Gastric cardia intestinal metaplasia: biopsy follow-up of 85 patients.
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BACKGROUND: Gastric cardia intestinal metaplasia (CIM), denoted by goblet cells is common. The frequency of persistent CIM is unknown. METHODS: 85 patients with CIM and follow-up endoscopies were prospectively identified during the time period of 10/6/94-12/21/97. The presence of goblet cells was the defining feature of CIM, other metaplastic cell types were not evaluated. AU 85 patients initially had biopsies that straddled the squamocolumnar junction (SCJ) showed CIM, an otherwise normal proximal stomach, lower esophagus, and squamocolumnar junction. The SCJ lay within the 2 cm of mucosa immediately proximal to the uppermost gastric fold and overlaid the junction of the tubular esophagus and the saccular dilatation of the stomach in all patients. The patients underwent endoscopy for many reasons. They were randomly identified based on the absence of a hiatal hernia and the presence of CIM. RESULTS: Ten of the 85 patients had CIM on repeat biopsy. Among patients with no CIM in the first repeat endoscopy, the degree of cardia inflammation decreased between the initial and first repeat endoscopy, whereas there was no change in the amount of inflammation among patients who had CIM in the first repeat endoscopy. The changes in mean inflammation score was significantly different between the two groups (P = .024). Twenty-two patients underwent a second repeat endoscopy and five had a third repeat endoscopy. Including all follow-up biopsies, six of the 85 patients (7%) had CIM. Four patients who did not have CIM on initial repeat endoscopy had CIM on their second repeat endoscopy, probably reflecting sampling issues. None of the biopsies had dysplasia. CONCLUSIONS: Cardia inflammation is a stimulus for cardia intestinal metaplasia, and a reduction in inflammation may allow the metaplastic mucosa to revert to normal. (+info)
Etiology, forms, and prognosis of gastrointestinal dysfunction resembling vagal indigestion occurring after surgical correction of right abomasal displacement.
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The objectives of this study were to determine the etiology and types of vagal indigestion (VI) occurring after right displacement of the abomasum or abomasal volvulus (RDA/AV), and the prognosis for each type. Data of cows presented for RDA/AV from a retrospective (n = 288) and a prospective (n = 132) study were used. Vagal indigestion occurred in 39 and 22 cows in each study, respectively. A necropsy was performed in 29 cases. Gastric compartment dilation compatible with VI type III or IV occurred in 23 cases. An abnormal gastric wall was detected in 22 cases. Peritonitis was present in 18 cows. Vagal nerve lesions were present in 5 out of 13 cases studied. Clinical, hematological, and necropsy results suggested a classification of VI with respect to presence or absence of peritonitis. Gastric wall damage, peritonitis and vagal nerve lesions appear important in the etiology. Considering peritonitis occurrence, antimicrobial therapy appears necessary in the treatment of RDA/AV. (+info)
The N-terminal 34 kDa fragment of Helicobacter pylori vacuolating cytotoxin targets mitochondria and induces cytochrome c release.
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The pathogenic bacterium Helicobacter pylori produces the cytotoxin VacA, which is implicated in the genesis of gastric epithelial lesions. By transfect ing HEp-2 cells with DNAs encoding either the N-terminal (p34) or the C-terminal (p58) fragment of VacA, p34 was found localized specifically to mitochondria, whereas p58 was cytosolic. Incubated in vitro with purified mitochondria, VacA and p34 but not p58 translocated into the mitochondria. Microinjection of DNAs encoding VacA-GFP and p34-GFP, but not GFP-VacA or GFP-p34, induced cell death by apoptosis. Transient transfection of HeLa cells with p34-GFP or VacA-GFP induced the release of cytochrome c from mitochondria and activated the executioner caspase 3, as determined by the cleavage of poly(ADP-ribose) polymerase (PARP). PARP cleavage was antagonized specifically by co-transfection of DNA encoding Bcl-2, known to block mitochondria-dependent apoptotic signals. The relevance of these observations to the in vivo mechanism of VacA action was supported by the fact that purified activated VacA applied externally to cells induced cytochrome c release into the cytosol. (+info)
Virulence factors of Helicobacter pylori responsible for gastric diseases in Mongolian gerbil.
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Helicobacter pylori infection induces various gastroduodenal diseases. We examined the role of two genes, vacA and cagE, in the gastric pathogenesis induced by H. pylori using a long-term (62 wk) animal model. Reportedly, both genes are associated with the virulence of H. pylori: vacA encodes vacuolating cytotoxin, and cagE, with other genes in the cag pathogenicity islands, encodes a type IV secretion system. Mongolian gerbils were challenged in this study by a wild-type TN2 strain and its isogenic mutants of cagE or vacA. The wild-type and vacA mutants induced severe gastritis, whereas cagE mutants induced far milder changes. Gastric ulcer was induced at the highest rate (22/23) by the wild-type TN2, followed by the vacA mutant (19/28). No ulcer was found in the gerbils infected with the cagE mutant (0/27) or in controls (0/27). Intestinal metaplasia was also found in the gerbils infected with the wild-type (14/23) or vacA mutant (15/28). Gastric cancer developed in one gerbil with wild-type infection and in one with vacA mutant infection. In conclusion, the knocking out of the cagE gene deprived wild-type H. pylori of the pathogenicity for gastritis and gastric ulcer, suggesting that the secretion system encoded by cag pathogenicity island genes plays an essential role. (+info)
Role of taurocholic acid in production of gastric mucosal damage after ingestion of aspirin.
