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)

'Gastro-esophageal reflux' is the passage of gastric content into the esophagus. Resulting typical symptoms are denoted as 'reflux like dyspepsia'. 'Reflux esophagitis' is the endoscopic or microscopic evidence of damage to the esophageal mucosa. Long-term intraesophageal pH-monitoring will establish 'pathologic gastroesophageal reflux' when 'acid exposure' time exceeds 5% of the monitoring time. GERD, 'gastro-esophageal reflux disease', is present when symptoms and/or esophagitis are caused by reflux. 'Columnar lined esophagus' is a better expression than 'Barret's esophagus'. Esophageal acid exposure increases during the day with a peak in the evening and little reflux after midnight. Treatment should probably be concentrated to evening time and not so much to night time.
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PMID:Gastro-esophageal reflux disease. 324 93

In these speculations of the future in gastro-esophageal reflux a hope is expressed that gastro-esophageal reflux disease is accepted as a separate entity. Treatment and diagnosis should not be confused with those of ulcer disease. Reflux disease is not a problem of too much acid in the stomach, but too much acid in the wrong place, the esophagus. The problem is mainly a leaking valve. Furthermore, the expression reflux like dyspepsia should be used when esophagitis or gastro-esophageal reflux disease is not established by endoscopy or pH-monitoring.
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PMID:Gastroesophageal reflux disease. 324 97

Dyspepsia, defined as chronic or recurrent upper abdominal pain or nausea, is a common occurrence. Dyspepsia without an ulcer (non-ulcer dyspepsia) is diagnosed in patients at least twice as often as peptic ulceration. Diseases that may present with similar symptoms include gastroesophageal reflux, biliary tract disease, chronic pancreatitis, and irritable bowel syndrome. A careful history and physical examination, supplemented by selected tests, usually lead to a correct diagnosis. The pathogenesis of non-ulcer dyspepsia remains unknown. Gastric acid secretion, duodenogastric reflux, psychological factors, environmental exposures, and heredity probably do not play a major role. Some patients may have motility disturbances, but whether these disturbances cause dyspepsia is unknown. Campylobacter pylori infection and associated gastritis are common in non-ulcer dyspepsia, but their etiologic role is controversial, as is the importance of chronic duodenitis. By recognizing the heterogeneity of patients who present with non-ulcer dyspepsia, more rational management may be possible. Although an empiric trial of antacids or H2 blockers has been recommended to treat dyspepsia, most controlled trials show that although these substances reduce severity of symptoms, they are no more effective than placebos in non-ulcer dyspepsia.
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PMID:Non-ulcer dyspepsia: potential causes and pathophysiology. 328 48

The effect of cimetidine and placebo was examined in 123 patients with non-ulcer dyspepsia (NUD) by means of a 12-day multi-crossover model with 5 regular interchanges between cimetidine and placebo. The evaluation of effect in individual patients was based on the number of times cimetidine was associated with less symptoms than the preceding or following placebo period. If cimetidine had no effect, the probability of being defined as a cimetidine responder was 25%. In general, cimetidine was associated with less symptoms than placebo (p less than 0.0001). Forty patients were identified as cimetidine responders (R) and the remaining patients were termed non-responders (NR). Symptoms compatible with gastroesophageal reflux were significantly more frequent in R than in NR, whereas the opposite was true for symptoms of the irritable colon syndrome. The ability of symptoms selected by stepwise logistic regression to predict response to cimetidine showed at best a sensitivity of 75% and a specificity of about 65%. No differences were found between R and NR with regard to acid secretion, endoscopic and histologic findings, or the result of an acid perfusion test. The present study supports the existence of a subgroup of cimetidine responders among patients with NUD characterized by symptoms suggestive of gastroesophageal reflux disease in the absence of confirmatory objective evidence.
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PMID:Cimetidine responders in non-ulcer dyspepsia. 329 Oct 85

The incidence of severe duodenal anomalies (MD) has been investigated in 458 patients submitted to barium meal examination and in 176 subjects comprising various clinical subgroups. The incidence of MD in patients submitted to barium meal examination was 11.6%. The incidence of MD in 25 normals was 4%, which was not significantly different from the incidence (10%) of MD in patients with gastroesophageal reflux symptoms. Compared with in normals, MD occurred with a significantly higher incidence in 45 patients with X-ray-negative dyspepsia (24%), in 36 patients with the irritable bowel syndrome (44%), and in 37 patients with asthma (38%). It is concluded that demonstration of MD in a patient is only indicative of a possible disorder.
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PMID:The incidence of severe duodenal anomalies in patients submitted to barium meal examination, in normals, and in different clinical subgroups. 343 6

