Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 38 year old female patient with a pancreatic mucinous cystadenocarcinoma. She presented at the onset with a peritoneal rupture that required emergency surgery. Five months later, the patient was subjected to a segmental pancreatectomy and splenectomy. One year later, the patient had a serious gastric bleeding secondary to a gastric ulcer. Due to a persistent increase in her CA 19-9 levels, a Positron Emission Tomography (PET) functional imaging with fluorine 18-deoxyglucose (F18FDG) was done. It showed an intense focal hypermetabolism in the gastric wall reported as a secondary tumour location. The patient was subjected to a total gastrectomy and Roux en Y anastomosis, with a good outcome. The pathological study confirmed the presence of a metastasis of an adenocarcinoma in the gastric wall. The relative value of CA 19-9 markers and FDG PET in pancreatic and gastric carcinomas is discussed.
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PMID:[Fluorodeoxiglucose F18 positron emission tomography imaging (F18FDG) for the assessment of rising levels of serum CA 19-9 in pancreatic mucinous cystadenocarcinoma. Report of one case]. 1537 72

Helicobacter pylori is prevalent worldwide, especially in developing countries, and is associated with several upper gastrointestinal diseases. Since it is present in over 90% of duodenal ulcer patients, empirical eradication in these patients is often recommended. In gastric ulcer patients, eradication is indicated only after the infection is confirmed. Testing for H. pylori infection should be carried out in patients with peptic ulcer hemorrhage, because eradication has been shown to reduce recurrent bleeding. Both H. pylori and NSAIDs are risk factors for peptic ulceration, and it is reasonable to screen for and eradicate H. pylori infection in peptic ulcer patients taking NSAIDs. H. pylori is a group I carcinogen for gastric adenocarcinoma, and should be eradicated for the primary prevention of this cancer. Eradication of this organism has been reported to result in regression of early low-grade mucosa-associated lymphoid tissue lymphoma. The role of H. pylori infection in the causation of gastroesophageal reflux and non-ulcer dyspepsia is not clearly established. Several tests are available for the diagnosis of H. pylori infection. These include invasive tests, such as histology, culture and urease test, and non-invasive tests, such as serology, urea breath test and stool antigen test. The choice of test is determined by clinical indication, pretest probability of infection, as well as the availability, cost, sensitivity and specificity of the test. H. pylori eradication therapy using proton pump inhibitor with clarithromycin and amoxycillin for 7 days has a success rate of 85-90%. Improved living standard and sanitation are vital in the control of H. pylori transmission and infection. Future development may include the use of vaccines against H. pylori, and therapies specifically targeting cagA strains of the bacteria.
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PMID:Eradication of Helicobacter pylori in clinical situations. 1559 83

Helicobacter pylori (H. pylori) colonizes the gastric mucosa of a half of the mankind. Duodenal ulcer is found in 15-25%, gastric ulcer in 13%, while gastric adenocarcinoma develops in 1% of all infected individuals. Pathogenesis of H. pylori infection is related to the virulence factors of the bacterium, environmental (dietary habits, hygiene, stress) and host factors (age, sex, blood type). Colonization of the gastric mucosa is related to the motility of the bacterium, presence of lipopolysaccharide (LPS) and various bacterial enzymes. Gastric mucosal injury is the result of H. pylori LPS, vacuolization cytotoxin (vacA), cytotoxin associated protein (cagA), heat shock proteins and factors responsible for neutrophil chemotaxis and activity. H. pylori colonizes the gastric mucosa and zones of ectopic gastric epithelium. H. pylori infection is transmitted via oral-oral, fecal-oral and iatrogenic way (during endoscopy). Higher prevalence of the infection is associated with lower socioeconomic level, lack of drinking water, and living in a community. Acute H. pylori gastritis is superficial pangastritis progressing into the chronic phase after 7-10 days. Gastric mucosal atrophy and intestinal metaplasia can develop during the course of H. pylori infection. Clearly defined factors that influence the outcome of H. pylori infection include bacterial strain, distribution of gastritis, acid secretion and gastric mucosal atrophy.
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PMID:[Pathogenesis of Helicobacter pylori infection--bacterium and host relationship]. 1579 58