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The possibility that aspirin-induced gastric mucosal damage may occur more readily in the presence of bile has been studied in man using measurement of transmucosal electrical potential difference as a marker of disruption of the gastric mucosal barrier. After the introduction of acetylsalicylic acid (600 mg) in suspension to seven subjects the mean electrical potential difference (plus or minus S.E. of mean) fell significantly from -33-3 plus or minus 2-0 mV to - 17-1 plus or minus 2-1 mV, and after the introduction of taurocholic acid (5 mmol/1) to seven other subjects the electrical potential difference fell significantly from -38-1 plus or minus 3-0 mV to-19-1 plus or minus 3-4 mV, the mean duration of these changes being 14-4 and 17-5 minutes respectively. When a combination of acetylsalicylic acid and taurocholic acid was introduced to eight subjects the mean electrical potential difference also fell significantly from -38-6 plus or minus 1-8 mV to -17-9 plus or minus 1-8 mV, but mean duration of this change (27 minutes) was significantly longer than that found after acetylsalicylic acid or taurocholic acid alone. These results indicate that the ingestion of aspirin, together with coincidental reflux of bile from duodenum, may be a factor in the pathogenesis of aspirin-induced gastric mucosal damage. (+info)
Characteristics of Helicobacter pylori infection in Jamaican adults with gastrointestinal symptoms.
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Helicobacter pylori infection is common in Jamaica. Describing its epidemiology in a population-based study depends largely on serology, but serologic assays have not been validated in this population. To address this issue, we examined the presence of H. pylori infection in 30 sequential adult patients with gastroduodenal symptoms by three biopsy-based methods (rapid urease test, histology, and culture) as well as by one research and two commercial enzyme-linked immunosorbent assays (ELISAs). A patient was considered H. pylori positive if the organism was detected by at least one biopsy-based method. Eighteen (60%) of the 30 patients were H. pylori positive by these criteria, whereas 21 (70%) were seropositive for H. pylori immunoglobulin G by our research ELISA. The presence of H. pylori infection in patients with gastric cancer and those with chronic gastritis was missed by biopsy-based methods but was detected by serologic assays. This observation indicates that serologic assays may be better suited for the detection of this infection in a population in which H. pylori-associated pathology is prevalent. The performance of our research ELISA in detecting biopsy-based H. pylori-positive cases was excellent, with a sensitivity and specificity of 100% and 75%, respectively. Molecular genotyping of the isolates revealed that the predominant H. pylori genotypes in this cohort of Jamaicans were cagA(+) vacA slb-m1, and iceA2. The validated serologic assay enables us to interpret epidemiologic data from population-based studies in Jamaica by comparison to those from other populations. (+info)
Ultrasonography of gastric volvulus: "peanut sign".
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We report a case of chronic gastric volvulus in which ultrasonography (US) was useful. An 81-year-old woman was hospitalized due to vomiting, and upper gastroduodenoscopy revealed that the stomach was spirally twisted and constricted. An upper gastrointestinal barium study demonstrated an organoaxial-mesenteroaxial combined type gastric volvulus. US showed constriction between the dilated upper stomach body and the lower stomach body similar to a "peanut". Thereafter, the patient's vomiting stopped and follow-up US demonstrated that the constriction of the stomach was loosened. Therefore, we believe that this characteristic US sign paralleled the symptoms of the patient. (+info)
Decreased concentration of serum apolipoprotein C-III in cows with fatty liver, ketosis, left displacement of the abomasum, milk fever and retained placenta.
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Apolipoprotein (apo) C-III is a low molecular mass protein mainly distributed in the high-density lipoprotein (HDL) fraction. In cows with postparturient diseases such as ketosis, concentrations of cholesterol, phospholipids and apoA-I and the activity of lecithin:cholesterol acyltransferase, which are mainly distributed in or functionally associated with HDL, are reduced. The purpose of the present study was to examine whether the serum concentration of apoC-III was similarly decreased in the postparturient diseases. Compared with healthy controls, the apoC-III concentration was significantly (P<0.01) decreased in cows with fatty liver, ketosis, left displacement of the abomasum, milk fever and retained placenta. Concentrations of apoC-III in the HDL fractions from diseased cows were also lower than in controls. Of the diseased cows, the decreased apoC-III concentration was particularly distinct in cows with milk fever. Increased nonesterified fatty acid and reduced free cholesterol, cholesteryl ester and phospholipid concentrations were observed in cows with milk fever, as in the other diseased cows. The decrease in the apoC-III concentration is suggested to be closely associated with the postparturient disorders, in particular with milk fever. (+info)