Evidence for hypomotility in non-ulcer dyspepsia: a prospective multifactorial study (original) (raw)
Related papers
Digestive diseases and sciences, 2000
Studies on the influence of Helicobacter pylori gastritis on gastric motility have produced inconclusive results. We investigated the effect of Helicobacter pylori eradication therapy on gastric emptying in patients with functional dyspepsia in a placebo-controlled double-blind study with one year follow-up. A standardized scintigraphic double-tracer examination was used. Of the 40 subjects, 29 were H. pylori-positive patients with functional dyspepsia and 11 were asymptomatic control subjects. Gastric emptying parameters were: postlag 50% retention time for solids (T50), gastric emptying half-time for liquids (T1/2), solid lag duration, and intragastric distribution of solids. At baseline, the scintigraphic examination was performed for all study subjects to detect any major alterations between dyspeptic patients and asymptomatic control subjects. Thereafter every patient was randomized to receive either H. pylori eradication therapy or placebo; in addition they also received omepr...
Dyspepsia Challenge in Primary Care Gastroenterology
Digestive Diseases, 2021
Background: The purpose of this review is to take a deep dive into general problems and challenges of diagnosis and treatment of patients with symptoms of dyspepsia in primary care practice. Summary: Primary care physicians become acquainted with a broad range of clinical problems and therefore require a wide span of knowledge in taking care of patients from their first medical examination within the health care system. Dyspepsia and Helicobacter pylori infection are two of the most frequent reasons of digestive-related health care issues, despite that in primary care practice, current recommendations for diagnosis and differential therapy are often not implemented. The “test-and-treat” strategy is the initial management of the condition, reserving gastroscopy for patients refractory to symptomatic treatment and for patients presenting with any of the following alarm signs: age of above 55, dysphagia, anemia, weight loss, frequent vomiting, family history of GI malignancy, or a phys...
Does Helicobacter pylori infection increase gastric sensitivity in functional dyspepsia
Gut, 1995
The role ofHelicobacterpylori infection in the pathogenesis of functional dyspepsia is debated. It is known that a substantial fraction of dyspeptic patients manifest a low discomfort threshold to gastric distension. This study investigated the symptomatic pattern in 27 Hpylori positive and 23 H pylori negative patients with chronic functional dyspepsia, and potential relations between infection and gastric hyperalgesia. Specific symptoms (pain, nausea, vomiting, bloating/fullness, early satiety) were scored from 0 to 3 for severity and frequency (global symptom scores: 0-15). The mechanical and perceptive responses to gastric accommodation were evaluated with an electronic barostat that produced graded isobaric distensions from 0 to 20 mm Hg in 2 mm Hg steps up to 600 ml. Gastric compliance (volume/pressure relation) and perception (rating scale: 0-10) were quantified. Standard gastrointestinal manometry and recorded phasic pressure activity at eight separate sites during fasting and postprandially were also assessed. H pylon positive and H pylon negative patients manifested similar severity and frequency of specific symptoms and global symptom scores (mean (SEM)) (severity: 9'5 (2.0) v 9.0 (2.1); frequency: 10-8 (2.0) v 9*7 (2.2)). No differences were seen either in gastric compliance (53 (4) mI/mm Hg v 43 (3) mi/mm Hg) or in gastric perception of distension (slope: 0.50 (0.05) v 0*53 (0.06)). Postprandial antral motility was significantly decreased in H pylori positive patients (two hours motility index: 10.4 (0.6) v 12.6 (0.5); p<0.05). It is concluded that H pylori infected patients with functional dyspepsia present no distinctive symptoms by comparison with H pylon negative counterparts and H pylorn infection is associated with diminished postprandial antral motility but it does not increase perception of gastric distension.
Digestive Diseases and Sciences, 1994
The pathogenesis of nonulcer dyspepsia (NUD) is unknown. Gas and postprandial bloating are frequent symptoms. The role of Helicobacterpylori (HP) in the pathogenesis of NUD is controversial. We studied the intestinal gas profile of NUD patients (N = 34) at baseline and after lactulose administration. The prevalence of hydrogen and methane producers was similar among HP+ and HP-patients. Breath H2 concentrations in response to lactulose showed significantly greater rise among HP+ subjects (P < 0.0001). HP positivity was associated with higher total breath excretion for 1-12 and methane combined (2984 ---1038 vs 1776 -521 ppm/hr) compared to HP-subjects (P < 0.05). There was no correlation between peak H 2 and methane levels. The role of alterations in intestinal gas in producing symptoms in HP+ patients with NUD needs further investigation.
Helicobacter pylori infection and gastric function in patients with chronic idiopathic dyspepsia
Gastroenterology
In the present study we evaluated the relation among histology, H. pylori, IgG to H. pylori, gastric emptying, and acid secretion in 43 patients with fundic atrophic gastritis. On the basis of gastric acid secretion, patients were divided into three subgroups: patients with preserved acid secretion (Group 1), patients with hypochlorhydria (Group 2), and patients with achlorhydria (Group 3). Fundic glandular atrophy was more severe in hypoachlorhydric patients than in those with preserved acid secretion (P Ͻ 0.05 vs Group 2, P Ͻ 0.005 vs Group 3). H. pylori colonization was found in 94% of patients in Group 1, in 61% of patients in Group 2, and in only 8% of patients in Group 3 (P Ͻ 0.001 vs Group 1, P Ͻ 0.05 vs Group 2). Conversely, serological positivity to H. pylori was high in all three subgroups of patients (100% in Group 1, 77% in Group 2, 92% in Group 3). Gastric emptying was delayed in atrophic patients, particularly in those with hypoachlorhydria. Our data suggest that fundic atrophic gastritis represents a possible end stage of H. pylori infection, characterized by a progressive disappearance of the bacterium and a progressive deterioration of gastric functions.