0.05). Özefajit gelişen ve gelişmeyen hastalardaki serum gastrin (sırasıyla 69.24±21.13 ve 65.41±19.85 pg/ml, p>0.05) ve TNF-α düzeyleri (13.52±5.2I ve. 14.64±5.39 pg/ml, p>0.05) arasında istatistiksel farklılık gözlenmedi. Anti-cagA IgG düzeyleri (21.00±12.3 ve 28.09±13.07) reflü özefajiti görülen ve görülmeyen gruplar arasında farklılık göstermezken: cinsiyet, gastritin lokalizasyonu ve şiddeti açısından da anlamlı farklılık saptanmadı(p>0.05). SONUÇ: H.pilori eradikasyon tedavisi sonrası reflü özefajit gelişme sıklığının yüksek olduğu gözlenmiş ancak: sözü edilen faktörler ile arasında bir ilişki kurulamamıştır. AIMS: In recent studies, it was suggested that a non-significant association was found between this esophageal disorder and Helicobacter pylori (H. pylori) infection. The aim of this study was to investigate whether cure of the H. pylori infection increases the risk of early onset of reflux esophagitis. METHODS: Patients with duodenal ulcer (DU) (n=74) and non-ulcer dyspepsia (NUD) (n=142) without reflux esophagitis at the time of Helicobacter treatment were followed up prospectively after the cure of the infection. All patients underwent esophagogastroduodenoscopy pre-entry and at 8<sup>th</sup> week. H. pylori infection was assessed by rapid urease test and histology. Biopsy specimens were sampled from the antrum, corpus, fundus and distal esophagus for histology. Serum samples for detection of gastrin, tumor necrosis factor-alpha (TNF-α), and cytotoxin-associated gene-A (cagA) were taken. The degree and localization of gastritis, gender and type of gastroduodenal diseases were also evaluated as risk factors for reflux esophagitis. Lansoprazole triple therapy regimens were used for the eradication of H. pylori. RESULTS: The incidences of reflux esophagitis within 8 wk were 32.8% in patients with DU and 31.6% in patients with NUD(p>0.05). Behveen groups who developed reflux esophagitis and not; serum gastrin (69.24±21.13 vs. 65.41±l9.85 pg/ml respectively, p>0.05) and TNF-α levels (13.52±5.21 vs. 14.64±5.39 pg/ml respectively, p>0.05) did not show statistically significant difference. Anti-cagA IgG levels (21.00±12.3 vs. 28.09±13.07) were also similar in both groups. The gender, localization and degree of gastritis were not found different between groups either(p>0.05). CONCLUSION: We found that reflux esophagitis may frequently develop after the cure of the H.pylori infection by-unknown risk factors and mechanism.">
[PDF] Helikobakter pilori eradikasyon tedavisi sonrası reflü özefajit gelişiminde risk faktörleri | [PDF] The risk factors of reflux esophagitis occurring after the cure of the Helicobacter pylori infection
0.05). Özefajit gelişen ve gelişmeyen hastalardaki serum gastrin (sırasıyla 69.24±21.13 ve 65.41±19.85 pg/ml, p>0.05) ve TNF-α düzeyleri (13.52±5.2I ve. 14.64±5.39 pg/ml, p>0.05) arasında istatistiksel farklılık gözlenmedi. Anti-cagA IgG düzeyleri (21.00±12.3 ve 28.09±13.07) reflü özefajiti görülen ve görülmeyen gruplar arasında farklılık göstermezken: cinsiyet, gastritin lokalizasyonu ve şiddeti açısından da anlamlı farklılık saptanmadı(p>0.05). SONUÇ: H.pilori eradikasyon tedavisi sonrası reflü özefajit gelişme sıklığının yüksek olduğu gözlenmiş ancak: sözü edilen faktörler ile arasında bir ilişki kurulamamıştır.">
0.05). Özefajit gelişen ve gelişmeyen hastalardaki serum gastrin (sırasıyla 69.24±21.13 ve 65.41±19.85 pg/ml, p>0.05) ve TNF-α düzeyleri (13.52±5.2I ve. 14.64±5.39 pg/ml, p>0.05) arasında istatistiksel farklılık gözlenmedi. Anti-cagA IgG düzeyleri (21.00±12.3 ve 28.09±13.07) reflü özefajiti görülen ve görülmeyen gruplar arasında farklılık göstermezken: cinsiyet, gastritin lokalizasyonu ve şiddeti açısından da anlamlı farklılık saptanmadı(p>0.05). SONUÇ: H.pilori eradikasyon tedavisi sonrası reflü özefajit gelişme sıklığının yüksek olduğu gözlenmiş ancak: sözü edilen faktörler ile arasında bir ilişki kurulamamıştır. AIMS: In recent studies, it was suggested that a non-significant association was found between this esophageal disorder and Helicobacter pylori (H. pylori) infection. The aim of this study was to investigate whether cure of the H. pylori infection increases the risk of early onset of reflux esophagitis. METHODS: Patients with duodenal ulcer (DU) (n=74) and non-ulcer dyspepsia (NUD) (n=142) without reflux esophagitis at the time of Helicobacter treatment were followed up prospectively after the cure of the infection. All patients underwent esophagogastroduodenoscopy pre-entry and at 8<sup>th</sup> week. H. pylori infection was assessed by rapid urease test and histology. Biopsy specimens were sampled from the antrum, corpus, fundus and distal esophagus for histology. Serum samples for detection of gastrin, tumor necrosis factor-alpha (TNF-α), and cytotoxin-associated gene-A (cagA) were taken. The degree and localization of gastritis, gender and type of gastroduodenal diseases were also evaluated as risk factors for reflux esophagitis. Lansoprazole triple therapy regimens were used for the eradication of H. pylori. RESULTS: The incidences of reflux esophagitis within 8 wk were 32.8% in patients with DU and 31.6% in patients with NUD(p>0.05). Behveen groups who developed reflux esophagitis and not; serum gastrin (69.24±21.13 vs. 65.41±l9.85 pg/ml respectively, p>0.05) and TNF-α levels (13.52±5.21 vs. 14.64±5.39 pg/ml respectively, p>0.05) did not show statistically significant difference. Anti-cagA IgG levels (21.00±12.3 vs. 28.09±13.07) were also similar in both groups. The gender, localization and degree of gastritis were not found different between groups either(p>0.05). CONCLUSION: We found that reflux esophagitis may frequently develop after the cure of the H.pylori infection by-unknown risk factors and mechanism.">
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