INTRODUCTIONDyspepsia is a common symptom ranging in prevalence from 26% in the USA to 41% in England. 1 While only one in four patients seeks medical help, 2 the condition results in signi®cant health care costs, 3 and an organic cause is found in only 40% of patients. The Rome criteria for diagnosing idiopathic or non-ulcer dyspepsia were originally put forward in 1991 and consist of chronic or recurrent upper abdominal pain or discomfort in the absence of obvious pathology. 4 The Rome group suggested subcategorizing non-ulcer dyspepsia into ulcer-like, re¯ux-like, dysmotility-like and nonspeci®c dyspepsia. The recent Rome II criteria provide a subgroup classi®cation based on the predominant symptom, and are supported by evidence suggesting SUMMARY Background: Dyspepsia is a common symptom for which an organic cause is found in only 40% of patients. When no cause is apparent and the dyspepsia is considered to be idiopathic, a diagnosis of non-ulcer dyspepsia is made. The pathophysiology of non-ulcer dyspepsia is poorly understood and numerous theories have been put forward, including a theory of enhanced central serotoninergic receptor sensitivity. Aim: To determine the sensitivity of serotonin receptors in non-ulcer dyspepsia. Methods: Using a randomized, double-blind, placebocontrolled design, we compared buspirone (a serotonin type 1a partial agonist)-stimulated prolactin release in 50 patients and 59 healthy comparison subjects. Buspirone, 30 mg, or matching placebo was administered on two separate occasions and prolactin release

Despite an increase in the rate of admission with IBD, there has been little change in the rates of surgical intervention and length of stay. The most dramatic increase was seen in the day-case admissions for patients with Crohn's disease and may reflect the use of anti-TNFalpha (infliximab) in the treatment of this disease.

H. pylori-related gastritis is associated with mucinous-type cardiac mucosa as well as with carditis. The former strongly points to expansion of mucinous cardiac mucosa in H. pylori gastritis. This probably represents metaplasia of oxyntic to mucinous mucosa and raises the possibility of a role in carcinogenesis of the gastro-oesophageal junction.