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)

Impaired gallbladder motility is common in gallstone patients and might be associated with other gastrointestinal defects. Twenty patients with small stones in an opacified gallbladder at oral cholecystography and 20 healthy subjects homogeneous for sex, age and body size were studied by ultrasonography to assess gallbladder and gastric emptying simultaneously in response to a standard liquid meal (120 kcal, 11 g fat, 200 mL). The same subjects underwent ambulatory 24-h gastro-oesophageal pH monitoring. Dyspeptic symptoms were specifically investigated using a questionnaire. Gallstone patients had a significantly larger fasting (P < 0.05) and residual (P < 0.005) gallbladder volume with slower (P < 0.05) and less complete (ANOVA, 0.001 < P < 0.05) gastric emptying than healthy control subjects. The speed of antral emptying was significantly correlated with the speed of gallbladder emptying (n = 40, r = +0.31, P < 0.05). Pathological gastro-oesophageal reflux was present in 75% and 15% of patients and control subjects respectively (P < 0.05). Overall, 95% of gallstone patients had abnormal pH profiles resulting from pathological gastro-oesophageal reflux and/or prolonged gastric alkalinization. The speed of post-prandial antral emptying was significantly correlated with the duration of the longest gastro-oesophageal reflux episode (r = +0.30, P < 0.03) and duodeno-gastric reflux episode (r = +0.80, P < 0.02). Best predictors for gastric alkalinization were the following indices of gallbladder function: large fasting volume (P = 0.03), large ejection volume (P = 0.009) and slower emptying (P = 0.032). Gallbladder and gastric motility were similar in patients with (n = 12) and without (n = 8) dyspeptic symptoms. Pathological gastro-oesophageal reflux was found in 83% of dyspeptic patients and in 25% of patients without dyspepsia (P < 0.01). When reflux was present, it was significantly less in asymptomatic than in dyspeptic patients [time at pH < 4, median (range): 6.4% (3.2-22.6%) vs. 47.8% (2.1-87%), P < 0.05]. This study shows that a subgroup of gallstone patients with small-mainly asymptomatic-stones have impaired gallbladder and gastric motility as well as abnormal gastro-oesophageal pH-profiles. These findings point to the existence of multiple functional defects of the upper gastrointestinal tract in gallstone disease.
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PMID:Impaired gallbladder and gastric motility and pathological gastro-oesophageal reflux in gallstone patients. 927 28

Anti-secretory drug use is common in patients with uninvestigated and functional dyspepsia, but the value of such agents has been controversial. Four large studies have evaluated the symptomatic outcome after a short course of acid inhibition in patients with uninvestigated dyspepsia presenting in primary care. All of these studies demonstrated a superior symptom response to proton pump inhibitor therapy compared with placebo and acid-alginates or H(2)-receptor antagonists. In patients with documented functional dyspepsia, 17 parallel group trials have evaluated an H(2)-receptor antagonist against placebo, with mixed results. A recent Cochrane review based on eight controlled trials concluded that there was a significant benefit of H(2)-blockers over placebo with a relative risk reduction of 30%, but as gastro-oesophageal reflux disease was not excluded, the conclusions are questionable. Six controlled studies have compared symptom relief after a short course of proton pump inhibitor therapy compared with placebo. Overall, there does appear to be a therapeutic gain with proton pump inhibitors over placebo, although how much of this is explained by undiagnosed gastro-oesophageal reflux disease remains unclear. There is conflicting evidence on the value of symptom subgrouping as a predictor of response to acid suppression. Overall, there is little convincing evidence that Helicobacter pylori infection influences the therapeutic outcome of acid-suppressant therapy. In conclusion, there appears to be a subgroup of patients with functional dyspepsia who will respond to acid suppression over and above placebo, but further work is required to characterize these responders.
Best Pract Res Clin Gastroenterol 2001 Jun
PMID:Current indications for acid suppressants in dyspepsia. 1140 34

Non-steroidal anti-inflammatory drugs (NSAIDs) are among the agents most frequently used against musculoskeletal and rheumatic disorders throughout the world. The gastroduodenal adverse effects include dyspepsia without endoscopically proven damage, asymptomatic endoscopic lesions of submucosal haemorrhage, erosions and ulcers, and-most important-ulcer complications. Established risk factors for NSAID-associated ulcer complications include patient-specific factors such as advanced age, female gender, a history of peptic ulcer, and drug-specific factors such as the use of non-selective NSAIDs (type, dose, duration, multiple use) and concomitant anticoagulant drugs or corticosteroids. Probable risk factors comprise Helicobacter pylori infection and heavy consumption of alcohol, whereas use of selective serotonin re-uptake inhibitors, smoking and a number of other factors have also been proposed to contribute. Knowledge of absolute risk estimates is important for clinical decision making. The aim of this chapter is to summarize the epidemiological data related to the broad spectrum of iatrogenic gastroduodenal mucosal injury.
Best Pract Res Clin Gastroenterol 2001 Oct
PMID:Epidemiology of NSAID-related gastroduodenal mucosal injury. 1156 36

