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1.
Turk J Gastroenterol ; 23(5): 478-84, 2012.
Article in English | MEDLINE | ID: mdl-23161322

ABSTRACT

BACKGROUND/AIMS: The risk of gastric cancer is increased in patients with intestinal metaplasia. Cyclooxygenase-2 activity is crucial for gastric cancer cell survival and proliferation. We aimed to assess cyclooxygenase-2 expression in patients with intestinal metaplasia or chronic active gastritis and in patients with or without a family history of gastric cancer, i.e. a first-degree relative with gastric cancer. MATERIALS AND METHODS: One hundred and six patients with histologically proven intestinal metaplasia, chronic active gastritis or normal gastric mucosa were included. Immunohistochemical staining was performed using the immunoperoxidase method. RESULTS: Cyclooxygenase-2 expression was detected in 23.1% of normal gastric mucosa, 70.6% of chronic active gastritis, and 90.5% of intestinal metaplasia patients. Cyclooxygenase-2 expression was significantly higher in intestinal metaplasia than in chronic active gastritis (p=0.018). Cyclooxygenase-2 expression was significantly more severe in the intestinal metaplasia group when compared to the chronic active gastritis group (p=0.017). Severe cyclooxygenase-2 expression (>60% of cells) was more frequent in the intestinal metaplasia group. Cyclooxygenase-2 expression was higher in the Helicobacter pylori-positive group when compared to the Helicobacter pylori-negative group (80.3% vs 57.1%, respectively; p=0.012). Cyclooxygenase-2 expression did not significantly differ according to presence of a first-degree relative with gastric cancer. CONCLUSIONS: Patients with intestinal metaplasia demonstrated increased presence and severity of cyclooxygenase-2 expression. Our findings suggest that cyclooxygenase-2 plays an important role in the stepwise process that eventually leads to gastric cancer. There was no statistically significant difference between the patients with and without a first-degree relative with a history of gastric cancer in terms of cyclooxygenase-2 expression.


Subject(s)
Cyclooxygenase 2/biosynthesis , Gastric Mucosa/metabolism , Gastritis/enzymology , Immunohistochemistry/methods , Precancerous Conditions/pathology , Adolescent , Adult , Aged , Aged, 80 and over , Biopsy , Chronic Disease , Endoscopy, Gastrointestinal , Female , Gastric Mucosa/pathology , Gastritis/pathology , Humans , Male , Metaplasia , Middle Aged , Precancerous Conditions/enzymology , Prognosis , Risk Factors , Severity of Illness Index , Young Adult
2.
Pathol Res Pract ; 208(2): 89-93, 2012 Feb 15.
Article in English | MEDLINE | ID: mdl-22277792

ABSTRACT

The primary aim is to compare individuals with intestinal metaplasia (IM), chronic active gastritis (CAG), and normal gastric mucosa (NGM) in terms of apoptosis, proliferation, and Bcl-2 expression. The secondary aim is to determine whether these parameters are different between patients with and without gastric cancer in first-degree relatives. We enrolled 106 patients whose histopathological results were consistent with IM (n: 42), CAG (n: 51), or NGM (n: 13). Antral biopsies were immunohistochemically stained for Bcl-2 and Ki-67 expression. Apoptosis was detected using TUNEL assay. While no significant difference was determined between three groups with regard to apoptosis and Bcl-2 expression (p>0.05), Ki-67 expression was significantly higher in the IM group when compared with the CAG and NGM groups (29.90±22.87 vs. 18.18±16.22 vs. 18.54±20, respectively; p=0.012). Helicobacter pylori was determined to increase apoptosis (49.3% vs. 25.7%, p<0.05), nevertheless, it had no significant effect on proliferation and Bcl-2 expression. Bcl-2 and Ki-67 expression and apoptosis were not different among patients with and without a history of gastric cancer in first degree relatives. Although intestinal metaplasia cases demonstrate an increase in proliferation, no elevation is observed in apoptosis. This can be an important factor in the progression to gastric cancer.


