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

Gastric dysplasia is generally accepted as a precancerous lesion. Ninety-nine patients with an initial diagnosis of gastric dysplasia, based on examination of endoscopic biopsies taken because of symptoms of dyspepsia, were followed to define the magnitude of the neoplastic risk. The degree of dysplasia in the initial biopsy was mild in 73 cases, moderate in 16, and severe in 10. Mild dysplasia was no longer detected in 74% of patients, persisted in 19%, and progressed in 7% (in four cases, to carcinoma). Moderate dysplasia regressed to mild dysplasia in 31% of cases, it was no longer found in 56%, and progressed to cancer in 13%. Our data show that both lesions can progress slowly, although in most instances they remain stable or regress. Thus, annual endoscopic and histologic controls appear to be advisable. Severe dysplasia was no longer detected in 20% of cases, regressed to moderate in 10%, persisted in 10%, and progressed to cancer in 60%; in half of these patients, carcinoma was detected within 3 months. Thus, severe dysplasia indicates a high risk of cancer, often a synchronous one, and it requires gastrectomy when it persists in repeated biopsies.
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PMID:Gastric dysplasia. A follow-up study. 821 13

A 52-year-old male presented with urinary symptoms of frequency and hesitation. X-rays, ultrasound, and computerized tomography investigations were performed that indicated the diagnosis and position of an enteric duplication cyst. Elective surgery was performed to completely remove the duplication cyst. Histological examination showed that the cyst was lined by stratified squamous, ciliated, and gastric-type epithelium, with a muscularis mucosae and a muscularis Propria. No malignancy or dysplasia was seen. Duplications of the alimentary tract are uncommon congenital abnormalities. They may be multiple and arise at any level from the mouth to the anus. Usually observed early in life, a minority may remain unsuspected until adulthood. The clinical presentations may be vague and diverse depending on their location. These include pain, distention, dysphagia, dyspepsia, and complications involve bleeding, perforation, malignancy, and obstruction of the alimentary tract and vessels. Plain x-rays are of limited use in the diagnosis of duplications but ultrasound findings may be diagnostic, with computerized tomography useful in delineating surrounding structures. Once the diagnosis is established, surgical correction is the treatment of choice, preferably with complete removal.
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PMID:An unusual presentation of intestinal duplication with a literature review. 861 48

Gastritis is a histopathologic diagnosis, which correlates poorly with both clinical symptoms of non-ulcer dyspepsia and endoscopic abnormalities. Worldwide, most cases of gastritis are due to Helicobacter pylori and are characterized by a diffuse superficial antral gastritis. Chronic inflammatory cells and lymphoid follicles are present in the lamina propria. Neutrophils are present in the surface and pit-lining epithelium. In North America and Western Europe, reactive gastropathy due to duodenal reflux or non-steroidal anti-inflammatory agents is also common. In this condition, there is no increase in inflammatory cells, but the pit-lining cells become hyperplastic, and the pits have a corkscrew appearance. Most examples of multifocal atrophic gastritis are the result of long standing Helicobacter gastritis, although there may be other causes as well. It is characterized by loss of glands in both pyloric and corpus mucosae with intestinal metaplasia of the surface epithelium. A subtype of intestinal metaplasia, in which sulphomucin (large bowel mucin) is present, has been associated with the development of distal gastric cancer. However, this association is relatively weak and is not considered useful for screening purposes. Gastric dysplasia may develop in areas of the stomach affected by intestinal metaplasia. High-grade dysplasia is a significant finding, with up to 60 percent of cases having coincident carcinoma and a further 25 percent of cases likely to develop an invasive malignancy within fifteen months.
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PMID:The morphology of gastritis. 904 89

There is a paucity of data on the long-term behavior of dyspepsia, endoscopic findings, and gastroduodenal histology in patients with or without Helicobacter pylori colonization. We evaluated these parameters during a period of 7 to 19 years (average, 12.3 years) by baseline and follow-up studies. In 36 patients studied, the pattern of gastroduodenal dyspepsia and esophagogastroduodenoscopy findings remained essentially unchanged in 67% and 56% respectively. Dyspepsia patterns did not correlate significantly with either endoscopic or histologic findings, including the severity or location of gastritis in the fundus or antrum, or the presence or absence of H. pylori gastritis. Of 36 patients with adequate biopsies of the fundus and antrum, H. pylori colonization with gastritis was present in 73% but not in 27%. Progression to various degrees of atrophic gastritis was noted in 100% with, and in none without, H. pylori gastritis. In the fundus, atrophy progressed from 14% to 56%, but intestinal metaplasia did not change. In the antrum, atrophy increased from 22% to 64% and intestinal metaplasia increased from 17% to 36%. No patient demonstrated dysplasia, but severe atrophy was seen in the fundus (6%) and antrum (11%). Only two patients (5%) had severe loss of glandular elements and very low pepsinogen I, and thus can be considered to have developed advanced gastric atrophy.
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PMID:Long-term symptom patterns, endoscopic findings, and gastric histology in Helicobacter pylori-infected and -uninfected patients. 956 20

