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)

A retrospective study was performed on patients diagnosed of gastric cancer, younger than 40 years old, in the Hospital Arzobispo Loayza, from January 1991 to December 1998.We found 81 patients younger than 40 years old, with confirmed diagnosis of gastric adenocarcinoma; we reviewed the records of 59 patients.There were 44 (74.6%) women and 15 (25.4%) men. The mean age was 31.644 +- 5.437 years and the mean duration of symptoms was 13.189 months.The most common symptoms were: epigastric pain (89.8%), weight loss (86.4%), dyspepsia (64.4%),vomiting (64.4%) and nausea (62.7%). The most frequent physical findings were pallor (62.7%), epigastric tenderness (40.7%) and emaciation (37.3%). 57.8% of patients had hemoglobine levels of less than 11 gr/dl.The most frequent location of the neoplasm was the antrum (31.1%) followed by the body (27.3%).On endoscopy, we observed that the most frequent lesion was advanced gastric cancer, Borrmann III (48%), followed by Borrmann IV (27.3%). The predominant histologic type was undifferentiated adenocarcinoma.
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PMID:[GASTRIC CANCER IN PATIENTS YOUNGER THAN FORTY YEARS OLD.HOSPITAL LOAYZA EXPERIENCE BETWEEN 1991 - 1998] 1214 May 86

Since the initial report 20 years ago by Marshall and Warren of an unidentified curved bacillus located on the gastric epithelium of patients with chronic active gastritis, the discovery of Helicobacter pylori and its association with a number of gastrointestinal diseases has revolutionized the field of gastroenterology. Although the association of H. pylori infection with peptic ulcer disease, chronic gastritis, mucosa-associated lymphoid tissue lymphoma, and gastric adenocarcinoma has been well documented over the past two decades, other areas remain less clear, including the role of H. pylori in gastropathy associated with nonsteroidal anti-inflammatory drugs, gastroesophageal reflux disease, and both uninvestigated and nonulcer dyspepsia. Although these areas still remain somewhat controversial, recent reports further clarify the role of H. pylori in these conditions. A review of the recent literature regarding H. pylori-associated diseases is presented along with recommendations for diagnosis and treatment of H. pylori infection.
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PMID:Helicobacter pylori-Associated Diseases. 1244 Oct 33

Helicobacter pylori infection has been recognized as the most important pathogenetic principal of peptic ulcer disease, atrophic gastritis, gastric adenocarcinoma and MALT lymphoma. At the moment efforts are made to clarify it's role in functional dyspepsia, and gastro-esophageal reflux disease. The complex interactions between H. pylori infection and NSAIDs is another field of ongoing research. Diagnosis and eradication therapy are standardized. Established indications are peptic ulcer disease, low-grade gastric MALT lymphoma, early gastric cancer treated by mucosal resection and partial gastrectomy for gastric cancer. Atrophic gastritis, known to be a precancerous lesion, as well as first degree relatives of patients with gastric cancer is another widely accepted indication for eradication therapy. The recommended eradication regimens combine a proton pump inhibitor with clarithromycin and either amoxicillin or metronidazole--for a week.
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PMID:[Helicobacter pylori. Update 2002]. 1250 73

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

About 50% of adults in the developed and 80-90% in the developing countries are estimated to be infected by Helicobacter pylori. Being 68% nationally, this rate is higher in the northern continental parts of Croatia, which also have higher gastric cancer rates. Low socio-economic status, poor living conditions in childhood (the age when Helicobacter pylori is typically acquired), and exposure to the stomach content of an infected person are risk factors for Helicobacter pylori. Most of the infected are symptomless, with 10 to 20% subsequently developing the disease, and this mainly from peptic ulcer, asymptomatic chronic gastritis and chronic dyspepsia. Less than 5/10,000 become affected with adenocarcinoma, MALT lymphoma or primary non-Hodgkin's gastric lymphoma. Helicobacter pylori is under intensive study for possible association with other diseases. As transmission route of the infection is still unclear, any mechanism allowing the bacteria entry into a non-infected individual's stomach is probably a possibility. In addition to improved socio-economic status, eradication or vaccination may be contributors to the reduction in the number of the infected.
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PMID:[Epidemiology of Helicobacter pylori infection]. 1259 7

Dyspepsia is a common clinical problem. Its causes include peptic ulcer disease, gastroesophageal reflux, and functional (nonulcer) dyspepsia. A detailed clinical description of pain does not reliably differentiate the cause. Approximately 80% of gastroscopies are performed for the investigation of dyspepsia. "Gastritis" is diagnosed endoscopically in 59% of all stomachs, although in only 3% are the changes severe. Pathologic examination of unselected gastric biopsy specimens reveals that abnormalities are present in 62-73%, but there is only a weak correlation between endoscopic and histologic findings. For these reasons, it is recommended that endoscopic examination should always be accompanied by biopsy. Ideally, biopsies should be taken in a systematic fashion to include sampling of antrum and corpus. Recent evidence suggests that gastric infection by Helicobacter pylori initially presents as a superficial gastritis. Later it may become atrophic with development of intestinal metaplasia. The onset of atrophic changes may be related to the duration of infection, the strain of the infecting organism, associated dietary factors, or as-yet undefined host factors related to immunity. Persistent superficial gastritis predisposes to duodenal ulcer and gastric mucosa-associated lymphoid tissue lymphoma. Atrophic gastritis predisposes to gastric ulcer and adenocarcinoma. Evidence is accumulating that in some patients, pernicious anemia may be an end result of H. pylori-induced atrophic gastritis. Reactive gastropathy is a relatively common finding in gastric biopsies; in most instances it is associated with either reflux of duodenal contents or therapy with nonsteroidal anti-inflammatory drugs. Lymphocytic gastritis, eosinophilic gastritis, and the gastritis associated with Crohn's disease are distinct morphologic entities. Lymphocytic gastritis and eosinophilic gastritis have a variety of clinical associations. Carditis is a controversial topic: currently opinions are divided as to whether it is the result of gastroesophageal reflux or a proximal extension of H. pylori infection from the remainder of the stomach.
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PMID:Gastritis and carditis. 1269 98

