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

Gastric neuromuscular disorders encompass a spectrum of dysfunction in nerve and smooth muscle that includes gastric visceral hypersensitivity, gastric dysrhythmias, fundic dysfunction, antral hypomotility, and gastroparesis. Patients with each disorder may present with such vague dyspepsia symptoms as early satiety, upper abdominal discomfort, bloating, or nausea with or without vomiting. A careful history and physical examination may suggest a gastric neuromuscular disorder, but symptoms are nonspecific. Gastroparesis is the most severe form of neuromuscular dysfunction. Such reversible causes of gastroparesis as mechanical obstruction of the stomach and chronic mesenteric ischemia must be excluded. Gastroparesis, gastric dysrhythmias, and hypersensitivity may follow viral infection or be due to degenerative processes that affect the gastric enteric neurons, smooth muscle, or interstitial cells of Cajal. Commonly, the cause of these gastric neuromuscular disorders is unknown. An approach to the diagnosis and treatment of gastric neuromuscular disorders is reviewed, including dietary counseling, drugs, and medical devices.
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PMID:Diagnosis and treatment of neuromuscular disorders of the stomach. 1286 63

Four cases of human infection by Echinochasmus japonicus (Trematoda; Echinostomatidae) were proven by the recovery of adult worms after a treatment with praziquantel (10 mg/kg in single dose) and purgation in February 1984 in Korea. The patients were 3 middle-aged men and 1 elderly woman residing in a riverside village of Kangjin-gun ( Tamjin river), Jeonranam-do, an ever-known endemic area of metagonimiasis. The treatment revealed numerous M. yokogawai worms together with 1-43 (total 54 ) specimens of E. japonicus and/or a few number of other kinds of trematodes or cestodes. The patients had gastrointestinal troubles such as indigestion and abdominal discomfort, probably due to these fluke infections. They have been eating some raw flesh of fresh water fishes such as cyprinoid ones or sweetfish caught from the river. This is the first record of human E. japonicus infection in the literature.
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PMID:Studies on intestinal trematodes in Korea XX. Four cases of natural human infection by Echinochasmus japonicus. 1288 63

Gastric dysrhythmias, such as tachy- or bradygastria, have been reported in patients with functional dyspepsia (FD), but their role in symptom production is uncertain. It is also not known whether gastric dysrhythmias in these patients can be elicited by physiological gastric distension with a meal. We investigated the relationships between symptoms after ingestion of different volumes of water following a test meal and gastric dysrhythmias in FD patients. Fourteen patients with dysmotility-like FD and 13 healthy volunteers underwent paired electrogastrography (EGG) studies. Fasted subjects ingested 150 ml of yoghurt with either 150 ml (low volume) or 300 ml (high volume) water in random order. Fasting and fed EGGs with monitoring of symptoms were performed in both studies. Ten FD patients (71.4%) reported upper abdominal discomfort and bloating after the low volume meal, but only one (7.1%) presented an abnormal EGG (dominant frequency in the 2-4-cpm range: 58%). Following the high volume meal, 7 patients (50%) had symptoms, but none had EGG abnormalities. No significant differences were found between FD patients and controls for any of the EGG variables, in any test. In FD patients with postprandial symptoms, the percentage of the EGG dominant frequency in the normal range (median, 84.6%; range, 76.0-100.0%) was similar (P>0.20) to that in those without symptoms (88.5%; 75.0-100.0%). We conclude that disturbances of gastric myoelectrical activity are unlikely to play a role in the origin of postprandial upper abdominal discomfort and bloating in dysmotility-like FD.
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PMID:Postprandial symptoms in dysmotility-like functional dyspepsia are not related to disturbances of gastric myoelectrical activity. 1468 43

Around 4% of primary care consultations are for dyspepsia, a term used for a specific group of upper gastrointestinal symptoms that includes abdominal discomfort, recurrent epigastric pain, bloating and heartburn. National guidelines recommend testing patients with uncomplicated dyspepsia for Helicobacter pylori infection, giving eradication therapy to those found to be infected and re-testing those who remain symptomatic after such treatment. Non-invasive tests for H. pylori avoid the need for endoscopy and biopsy to confirm infection, and several are now available for use in primary care. Here we review these tests and consider their role in the management of adults with dyspepsia.
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PMID:Which test for Helicobacter pylori in primary care? 1537 28

