Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although manometric antral hypomotility and delayed gastric emptying have been reported separately in patients with dyspepsia, relationships between symptoms, antral contractility and emptying rate have not been sought. The present study therefore aimed to evaluate, simultaneously, gastric antral excursion characteristics and emptying in a sub-group of patients with severe functional dyspepsia using high-resolution real-time ultrasound. The circumference of the relaxed and contracted antrum was measured at 15-min intervals after ingestion of a 360 mL mixed nutrient meal in 36 chronic dyspepsia patients with symptoms of post-prandial bloating and epigastric distension, and in 25 healthy volunteers. Antral emptying (measured as the rate of decrease in circumference of the relaxed antrum) was slower in patients than normals (P = 0.02). In both groups, the average values for antral excursion were similar but the range of excursion in patients was significantly wider than in controls (F < 0.001), with 11 patients showing values above, and 8 showing values below the normal range. There was no relationship between antral emptying and antral excursion in either patients or volunteers. In conclusion, patients with severe functional dyspepsia show a wide range of antral performance characteristics, suggesting not only that the mechanisms responsible for the control of antral motor function are disturbed but also that the cause of the symptoms and the disturbed antral motor function are probably not directly related.
 ...
PMID:Evaluation of gastric antral motor performance in patients with dysmotility-like dyspepsia using real-time high-resolution ultrasound. 934 77

In the present double-blind placebo-controlled study the effect of cisapride on functional dyspepsia was evaluated in patients with and without histological gastritis. Patients with functional dyspepsia and whose symptoms persisted after a 2 week run-in period with antacid treatment were randomized to receive cisapride (10 mg) or matching placebo three times daily for 4 weeks. Symptoms of epigastric pain, bloating, nausea, belching, early satiety and heartburn were graded on a four-point scale based on patients' feedback and diary card recording. A global response was also formulated by the investigators. One hundred and four patients entered the study and 76 completed the trial, comprising 36 patients with histological gastritis and 40 patients without gastritis. Symptom scores in both gastritis and non-gastritis groups were significantly improved by both cisapride and placebo; however, the improvement was not statistically different between the two treatment groups. Cisapride produced a good or better global response in 58% of subjects with histological gastritis and in 53% of subjects without gastritis compared with 47% and 52%, respectively, of patients on placebo; this difference was not statistically significant. Gastric histology did not influence the effect of cisapride on the symptoms of functional dyspepsia.
 ...
PMID:Effect of cisapride on functional dyspepsia in patients with and without histological gastritis: a double-blind placebo-controlled trial. 907 16

Cisapride is a substituted benzamide with gastrointestinal prokinetic effects presumed to be due to the enhancement of the physiological release of acetylcholine at the myenteric plexus. In a multicentre study, 189 patients with nonulcer dyspepsia (NUD) received single-blind placebo treatment for two weeks. A total of 123 patients with no or minimal response to placebo and epigastric pain of at least moderate severity and frequency were randomly assigned to one of the three parallel double-blind treatments for six weeks: cisapride 10 mg tid, cisapride 20 mg tid or placebo. The severity and frequency of individual symptoms (epigastric pain, heartburn, nausea, vomiting anorexia, postprandial discomfort, regurgitation, lower abdominal pain, bloating and constipation) were assessed on a four- and five-point categorical scale, respectively, by the investigator at three on treatment visits and by patients in a daily diary. Analysis of investigator and patient assessments for differences in symptom severity x frequency composite scores among the three treatment groups showed no statistically significant differences for individual symptoms or symptom clusters. As assessed by the investigator, and compared with baseline, cisapride 20 mg tid significantly (P < 0.05) improved epigastric pain, bloating and early satiety as well as improved the total symptom cluster. Investigator evaluation of the five most severe and frequent symptoms for each patient showed statistically significant improvement in each treatment group. For patient diary assessments, statistically significant within-treatment improvement of the total symptom cluster, the five most severe symptoms cluster, bloating and early satiety was observed for both cisapride 20 mg and placebo, whereas epigastric pain significantly (P < 0.05) improved in all three treatment groups. Investigator evaluation of global response (good+excellent) rate at the end of the six week treatment period was 38% for cisapride 20 mg, 47% for cisapride 10 mg and 33% for placebo. No statistically significant difference in this parameter among treatments was noted. Cisapride was well tolerated at both doses with a side effect profile comparable with that of placebo. It is concluded that in this double-blind multicentre study with a single-blind two-week placebo run in phase, cisapride 10 mg tid and 20 mg tid were not effective compared with placebo in improving symptoms in NUD patients. This study re-emphasizes the good prognosis of patients with NUD, with 14% of patients improving in the two-week placebo run-in phase and a further 33% improving in the next six weeks while on placebo. Within-treatment analysis of investigator assessments showed improvement for cisapride 20 mg tid suggesting a trend of efficacy at this dose.
 ...
PMID:A double-blind randomized study of cisapride in the treatment of nonulcer dyspepsia. The Canadian Cisapride Nud Study Group. 911 11

