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Sydney System (sydney + system)
Kinds of Sydney System Selected AbstractsHIF-1, protein expression is associated with the environmental inflammatory reaction in Barrett's metaplasiaDISEASES OF THE ESOPHAGUS, Issue 8 2009F. C. Ling SUMMARY The oxygen-regulated transcription factor subunit hypoxia inducible factor-1, (HIF-1,) is involved in angiogenesis, energy metabolism, cell survival, and inflammation. We examined the protein expression of HIF-1, within the progression of Barrett's sequence as well as the type and degree of the environmental inflammatory reaction. Squamous epithelium (SE), metaplastic, low- and high-grade dysplastic lesions, and tumor tissue of 57 resection specimens from patients with Barrett's adenocarcinoma were immunohistochemically analyzed. Active and chronic inflammatory reactions were classified according to the Updated Sydney System. HIF-1, protein expression increased significantly from SE to Barrett's metaplasia (BM) (P < 0.0001). From metaplasia through low- and high-grade dysplasia to cancer, no further increase could be detected. Active and chronic inflammation were also significantly different between SE and BM (P < 0.0001) but not during further progression in the sequence. HIF-1, protein expression did not correlate with histopathologic parameters or survival. HIF-1, protein expression pattern resembles the active and chronic environmental inflammatory reaction. All were significantly increased in metaplasia compared to SE without further change in tumor development. HIF-1, protein expression appears to be associated with inflammatory processes in the development of BM. [source] Helicobacter pylori -Associated Chronic Gastritis and Unexplained Iron Deficiency Anemia: a Reliable Association?HELICOBACTER, Issue 6 2003Stéphane Nahon Abstract Background and aim., About 35% of iron deficiency anemia cases remain unexplained after a gastrointestinal evaluation. An association between Helicobacter pylori and iron malabsorption has been suggested. The aim of this study was to determine whether H. pylori -associated chronic gastritis is linked to unexplained iron deficiency anemia in adults. Methods., From 1996 to 2001, we identified 105 patients with unexplained iron deficiency anemia after upper endoscopy, colonoscopy, small bowel radiographic examination and duodenal biopsies. Two biopsies were obtained from the gastric antrum and two from the corpus of each patient. Gastritis status was described according to the Sydney System and H. pylori infection was assessed by an immunohistochemical test on biopsy specimens. This group was compared to a control group matched for sex and age. Results., There were 76 women and 29 men (mean age 57.4 ± 21.4 years) examined in the study. A H. pylori -associated chronic gastritis was identified in 63 cases (60%) vs. 45 cases (43%) cases in the control group (p < .01). Atrophic gastritis was significantly associated with iron deficiency anemia compared with the control group [16 (15%) vs. 6 (6%); p < .03]. In the unexplained iron deficiency anemia group, (1) patients with chronic gastritis were significantly younger (52 ± 22 vs. 64 ± 20 years; p < .005), and (2) chronic gastritis was not linked to sex [sex ratio (male/female): 0.5 vs. 0.34, p = .34]. The prevalence of H. pylori infection was similar between premenopausal and postmenopausal women [28 (27%) vs. 26 (25%); p = .7] with iron deficiency anemia. Conclusion.,H. pylori infection and chronic gastritis, especially atrophic gastritis, are significantly associated with unexplained iron deficiency anemia. Relationships between H. pylori -associated chronic gastritis and unexplained iron deficiency anemia should be considered. [source] cag Pathogenicity Island of Helicobacter pylori in Korean ChildrenHELICOBACTER, Issue 4 2002Jae Sung Ko Abstract Background.cag pathogenicity island is reported to be a major virulence factor of Helicobacter pylori. The aim of this study was to investigate the status of cag pathogenicity island genes and gastric histology in Korean children with H. pylori gastritis. Methods.Helicobacter pylori DNA was extracted from antral biopsy specimens from 25 children with H. pylori gastritis. Specific polymerase chain reaction assays were used for four genes of cag pathogenicity island. The features of gastritis were scored in accordance with the updated Sydney System. Results.cagA was present in 23 (92%) of 25 children, and cagE in 24 (96%). Twenty-two (88%) children were cagT positive and 19 (76%) virD4 positive. All of the selected genes of the cag pathogenicity island were present in 17 (68%) children and completely deleted in one child. There were no differences in neutrophil activity and chronic inflammation between children infected with intact cag pathogenicity island strains and those with partially or totally deleted- cag pathogenicity island strains. Conclusion.cag pathogenicity island is not a uniform, conserved entity in Korea. Completeness of cag pathogenicity island may not be the major factor to determine the severity of H. pylori gastritis in children. [source] Pathological development of the gastric mucosa in Helicobacter pylori -related diseasesJOURNAL OF DIGESTIVE DISEASES, Issue 4 2001Tianshu Liu OBJECTIVE: To study the relationship between Helicobacter pylori eradication and the pathological development of the gastric mucosa in H. pylori -related diseases. METHODS: One hundred and ninety-one H. pylori -infected patients were randomly given anti- H. pylori or non-anti- H. pylori medications. Endoscopic examination was carried out 1 year after treatment. Pathological classifications followed the Sydney System. RESULTS: Of the 191 patients, those with chronic inflammation of the gastric mucosa improved (P < 0.05), as did those with atrophy and intestinal metaplasia (P < 0.05). Helicobacter pylori was eradicated in 107 patients, but not in 84 patients. Compared with those patients in whom H. pylori was not eradicated, those with H. pylori eradicated had ameliorated chronic inflammation of the gastric mucosa (P < 0.05) and active inflammation reduced in some cases (P < 0.05). Notwithstanding a stratification of different gastric diseases and different treatments, patients with H. pylori eradicated showed a more marked improvement in mucosal chronic inflammation than did patients in whom H. pylori was not eradicated (P < 0.05). CONCLUSIONS: These results suggest that H. pylori infection is closely related to active inflammation of the gastric mucosa. Helicobacter pylori eradication is beneficial in improving chronic inflammation of the gastric mucosa. [source] CORRELATION OF GASTRIC INTESTINAL METAPLASIA AND HELICOBACTER PYLORI INFECTION AMONG FUNCTIONAL DYSPEPTIC PATIENTSJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2000Murdani Abdullah Background: It is generally accepted that intestinal metaplasia (IM) is a pre cursor of gastric cancer and is associated with Helicobacter pylori (Hp) infection. But still little data available about association of IM and Hp in different clinical groups of patients, especially in areas with high Hp prevalence. Aim: to evaluate the IM and itís correlation with Hp infection in consecutive patients with functional dyspepsia (FD). Methods: a retrospective review of our endoscopy database and histological data from January 1997 to December 1999 was made. In this period we performed 3083 upper intestinal endoscopy in patients with FD. Endoscopy procedure was done without any specific preparation for Hp evaluation. Biopsy specimen were taken from antrum and corpus and were stained with Giemsa, H&E and Alcian Blue. Histological data was evaluated by pathologist from Department of Pathology, Medical Faculty, University of Indonesia according to the Sydney System. IM was evaluated as present or absent. One hundred and fourteen consecutive data were eligible for statistical analysis. Results: Histological data of 114 patients with FD was analyzed. Average age was 45.47 years (SD 14.32), male 62.3 % (71/114), and female 37.7 % (43/114). Forty-eight (42.11%) patients with FD were Hp positive on histology and were significantly older than Hp negative. (48.74 +12.65/43.25+15.04; p < 0.05). IM was present in 13 ( 11.4%) patients with FD. They were significantly older than the patients without IM (mean age 55.08+11.98/44.23+14.18; p <0.05) Frequency of IM was similar both in Hp positive and Hp negative patients with FD (12.5%/10.6%; p>0.05). Conclusions: IM among patients with FD was 11.4%. IM was significantly more frequent found in older age but our data suggest that IM is not related to Hp status in FD patients. [source] Seropositivity to Helicobacter pylori heat shock protein 60 is strongly associated with intensity of chronic inflammation, particularly in antrum mucosa: an extension of an 18-year follow-up study of chronic gastritis in Saaremaa, EstoniaFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2001Tamara Vorobjova Abstract Helicobacter pylori is a cause of chronic gastritis and leads to development of atrophy in