Delayed gastrojejunocolic fistulas in patients previously operated for gastric cancer are often caused by local recurrence of the tumour. We present two cases of delayed gastrojejunocolic fistula without neoplastic recurrence. Both patients had been operated for adenocarcinoma several months earlier; a gastric Billroth 2 resection was performed in both cases. The first patient arrived at our hospital for chest pain, dyspepsia, weight loss, vomiting and diarrhoea. Blood tests showed low levels of vitamin B, proteins and cholesterol. The second patient was admitted for lipothymia, hyporexia, proctorrhagia, diarrhoea and weight loss. Blood tests showed macrocytic anaemia and hypoproteinaemia. The radiological and endoscopic examinations revealed a gastrojejunocolic fistula in both cases. Since gastrojejunocolic fistulas are rarely resolved by conservative treatment, we performed a gastric resection with a histological examination to exclude tumour recurrence in both patients. The aetiopathogenesis of gastrojejunocolic fistulas is unknown. It is conceivable that some agents (such as bile) may damage a mucosa that has been weakened by nutritional deficiency and/or postsurgical microvascular damage. Early and delayed gastrojejunocolic fistulas present the same clinical manifestations, namely, diarrhoea, abdominal pain, weight loss and hypoproteinaemia.
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PMID:[Benign gastrojejunocolic fistula as a complication of gastric resection for adenocarcinoma]. 1472 37

Population Helicobacter pylori screening and treatment has the potential to dramatically reduce global gastric cancer mortality. There is overwhelming evidence that the infection is a major cause of distal gastric adenocarcinoma. There is also randomized controlled trial evidence that H. pylori eradication reverses or ameliorates histological changes in the gastric mucosa that are important in carcinogenesis. Preliminary randomized controlled trial data suggest that screening and treatment may reduce the risk of gastric cancer although the number of cancer cases was small. Population H. pylori screening and treatment will also reduce mortality from peptic ulcer complications and reduce the burden of dyspepsia in the community. The reduction in health service dyspepsia costs means that this could be the first programme to pay for itself. From a scientific perspective, we still have insufficient evidence to conclude the benefits of population H. pylori screening are greater than the possible harms and we need more randomized controlled trial data. From a public health perspective however, sometimes screening programmes are developed with imperfect information. The medical community should be consistent and if we are instituting other population screening programmes without randomized controlled trial evidence then H. pylori testing and treatment should also be considered.
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PMID:Helicobacter pylori public health implications. 1534 8

Helicobacter pylori is the most frequent infection of the stomach worldwide. Some of the people infected with H. pylori develop symptoms of dyspepsia that correlate with pathologic evidence of gastritis and peptic ulcers. In addition, H. pylori has been associated with preneoplastic lesions and with two neoplasias: intestinal-type gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma. Rarely, gastric pathology can also be caused by other infectious agents, including fungi, other bacteria, parasites, and viruses. This review describes H. pylori-associated pathology and pathologies related to other infectious agents.
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PMID:The spectrum of gastric disease associated with Helicobacter pylori and other infectious gastritides. 1552 73

Barrett's esophagus (BE) is an acquired disease of the esophagus, in which esophageal squamous epithelium is changed by injury from reflux to metaplastic intestinal type columnar epithelium. BE is the premalignant lesion of adenocarcinoma of the esophagus. It is widely accepted that the long-standing reflux of gastric acid is a catalyst for the development of BE. More recent work points toward the reflux of duodenal secretions as a catalyst in this disease process as well. Moreover, the time course for the development of BE once a patient has reflux is not known. Our case challenges the currently defined time course of "long-standing" reflux symptoms for the development of BE, and supports the role of duodenal secretions alone in the development of BE. A 68-yr-old Caucasian man was admitted with weight loss, left upper quadrant pain, a hemoglobin of 6.8, and heme-positive stool. Esophagogastroduodenoscopy (EGD) revealed normal esophageal mucosa and a mass in the gastric cardia. Biopsies showed moderately differentiated gastric adenocarcinoma. The patient underwent a total gastrectomy, distal esophagectomy, and a Roux-en-Y esophagojejunostomy. Pathology confirmed gastric adenocarcinoma (T1 N0 Mx). The distal esophagus and gastroesophageal junction in the resected specimen were grossly and microscopically normal. Six months later an EGD, prompted by new complaints of regurgitation and dyspepsia, revealed distal esophageal mucosa lined by red-colored columnar tissue. Biopsies showed intestinal type epithelium. Thus, our case report's contribution to the current literature is twofold. It provides evidence of development of BE solely from duodenal reflux, and it documents a relatively short time span to development of BE.
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PMID:Development of Barrett's esophagus six months after total gastrectomy. 1555 10


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