The purpose of this study was to investigate whether sublingual glyceryl trinitrate influences the size of the proximal stomach and postprandial symptoms in patients with functional dyspepsia. Twenty patients with functional dyspepsia were included in a double-blind, placebo-controlled crossover study with sublingual glyceryl trinitrate. All patients were scanned twice on consecutive days, receiving either placebo or 0.5 mg glyceryl trinitrate randomly 5 min prior to ingestion of 500 ml meat soup. Total symptoms, pain, nausea, and bloating were scored on a visual analog scale before and after the meal. Standardized ultrasonograms were obtained 1, 10, and 20 min postprandially of the proximal and distal stomach. The proximal stomach was larger in the sagittal section at 1 min postcibally (26.5 +/- 3.9 vs 24.8 +/- 4.9 cm2, P = 0.036) and 10 min postprandially (22.0 +/- 5.1 vs 19.8 +/- 5.3 cm2, P = 0.009) after administration of glyceryl trinitrate compared with placebo, whereas a tendency was observed after 20 min (18.7 +/- 5.5 vs 17.3 +/- 5.7 cm2, P = 0.076). The corresponding changes in the frontal diameters were 8.3 +/- 1.1 vs 7.8 +/- 1.2 cm (P = 0.067) after 1 min, 7.2 +/- 0.9 vs 6.4 +/- 0.8 cm (P = 0.001) after 10 min, and 6.3 +/- 1.1 vs 5.6 +/- 1.2 cm (P = 0.016) after 20 min. The area of the distal stomach was not different (P > 0.31) in the two groups. After administration of glyceryl trinitrate, the patients reported less pain (P = 0.048) and nausea (P = 0.023) 5 min postprandially, but this effect was reduced 15 min later. Total symptom score was improved by glyceryl trinitrate treatment (P < 0.042). Sublingual glyceryl trinitrate improves accommodation of the proximal stomach to a meal and reduces postprandial symptoms in a group of patients with functional dyspepsia.
 ...
PMID:Effect of glyceryl trinitrate on gastric accommodation and symptoms in functional dyspepsia. 936 47

Dyspepsia is a vague term for the nonspecific symptoms of upper abdominal discomfort, prolonged postprandial fullness or early satiety, nausea, vomiting, and upper abdominal bloating. Many common and accepted diseases and disorders such as gastroesophageal reflux and irritable bowel syndrome cause dyspepsia symptoms; these disorders should be identified and treated. However, many patients with dyspepsia symptoms have normal radiographic and endoscopic evaluations; in these patients, neuromuscular of functional disorders of the stomach ranging from gastric dysrhythmias to gastroparesis may be the cause of dyspepsia symptoms. A practical approach to the evaluation and treatment of dyspepsia symptoms attributed to gastric neuromuscular dysfunction of unknown origin is described.
 ...
PMID:Dyspepsia of unknown origin: pathophysiology, diagnosis, and treatment. 943 96

The expectation that cholecystectomy is effective treatment for symptomatic gallstones is not always achieved in surgical practice. The impact of cholecystectomy on the relief of gastrointestinal symptoms was evaluated in 92 patients followed up after surgery for a mean of 31.1 months (range 12-83 months). Abdominal pain continued to be present, or arose de novo, in 28 (30.4%) patients. Pain-free outcome after cholecystectomy was associated with a preoperative clinical diagnosis of biliary colic, fatty food intolerance, and a thick-walled gallbladder on ultrasound (P = 0.02). Logistic regression associated a thick-walled gallbladder, elevated gamma-glutamyl transpetidase, body mass index < 26, fat intolerance, and normal bowel habit with good postoperative results (P = 0.001). Application of each of these five factors to a clinical index failed to predict long-term pain-free outcome after cholecystectomy. Abdominal bloating (P = 0.03), dyspepsia (P < 0.001), heartburn (P < 0.007), fat intolerance (P < 0.001), nausea (P = 0.001) and vomiting (P < 0.001) were significantly improved after cholecystectomy, but diarrhoea, constipation and excessive flatus were not. Outcome benefit ratios confirmed that vomiting (0.96), nausea (0.87), dyspepsia (0.67), fat intolerance (0.57) and heartburn (0.51) were relieved by surgery. Cholecystectomy improved symptoms compared with a matched control group, suggesting that surgery remains the gold standard treatment of symptomatic gallstones.
 ...
PMID:Is cholecystectomy effective treatment for symptomatic gallstones? Clinical outcome after long-term follow-up. 984 45