The aim of this study was to describe the clinical features of patients with chronic unexplained dyspepsia and compare the symptoms with peptic ulcer and biliary pain, and determine the prevalence of symptoms that may indicate psychoneurotic traits and measure chronic illness behaviour (days lost from work and doctor visits). Studied were: 113 patients with essential dyspepsia, defined as endoscopically confirmed non-ulcer dyspepsia where gallstones, the irritable bowel syndrome and gastro-esophageal reflux have been excluded and there is no ascertainable cause for the dyspepsia; 55 patients with dyspepsia and peptic ulceration at endoscopy; and 53 patients with diagnosed biliary pain and cholelithiasis, proven at cholecystectomy. All patients completed a detailed structured history questionnaire in the presence of one investigator. More patients with peptic ulcer than with essential dyspepsia experienced night pain, pain relieved by food, and vomiting, while more patients with essential dyspepsia than with cholelithiasis experienced epigastric pain, lack of radiation of pain, continuous pain, mild to moderate pain, pain before meals, pain relieved by food and antacids, pain aggravated by food and alcohol, and an absence of vomiting (all p less than 0.01). Symptoms suggesting psychoneurosis, aerophagy symptoms, and chronic illness behaviour were similar in all groups. We conclude that certain symptoms may be of value in diagnosing the underlying cause of dyspepsia.
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PMID:Comparison of the clinical features and illness behaviour of patients presenting with dyspepsia of unknown cause (essential dyspepsia) and organic disease. 346 12

Non-ulcer dyspepsia (NUD) is a poorly defined heterogenous condition less well suited for the conventional randomized and placebo controlled parallel type trials. We have designed a multi cross-over model (MCO-model) with the facility of providing information about drug responses in individual patients. A pilot study suggested that the model may identify individual cimetidine responders among patients with dyspepsia. Preliminary findings from an ongoing study in patients with NUD supports the existence of a subgroup of cimetidine responders characterized by gastroesophageal reflux symptoms and possibly an increased basal acid secretion.
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PMID:Dyspepsia: Therapeutic response as a diagnostic tool. 347 94

Nonulcer dyspepsia remains a difficult disorder to treat because it is a heterogeneous syndrome. Once patients with the irritable bowel syndrome, esophagitis, and other organic diseases are excluded, there remain patients with dyspepsia of unknown cause (termed "essential dyspepsia") and patients with dyspepsia plus symptoms of gastroesophageal reflux without esophagitis. The aim of this study was to determine whether cimetidine or pirenzepine is efficacious in relieving the symptoms of these latter subgroups. Sixty-two consecutive patients were studied who had chronic upper abdominal pain or nausea where endoscopy had shown no evidence of peptic ulceration, esophagitis, or malignancy; 47 had essential dyspepsia, and 15 had dyspepsia plus gastroesophageal reflux. They were initially randomized to either cimetidine or placebo, or pirenzepine or placebo. Patients continued each medication for 1 mo, and, after a washout period, crossed over when again symptomatic; 51 patients completed cimetidine and placebo, and 50 completed pirenzepine and placebo. The results showed that cimetidine was superior to placebo in decreasing the number of upper abdominal pain episodes weekly and the severity of pain, but the absolute improvement was small. Pirenzepine was not superior to placebo in decreasing symptoms.
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PMID:Randomized, double-blind, placebo-controlled crossover trial of cimetidine and pirenzepine in nonulcer dyspepsia. 351 48

Dyspepsia or indigestion is one of the most common disorders that is managed by general practitioners and gastroenterologists. Non-ulcer dyspepsia can be defined as upper abdominal pain or nausea in patients in whom endoscopy reveals no evidence of peptic ulceration or gastric cancer. Non-ulcer dyspepsia is a heterogeneous disorder and can be the result of such diverse entities as the irritable bowel syndrome, duodenitis or gastro-oesophageal reflux, or may be idiopathic ("essential" dyspepsia). This review traces the development of modern thought on dyspepsia and non-ulcer dyspepsia, from the 16th century to the present.
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PMID:Dyspepsia and non-ulcer dyspepsia: an historical perspective. 354 May 42

The aim of this study was to determine if there were predictors of the symptomatic course of patients with chronic unexplained (essential) dyspepsia. After endoscopic assessment, 111 patients with essential dyspepsia were followed up by telephone interview every second month. Data were gathered, for a mean of 17 mo per patient, on the number of days of upper abdominal pain (the response variable) each month. In the 6-mo period before entry to the study the following predetermined predictor variables were collected: demographic factors (age, sex, social grade), number of pain days in the 6 mo before diagnosis, environmental factors (analgesics, nonsalicylate nonsteroidal antiinflammatory drugs, alcohol, smoking, coffee, tea), length of dyspepsia history, and past history of peptic ulcer. Prospectively for each month of follow-up, the following additional variables were recorded: environmental factors, treatment, and development of gastroesophageal reflux symptoms. It was found that patients with more pain before diagnosis were significantly more likely to have pain over the follow-up, and the taking of medications for dyspepsia and development of gastroesophageal reflux were associated with more days of pain over the follow-up (all p less than 0.001). Demographic and environmental factors, length of dyspepsia history, and a past history of ulcer were of no significant predictive value. There was a decrease in pain over the follow-up period (p = 0.002), but this effect was limited to the first two periods after endoscopic diagnosis.
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PMID:Prognosis of chronic unexplained dyspepsia. A prospective study of potential predictor variables in patients with endoscopically diagnosed nonulcer dyspepsia. 355 87


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