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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dyspepsia can be defined as the presence of upper abdominal pain or discomfort; other symptoms referable to the proximal gastrointestinal tract, such as nausea, early satiety, and bloating, may also be present. Symptoms may or may not be meal related. To be termed chronic, dyspepsia should have been present for three months or longer. Over half the patients who present with chronic dyspepsia have no evidence of peptic ulceration, other focal lesions, or systemic disease and are diagnosed as having non-ulcer (or functional) dyspepsia. Non-ulcer dyspepsia is a heterogeneous syndrome. It has been proposed that this entity can be subdivided into a number of symptomatic clusters or groupings that suggest possible underlying pathogenetic mechanisms. These groupings include ulcer-like dyspepsia (typical symptoms of peptic ulcer are present), dysmotility (stasis)-like dyspepsia (symptoms include nausea, early satiety, bloating, and belching that suggest gastric stasis or small intestinal dysmotility), and reflux-like dyspepsia (heartburn or acid regurgitation accompanies upper abdominal pain or discomfort). The aetiology of non-ulcer dyspepsia is not established, although it is likely a multifactorial disorder. Motility abnormalities may be important in a subset of dyspepsia patients but probably do not explain the symptoms in the majority. Epidemiological studies have not convincingly demonstrated an association between Helicobacter pylori and non-ulcer dyspepsia. Other potential aetiological mechanisms, such as increased gastric acid secretion, psychological factors, life-event stress, and dietary factors, have not been established as causes of non-ulcer dyspepsia. Management of non-ulcer dyspepsia is difficult because its pathogenesis is poorly understood and is confounded because of a high placebo response rate. Until more data are available, it seems reasonable that treatment regimens target the clinical groupings described above. Antacids are no more effective than placebo in non-ulcer dyspepsia, although a subgroup of non-ulcer dyspepsia patients with reflux-like or ulcer-like symptoms may respond to H2-receptor antagonists. However, there is no significant benefit of these agents over placebo in many cases. Bismuth has been shown to be superior to placebo in patients with H. pylori in a number of studies, but these trials had several shortcomings and others have reported conflicting findings. Sucralfate was demonstrated in one study to be superior to placebo, but this finding was not confirmed by another group of investigators. Prokinetic drugs appear to be efficacious, and may be most useful in patients with dysmotility-like and reflux-like dyspepsia.
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PMID:Non-ulcer dyspepsia: myths and realities. 188 33

Nonulcer (functional) dyspepsia is a common heterogenous disease resulting in upper gastrointestinal tract symptoms. Evidence would support that a subset of this disease is caused by H. pylori-induced gastritis. Despite the conflicting evidence, most studies evaluating H. pylori clearance and eradication, particularly the long-term studies, have observed clinical improvement in most subjects. Hill's concepts to distinguish causal from noncausal associations of an agent to a specific disease include the strength of association, consistency, specificity, temporality, biologic gradient, plausibility, coherence, experimental evidence, and analogy. There is considerable criticism of these nine aspects of epidemiologic evidence to judge whether an association is causal. These epidemiologic criteria to support that an association is causal are inappropriate when applied to H. pylori and NUD. First, the disease definition, based on clinical criteria, is imprecise, with poorly defined end points and considerable individual variability in interpretation. Second, it would appear that the cause is multifactorial, and thus, evaluation of one etiologic agent is inappropriate. In view of the potential factors to cause NUD, a scheme of treatment with a subset of eradication of H. pylori if present is advocated (Fig. 1). It is suggested that, because of the conflicting data in this area, subjects be entered into clinical trials, with eradication of H. pylori evaluated and long-term follow-up of symptoms accurately monitored.
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PMID:The role of Helicobacter pylori in nonulcer dyspepsia. A debate--for. 844 63

Dyspepsia, defined as "pain or discomfort centered in the upper abdomen" is reported by one in four adults in Western societies. The most important causes are non-ulcer (functional) dyspepsia, peptic ulcer, gastroesophageal reflux, and, rarely, gastric cancer. Persons with heartburn alone are not considered to have dyspepsia. The division of dyspepsia into symptom-based subgroups (ulcer-like, dysmotility-like, reflux-like, and unspecified dyspepsia) has proven to be of doubtful value for the clinician, as it has a low predictive value for identifying the causes of dyspepsia. Upper endoscopy remains the "gold standard" test; ultrasound and blood tests have a low yield. The role of Helicobacter pylori in peptic ulcer disease is well known, but the clinical role of the infection in non-ulcer dyspepsia remains very controversial. In uninvestigated dyspeptic patients who are H. pylori infected based on a non-invasive test, empiric anti-H. pylori therapy is a reasonable and probably cost-effective option. In documented non-ulcer dyspepsia, prokinetics are superior to placebo while antisecretory therapy is of less certain efficacy.
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PMID:Dyspepsia: current understanding and management. 950 76

