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%. 1. Introduction The discovery of Helicobacter pylori (Hp) in 1983, by Warren and Marshall, was one of the most exciting advances in the history of peptic ulcer disease (PUD) which has dramatically changed the management of this clinical entity [1, 2]. Until a few years ago, Hp was found to be present in more than 90% of patients with duodenal ulcer (DU) that resulted in the famous dictum “no Hp, no DU” [3]. Hence, eradication of HP infection even empirically without confirmation of the infection became the mainstay of treatment for PUD resulting in very high ulcer healing rates and a dramatic reduction in recurrence rates [2]. However, it has been suggested that the epidemiology of PUD has begun to change dramatically with an increase reported in the proportion of DUs in recent years that are Hp-negative [4, 5]. Since the prevalence of Hp-negative ulcers has been likely to depend upon the background prevalence of Hp in the general population, it has been suggested that as the prevalence of Hp infection continues to fall over the next decades, the proportion of Hp-negative ulcers will progressively increase [2]. In this regard, as demonstrated in 25–75% of the Hp-negative DU patients, several observations suggest that non-steroidal
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