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)

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

With rare exception, peptic ulcers can now be classified as either Helicobacter pylori-related, induced by nonsteroidal anti-inflammatory drugs (NSAIDs), or related to Zollinger-Ellison syndrome. Helicobacter pylori-related ulcers can be treated by eradication of H pylori or by traditional therapies, including antisecretory drugs or sucralfate. Successful eradication of H pylori requires compliance with a multidrug regimen. Therefore, candidates should demonstrate substantial motivation. In general, the greater the degree of ulcer recurrence or resistance, the stronger the indication for H pylori eradication. Sucralfate is effective in healing H pylori-related duodenal ulcers, and H2 receptor antagonists heal H pylori-related duodenal and gastric ulcers. Omeprazole provides faster healing of H pylori-related ulcers, and is particularly useful in treating large gastric ulcers. Dyspepsia induced by NSAIDs and NSAID-related endoscopic erosions are managed by stopping NSAID use or reducing the dosage; administering NSAIDs with meals; and administering H2 receptor antagonists in full split-doses. NSAID-induced duodenal ulcers and small gastric ulcers can be healed with full split-doses of H2 receptor antagonists, even while the NSAID is continued. Large (> 5 mm) NSAID-induced gastric ulcers are most efficiently treated with omeprazole, particularly if the patient continues to take the NSAID.
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PMID:An etiologic approach to management of duodenal and gastric ulcers. 828 53

Sucralfate is a cytoprotective drug widely used in clinical practice to prevent or treat several gastrointestinal diseases such as gastro-esophageal reflux, gastritis, peptic ulcer, stress ulcer and dyspepsia. Sucralfate is a safe and well tolerated drug, as demonstrated by the quite complete lack of side effects and it is, for this reason, one of the most important therapeutic choices in the management of acid related diseases during pregnancy. Moreover, sucralfate has recently been shown to be useful in non-acid related gastrointestinal disease as well. In fact, sucralfate has also been administered topically in patients with radiation-induced mucosal procto-sigmoiditis or ulcerative colitis with surprising results. The drug is actually able to form a physical barrier between epithelium and damaging agents (-bile salts, drugs, refluxate...). Moreover, sucralfate increases the local levels of fibroblast growth factors and induces a rise in the mucosal concentration of prostaglandins which are considered important factors in mucosal healing. The aim of this paper is to describe the current and probably forthcoming uses of sucralfate in the field of gastrointestinal disorders. Moreover, we investigate the role of sucralfate as a reliable means to prevent the occurrence of reflux-like symptoms after Helicobacter pylori eradication and in the management of Helicobacter pylori negative patients affected by non-ulcer dyspepsia.
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PMID:Role of sucralfate in gastrointestinal diseases. 1101 6

Non-ulcer dyspepsia is common and is often confused with other diagnoses. It remains a condition identified by exclusion, and continues to be a challenge to manage. Currently, only a limited number of pharmacological options are available. Antacids are no more effective than placebo in treating nonulcer dyspepsia. H2-receptor antagonists appear to be superior to placebo in efficacy, but many of the studies suggesting this finding have had a suboptimal study design. Proton pump inhibitors have been shown to be superior to placebo, although questions remain as to whether the only subgroup that responds is comprised of patients with unrecognized gastroesophageal reflux disease. Studies have found that prokinetic agents are superior to placebo, but currently only a very limited number of agents within this class can be prescribed in the United States. Sparse data support the role of metoclopramide and its side effects limit its use even further. The eradication of Helicobacter pylori has a small but positive therapeutic benefit in non-ulcer dyspepsia, and can be considered in those confirmed to be infected. Sucralfate is unlikely to be effective, and misoprostol is ineffective. Bismuth alone is probably not efficacious. Tricyclic antidepressants may have a therapeutic role, but this is not firmly established and this class of medication should be reserved for resistant cases. Emerging therapies include drugs that relax the gastric fundus, such as buspirone or sumatriptan, and the new prokinetic tegaserod. Psychological therapies may play a role but studies of these therapies are limited. Therapy for non-ulcer dyspepsia remains challenging and is usually empiric; it will remain so until the mechanisms that induce symptoms of dyspepsia are better understood.
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PMID:Update on the role of drug therapy in non-ulcer dyspepsia. 1268 90

Venous leg ulcers are an important medical issue due to their high incidence in the elderly and the lack of a standard curative approach. Apart from surgical therapy, different medical treatments to effect ulcer wound repair and regeneration are currently being investigated. Sucralfate is a cytoprotective agent employed to prevent or treat several gastrointestinal diseases such as gastroesophageal reflux, gastritis, peptic ulcer, stress ulcer and dyspepsia. In this study we evaluated the efficacy, safety and tolerability of topical sucralfate (SUC-LIS 95) on the healing of chronic venous leg ulcers in 50 patients by a double-blind, placebo-controlled, randomized study. Our results indicated that the daily application of SUC-LIS 95 to non-infected post-phlebitis/vascular ulcers, for a median period of 42.0 days, led to complete healing in 95.6% of patients, against only 10.9% of cases with a matched placebo. A significant improvement was obtained in the SUC-LIS 95-treated patient group with regard to local tissue inflammation as well as pain and burning, and consequently, in ulcer size and the evolution of granulation tissue. Our findings were corroborated for selected patients by the morphological analysis of biopsies obtained before and after treatment. Using ultrastructural analysis we demonstrated that the topical use of SUC-LIS 95 was able to affect neoangiogenesis, increase wound contraction, promote re-epithelialization of the wound area and diminish the inflammatory reaction. Overall, our results indicated that patients with chronic venous ulcers show improvement after the use of topical sucralfate.
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PMID:Topical treatment of chronic venous ulcers with sucralfate: a placebo controlled randomized study. 1857 71