Disease relevance of Dyspepsia

• Lack of effect of treating Helicobacter pylori infection in patients with nonulcer dyspepsia. Omeprazole plus Clarithromycin and Amoxicillin Effect One Year after Treatment (OCAY) Study Group [1].
• Five-year study of cimetidine or surgery for severe duodenal ulcer dyspepsia [2].
• Adjusting for age, community rheumatoid arthritis patients with H. pylori were not more likely to have visible mucosal damage or dyspepsia, but were significantly more likely to have histological gastritis (P less than 0.01) [3].
• Subgroups were as follows: those with symptoms suggestive of peptic ulceration (ulcerlike dyspepsia), those with gastric stasis (dysmotilitylike dyspepsia), those with gastroesophageal reflux (refluxlike dyspepsia), and the remainder (unspecified dyspepsia) [4].
• An enzyme-linked immunosorbent assay (ELISA) for detection of IgG antibodies against Campylobacter pylori was used to examine sera from 70 patients with non-ulcer dyspepsia [5].

Psychiatry related information on Dyspepsia

• In early therapy, the emergent adverse experiences more common with the ropinirole group compared with placebo were nausea, somnolence, leg edema, abdominal pain, vomiting, dyspepsia, and hallucinations [6].

High impact information on Dyspepsia

• METHODS: We randomly assigned 170 H. pylori-infected patients with nonulcer dyspepsia to receive twice-daily treatment with 20 mg of omeprazole, 1000 mg of amoxicillin, and 500 mg of clarithromycin for 14 days and 167 such patients to receive identical-appearing placebos; all patients were then followed through regular visits for 12 months [7].
• CONCLUSIONS: In patients with H. pylori infection and nonulcer, or functional, dyspepsia, treatment with omeprazole and antibiotics to eradicate the infection is more likely to resolve symptoms than treatment with omeprazole alone [8].
• Absence of therapeutic benefit from antacids or cimetidine in non-ulcer dyspepsia [9].
• The most common adverse events were headache (11% sildenafil, 2% placebo), dyspepsia (9% sildenafil, 0% placebo), and respiratory tract disorder (6% sildenafil, 2% placebo), predominantly sinus congestion or drainage [10].
• CONCLUSIONS: Prompt endoscopy confers a small benefit in terms of cure of dyspepsia but costs more than "test and treat" and is not a cost-effective strategy for the initial management of dyspepsia [11].

Chemical compound and disease context of Dyspepsia

• METHODS: Patients were enrolled if they were NSAID naïve, had a positive urea breath test, had dyspepsia or an ulcer history, and required long-term NSAID treatment [12].
• Endoscopy was repeated after 8 weeks of naproxen treatment or when naproxen treatment was stopped early because of bleeding or intractable dyspepsia [13].
• Dicyclomine for idiopathic dyspepsia [14].
• The results showed that whereas pentagastrin caused a significant increase in gastric secretion, only the patients with nonulcer dyspepsia reported any appreciable pain before or after the injection [15].
• While NSAIDs also cause dyspepsia, inhibition of prostaglandin synthesis may reduce this from even higher levels that would otherwise prevail and mask ulcer-related dyspepsia, making anticipatory management difficult [16].

Biological context of Dyspepsia

• A dual isotopic technique was used to evaluate patients with non-obstructive dyspepsia (idiopathic and secondary) (part 1) and to assess the effects of a new gastrokinetic agent: cisapride, on gastric emptying in such patients (part 2) [17].
• The aim of this study was to determine the effect of colloidal bismuth subcitrate (De Nol) on symptoms and gastric histology in patients with non-ulcer dyspepsia [18].
• The management of acid-related dyspepsia in general practice: a comparison of an omeprazole versus an antacid-alginate/ranitidine management strategy. Compete Research Group [corrected] [19].
• Effects of oral clarithromycin and amoxycillin on interdigestive gastrointestinal motility of patients with functional dyspepsia and Helicobacter pylori gastritis [20].
• The effects of levosulpiride on gastric and gall-bladder emptying in functional dyspepsia [21].

Anatomical context of Dyspepsia

• One patient with dyspepsia, high basal plasma gastrin, negative secretin and calcium infusion studies, and a positive meal test was diagnosed as having G-cell hyperplasia; this was confirmed by biopsy and antral gastrin extraction [22].
• A patient with a somatostatin (SRIH)-secreting islet cell tumor, whose only symptoms were dyspepsia and anemia, is described [23].
• Gallbladder volume as a biomarker for the motilin effect in healthy volunteers and patients with functional dyspepsia [24].
• Fourteen patients with polycythaemia rubra vera (PRV) and four with chronic granulocytic leukaemia (CGL) were studied to examine the relationship between basophil counts, blood histamine, gastric acid secretion and dyspepsia or peptic ulceration [25].
• Aspirin-related side effects were dyspepsia (reported by four patients), heartburn (by seven), nausea and vomiting (by four), and melena (by five); nicardipine-related side effects were transient hypotension (by two), headache (by four), ankle edema (by three), and constipation (by four) [26].

Gene context of Dyspepsia

• BACKGROUND & AIMS: In patients with functional dyspepsia, altered alpha-adrenoreceptor function and depression are prevalent, features that are linked to a G-protein beta 3 (GNB3) subunit gene polymorphism (C825T) [27].
• Role of duodenal lipid and cholecystokinin A receptors in the pathophysiology of functional dyspepsia [28].
• RESULTS: COX-2 expression in corpus was significantly higher in H. pylori positive than in negative non-ulcer dyspepsia (NUD) (p <.05) [29].
• CCK is a major mediator of the sensitisation of gastric perception by lipids in patients with functional dyspepsia as the CCK-A receptor antagonist dexloxiglumide markedly diminishes this effect [30].
• Similarly, the 120 kDa antigen (cagA) tended (p < 0.15) to be more prevalent in DU patients (82%; 95% CI, 69-91) compared with controls (69%; 95% CI, 57-80) but not functional dyspepsia (77%; 95% CI, 57-90) [31].

Analytical, diagnostic and therapeutic context of Dyspepsia

• Unadjusted rates of GI hospitalization, ulcer, and dyspepsia were higher for patients in the acetaminophen cohort than for those in the NSAID cohort [32].
• METHOD: Patients with a clinical diagnosis of functional dyspepsia according to the Rome II criteria and normal upper gastrointestinal endoscopy were recruited and randomised to receive: (1) lansoprazole 30 mg, (2) lansoprazole 15 mg, or (3) placebo, all given daily for four weeks [33].
• The total incidence of nausea, vomiting, diarrhoea and dyspepsia in a double-blind study was 12% in patients who received tranexamic acid 1g four times daily for 4 days for two cycles (not significantly different to the incidence in placebo recipients) [34].
• Although originally developed for the assessment of uninvestigated dyspepsia, the validation of SODA for use in clinical trials suggested its ability to compare treatment effects of non-specific non-steroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase (COX)-2-specific inhibitors [35].
• METHODS: Forty-three healthy volunteers and 10 patients with functional dyspepsia received motilin (4 pmol.min/kg) or placebo in four separate double-blind, randomized, placebo-controlled, cross-over studies [24].

References