Symptoms of functional dyspepsia are characterized by upper abdominal discomfort or pain, early satiety, postprandial fullness,bloating, nausea and vomiting. It is a chronic disorder, with symptoms more than 3 mo per year,and no evidence of organic diseases. Dysfunctional motility, altered visceral sensation, and psychosocial factors have all been identified as major pathophysiological mechanisms. It is believed that these pathophysiological mechanisms interact to produce the observed symptoms. Dyspepsia has been categorized into three subgroups based on dominant symptoms. Dysmotility-like dyspepsia describes a subgroup of patients whose symptom complex is usually related to a gastric sensorimotor dysfunction. The brain-gut peptide cholecystokinin (CCK) and serotonin (5-HT) share certain physiological effects. Both have been shown to decrease gastric emptying and affect satiety. Furthermore the CCK induced anorexia depended on serotonergic functions probably acting via central pathways. We believe that abnormalities of central serotonergic receptors functioning together with a hyper responsiveness to CCK or their interactions may be responsible for the genesis of symptoms in functional dyspepsia (FD).
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PMID:Role of cholecystokinin and central serotonergic receptors in functional dyspepsia. 1655 97

Functional dyspepsia is a symptom complex characterised by upper abdominal discomfort or pain, early satiety, motor abnormalities, abdominal bloating and nausea in the absence of organic disease. The central nervous system plays an important role in the conducting and processing of visceral signals. Alterations in brain processing of pain, perception and affective responses may be key factors in the pathogenesis of functional dyspepsia. Central serotonergic and noradrenergic receptor systems are involved in the processing of motor, sensory and secretory activities of the gastrointestinal tract. Visceral hypersensitivity is currently regarded as the mechanism responsible for both motor alterations and abdominal pain in functional dyspepsia. Some studies suggest that there are alterations in central serotonergic and noradrenergic systems which may partially explain some of the symptoms of functional dyspepsia. Alterations in the autonomic nervous system may be implicated in the motor abnormalities and increases in visceral sensitivity in these patients. Noradrenaline is the main neurotransmitter in the sympathetic nervous system and again alterations in the functioning of this system may lead to changes in motor function. Functional dyspepsia causes considerable burden on the patient and society. The pathophysiology of functional dyspepsia is not fully understood but alterations in central processing by the serotonergic and noradrenergic systems may provide plausible explanations for at least some of the symptoms and offer possible treatment targets for the future.
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PMID:Central serotonergic and noradrenergic receptors in functional dyspepsia. 1671 53

The purpose of this study was to evaluate the efficacy and safety of commonly used probiotics and nutrients available for functional gastrointestinal disorders (FGID). Five different combinations of probiotics and nutrients, or placebo, were taken daily over 12 weeks. In this randomized controlled clinical trial, men and women 21 to 72 years of age with FGID symptoms of indigestion, bloating, and abdominal discomfort were assigned to one of six groups, 12 patients per group. Gastrointestinal Quality of Life Index (GIQLI) and visual analogue scale (VAS) for GI symptoms, SF-36, lactulose and mannitol test (LMT), and urine indican levels were evaluated. GIQLI, VAS scores, and LMT did not change significantly (P > 0.05). There were clinically notable improvements in two of the combination formulations. While the nonsignificant improvements in GI symptoms could suggest that combination probiotics and nutrients may be beneficial in conditions such as FGID, no conclusive evidence was found in this pilot trial. Further investigations to explore the findings are discussed.
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PMID:Efficacy of probiotics and nutrients in functional gastrointestinal disorders: a preliminary clinical trial. 1707 6

Lower dyspeptic syndrome is a bowel disease manifesting namely with pain or sensation of abdominal discomfort and bowel movement problems (changes in the frequency and stool consistency). Symptoms include sensation of intraabdominal pressure and fullness, diarrhoea (with or without pain), sensation of incomplete defecation, constipation or bowel movement problems (with or without pain), irregular stool, collywobbles and bowel content flow (borborygia with spasms), meteorism, flatulency. Prevalence of the Irritable Bowel Syndrome in the European population is estimated to be 5 to 25 %. In the Czech Republic the total prevalence of dyspepsias is about 13 %. To the pathogenesis of the lower dyspeptic syndrome contribute: 1. abnormal motility, 2. abnormal visceral perception, 3. psychosocial factors, 4. luminal factors, 5. imbalance of neurotransmitters and/or intestinal bacteria and 6. possible inflammatory changes of the intestinal mucosa. Infectious diarrhoea is one of the causes. Functional bowel defects represent various combinations of chronic and recurrent symptoms from the digestive tract which cannot be explained by structural or biochemical abnormalities. Irritable bowel syndrome is a functional defect manifesting with abdominal pain, intestinal dyspepsia and compulsive defecations. Subtypes with typical symptomatology are characterized by circumstances which bring about pain and compulsive defecations (morning fractional defecation, postprandial defecation, debacles). Functional diarrhoea manifests with diarrhoea without intensive pain. Spastic obstipation manifests by abdominal pain, obstipation, compulsive defecations are absent, stool is cloddish, fragmented by spastic haustration, or it has a ribbon-form. Changes in the intestinal chemism include fermentative and putrefactive dyspepsia. Among the incomplete and atypical forms the isolated meteorism, irregular defecation, flatulency, abdominal pain--syndrome of the left or right epigastium or the syndrome of the right hypogastrium can be included. In patients with typical set of symptoms the working diagnose of the lower dyspeptic syndrome can be done by general practitioner. Complete history of the disease can reveal possible extra abdominal cause of dyspepsia, recognise alarming symptoms and consider circumstances elevating or lowering the probability of functional problems. Functional bowel problems have usually long-term character and represent clinically demanding challenge. Only few therapeutic regimens are successful and the therapy aimed at the abolishment of one symptom need not bring general improvement. For the clinical studies of the therapy of functional bowel problems significant placebo effect is typical. Quoad vitam prognosis is good, quoad sanationem it is rather doubtful.
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PMID:[Lower dyspeptic syndrome. Recommended diagnostic and therapeutic procedures for general practitioners 2006]. 1731 May 80