Subject(s)
Apoptosis , Cell Proliferation , Gastric Mucosa , Gastritis , Ki-67 Antigen/analysis , Precancerous Conditions , Proto-Oncogene Proteins c-bcl-2/analysis , Stomach Neoplasms , Adolescent , Adult , Aged , Aged, 80 and over , Analysis of Variance , Biopsy , Case-Control Studies , Chi-Square Distribution , Chronic Disease , Disease Progression , Female , Gastric Mucosa/chemistry , Gastric Mucosa/microbiology , Gastric Mucosa/pathology , Gastritis/metabolism , Gastritis/microbiology , Gastritis/pathology , Helicobacter pylori/isolation & purification , Heredity , Humans , Immunohistochemistry , In Situ Nick-End Labeling , Male , Metaplasia , Middle Aged , Pedigree , Precancerous Conditions/chemistry , Precancerous Conditions/microbiology , Precancerous Conditions/pathology , Stomach Neoplasms/chemistry , Stomach Neoplasms/genetics , Stomach Neoplasms/microbiology , Stomach Neoplasms/pathology , Turkey , Young Adult
3.
J Clin Gastroenterol ; 38(9): 750-5, 2004 Oct.
Article in English | MEDLINE | ID: mdl-15365399

ABSTRACT

BACKGROUND: The effect of Helicobacter pylori (H. pylori) eradication on gastroesophageal reflux disease is controversial. We aimed to investigate the effect of H. pylori eradication in this group of patients. MATERIALS AND METHODS: Thirty-four consecutive patients with H. pylori infection and reflux esophagitis (grade 1 or 2) were enrolled into the study. Twenty-four hour intra-esophageal pH recording and esophageal manometry were performed before and 3 months after eradication of H. pylori, which was achieved using lansoprazole 30 mg b.i.d., amoxycillin 1 g b.i.d., and clarithromycin 500 mg b.i.d. for 14 days. H. pylori was evaluated in biopsy specimens taken from the antrum and corpus by rapid urease test and by histopathologic examination before and 3 months after eradication. RESULTS: Eighteen patients (11 men and 7 women, median age 42 years) completed the study. Three months after the treatment, there was no significant change in any of the 24-hour esophageal pH recording parameters and mean lower esophageal sphincter resting pressure (P > 0.05). The percentage of total time esophageal pH <4 increased in 10 patients, and decreased in 8 patients. There was a significant decrease in the scores of heartburn and regurgitation (P < 0.01). Esophagitis persisted in 16 patients and disappeared in 2 patients. Esophagitis score decreased in 6 patients, and did not change in 12 patients (P < 0.05). CONCLUSION: H. pylori eradication does not have any effect on gastroesophageal acid reflux in patients with reflux esophagitis 3 months after eradication, but significant improvement is achieved in some reflux associated symptoms.


Subject(s)
Gastroesophageal Reflux/drug therapy , Helicobacter Infections/drug therapy , Omeprazole/analogs & derivatives , 2-Pyridinylmethylsulfinylbenzimidazoles , Adult , Amoxicillin/therapeutic use , Anti-Bacterial Agents/therapeutic use , Anti-Ulcer Agents/therapeutic use , Clarithromycin/therapeutic use , Drug Therapy, Combination , Endoscopes, Gastrointestinal , Female , Gastroesophageal Reflux/etiology , Gastroesophageal Reflux/pathology , Heartburn/drug therapy , Heartburn/etiology , Helicobacter Infections/complications , Helicobacter Infections/pathology , Helicobacter pylori/isolation & purification , Humans , Hydrogen-Ion Concentration/drug effects , Lansoprazole , Male , Middle Aged , Monitoring, Physiologic , Omeprazole/therapeutic use , Treatment Outcome , Urease/analysis , Urease/metabolism
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