Biomedical subjects

Zsolt Tulassay

Publications and source records attributed to Zsolt Tulassay.

93 records · Page 6Linked to original sources

PubMedDate not supplied

Superoxide-dismutase activity of the gastric mucosa in patients with Helicobacter pylori infection.

BACKGROUND: Helicobacter pylori (HP) is a pathogenic factor in the development of different alterations in the gastric mucosa. Superoxide-dismutase (SOD) is a key enzyme of mucosal antioxidant protection. We have detected changes in the activity of mucosal SOD in different diseases caused by HP. MATERIALS AND METHODS: Biopsies were taken upon gastroscopy (n = 131). Activity of SOD was measured by photometry, referred to the amount of protein in the sample. RESULTS: SOD activity of the antrum of HP-positive patients was significantly higher than that of HP-negative ones. There was a significant increase in erosive gastritis. CONCLUSION: In the presence of HP there was a significant increase of the SOD activity in the antrum but not in the corpus. In chronic antral gastritis there was a positive relationship between the SOD activity and both the severity and activity of inflammation. We presume that HP-associated gastritis is predominant in the antrum.

Adolescent↗

PubMedDate not supplied

Clinical presentation of Crohn's disease. association between familial disease, smoking, disease phenotype, extraintestinal manifestations and need for surgery.

BACKGROUND/AIMS: Recent molecular data suggest that genetic factors may underlie the disease heterogeneity observed in Crohn's disease (CD). It was also suggested that familial inflammatory bowel disease (IBD) is a homogenous subgroup, phenotypically different from sporadic disease. Our aim was to determine the clinical presentation in a large CD population. METHODOLOGY: 564 CD patients (m/f: 278/286, age: 37.4 (SD 12.7) yrs, duration: 8.4 (7.1) yrs) were included. Disease phenotype was determined according to Vienna classification. Familial disease, extraintestinal manifestations (EIM), need for surgery and smoking habits were also analyzed. RESULTS: Familial IBD was present in 73 (12.9%) patients. Age at onset and presence of EIMs was associated with familial disease. Penetrating (44.6% vs. <10 yrs: 29.1%, P<0.0001) and ileocolonic disease (54.4% vs. 42.8%, P=0.03) were more common in patients with a disease duration of > or =10 yrs. In a logistic regression model female gender, colonic/ileocolonic location, smoking and familial IBD were independent risk factors for EIMs, while ileal and non-inflammatory disease increased the risk for resections. Smoking was also associated with frequent relapses. CONCLUSIONS: Familial IBD was associated with the presence of EIMs, while ileal involvement and noninflammatory behavior independently increased the risk for surgery. Since penetrating and extensive disease was more frequent in patients with longer disease duration our data support a possible change in location and behavior during the course of disease.

Adult↗

PubMedDate not supplied

Relationship between eradication of Helicobacter pylori and gastric mucosal superoxide dismutase activity.

BACKGROUND: Helicobacter pylori (HP) is the main pathogenic factor in the development of gastritis and gastric cancer. Superoxide-dismutase (SOD) is a key enzyme of mucosal antioxidant protection. In the presence of HP there is a significant increase of SOD activity in the antrum. Changes in gastric mucosal SOD activity were detected in response to eradication treatment of HP infection. PATIENTS AND METHODS: Biopsies were taken from 13 patients upon gastroscopy performed prior to and 88.3 +/- 12.6 days after treatment. The activity of SOD was determined by spectrophotometry. RESULTS: The activity of SOD in the gastric mucosa decreased significantly following the successful eradication, whereas in the corpus activity did not change significantly. CONCLUSION: In the presence of HP there is an oxidative stress in the gastric mucosa triggered by the bacterium. It may represent the final common path of HP carcinogenesis. Successful eradication treatment prevents the production of reactive oxygen metabolites.

Adult↗