Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Functional dyspepsia (FD) is very common, but the pathogenesis of Helicobacter pylori leading to FD is still debated. The aim of this study was first to evaluate the impact of H. pylori colonization on the efficacy of Paspertase (a metoclopramide plus exogenous enzymes regimen for FD patients) and, second, to compare the prevalence of H. pylori infection in FD patients with the general population. Seventy-four consecutive FD patients were enrolled undergoing Paspertase treatment. The symptomatic response was evaluated according to 1-4 scales of six main dyspeptic symptoms (i.e. epigastric pain/discomfort, early satiety, heartburn, nausea/vomiting, abdominal fullness/bloating, and belching). Nine hundred and seventy healthy subjects undergoing a paid physical check-up were included to study the status of H. pylori colonization. The demographic data and basal symptom scores between 43 H. pylori-positive and 31 H. pylori-negative patients were not significantly different. Total and individual symptom scores improved significantly after 4 weeks of Paspertase therapy (P < 0.05), irrespective of H. pylori infection. The prevalences of H. pylori were very similar in FD patients and the general population (58.1 vs 58.0%, NS). In conclusion, these observations suggest that H. pylori colonization is not significant in FD patients of Taiwan while a short-term prokinetic medication is effective for these patients, irrespective of H. pylori status.
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PMID:Helicobacter pylori colonization does not influence the symptomatic response to prokinetic agents in patients with functional dyspepsia. 964 48

The purpose of this clinical study was to determine the efficacy, tolerability, and impact on quality of life of domperidone--a specific peripherally acting dopamine antagonist--in the management of symptoms of gastroparesis, a common and potentially debilitating condition in patients with diabetes mellitus. In the first phase of this multicenter, two-phase withdrawal study, 287 diabetic patients with symptoms of gastroparesis of at least 6 months' duration received domperidone 20 mg QID in a single-masked fashion for 4 weeks. Efficacy was evaluated using a four-point rating scale (0 = none, 1 = mild, 2 = moderate, 3 = severe) for each of the following symptoms: nausea, abdominal distention/bloating, early satiety, vomiting, and abdominal pain. At the end of the first phase, patients with sufficient improvement in their total symptom score (a score < or = 6 and a decrease in score of > or = 5 units from the baseline [selection] visit) were eligible for the 4-week, randomized, placebo-controlled, double-masked withdrawal phase of the study. The impact of domperidone on quality of life was determined using the Medical Outcomes Study Short Form-36 (SF-36). Of 269 patients with data from the single-masked phase, 208 (77%) qualified for entry into the double-masked phase based on a statistically significant improvement in total symptom score, from a mean score of 10.32 at baseline (initial visit) to 3.79 after 4 weeks of single-masked domperidone therapy. During the double-masked phase, patients in the placebo group had significantly greater deterioration in total symptom scores compared with patients in the domperidone group (mean changes of 1.84 and 0.85, respectively). Similar significant differences in favor of domperidone were seen in the secondary efficacy variables (i.e., patients' diary scores and global assessments of symptoms). The tolerability profile of domperidone was similar to that of placebo. Patients who responded to domperidone experienced significant improvements in quality of life, as indicated by the SF-36 physical and mental component summary scores. During the double-masked phase, patients who were randomized to placebo experienced a significant deterioration in the physical component summary score compared with patients in the domperidone group. The results of this study suggest that domperidone 20 mg QID provides significant improvement in the upper gastrointestinal symptoms of diabetic gastroparesis and is well tolerated in patients with this condition.
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PMID:Domperidone in the management of symptoms of diabetic gastroparesis: efficacy, tolerability, and quality-of-life outcomes in a multicenter controlled trial. DOM-USA-5 Study Group. 966 60