Non-steroidal anti-inflammatory drugs (NSAIDs) are some of the most widely consumed medications. They are available by prescription and 'over the counter'. The same pharmacological properties which make them effective in the treatment of a variety of painful and/or arthritic conditions are responsible for a variety of adverse gastrointestinal effects, ranging from relatively mild dyspepsia to potentially lethal gastrointestinal (GI) bleeding and perforated ulcers. Yearly medical costs of GI complications associated with the use of NSAIDs are very high and likely to increase with the growth of the ageing US population. A review of the literature (1970-2000) on consequences and costs of NSAID-associated GI adverse effects, including iatrogenic cost factors of NSAIDs, was performed. The results were tabulated and compared. Knowledge and comparison of the consequences and costs of NSAID-associated GI adverse effects in various populations and across various health care systems are important for clinical care, pharmacoeconomics and policy arenas.
Best Pract Res Clin Gastroenterol 2001 Oct
PMID:Adverse gastrointestinal effects of NSAIDs: consequences and costs. 1156 38

The mechanisms by which aspirin(ASA) and non-steroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal symptoms are poorly understood. They probably arise from several causes, including direct and indirect mucosal injury, exacerbation of underlying peptic ulcer disease or non-ulcer dyspepsia, exacerbation of Helicobacter pylori gastritis, and possibly motility disorders. No single form of therapy has been generally successful. Because, in most cases, symptoms abate fairly rapidly with continued treatment, there is little evidence that benefit associated with any symptom-directed drug therapy is superior to placebo beyond 4 weeks. Exceptions may be the subsets of patients with pre-existing ulcer disease or heartburn, exacerbated by the NSAID therapy, who usually benefit from acid-suppressive drug treatment. Different NSAIDs vary in the frequency with which their use leads to gastrointestinal(GI) complications such as haemorrhage, perforation, obstruction, or the symptomatic ulcers from which about 40% of the complications arise. Most gastroduodenal ulcers heal over time, albeit more slowly, with conventional doses of any of the available anti-ulcer drugs. Maintenance therapy may be needed in many patients who continue NSAID therapy. Anti-ulcer drugs have not, thus far, been shown to be more effective than placebo in preventing ulcer complications or their recurrence. The use of COX-2-selective inhibitors appears, in outcome studies, to reduce gastrointestinal bleeding, including bleeding from ulcers, but it is not established that the ulcers protected were caused by NSAIDs, as distinct from ulcers exacerbating or recurring from antecedent peptic ulcer disease. To-date, perforation or obstruction have not been shown to be affected by selective COX-2 inhibitor drugs. If the major problem giving rise to severe NSAID complications is pre-existing peptic ulcer disease, it may yet emerge that the most effective approach will be the use of proton pump inhibitor drugs, for the duration of NSAID therapy, in a small subset of high-risk patients. Most other low-risk patients may not need any special care. Co-morbid conditions have a major impact on outcome of NSAID therapy. Morbidity or even death attributable solely to NSAIDs is probably small in normal patients, and requires little in the way of prophylaxis.
Best Pract Res Clin Gastroenterol 2001 Oct
PMID:Prevention and treatment of gastrointestinal symptoms and complications due to NSAIDs. 1156 39

Gastrointestinal diseases in pregnancy can be divided into diseases specific to pregnancy, for example, hyperemesis gravidarum, obstetric cholestasis, HELLP syndrome and acute fatty liver of pregnancy, and diseases incidental to pregnancy, for example, inflammatory bowel disease, dyspepsia, peptic ulcer disease and viral hepatitis. Disorders in the second category may present for the first time in pregnancy. This chapter considers the drug management of each of these conditions, with the exception of HELLP syndrome and acute fatty liver. The preferred drug treatment and the known complications associated with their use in pregnancy are also described. Where possible, studies relating to the safety of different therapeutic options are discussed.
Best Pract Res Clin Obstet Gynaecol 2001 Dec
PMID:Drugs in pregnancy. Gastrointestinal disease. 1180 May 34