Recognition of Helicobacter pylori (Hp) as the major cause of peptic ulcer disease has profoundly changed treatment and prognosis of this disease. The diagnostic tests are invasive (i.e. via the endoscopy) or non-invasive. The invasive tests are: urease test, histology, culture and PCR. Non invasive tests are: breath test, serology and Hp-antigens in faeces. The performance of the tests are almost similar. Sensitivities and specificities usually are > 90%, however the sensitivities and specificities of serological tests may be lower. Choice of diagnostic test depends on the clinical situation, sensitivity and specificity of test and the prevalence of Hp. Patients who should be examined for Hp: 1. The peptic ulcer patient who has used ASA/NSAID (urease test). 2. MALT-lymphoma, (histology). 3: The young (< 45 years) dyspeptic patient with no alarm symptoms and not taking NSAID/ASA (breath test). 4. Recurrence of upper dyspepsia after former eradication of Hp in peptic ulcer patients (if malignancy is not suspected breath test is first choice). 5. Verification of Hp eradication is necessary only in patients with MALT-lymphoma (histology) or patients with complicated peptic ulcer. Breath test will be the first choice in patients with complicated peptic ulcer when endoscopy is not performed. When endoscopy is performed, the urease test is the first choice. Diagnosis of Hp status not indicated: 1. There is no documentation that Hp eradication is of benefit in patients with non organic dyspepsia. Therefore, there is no indication for diagnosis of Hp. 2. Although there is some association between Hp positivity and chronic active gastritis and carcinoma of the stomach, there is at present no indication for diagnosis of Hp, as treatment of the infection has not proved effective in reversing atrophy or dysplasia. 3. The relationship between Hp and ASA/NSAIDs in peptic ulcer disease is far from clear. There is no indication for diagnosis and treatment of the infection prior to treatment with these medications. 4. For patients treated with longterm proton pump inhibitors there is no indication for diagnosis and treatment.
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PMID:[Diagnosis of Helicobacter pylori infections--how, when and in whom?]. 1101 47

A bacterium is associated with a specific gastritis. Neutrophils infiltrate the necks of the glands, just deep to the infected foveolae. This infiltration rarely, if ever, occurs without H. pylori infection. Foveolar epithelial damage is common, with loss of cell structure. Electron microscopy suggests that the bacteria cause this damage as they attach to the superficial cell membrane. These features, defined by Whitehead et al as active changes, appear specific for H. pylori infection. The neutrophils and specific epithelial changes disappear within days of starting treatment for Helicobacter. They rapidly recur if the treatment is unsuccessful. Without treatment, the changes remain for decades and are severe in 10% to 20% of cases. Other changes occur in the mucosa. Reduced mucus secretion occurs in damaged or proliferating epithelium. This reduced secretion occurs near healing ulcers or with other types of inflammation but is often severe when Helicobacter is present. It returns to normal within weeks of treating the infection. The bacteria adhering to the cell membrane may cause this change directly. Lymphoid infiltration occurs with any type of chronic inflammation or immune reaction. The infiltration is not specific for Helicobacter, and it reduces slowly in months or years after eradication of H. pylori. Peptic ulceration, particularly duodenal ulceration, although not specific, is particularly common with H. pylori infection. The long-term inflammation probably causes other gastric pathology. Atrophy is common. Epithelial metaplasia occurs in about 20% of patients, usually mild. Other features, such as scarring, epithelial dysplasia, and in situ malignant change, are less common. They show little improvement after eradicating H. pylori. The part played by the bacteria in their cause remains uncertain. Pathologists see a long-standing chronic gastritis clearly related to a bacterium. The inflammation often is severe and commonly damages the mucosa, with ulceration, atrophy, metaplasia, and occasional premalignant changes. Physicians would treat inflammation of this degree in most other parts of the body. This disease is usually symptomless. There is some controversy, but eradicating Helicobacter often fails to improve nonulcer dyspepsia. This failure results in a continuing argument over whether or not to treat the infection. Meanwhile the pathology continues. A temporary solution to the problem is suggested: Patients infected with Helicobacter can give informed consent. Patients can be told about the infection, the pathology, the poor relationship to symptoms, and side effects of therapy, and they can decide.
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PMID:Gastric pathology associated with Helicobacter pylori. 1103 82

