiological mechanisms still largely unknown. Besides, Helicobacter pylori infection is often present in these patients and contributes to complicate the clinical presentation. One of the main problem in the management of these patients is the lack of reliable biohumoral markers. Thus, functional disorders are usually diagnosed on the bases of symptomatic patterns. The Rome consensus has proposed to further subdivide FD into two diagnostic categories of meal-induced dyspeptic symptoms: postprandial distress syndrome (PDS), characterized by postprandial fullness and early satiation, and epigastric pain syndrome (EPS), characterized by epigastric pain and burning.~Central processing of visceral stimuli, and its role in the pathogenesis of functional dyspepsia, as well as low-grade inflammation in the duodenum are important emerging topics in pathophysiology research. In this framework, disorders of gastric electric activity and abnormal gastric emptying are probably actively involved in the onset of symptomatology. Different noninvasive procedures may be applied in order to evaluate the gastric motor functions. Among them, gastric emptying time evaluation by 13C breath testing and cutaneous electrogastrography have raised attention for their reliability and potentiality. Another important pathophysiological concern of FD is represented by the possible alterations in circulating concentrations of different gastrointestinal peptides at various degree involved in the control of gastroduodenal motility [namely Cholecystokinin (CCK), peptide YY, Neurotensin, Somatostatin, Leptin, Ghrelin, Motilin, Gastrin, Pepsinogen I and II]. In previous studies significant lower levels of motilin was found in dyspeptic patients with altered antroduodenal motility was found. CCK mediates satiety by acting on the CCK receptors distributed widely throughout the central nervous system as well as effects on the vagus nerve. Other experimental data suggest that somatostatin and neurotensin may affect muscle contractility and delay the intestinal transit.~On these bases aims of the study will be: 1) to evaluate the GI peptide circulating concentrations, the gastric electrical activity and gastric emptying time by applying noninvasive procedures in patients suffering from functional dyspepsia and 2) to test whether a significant difference exists between the two diagnostic categories of meal-induced dyspeptic symptoms
Rome III criteria defined functional dyspepsia (FD) as the presence of symptoms from the gastroduodenal region in the absence of any organic, systemic or metabolic disease that is likely to explain the symptoms. FD can be further subdivided into two diagnostic categories: postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS).~Disorders of gastric electric activity and abnormal gastric emptying are probably actively involved in the FD onset. Different noninvasive procedures may be applied in order to evaluate the gastric motor functions such as 13C breath testing and cutaneous electrogastrography. Besides, different gastrointestinal peptides (i.e. CCK, peptide YY, Neurotensin, Somatostatin, Leptin, Ghrelin, Motilin, Gastrin, Pepsinogen I and II) are involved in the control of gastroduodenal motility.~Aims of the present study are: 1) to evaluate the GI peptide circulating concentrations, the gastric electrical activity and gastric emptying time by applying noninvasive procedures in patients suffering from functional dyspepsia and 2) to test whether a significant difference exists between the two diagnostic categories of meal-induced dyspeptic symptoms