(1) Pain relieved by antacids, age above 40 years, previous peptic ulcer disease, male sex, symptoms provoked by berries, and night pain relieved by antacids and food were found to predict organic dyspepsia with a sensitivity and specificity of approximately 70%, when applied on the observed material.
(2) Antibody to cytomegalovirus was found in 83% of duodenal ulcer, 85% of gastric ulcer and 75% of non-ulcer dyspepsia patients; differences were not significant.
(3) Peptic ulcers were identified in 14 patients, mostly those with new dyspepsia, during the study period.
(4) A follow-up study of erosive prepyloric changes (EPC) was undertaken in 60 patients who originally presented with non-ulcer dyspepsia and EPC grade 2 or 3.
(5) Biopsy samples were taken from the gastric mucosa of 209 patients endoscoped for dyspepsia symptoms.
(6) Bacteriological studies on gallbladder bile from 39 patients suggested that infection within the gallbladder may be a factor in the causation of flatulent dyspepsia.
(7) To be termed chronic, dyspepsia should have been present for three months or longer.
(8) In order to exclude physician bias in history taking, 18 patients (9 female) diagnosed as non-ulcer dyspepsia, after endoscopy and gallbladder ultrasonography, underwent computer interrogation using the Glasgow Diagnostic System for Dyspepsia (GLADYS).
(9) Gastric biopsy specimens from 109 patients with non-ulcer dyspepsia were retrospectively examined.
(10) Four patients had severe dyspeptic symptoms and four severe dyspepsia plus dumping.
(11) 4 cases of drug-induced side effects were reported: dizziness and mild dyspepsia.
(12) We also assessed observer variation among endoscopists prospectively in 38 patients investigated for dyspepsia after operation for peptic ulcer.
(13) The purpose of our study was to carry out a thorough gastroenterologic investigation of all patients consulting their general practitioner and reporting dyspepsia during 1 full year, from a population within a defined geographic area.
(14) Select patients with dyspepsia receiving a combination of reassurance and empiric antacid therapy do as well as patients whose initial management strategy includes upper gastrointestinal radiography, at a substantially lower cost.
(15) How much the esophagus contributes to the clinical symptomatology of dyspepsia awaits further elucidation.
(16) A conception of ++non-ulcerative dyspepsia is suggested.
(17) Chronic idiopathic gastric stasis can be responsible for unexplained dyspepsia.
(18) To determine the prevalence of Helicobacter pylori in patients with non-ulcer dyspepsia and ulcer disease as well as in a control population undergoing endoscopic retrograde cholangiopancreatography (ERCP) for suspected pancreatic or biliary disease.
(19) Thirty-eight patients with non-ulcer dyspepsia served as controls.
(20) At follow-up 19-35 years later, 296 of the patients could be traced, and 284 replied to a questionnaire concerning ulcer dyspepsia.