The aim of this study was to evaluate the reasons for trial exclusion among dyspeptic patients and estimate the proportion that may have benefited from proton pump inhibitor (PPI) therapy. Stringent inclusion criteria for enrollment in two multicenter functional dyspepsia trials included dyspepsia (predominant persistent/recurrent upper abdominal discomfort [UAD] during the prior 3 months) of at least moderate intensity during > or =30% of days during the prior 2 to 3 weeks. Exclusion criteria were mild/infrequent UAD; heartburn and UAD of equal frequency; predominant heartburn with UAD; endoscopic evidence of erosive esophagitis or Barrett's or gastric and/or duodenal erosions (>5) or ulcers; irritable bowel syndrome (IBS); other gastrointestinal diagnoses; or other "non-categorized" disorders. Of 2,588 screened patients, 1,667 were excluded. Excluded patients by category had mild/infrequent UAD (12.5%, n=324), heartburn and UAD of equal frequency (1.1%, n=29), predominant heartburn with UAD (11.6%, n=300), endoscopic evidence of erosive esophagitis or Barrett's (6.2%, n=160), gastric and/or duodenal erosions (1.4%, n=36), gastric and/or duodenal ulcers (2.0%, n=53), IBS (7%, n=180), "other" gastrointestinal diagnoses (2.8%, n=73), or other "non-categorized" disorders (19.8%, n=512). Fifty-four percent of patients (902/1,667) had symptoms/diagnoses that would be expected to improve with PPI therapy. Individuals with IBS, "other," or "non-categorized" disorders were considered to have symptoms unlikely to respond to PPI treatment. Empiric PPI treatment would be expected to provide symptom relief to the majority of dyspepsia sufferer who present in clinical practice. PPIs represent the best currently available therapy for acid-related disorders and should be considered the first-line management approach in patients with uninvestigated dyspepsia.
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PMID:Proton pump inhibitors: effective first-line treatment for management of dyspepsia. 1734 2

The enteric-coated mycophenolate sodium (EC-MPS) is a new formulation of mycophenolic acid with a gastro-resistant enteric coating, which releases the drug in the intestine, reducing the incidence of the gastrointestinal (GI) adverse effects. The present work provided a summary of 20 patients with liver transplantation and more than a 1 year of treatment with mycophenolate mofetil (MMF) who, after presentation of GI complications, were converted to EC-MPS. The patients were followed over a 3-month period after beginning EC-MPS treatment. The mean age of the cohort was 53 +/- 10 years and included 75% men. The reasons for transplantation were ethanol cirrhosis (70%), hepatitis C cirrhosis (30%), hepatocarcinoma (5%), and Wilson's disease (5%). At baseline, all patients were being treated with cyclosporine (CsA). CsA doses and levels were reduced during follow-up: baseline dose 179 mg/day versus 143 mg/day at 3 months; levels: 90.4 ng/mL versus 85.8 ng/mL, respectively (P = .017). The administered dose of EC-MPS was 720 mg/day in all cases. The GI complications at baseline were: diarrhea 60% (92% moderate-severe), abdominal discomfort 60% (58% moderate), abdominal pain 45% (44% moderate-severe), gas 40% (38% moderate-severe), nausea 20% (25% moderate), and dyspepsia 20% (mild). After 3 months of EC-MPS treatment, only two patients (10%) displayed moderate diarrhea. The renal evolution was favorable, serum creatinine was reduced, and 24-hour creatinine clearance significantly increased (creatinine: 1.78 +/- 1.6 mg/dL at baseline versus 1.30 +/- 0.3 mg/dL at 3 months, P = .002; creatinine clearance: 72.8 +/- 18 mL/min versus 79.6 +/- 13 mL/min, P = .001). Conversion of MMF to EC-MPS in liver transplant recipients solved the GI tolerability problems and improved renal function during the first 3 months, probably due to the concomitant reduction of anticalcineurinic dose.
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PMID:Clinical evolution in the first 3 months of patients after liver transplantation in maintenance phase converted from mycophenolate mofetil to mycophenolate sodium due to gastrointestinal complications. 1788 75


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