Wos İndeksli Açık & Kapalı Erişimli Yayınlar

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search.filters.applied.f.rights: search.filters.rights.info:eu-repo/semantics/closedAccessSubject: search.filters.subject.Helicobacter pylori

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    Interactions between Helicobacter pylori and gastroesophageal reflux disease
    (2019) Yucel, Oya; 0000-0001-5752-7493; 30151653; AAU-1657-2020
    Interactions between Helicobacter Pylori (HP) and gastroesophageal reflux disease (GERD) are a complex issue. Several pathophysiological factors influence the development and the course of GERD, HP infection might be only one of these. Many studies emphasize the co-existence of these diseases. HP infection could contribute to GERD through both a protective and an aggressive role. Gastric acid secretion is a key factor in the pathophysiology of reflux esophagitis. Depending on the type of gastritis related to HP, acid secretion may either increase or decrease. Gastritis in corpus leads to hypoacidity, while antrum gastritis leads to hyperacidity. In cases of antral gastritis and duodenal ulcers which have hyperacidity, the expectation is an improvement in pre-existing reflux esophagitis after eradication of HP. In adults, HP infection is often associated with atrophic gastritis in the corpus. Atrophic gastritis may protect against GERD. Pangastritis which leads to gastric atrophy is commonly associated with CagA strains of HP and it causes more severe gastric inflammation. In case of HP-positive corpus gastritis in the stomach, pangastritis, and atrophic gastritis, reflux esophagitis occurs frequently after eradication of HP. Nonetheless, as a predisposing disease of gastric cancer, HP should be treated. In conclusion, as the determinative factors affecting GERD involving in HP, detailed data on the location of gastric inflammation and CagA positivity should be obtained by the studies at future.
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    Is Human Papillomavirus and Helicobacter pylori Related in Gastric Lesions?
    (2019) Bozdayi, GUlendam; Dinc, Bedia; Avcikucuk, Havva; Turhan, Nesrin; Altay-Kocak, Aylin; Ozkan, Secil; Ozin, Yasemin; Bostanci, Birol; 31625359
    Background: Human papillomavirus (HPV), the causative agent of cervical cancer, is also suggested as a risk factor for gastric adenocarcinoma. Many infectious agents besides Helicobacter pylori have been associated with gastritis. The aim of this study was to investigate HPV DNA and genotyping HPV type 16 DNA in gastric adenocarcinoma and Helicobacter pylori gastritis cases. Methods: A hundred and six gastric adenocarcinoma and Helicobacter pylori gastritis samples and 26 controls were included. After deparaffinization by xylene, DNA extraction was performed by the phenol-chloroform-isoamyl alcohol method and 106 samples were studied with a G6PDH control kit (Eurogentec, Seraing, Belgium). Fifty-three adenocarcinoma and 43 Helicobacter pylori samples were thought to have enough tissue and were studied for HPV DNA. HPV types other than 16 and HPV type 16 DNA were detected by Real Time PCR using the L1 region. Amplifications of MY09/11 products were done by GP5+/GP6+ primers and Cyanine-5 labeled HPV DNA and HPV 16 DNA specific probe in Light Cycler 2.0 (Roche Diagnostics, Germany) device. Results: Among gastric adenocarcinoma and Helicobacter pylori gastritis samples, 20/53 (38%) and 18/43 (41.8%) were HPV DNA positive, respectively. Five (19.2%) of 26 controls were HPV DNA positive. Conclusions: Our 38% positive result in the gastric carcinoma group is in concordance with previous reports. This is the first study revealing the HPV-H. pylori relationship in gastritis cases and we concluded that with regard to the nearly three-fold higher HPV DNA (41.8%) in gastritis cases compared to controls, Helicobacter pylori positive cases should also be evaluated in favor of HPV in the gastritis group.
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    Is there any association between colonic polyps and gastric intestinal metaplasia?
    (2016) Unler, Gulhan Kanat; Ozgur, Gulsum Teke; Gokturk, Huseyin Savas; Korkmaz, Huseyin; Erinanc, Ozgur Hilal; 27210777
    Background/Aims: Chronic gastritis progression is a multistep process of atrophy, intestinal metaplasia (IM), and dysplasia, which may lead to invasive carcinoma. In this study, we identified an association of colonic polyps with gastric IM in patients undergoing colonoscopy. Materials and Methods: This retrospective case-control, cross-sectional study was conducted in a tertiary-care institution in Turkey. Pathology and endoscopy reports were reviewed. The study group comprised 400 patients with colonic adenomatous polyps, and the control group comprised 360 patients without colonic adenomatous polyps on colonoscopy. Results: The risk of gastric IM was 1.42-fold higher in the study group (p<0.05). The risk of IM in patients aged >= 50 years with colonic polyps was 3.35-fold higher than in those aged <50 years (p<0.05). The risk of Helicobacter pylori infection in the study group was 1.07-folder higher than that in the control group (p<0.05). H. pylori infection prevalence was higher only in patients with high-grade colonic polyp dysplasia (p<0.05). There were no statistically significant differences in the proportion of incomplete IM between the groups (p<0.05). Conclusion: This study observed increased rates of gastric IM with colonic polyps. An increased risk of gastric IM was associated with higher grades of polyp dysplasia.