It is clear that non-ulcer (or functional) dyspepsia is a heterogeneous syndrome that includes a subset of patients with unrecognized gastroesophageal reflux. Patient heterogeneity combined with inadequate study methodology has led to enormous confusion in interpreting the relationship between Helicobacter pylori and non-ulcer dyspepsia. The possibility that H. pylori is associated with gastroesophageal reflux disease may explain, in part, the difficulty in establishing a link between non-ulcer dyspepsia and H. pylori infection. It is unclear whether the prevalence of H. pylori is increased in non-ulcer dyspepsia over and above the background population. H. pylori does not appear to be linked to heartburn or other specific upper gastrointestinal tract symptoms. The results of eradication trials in H. pylori-infected patients with non-ulcer dyspepsia have been equivocal and generally flawed. There is no doubt that H. pylori is not a sufficient cause of non-ulcer dyspepsia, because it is well documented in the literature that dyspepsia can occur in the absence of infection and infection can occur in the absence of symptoms. At this stage, there is insufficient evidence to support the hypothesis that H. pylori is etiologically linked to non-ulcer dyspepsia, but data from well designed large randomized controlled trials of eradication therapy, are awaited with great interest.
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PMID:Helicobacter pylori and dyspepsia. 1078 May 76

The role of psychological factors or symptom pattern for the response to treatment in patients with unexplained (functional) dyspepsia is unknown. We hypothesized that patients with reflux- and ulcer-like symptoms would be more likely to respond to acid-lowering therapy, while psychological disturbances would be associated with a less favorable response to treatment. Seventy-eight patients with a diagnosis of functional dyspepsia were recruited and 75 completed the trial. Patients were treated for 4 weeks in a double-blind, placebo-controlled crossover trial starting in random order with either active drug (ranitidine, 150 mg b.d.) or placebo. Every 7 days, medication was switched from active drug to placebo, or vice versa. At entry, patient characteristics were assessed utilizing a semistructured standardized interview and standardized questionnaires, and weekly intensity of symptoms was assessed utilizing a visual analogue scale. Patients with a greater reduction of the symptom score during active treatment and an overall reduction of the global symptom score by more than 50% at the end of the study period were categorized as responders. Logistic regression analysis was utilized to assess the influence of symptom type and presence of psychological disturbances on the treatment response. During treatment the symptom score decreased significantly, from 32.1 +/- 1.44 (SD) to 21.3 +/- 1.9 at the end of the trial (P < 0.001). Twenty of 75 were responders. High scores for somatization (OR, 3.6; 95% Cl, 1.2-11.4), anxiety (OR, 3.3; 95% Cl, 0.9-11.8), and reflux-like symptoms (OR, 5.3; 95% Cl, 1.7-16.7) were associated with response to treatment, while dysmotility-like symptoms were associated with an unfavorable response (OR, 0.3; 95% Cl, 0.1-0.9). Symptom pattern and psychological disturbances are independent predictors of treatment response. Patients with reflux-like symptoms and greater psychological disturbances are more likely to respond to an acid-lowering compound.
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PMID:Clinical presentation and personality factors are predictors of the response to treatment in patients with functional dyspepsia; a randomized, double-blind placebo-controlled crossover study. 1518 77

There is increasing concern in identifying the mechanisms underlying the intimate control of the intestinal barrier, as deregulation of its function is strongly associated with digestive (organic and functional) and a number of non-digestive (schizophrenia, diabetes, sepsis, among others) disorders. The intestinal barrier is a complex and effective defensive functional system that operates to limit luminal antigen access to the internal milieu while maintaining nutrient and electrolyte absorption. Intestinal permeability to substances is mainly determined by the physicochemical properties of the barrier, with the epithelium, mucosal immunity, and neural activity playing a major role. In functional gastrointestinal disorders (FGIDs), the absence of structural or biochemical abnormalities that explain chronic symptoms is probably close to its end, as recent research is providing evidence of structural gut alterations, at least in certain subsets, mainly in functional dyspepsia (FD) and irritable bowel syndrome (IBS). These alterations are associated with increased permeability, which seems to reflect mucosal inflammation and neural activation. The participation of each anatomical and functional component of barrier function in homeostasis and intestinal dysfunction is described, with a special focus on FGIDs.
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PMID:Abnormal Barrier Function in Gastrointestinal Disorders. 2799 92