Helicobacter pylori colonizes the mucus layer of the human stomach and duodenum, causes chronic gastritis, gastric ulcer, and is a risk factor for gastric adenocarcinoma. There is a 20% failure rate in antibiotic therapy, which is increasingly due to antibiotic resistance and necessitates the search for alternative antimicrobial methods. We have discovered that H. pylori when cultured in liquid medium, accumulates significant quantities of coproporphyrin and protoporphyrin IX, both in the cells and secreted into the medium. These photoactive porphyrins lead to cell death (up to 5 logs) by photodynamic action upon illumination with low doses of visible light, with blue/violet light being most efficient. The degree of killing increases with the age of the culture and is greater than that found with Propionibacterium acnes (another bacterium known to be photosensitive due to porphyrin accumulation). Both virulent and drug-resistant strains are killed. The data suggest that phototherapy might be used to treat H. pylori infection in the human stomach.
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PMID:Helicobacter pylori accumulates photoactive porphyrins and is killed by visible light. 1598 Mar 55

In the recent years, the prevalence of adenocarcinomas of the esophagus has substantially increased. At present its prevalence in the USA is comparable to that of squamous carcinoma (5/100,000 a year). In 80-90% of cases esophageal adenocarcinoma is located in 1/3 of the lower esophagus and is mainly derived from Barrett's esophagus (BE). The role of Helicobacter pylori (Hp) infection in the pathogenesis of gastritis and gastric ulcer disease has been well known and documented. However, its role in the pathogenesis of esophageal reflux disease, its complications, particularly regarding the risk of Barrett's esophagus and adenocarcinoma is still being studied. The relation between Hp infection and BE has been discussed for many years. The importance of the problem is warranted by the wide prevalence of both Hp infection and reflux disease in the population. The above mentioned findings confirm the protective effects of Hp infection in BE. Despite numerous studies some doubts concerning the relations between Hp infection and BE are still to be explained.
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PMID:Helicobacter pylori infection and the risk of adenocarcinoma of the esophagus. 1614 24

Helicobacter pylori is a unique organism which is pathogenic for stomach-duodenum (chronic gastritis, duodenal ulcer, gastric ulcer, gastric malignancy, mucosa-associated lymphoid tissue (MALT) lymphoma) and protective for oesophagus (Barrett's oesophagus, oesophageal adenocarcinoma) at the same time in an individual. For prevention of diseases, the necessity of presence of some bacteria throughout the gastrointestinal lumen needs to be emphasized. The concept--only good Helicobacter pylori is a dead Helicobacter pylori, is dangerous and humans should learn to live in harmony with a few bacteria throughout the gastrointestinal tract.
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PMID:Is the presence or absence of Helicobacter pylori in gastric mucosa a greater risk? 1664 44

Helicobacter pylori is one of the most common bacterial infections worldwide. It is associated with chronic gastritis, peptic ulcer disease and constitutes a major risk factor for gastric adenocarcinoma and lymphoma. The aim of this study was to evaluate the specific serologic immunoglobulin G (IgG) response to whole cells proteins, CagA and urease antigens of Helicobacter pylori in a Venezuelan population. We evaluated 66 patients from the Hospital Universitario de Caracas, attending in the gastroscopy service. H. pylori infection was detected by culture and rapid urease test. IgG antibodies against, CagA and ureases were tested by enzyme-linked immunosorbent assay method using highly purified recombinant antigens. We demonstrated the presence of H. pylori in 48/66 (72.7%), by culture and rapid urease test. We found a seroprevalence of 45 (68%) to whole cells, 34/66 (51%) to CagA and 18/66 (27%) to urease. The positive rates of CagA antibodies in patients with gastric ulcer, gastric cancer and chronic gastritis were 87.8%, 77.7% y 40.8% respectively. The serum antibodies anti-CagA were similar between peptic ulcer disease and gastric cancer patients.
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PMID:[Importance of IgG anti-CagA antibodies of Helicobacter pylori in Venezuelan patients with gastric diseases]. 1635 43

