Helicobacter pylori negative, non-steroidal anti-inflammatory drug-negative peptic ulcers in India

Goenka, Mahesh Kumar; Majumder, Shounak; Sethy, Pradeepta Kumar; Chakraborty, Madhurima

doi:10.1007/s12664-011-0085-9

Cited by 17 publications

(11 citation statements)

References 32 publications

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“…The possible causes of IPUD are hypergastrinemia, gastric acid hypersecretion, or rapid gastric empting 15,18,19. However, some controversies have existed concerning these hypotheses 16,20. Furthermore, these hypotheses cannot explain development of gastric ulcer.…”

Section: Discussionmentioning

confidence: 99%

High Recurrence Rate of Idiopathic Peptic Ulcers in Long-Term Follow-up

Yoon¹,

Kim²,

Jung³

et al. 2013

Gut Liver

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Background/AimsOur aim was to compare the long-term clinical outcomes of idiopathic peptic ulcer disease (IPUD) with those of Helicobacter pylori-positive and nonsteroidal anti-inflammatory drug (NSAID)-induced peptic ulcer disease (PUD).MethodsPatients with endoscopically diagnosed PUD were retrospectively reviewed. According to their H. pylori-infection status and history of NSAIDs use, patients were categorized into three groups: H. pylori-positive PUD, NSAID-induced PUD, and IPUD. Clinical outcomes were analyzed, and the recurrence rate of PUD was compared among the three groups.ResultsA total of 238 patients were enrolled. Those with IPUD, NSAID-induced PUD, and H. pylori-positive PUD comprised of 56, 60, and 122 patients, respectively. The 5-year cumulative incidences of recurrent ulcers were 24.3% (95% confidence interval [CI], 11.6% to 37.0%) in IPUD, 10.9% (95% CI, 2.6% to 19.2%) in NSAID-induced PUD, and 3.8% (95% CI, 0.1% to 7.5%) in H. pylori-positive PUD (IPUD vs NSAID-induced PUD/H. pylori-positive PUD, p=0.43/p<0.001 by log-rank test). In the Cox-proportional hazards model, only IPUD remained as an independent risk factor associated with recurrent ulcers (hazard ratio, 5.97; 95% CI, 1.94 to 18.34; p=0.002).ConclusionsIPUD exhibited a higher recurrence rate than H. pylori-positive and NSAID-induced PUD in long-term follow-up and was an independent risk factor for ulcer recurrence.

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Section: Discussionmentioning

confidence: 99%

High Recurrence Rate of Idiopathic Peptic Ulcers in Long-Term Follow-up

Yoon¹,

Kim²,

Jung³

et al. 2013

Gut Liver

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“…NSAIDs such as aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity and reducing levels of mucosal prostaglandins. Many people with H. pylori colonization or taking NSAIDs do not suffer from gastritis or peptic ulcer disease, which indicates that other important causative factors can be involved [3]. …”

Section: Introductionmentioning

confidence: 99%

Inhibitory Effects of ECQ on Indomethacin-Induced Gastric Damage in Rats

Jung

Nam

Sohn

2012

Korean J Physiol Pharmacol

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We investigated inhibitory effects of extract containing quercetin-3-O-β-D-glucuronopyranoside (ECQ) extracted from Rumex Aquaticus Herba on indomethacin-induced gastric damage in Rats. Gastritis was induced in male Sprague-Dawley rats (200~220 g) by oral administration of indomethacin at a dose of 40 mg/kg. One hour before administration of indomethacin, animals were orally pretreated with ECQ at doses of 0.3, 1, 3 or 10 mg/kg. Six hours after indomethacin administration, the rats were sacrificed and the stomach was excised and opened along the greater curvature, and the surface area of gastric lesion was measured using optical microscope. Superoxide dismutase (SOD), catalase (CAT), myeloperoxidase (MPO) activities and malondialdehyde (MDA) levels were measured by ELISA. Western blot analysis was performed to detect protein expression of SOD-2. Linear hemorrhagic mucosal lesions were observed in the stomach 6 hours after oral administration of indomethacin. Pretreatment with ECQ significantly reduced the severity of the lesions in a dose-dependent manner. It also inhibited the reductions in SOD and CAT activities and SOD expression by the indomethacin-induced gastric damage. In addition, the pretreatment with ECQ significantly suppressed the elevation of the MPO activity and the MDA levels induced by indomethacin. These results suggest that ECQ has the inhibitory effects via antioxidative action against indomethacin-induced gastritis in rats.

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“…Although Hp infection and NSAIDs have for long been considered to be the major etiological factors in the causation of PUD, recent years have witnessed a paradigm shift in the epidemiology of the disease with an increase in proportion of Hp -negative PUD in developed countries [15]. …”

Section: Discussionmentioning

confidence: 99%

“…Besides higher incidence of mortality and recurrent bleeding associated with Hp -negative duodenal ulcers were reported to make their documentation important [15]. …”

Section: Introductionmentioning

confidence: 99%

The Role ofHelicobacter pyloriand NSAIDs in the Pathogenesis of Uncomplicated Duodenal Ulcer

Çekın

Taskoparan²,

Duman³

et al. 2012

Gastroenterology Research and Practice

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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 (n = 152; median age: 41.0 (16–71) years; 58.6% males) or control group (n = 70; 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; P < 0.001), incisura (75.7 versus 60.0%; OR = 2.07; 95% CI: 1.13–3.79; P = 0.017), and antrum (80.3 versus 60.0%; OR = 2.71; 95% CI: 1.45–5.05; P = 0.001) 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%.

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Helicobacter pylori negative, non-steroidal anti-inflammatory drug-negative peptic ulcers in India

Abstract: The current study indicates existence of high proportion of non-NSAID, non-H. pylori peptic ulcer disease in Indian patients.

Cited by 17 publications

References 32 publications

High Recurrence Rate of Idiopathic Peptic Ulcers in Long-Term Follow-up

High Recurrence Rate of Idiopathic Peptic Ulcers in Long-Term Follow-up

Inhibitory Effects of ECQ on Indomethacin-Induced Gastric Damage in Rats

The Role ofHelicobacter pyloriand NSAIDs in the Pathogenesis of Uncomplicated Duodenal Ulcer

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