some cases. There is evidence that the heat shock protein 60 (HSP60) of H. pylori is involved in induction of chronic inflammation. Seroprevalence of IgG antibodies to H. pylori HSP60 in an adult cohort from Saaremaa, Estonia (68 persons, median age 57 years), with a high prevalence of antibodies to cell surface proteins of H. pylori (92%) and a well characterized dynamics of chronic gastritis in an 18-year follow-up study, was tested using purified H. pylori HSP60 at a concentration of 1 ,g ml,1 with ELISA. The state of the gastric mucosa and the presence of H. pylori in histological sections in the samples of 1979 and 1997 were assessed in accordance with the Sydney system. Seropositivity for H. pylori HSP60 was 65%. Immunological response to H. pylori HSP60 is associated with the morphological presence of H. pylori in the antrum and corpus (P=0.01) and is strongly correlated with the grade of chronic inflammation, particularly in the antrum mucosa (r=0.34; P=0.003; OR=5.97 (95% CI 1.21,29.3)), but is not associated with development of atrophy during 18 years of follow-up, or with the activity of gastritis. This finding supports the evidence that immunological response to H. pylori HSP60 may play a role in triggering of the inflammatory process in the gastric mucosa. [source] Effect of Helicobacter pylori infection on cyclooxygenase-2 expression in gastric antral mucosaJOURNAL OF DIGESTIVE DISEASES, Issue 2 2002Hong LU OBJECTIVE: Helicobacter pylori infection is a major etiological cause of chronic gastritis. Inducible cyclooxygenase (COX-2) is an important regulator of mucosal inflammation. Recent studies indicate that expression of COX-2 may contribute to gastrointestinal carcinogenesis. The aim of this study was to investigate the effects of H. pylori infection and eradication therapy on COX-2 expression in gastric antral mucosa. METHODS: Antral biopsies were taken from 46 H. pylori- infected patients, who also had chronic gastritis, both before and after anti- H. pylori treatment. The COX-2 protein was stained by using immunohistochemical methods and COX-2 expression was quantified as the percentage of epithelial cells expressing COX-2. Gastritis and H. pylori infection status were graded according to the Sydney system. RESULTS: Cyclooxygenase-2 expression was detected in the cytoplasm of gastric antral epithelial cells both before and after the eradication of H. pylori. Cyclooxygenase-2 expression in mucosa with H. pylori infection was compared with the corresponding mucosa after successful H. pylori eradication (20.1 ± 13.1%vs 13.8 ± 5.9%; P < 0.05). At the same time, COX-2 expression in H. pylori -infected mucosa was compared with the normal controls (18.0 ± 14.1%vs 12.3 ± 4.6%, P < 0.05). Expression of COX-2 was correlated with the degree of chronic inflammation (r= 0.78, P < 0.05). CONCLUSIONS: Our results showed that H. pylori infection leads to gastric mucosal overexpression of COX-2 protein, suggesting that the enzyme is involved in H. pylori -related gastric pathology in humans. [source] Peroxiredoxin I protects gastric mucosa from oxidative injury induced by H. pylori infectionJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 4 2008Daisuke Sato Abstract Background and Aim:, Helicobacter pylori (H. pylori) infection enhances the production of reactive oxygen species and peroxynitrite, thereby resulting in oxidative tissue damage. In this study, we examined the role of peroxiredoxin I (Prx I), a stress-induced antioxidant enzyme, in protecting gastric mucosa from H. pylori -induced gastric mucosal injury. Methods:, Wild type (Prx I+/+) and Prx I-deficient type (Prx I,/,) mice were maintained for 2 to 12 months with or without infection of H. pylori, Sydney strain-1. Gastric mucosal expression of Prx I was assessed by immunoblot analysis and immunohistochemistry. The degree of gastritis was evaluated by the updated Sydney system and by mucosal levels of inflammatory cytokines (MIP-2, IL-1,, and TNF-,). Oxidative DNA injury and apoptosis were analyzed by mucosal level of 8-hydroxy-2,-deoxyguanosine, and the number of apoptotic cells stained with a single-stranded DNA antibody, respectively. Results:,H. pylori infection upregulated gastric mucosal Prx I expression in the Prx I+/+ but not the Prx I,/, mice. H. pylori infection also induced more severe gastritis and a more prominent increase in MIP level, more marked oxidative DNA injury, and apoptosis in the Prx I,/, than the Prx I+/+ mice. In the absence of H. pylori infection, no changes were demonstrated in gastric