BACKGROUND: Duodenal hypersensitivity to acid and decreased duodenal clearance of exogenous acid have been reported in functional dyspepsia (FD). However, the relevance of these abnormalities to spontaneous duodenal acid exposure and dyspeptic symptoms in FD is unknown. AIMS:To determine spontaneous duodenal acid exposure and its relationship with symptoms, duodenal sensitivity to acid, and the effects of a 5-HT 3 receptor antagonist on duodenal responses to acid in FD. METHODS:Eleven FD patients with prominent nausea and 11 healthy controls underwent 24-h ambulatory duodenal pH monitoring with assessment of dyspeptic symptoms. On the next day, duodenal bolus infusions of 5 ml of acid and normal saline were given in a randomized double-blind manner and repeated after ondansetron or a placebo. RESULTS:Nighttime duodenal acid exposure was similar, but FD patients had lower duodenal pH and higher duodenal % time (pH < 4) than controls during the daytime and in the second postprandial 2 h (p < 0.05). Seven patients (64%) with duodenal acid exposure above the normal range had higher severity scores for several dyspeptic symptoms including nausea. However, the symptom severity was poorly or weakly correlated to duodenal pH, and brief duodenal acid infusion did not affect any symptoms. Duodenal responses to exogenous acid were unaffected by 5-HT 3 receptor antagonism.CONCLUSIONS: Spontaneous duodenal acid exposure is increased in a subset of FD patients with prominent nausea, and this is associated with more severe dyspeptic symptoms. However, a direct relationship between duodenal acid exposure and symptom severity is lacking.

In our experience, intestinal ultrasound seems important as a first diagnostic tool in young patients without clear symptoms or signs of organic diseases, and can be used as an indication that subsequent invasive tests are required.

Functional dyspepsia is a clinical syndrome defined by upper abdominal symptoms without identifiable cause by conventional diagnostic means. Recent studies have established that functional dyspepsia is a heterogeneous disorder in which different pathophysiologic disturbances underlie different symptom profiles. Delayed gastric emptying is associated with postprandial fullness, nausea, and vomiting; impaired accommodation is associated with early satiety and weight loss; and hypersensitivity to gastric distention is associated with epigastric pain, belching, and weight loss. The pathogenesis of functional dyspepsia is unknown but may be postinfectious in a subgroup of patients. The role of psychological disturbances and of duodenal hypersensitivity requires further study. Treatment of the underlying pathophysiologic abnormality seems logical, but options for pharmacotherapy are limited to acid suppression, prokinetic drugs, and antidepressants. Psychotherapy can be considered for refractory patients. Several novel drug therapies are under evaluation.

SUMMARYBackground: Intraduodenal administration of lipids, through lipid digestion and release of cholecystokinin (CCK), induces viscero-visceral reflexes that affect gastric tone and sensitivity. It is unclear whether the same mechanisms control gastric function after an orally ingested meal. Aim: To evaluate the effect of orlistat, a selective lipase inhibitor, on gastric response to an orally administered meal. Methods: Eighteen healthy volunteers participated in this study. They were treated for 5 days with orlistat (120 mg) or placebo t.d.s. in a double-blind randomized crossover design. During treatment, all subjects underwent a gastric barostat study, measurement of plasma CCK levels and a satiety drinking test.

Background: It has been shown that azathioprine prolongs the response to ciclosporin of steroid‐refractory ulcerative colitis, but no specific data are available concerning its toxicity in this indication. Aim and methods: The charts of 21 patients with steroid‐refractory ulcerative colitis who received azathioprine overlapping with a successful ciclosporin course were reviewed for the onset of toxicity. The controls consisted of 48 initial responders to steroids who received azathioprine for steroid‐dependence or resistance/toxicity. Results: Two of the 21 patients were withdrawn because of hypersensitivity to azathioprine. The remaining 19 were treated for a median of 18 months together with a median daily steroid dose of 35 mg (10–75 mg) to be tapered off. Toxicity (31%) included leukopenia alone (two cases), cholestasis alone (one case), cholestasis and increased amylase (one case), increased amylase alone (one case), and cutaneous infection (one case). The frequency of withdrawal was 21%. The mean daily steroid doses were reduced from 38 mg to 3.8 mg in the study cohort, and from 25 mg to 8 mg in the controls, among whom toxicity (27%) included four cases each of leukopenia and increased amylase, two cases each of alteration of liver enzymes and infection, and one case of gastric intolerance. Ten of the 48 controls (20%) were withdrawn from the study. Conclusion: Azathioprine is as effective and safe in the maintenance of the response of patients with steroid‐refractory ulcerative colitis to ciclosporin as it is in the treatment of those who respond to steroids.