Nausea and gastric dysrhythmias occur in conditions associated with gastric distension. The roles of distal and proximal gastric mechanoreceptors in these responses are unexplored. Because antral distension induces vomiting in animals and antral and fundic vagal afferent discharges differ, we hypothesized that distal gastric distension in humans leads to greater symptomatic and dysrhythmic responses than proximal distension. Symptoms and electrogastrograms were recorded in healthy humans during distal and proximal gastric distension with a barostat. Distal but not proximal distension induced nausea and a 747 +/- 250% increase in dysrhythmic power (P < 0.05), responses not affected by granisetron, indomethacin, or atropine, agents that block dysrhythmias in other settings. In the distal stomach, bloating and pain developed at lower pressures (P < 0.05) not modified by granisetron, and compliance was significantly lower (P < 0.05). In conclusion, gastric mechanoreceptor activation in the less-compliant distal stomach produces nausea and dysrhythmias via non-5-hydroxytryptamine3 (5-HT3), non-prostaglandin-dependent, and noncholinergic pathways. Distal mechanoreceptor activation induces greater bloating and pain than proximal mechanoreceptor activation via 5-HT3-independent pathways.
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PMID:Differential symptomatic and electrogastrographic effects of distal and proximal human gastric distension. 972 52

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.
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PMID:Definitions of dyspepsia: time for a reappraisal. 1002 67

Patients with fat intolerance complain of early satiety, bloating, nausea, and vomiting. Since these symptoms are similar to those of patients with postgastrectomy dumping syndrome, we hypothesized that fat intolerance may be associated with early, rapid gastric emptying. Using a three-meal gastric emptying study, we compared gastric emptying in nine patients with a history of fat intolerance and nine normal volunteers. On three separate days, 500-ml radiolabeled test meals containing 0, 15, or 60 g of fat were studied. The percentages of the test meal emptied at 15 and 60 min were analyzed by repeated measures two-way ANOVA. At 15 min (p < 0.05) but not 60 min, gastric emptying was faster in patients than normals. Gastric emptying at 15 min (p < 0.001) and 60 min (p < 0.001) depended on the dose of fat. We conclude that fat intolerance is associated with early, rapid gastric emptying.
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PMID:Fat intolerance depends on rapid gastric emptying. 1006 19

Since Helicobacter pylori (Hp) was first isolated in 1983, much work has been carried out on the pathogenic effects of this organism. Hp infection is common in humans and currently is the most important etiologic agent in the development of chronic active gastritis, gastric and duodenal ulcers, carcinoma and Malt-lymphoma of the stomach. Moreover Hp infection has also been associated with various extradigestive diseases. At present, a role of Hp infection in dyspepsia is discussed. Dyspepsia is defined by persistence of pain, burning or discomfort localised to the upper abdomen; some authors include in dyspepsia symptoms such as belching, bloating, alitosis, nausea, postprandial repletion, vomiting and regurgitation. In absence of any underlying pathologies, such as peptic ulcer, gastroesophageal reflux, pancreatitis, biliary tract disease or others, dyspepsia is defined as functional or idiopathic dyspepsia. Functional dyspepsia may be distinct in ulcer, reflux or dysmotility-like dyspepsia and unspecified dyspepsia. Hp infection is common in dyspeptic patients and a role of this bacterium has been postulated mostly in ulcer-like dyspepsia. Mechanisms by when Hp induces dyspeptic symptoms are uncertain; bacterial cytotoxins, phlogosis mediators, activity of chronic gastritis Helicobacter-related and host immune response probably play an important role in pathogenesis of functional dyspepsia. However, dyspepsia is not present only in infected patients; therefore other pathogenic factors may be implicated in expression of dyspeptic symptoms in uninfected subjects, such as gastric dysmotility, modifications of gastric output or altered visceral sensibility, psychological factors, gastroesophageal reflux and irritable bowel.
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PMID:[Dyspepsia and Helicobacter pylori]. 1036 46