mucosa in either the Prx I+/+ or the Prx I,/, mice. Conclusion:, These data suggest that H. pylori infection upregulates gastric mucosal Prx I expression, and further, that Prx I plays an important role in gastric mucosal protection against oxidative injury induced by H. pylori infection. [source] Reflux esophagitis facilitates low Helicobacter pylori infection rate and gastric inflammationJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 8 2002Tae Jung Jang Abstract Background:Helicobacter pylori is regarded as an important pathogen in upper gastrointestinal diseases. However, little is known about the relationship between H. pylori infection and reflux esophagitis. Therefore, an investigation was undertaken in Korean subjects regarding the incidence of H. pylori infection, and a histopathological study of reflux esophagitis was also carried out. Methods: Analysis of gastric biopsy specimens was conducted for 73 patients with reflux esophagitis and 132 control subjects without reflux esophagitis. The H. pylori infection was assessed by using rapid urease test and the immunohistochemical method, and gastric mucosal morphologic change was analyzed according to the updated Sydney system. Results: The prevalence of H. pylori infection was significantly lower in patients with reflux esophagitis than in the non-reflux group. Grade of inflammation and glandular atrophy in the antrum and body were higher in patients in the non-reflux group compared with those in the reflux esophagitis group. Conclusions: It is suggested that H. pylori infection decreases the risk of reflux esophagitis by inducing atrophic gastritis. © 2002 Blackwell Publishing Asia Pty Ltd [source] Alteration of histological gastritis after cure of Helicobacter pylori infectionALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 11 2002M. Hojo Summary Background : It is still disputed whether gastric atrophy or intestinal metaplasia improves after the cure of Helicobacter pylori infection. Aim : To clarify the histological changes after the cure of H. pylori infection through a literature survey. Methods : Fifty-one selected reports from 1066 relevant articles were reviewed. The extracted data were pooled according to histological parameters of gastritis based on the (updated) Sydney system. Results : Activity improved more rapidly than inflammation. Eleven of 25 reports described significant improvement of atrophy. Atrophy was not improved in one of four studies with a large sample size (> 100 samples) and in two of five studies with a long follow-up period (> 12 months), suggesting that disagreement between the studies was not totally due to sample size or follow-up period. Methodological flaws, such as patient selection, and statistical analysis based on the assumption that atrophy improves continuously and generally in all patients might be responsible for the inconsistent results. Five of 28 studies described significant improvement of intestinal metaplasia. Conclusions : Activity and inflammation were improved after the cure of H. pylori infection. Atrophy did not improve generally among all patients, but improved in certain patients. Improvement of intestinal metaplasia was difficult to analyse due to methodological problems including statistical power. [source] 1322: History of disease, facial nerve grading systems & clinical evaluationACTA OPHTHALMOLOGICA, Issue 2010I MAVRIKAKIS Obtaining an accurate history of the onset, progress and associated symptoms of newly acquired facial nerve palsy is extremely helpful in determining the potential cause of the palsy. More importantly it serves as a guide for prognosis and timing of any necessary surgical intervention. Acute versus chronic facial nerve palsy, complete versus incomplete facial nerve palsy, recovery and recurrence of the disease will be discussed. The gold standard for grading facial nerve function is the House-Brackmann grading scale. Due to the limitations and subjectivity of this scale, several new scales of various degrees of objectivity and ease of use have been introduced. These include the Nottingham system, the Sunnybrook scale, the Yanagihara and the Sydney system, all with their advantages and disadvantages. Clinical evaluation of a patient with facial nerve palsy include evaluation of upper eyelid retraction, blink reflex, lagophthalmos, brow ptosis, paralytic ectropion, midface ptosis, mouth symmetry, platysma muscle strength, hearing, corneal sensation, Bell's phenomenon, tear function and synkinesis. [source] | ||||||||||||||||||||||