In patients with celiac axis occlusion, performance of pancreaticoduodenectomy involves sacrifice of the gastroduodenal artery which results in a risk of hepato-pancreato-biliary and other organic ischemia. Celiac axis occlusion does not recently seem an uncommon finding in cases of pancreaticoduodenectomy but diagnosis of celiac axis occlusion may be difficult in patients with former abdominal surgery. The present case report shows a patient with pancreatic head adenocarcinoma, in whom a preoperative diagnosis of celiac axis occlusion was not proved because of displacement of the celiomesenteric arterial branches based on former distal gastrectomy with Kocher's maneuver. A 56-year-old man with malignant obstruction of the lower bile duct was referred to our hospital for undergoing pancreaticoduodenectomy. In his past history, the patient had undergone distal gastrectomy reconstructed with Billroth I method due to gastric ulcer. In preoperative abdominal angiography, the celiac axis was not detected at the normal position and was incorrectly recognized to be anomalously originated from the superior mesenteric artery. During surgery, hepatic arterial flow was markedly diminished by clamping of the gastroduodenal artery. Celiac axis occlusion was then proved and the thick and tight median arcuate ligament was detected. Hepatic arterial blood flow was recovered by a complete division of the median arcuate ligament. Postoperative course of the patient was uneventful. In cases of pancreaticoduodenectomy, careful preoperative angiographic diagnosis is needed for patients with celiac axis occlusion who have undergone former gastric surgery because the celio-mesenteric arterial branches have been displaced by Kocher's maneuver. The present report also demonstrates another patient with a typical celiac axis stenosis.
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PMID:Celiac axis occlusion of a patient undergoing pancreaticoduodenectomy after distal gastrectomy. 1752 29

Apoptosis has an essential function in maintaining the integrity of the gastrointestinal mucosa. Its deregulation is associated with the occurrence of lesions such as in atrophic gastritis, peptic ulcers, intestinal metaplasia, and stomach tumorigenesis. Thus, the aim of the present study was to investigate the frequency of apoptotic cells (apoptotic index, AI) by using two different immunohistochemical techniques, TUNEL and anti-activated caspase-3 antibody (CPP32), in gastric dyspepsia [chronic gastritis (CG, N = 34), chronic atrophic gastritis (CAG, N = 11), gastric ulcer (GU, N = 17), and intestinal metaplasia (IM, N = 15)], normal gastric mucosae (NM, N = 8), and gastric adenocarcinoma (GC, N = 12). The relationship was investigated between the AI and Helicobacter pylori infection, diagnosed by PCR, overexpression of p53 protein determined by immunohistochemistry, and aneuploidy by fluorescence in situ hybridization, as performed by our laboratory in previous studies. No significant differences were observed in AI between the different groups, whether by the TUNEL technique (F = 1.60; p = 0.1670) or by CPP32 antibody (F = 1.70; p = 0.1420). Nonetheless, CAG and CG groups had AI statistically higher than those of normal mucosae. These two groups (CAG and CG) also showed a higher frequency of apoptosis-positive cases (TUNEL+ or CPP32+). Generally, there was no correlation between the AI detected by the TUNEL and CPP32 techniques in the groups studied, except in the GC group (r = 0.70). Moreover, there was no significant association between apoptosis and H. pylori infection, overexpression of p53 protein and aneuploidy, but the H. pylori-positive cases only of GU (p = 0.0233) and IM (p = 0.0253) groups displayed a statistically higher AI compared to H. pylori-negative NM, when the CPP32 antibody technique was used. Thus, CG and CAG have increased apoptosis, which may occur independent of an association with H. pylori infection, aneuploidy and overexpression of p53 protein.
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PMID:Apoptosis in different gastric lesions and gastric cancer: relationship with Helicobacter pylori, overexpression of p53 and aneuploidy. 1798 8

Metastatic adenocarcinoma presenting as microangiopathic hemolytic anemia (MAHA) and leukoerythroblastic blood picture is rare. We report three patients who presented with MAHA as the initial symptom of metastatic signet ring cell gastric adenocarcinoma. One patient had past history of gastric ulcer. In all these patients the initial diagnosis was based on peripheral blood smear followed by bone marrow biopsy; upper GI endoscopy showed presence of gastric ulcers with focally scattered neo-plastic signet ring cells on histopathology. All patients died within a week of diagnosis.
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PMID:Metastatic signet ring gastric adenocarcinoma presenting with microangiopathic hemolytic anemia. 1798 49


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