The histopathology of the antral mucosa of patients with acid peptic disease was studied in relation to Helicobacter pylori infection. Three hundred and fifty-five patients underwent gastroscopy and biopsy on 443 occasions. During each gastroscopy, two antral samples were taken for Rapid Urease Test (RUT) for H. pylori and two antral samples for histopathology. Haematoxylin and Eosin and modified Giemsa stained sections were studied. Histopathological changes in the antrum and the density of H. pylori were graded according to the Sydney System criteria. There was a significant association between the RUT and histology results for detection of H. pylori. The overall prevalence of H. pylori was 61.4% with a maximum incidence in the third and fourth decades of life, and an equal sex distribution. H. pylori colonisation was seen in 90.7% of patients with duodenal ulcer, 66.7% with gastric ulcer and 44.3% with non-ulcer dyspepsia. H. pylori colonisation was associated with more severe antral chronic active gastritis, lymphoid follicles, intestinal metaplasia and dysplasia. Elimination of H. pylori by treatment with anti-H. pylori regimens resulted in regression of the changes.
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PMID:Antral histopathological changes in acid peptic disease associated with Helicobacter pylori. 1112 73

Reliable data regarding the efficacy of different schemes of triple therapy for the eradication of Helicobacter pylori in our country, are not available. Patients with Helicobacter pylori infection and non-ulcer dyspepsia or active peptic ulcer disease were randomized in three different groups for therapy with, omeprazole 20 mg, clarithromycin 500 mg and amoxicillin 1000 mg, twice daily for one week (OCA 1, 40 patients) and the same treatment but for two weeks in a second group (OCA 2, 40 patients). The third group received omeprazole 20 mg, clarithromycin 500 mg and metronidazole 500 mg twice daily during one week (OCM, 40 patients). The primary efficacy end point was the eradication of Helicobacter pylori as confirmed by negative urea breath test, 4 weeks after the completion of treatment. Of 120 patients enrolled in the study, 113 met the entry criteria. Of them, 103 completed the treatment. When analyzed by intention to treat, after 4 weeks of finishing the treatment, Helicobacter pylori was eradicated in 92.3% of patients in OCA 1, 89.7% in OCA 2, and 82.8% in OCM. There was no significant difference between the three groups, regarding the eradication efficacy. Side effects were observed more frequently in OCA 2 and OCM groups. Primary resistance to amoxicillin and clarithromycin was not demonstrated, while 20% of cultured strains were resistant to metronidazole. In patients with peptic ulcer disease or non-ulcer dysplasia, triple therapy with omeprazole and two antibiotics is highly effective in the eradication of Helicobacter pylori. One week of OCA therapy is as effective as two weeks of OCA or one week of OCM, with less side effects.
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PMID:[Diagnosis and treatment of Helicobacter pylori infection. Its relationship with gastrointestinal ulcer and antimicrobial resistance]. 1172 21

The histopathological changes due to chronic Helicobacter pylori infection are well characterized. Nevertheless, the clinical and pathological outcomes resulting from the cure of this infection remain incompletely described. In particular, the influence of eradication of H. pylori on nonulcer dyspepsia, the long-term effects of H. pylori eradication on gastric atrophy and intestinal metaplasia, and the role of H. pylori eradication in the prevention of gastric cancer are still unclear. We reviewed 38 studies reported between 1993 and 1999 on the outcome of various disorders related to H. pylori infection after successful eradication. There is general agreement concerning the regression of chronic gastritis, lymphoid follicles, and limited-stage low-grade MALT lymphomas of the gastric mucosa after eradication of H. pylori infection. Conversely, there are still major questions on whether H. pylori eradication improves the outcome of premalignant lesions, such as atrophy, intestinal metaplasia, and dysplasia. Finally, some extragastric idiopathic diseases seem to improve in consequence of the eradication of the infection, although there are still no definitive data to support this.
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PMID:Gastric mucosa: long-term outcome after cure of Helicobacter pylori infection. 1210 60

Gastroesophageal reflux disease (GERD) is one of the most prevalent gastrointestinal disorders. The key feature of GERD is reflux of gastric contents into the esophagus. Medical treatment with proton-pump inhibitors (PPIs) is well established and is considered the standard treatment. Given the high prevalence of the condition and the excellent response to medical therapy, antireflux surgery is an option for patients with volume reflux that is not properly controlled by medical therapy. Adenocarcinoma is a rare but life-threatening complication of GERD. The only known precursor lesion for esophageal adenocarcinoma is Barrett's esophagus. In recent years, a clearer understanding of the development of Barrett's and of its progression toward invasive cancer has developed. Genetic factors almost certainly determine the individual risk. The length of the Barrett's esophagus segment and the size of a hiatal hernia are associated with the risk of developing high-grade dysplasia and esophageal adenocarcinoma.With regard to the clinical management of GERD patients with Barrett's, endoscopic surveillance at 3-year intervals is now considered appropriate in the absence of dysplasia. In patients with high-grade dyspepsia, the situation is more difficult. While a considerable proportion of these patients may already have invasive cancers, there is also the possibility that there is only focal dysplasia. For this reason, it is justifiable to carry out curative endoscopic resection. Mucosal ablation procedures may also be appropriate, but these still need to be properly investigated in clinical trials.
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PMID:Reflux disease and Barrett's esophagus. 1256 Oct 4


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