While widely used in research, the 1991 Rome criteria for the gastroduodenal disorders, especially symptom subgroups in dyspepsia, remain contentious. After a comprehensive literature search, a consensus-based approach was applied, supplemented by input from international experts who reviewed the report. Three functional gastroduodenal disorders are defined. Functional dyspepsia is persistent or recurrent pain or discomfort centered in the upper abdomen; evidence of organic disease likely to explain the symptoms is absent, including at upper endoscopy. Discomfort refers to a subjective, negative feeling that may be characterized by or associated with a number of non-painful symptoms including upper abdominal fullness, early satiety, bloating, or nausea. A dyspepsia subgroup classification is proposed for research purposes, based on the predominant (most bothersome) symptom: (a) ulcer-like dyspepsia when pain (from mild to severe) is the predominant symptom, and (b) dysmotility-like dyspepsia when discomfort (not pain) is the predominant symptom. This classification is supported by recent evidence suggesting that predominant symptoms, but not symptom clusters, identify subgroups with distinct underlying pathophysiological disturbances and responses to treatment. Aerophagia is an unusual complaint characterized by air swallowing that is objectively observed and troublesome repetitive belching. Functional vomiting refers to frequent episodes of recurrent vomiting that is not self-induced nor medication induced, and occurs in the absence of eating disorders, major psychiatric diseases, abnormalities in the gut or central nervous system, or metabolic diseases that can explain the symptom. The current classification requires careful validation but the criteria should be of value in future research.
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PMID:Functional gastroduodenal disorders. 1045 43

An athlete's ability to reach maximum performance is a direct result of physical and muscular performance, muscular and systemic stress tolerance, control and regulation of immune function, and adaptation to physical stress. In this complex sense, the gastrointestinal (GI) tract is also part of the system that controls and regulates adaptation and regeneration of the athlete. A well-balanced GI immune system and an optimized immune competence may protect the athlete from harmful pathogens; it may also protect against dietary as well as inhaled antigens. However, under conditions of mechanical and biochemical stress, the integrity of the GI mucosal block, particularly the epithelial hood, can be damaged, leading to a pathological uptake of toxic or immunogenic substrates. This may occur in endurance athletes, since gut symptomatology, nausea, vomiting, pain, bloating, diarrhea, cramping, and bleeding can be observed in up to half of all participants in endurance events. In addition, composition of stool and fecal microflora in endurance athletes has shown that there may be a specific need for nutritional support for mucosal immunity in highly trained but chronically stressed athletes. Proper diet during training and competition is a significant factor in guarding against GI symptoms and exercise-induced gastrointestinal side effects that may compromise immune competence and physical performance. The present review presents some important suggestions on the possible role of the GI tract in human performance and stress tolerance, and offers new insights about the influence of food quality on the immune system of the gut.
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PMID:The gastrointestinal system--an essential target organ of the athlete's health and physical performance. 1051 63

Gastroparesis-or delayed gastric emptying--is associated with upper gastrointestinal symptoms that include early satiety, nausea, vomiting, regurgitation, fullness, and bloating. Gastroparesis should be considered in the diagnosis of a patient with these symptoms after mechanical and structural lesions have been ruled out. This review briefly summarizes gastric motor physiology and discusses the etiology and diagnostic approach to the treatment of a patient with possible gastroparesis. We highlight the methods available to measure gastric motility and describe their relative advantages and disadvantages.
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PMID:The diagnosis and work-up of the patient with gastroparesis. 1073 Sep 17

About 30% of patients who have a Roux-en-Y gastrojejunostomy after gastrectomy suffer from abdominal pain, nausea, vomiting of food and bloating made worse by eating. This syndrome, called the Roux stasis syndrome, is caused, in part, by a motility disorder of the Roux limb. Transection of the jejunum during the construction of the limb separates the limb from the natural small intestinal pacemaker located in the duodenum. Ectopic pacemakers then appear in the limb and trigger retrograde contractions in its proximal portion. These contractions slow transit through the limb and result in Roux stasis. Current nonsurgical treatment of the syndrome includes the use of prokinetic agents and intestinal pacing, neither of which has demonstrated long-term benefits. A near-total gastrectomy may speed upper gastrointestinal transit somewhat, but stasis in the Roux limb often persists. Our current approach alms at preventing the syndrome by the use of an 'uncut' Roux limb, an operation which preserves myoneural continuity between the duodenal pacemaker and the Roux limb and so prevents the appearance of ectopic pacemakers and stasis in the limb.
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PMID:Motility Disorders after Roux-en-Y Gastrojejunostomy. 1074 77


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