The term 'functional gastrointestinal disorder (FGID)' is used to define several variable combinations of chronic or recurrent gastrointestinal (GI) symptoms that do not have an identified underlying pathophysiology. In the absence of any objective marker, the identification and classification of FGIDs are based on symptoms. The most widely accepted classification is based on the 'Rome diagnostic criteria,' which have classified 24 FGIDs into oesophageal, gastroduodenal, bowel, biliary, anorectal and abdominal pain subcategories. Classification into mutually exclusive categories has been useful for performing epidemiological studies in homogeneous populations, but has inevitably lead to disregarding subjects with overlapping FGIDs, or with a not sufficiently standardised symptom presentation. The epidemiology of FGID is still in its infancy, as indicated by the lack of epidemiological data for many FGIDs and the widely different incidence and prevalence rates reported for the most frequently occurring and investigated FGIDs: irritable bowel syndrome (IBS), dyspepsia, constipation and oesophageal disorders. Epidemiological studies and the definitions of the various FGIDs need to be further improved and standardised.
Best Pract Res Clin Gastroenterol 2004 Aug
PMID:Definition and epidemiology of functional gastrointestinal disorders. 1532 3

The term 'Functional diseases' implies symptoms arising from an organ without overt pathology. However this is more apparent than real since inflammation often leaves changes in nerves and mucosal function only apparent with specialised techniques. Acute onset functional dyspepsia accounts for around 1/5 of functional dyspepsia and is characterised by early satiety, nausea, vomiting and weight loss. Impaired postcibal fundal accommodation may underlie some of these symptoms. Post infectious gastroparesis is much rarer and is associated with markedly delayed gastric emptying and antral hypomotility. Approximately 1/10 of IBS cases describe a post infectious onset. Post infectious IBS is typically of the diarrhoea-predominant type. Post inflammatory functional diseases tend to be associated with less psychological abnormalities and have a better prognosis than other functional diseases. There are isolated anecdotal reports of symptom response to anti-inflammatory treatments but larger controlled trials are needed.
Best Pract Res Clin Gastroenterol 2004 Aug
PMID:Inflammation as a basis for functional GI disorders. 1532 5

The optimal diagnostic approach to the dyspeptic patient in primary care is still debated. Early endoscopy continues to be the diagnostic gold standard but competing non-invasive strategies challenge this. The most important approaches are empiric antisecretory treatment reserving endoscopy for unresponsive patients and patients with an early symptomatic relapse and helicobacter-based strategies reserving endoscopy for infected patients (test-and-scope) or for failures after eradication therapy (test-and-treat). Early endoscopy is recommended in patients with alarm features and should be considered in patients with new onset dyspepsia after age 50. In the remaining patients, early investigation can only be recommended in areas providing endoscopy at a low cost and with a short waiting list. The test-and-scope strategy may lead to a rise in the referral rates for endoscopy and cannot be recommended. The test-and-treat strategy is well documented in clinical trials as a safe and cost-effective approach. Helicobacter-based strategies are challenged by a decreasing prevalence of peptic ulcer disease and of the infection. In the near future, the empirical acid inhibition strategy will probably be cost-effective as gastro-oesophageal reflux becomes the predominant disorder in dyspeptic patients.
Best Pract Res Clin Gastroenterol 2004 Aug
PMID:Diagnostic approach to dyspepsia. 1532 7

As the incidence of both gastric cancer and peptic ulcer disease have declined, that of gastro-oesophageal reflux disease (GORD) and non-ulcer, or functional dyspepsia (FD) have reached virtually epidemic proportions. As we come to appreciate the expression of these disorders in the community, the real spectrum of each disease has become evident. FD and non-erosive reflux disease (NERD), the most prevalent manifestation of GORD, frequently overlap. Where then does GORD end and FD begin? Is it realistic, or even clinically relevant, to attempt a clear separation between these entities? These are more than issues of mere semantics; therapeutic options may be dictated by the classification of the patient as one or the other. Recent work indicates clearly that NERD is a heterogeneous disorder incorporating some patients who may well harbour subtle manifestations of oesophagitis and others who have entirely normal 24-hour pH studies. These differences may be crucial to the concept of NERD/FD overlap. While evidence in support of this concept is far from complete, it would appear that this overlap is most relevant to those NERD patients who do not exhibit abnormal esophageal acid exposure. These patients truly belong in the spectrum of functional gastrointestinal disorders rather than in GORD; attempts to shoe-horn these individuals into the spectrum of GORD will result in therapeutic disappointment and surgical disaster.
Best Pract Res Clin Gastroenterol 2004 Aug
PMID:Functional dyspepsia (FD) and non-erosive reflux disease (NERD): overlapping or discrete entities? 1532 8


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