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Gastroenterology Research and Practice
Volume 2012 (2012), Article ID 189373, 6 pages
http://dx.doi.org/10.1155/2012/189373
Clinical Study

The Role of Helicobacter pylori and NSAIDs in the Pathogenesis of Uncomplicated Duodenal Ulcer

1Department of Gastroenterology, Antalya Training and Research Hospital, 07050 Antalya, Turkey
2Department of Gastroenterology, Adiyaman State Hospital, Adiyaman, Turkey
3Department of Pathology, Antalya Training and Research Hospital, 07050 Antalya, Turkey
4Department of Microbiology, Antalya Training and Research Hospital, 07050 Antalya, Turkey
5Department of Biostatistics and Medical Informatics, Faculty of Medicine, Akdeniz University, 07050 Antalya, Turkey
6Department of Internal Medicine, Antalya Training and Research Hospital, 07050 Antalya, Turkey
7Department of Pathology, Adiyaman State Hospital, Adiyaman, Turkey

Received 7 July 2012; Accepted 27 August 2012

Academic Editor: Y. Yamaoka

Copyright © 2012 Ayhan Hilmi Cekin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background/Aim. To identify the etiological role of Helicobacter pylori (Hp) and nonsteroidal anti-inflammatory drugs (NSAIDs) in endoscopically diagnosed duodenal ulcers (DUs). Methods. Patients undergoing esophagogastroduodenoscopy in two major hospitals in Antalya and Adiyaman were included in this study and assigned as duodenal ulcer ( ; median age: 41.0 (16–71) years; 58.6% males) or control group ( ; median age: 41.0 (18–68) years; 57.1% males). Patient demographics, risk factors, and NSAID/acetylsalicylic acid (ASA) use were recorded. Results. HP was more commonly located in the corpus (75.0 versus 50.0%; odds ratio [OR] = 3.00; 95% confidence interval [CI]: 1.66–5.44; ), incisura (75.7 versus 60.0%; ; 95% CI: 1.13–3.79; ), and antrum (80.3 versus 60.0%; ; 95% CI: 1.45–5.05; ) among DU patients than controls. Hp positivity was 84.9% while Hp was negative in 15.1% of patients including those accompanied with NSAID and/or ASA use (9.2%), and those were negative for all three etiological factors (5.9%). Conclusion. Our findings indicate the substantial role of Hp in the pathogenesis of DU disease as identified in 84.9% of DU patients compatible with the background prevalence of 61.4% among age-matched control subjects. Hp was the single causative factor in 44.1% of our patients, while NSAID/ASA exposure was in 9.2%.