Functional gut disorders include several clinical entities defined on the basis of symptom patterns (e.g., functional dyspepsia, irritable bowel syndrome, functional abdominal pain, functional abdominal bloating), for which there is no established pathophysiological mechanism. Because there is no well-defined pathophysiological target, treatment should be aimed at symptom improvement. Prokinetics and antispasmodics have been widely used in the treatment of functional gut disorders on the assumption that disordered motility is the underlying cause of symptoms, and symptom improvement is indeed achievable with these compounds in some, but not all, patients with features of hypo- or hypermotility, respectively. In the first part of this review, we cover the basic pharmacology and discuss the rationale for the clinical use of prokinetics and antispasmodics. On the other hand, in the past few years, the explosive growth in the research focusing on visceral sensitivity and visceral reflexes has suggested that at least some patients with functional gut disorders have altered visceral perception. Thus, the second part of the review covers these developments and focuses on studies addressing the issue of drugs modulating visceral sensitivity.
 ...
PMID:Functional gut disorders: from motility to sensitivity disorders. A review of current and investigational drugs for their management. 980 54

Symptoms of functional dyspepsia, such as epigastric pain, bloating or early satiety and nausea, are non-specific and are likely to arise from different mechanisms. Current evidence suggests the presence of at least two subgroups: patients who respond to a prolonged course of acid suppression and patients who show a significant overlap of symptoms with other functional gastrointestinal disorders such as irritable bowel syndrome. An enhanced sensitivity of visceral afferent pathways with or without associated autonomic dysregulation appears to play an important role in the aetiology of symptoms in the second group. In the absence of visceral hypersensitivity, neither the slowing of gastric emptying nor the presence of chronic gastritis appears to be sufficient to cause symptoms of functional dyspepsia. The mechanisms and aetiology of visceral hypersensitivity are incompletely understood. An alteration in the interplay between vagal and spinal afferents, and the inadequate activation of antinociceptive systems in response to tissue irritation, may play a role in symptom generation.
 ...
PMID:Gastrointestinal sensory abnormalities in functional dyspepsia. 989 87

The term "functional dyspepsia" represents a complex of symptoms related to the upper gastrointestinal tract, including epigastric pain, upper abdominal bloating/distension, regurgitation, postprandial fullness, early satiety, nausea and vomiting and frequently reported to occur in connection with food intake. Particularly foods containing fat appear to potently provoke dyspeptic symptoms. Despite all the anecdotal reports from patients as to which food groups or even particular nutrients evoke symptoms, it is rather surprising that only few studies have been published which systematically investigate the effects of these foods or the exclusion of certain foods on symptom development and improvement. The results from these studies were not clear-cut: although some patients report to experience dyspeptic symptoms after foods rich in fat, they tolerate these foods if the fat is well disguised [1]. In addition, food consistency or preparation appears to be a determinant for symptoms: solid food containing fat is less likely to induce symptoms than fat-containing liquids [2]. The following discussion will be focussed on the role of gastric motility and gastrointestinal sensitivity to nutrients and a possible interaction between the two in the origin of symptoms of functional dyspepsia.
 ...
PMID:Duodenal sensitivity to lipids and gastric motility: contribution to functional dyspepsia. 1002 57

While many definitions exist, dyspepsia is best considered a symptom complex (not a diagnosis) thought to arise in the upper gastrointestinal tract, unrelated to defecation. The symptom complex includes: upper abdominal/epigastric pain or discomfort, postprandial fullness, bloating, belching, early satiety, anorexia, nausea, retching, vomiting, heartburn and regurgitation. Patients with typical gastroesophageal reflux, biliary colic and irritable bowel syndrome should not be considered to have dyspepsia. After investigations, if a cause of dyspepsia is found, this is 'organic or structural' dyspepsia. If no structural cause is found, this is best called 'functional dyspepsia', subclassified into a) ulcer-like b) dysmotility-like c) reflux-like and d) unspecified dyspepsia. This symptom guided classification should be shifted to the first presentation with uninvestigated dyspepsia, prior to any investigations, to define a clinically useful guide to patient care. As there is considerable symptom overlap, it may be useful to combine together the ulcer and reflux-like groups into an acid-related dyspepsia group. In 1998, another approach would be to screen dyspeptic patients with an H. pylori test and classify them as H. pylori positive and negative dyspepsia.
 ...
PMID:Definitions of dyspepsia: time for a reappraisal. 1002 67


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>