scholarly journals What Do We Do aboutHelicobacter pylori?

1999 ◽  
Vol 13 (2) ◽  
pp. 143-145 ◽  
Author(s):  
CJ Hawkey
Keyword(s):  
Past History ◽  
Ulcer Disease ◽  
History Of ◽  
Inflammatory Drugs ◽  
Heliobacter Pylori ◽  
Anti Inflammatory ◽  
H Pylori

Heliobacter pyloriand nonsteroidal anti-inflammatory drugs (NSAIDs) cause ulcers by different mechanisms. Under some circumstances, patients infected withH pylorimay be less prone to NSAID-associated ulcers than those who areH pylori-negative. Eradication trials have yielded differing results. However, those who have studied patients who have a past history of ulcer disease and are already established on NSAIDs have shown no benefit fromH pylorieradication.

scholarly journals Risk of Recurrent Peptic Ulcer Disease in Patients Receiving Cumulative Defined Daily Dose of Nonsteroidal Anti-Inflammatory Drugs

2019 ◽  
Vol 8 (10) ◽  
pp. 1722
Author(s):  
Chih-Ming Liang ◽  
Shih-Cheng Yang ◽  
Cheng-Kun Wu ◽  
Yu-Chi Li ◽  
Wen-Shuo Yeh ◽  
...  
Keyword(s):  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
Eradication Therapy ◽  
Case Control ◽  
Defined Daily Dose ◽  
Ulcer Disease ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
H Pylori

The purpose of this population-based case–control study was to clarify the impact of cumulative dosage of nonsteroidal anti-inflammatory drugs (NSAIDs) on recurrent peptic ulcers among chronic users after Helicobacter pylori (H. pylori) eradication. We analyzed data of 203,407 adult peptic ulcer disease (PUD) patients from the National Health Insurance Research Database in Taiwan entered between 1997 and 2013. After matching for age/gender frequencies and the length of follow-up time in a ratio of 1:1, the matched case–control groups comprised 1150 patients with recurrent PUD and 1150 patients without recurrent PUD within 3 years of follow-up. More recurrent PUDs occurred in NSAID users than in the control group (75.30% versus 69.74%; p = 0.0028). Independent risk factors for recurrent PUD included patients using NSAIDs (adjusted OR (aOR): 1.34, p = 0.0040), H. pylori eradication (aOR: 2.73; p < 0.0001), concomitant H2 receptor antagonist (aOR: 1.85; p < 0.0001) and anti-coagulant (aOR: 4.21; p = 0.0242) use. Importantly, in the initial subgroup analysis, the risk ratio of recurrent PUD did not increase in NSAID users after H. pylori eradication compared with that in non-users (p = 0.8490) but a higher risk for recurrent PUD with the increased doses of NSAIDs without H. pylori eradication therapy (aOR: 1.24, p = 0.0424; aOR: 1.47, p = 0.0074; and aOR: 1.64, p = 0.0152 in the groups of ≤28, 29–83, and ≥84 cumulative defined daily doses, respectively). The current study suggested that H. pylori eradication therapy could decrease the risk of recurrent PUD among patients with high cumulative doses of NSAIDs.

scholarly journals Double Pylorus in Upper Gastrointestinal Bleeding

2021 ◽  
pp. 332-337
Author(s):  
Heasty Oktaricha ◽  
Muhammad Miftahussurur
Keyword(s):  
Duodenal Bulb ◽  
Rare Condition ◽  
High Dose ◽  
Protective Agent ◽  
Gastrointestinal Fistula ◽  
Double Pylorus ◽  
History Of ◽  
Inflammatory Drugs ◽  
H Pylori ◽  
Upper Gastrointestinal

Double pylorus, also known as acquired double pylorus, is a rare condition defined as a gastrointestinal fistula connecting stomach antrum and duodenal bulb. The prevalence of double pylorus ranges from 0.001 to 0.4% by esophagogastroduodenoscopy (EGD). Although the etiology is unknown, the formation of double pylorus is related to Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAID). The development of the occurrence of double pylorus is still unknown, but many systemic diseases play a role. We present the case of a 59-year-old man who was admitted to Dr. Soetomo General Hospital with hematemesis and melena. The patient had a history of diabetes mellitus since 3 years and consumption of medicinal herbs for myalgia, which was suspected of NSAIDs for the past 5 months. The patient had anemia with hemoglobin at 8.3 g/dL, enterogenous azotemia with blood urea nitrogen 28 mg/dL and serum creatinine 1.14 mg/dL. At EGD, double pylorus was found and accompanied by gastric ulcer, a giant white base ulcer, part of it covered by clotting without any sign of active bleeding. Biopsy revealed chronic inactive gastritis, and no H. pylori was found. Treatment mainly depends on gastrointestinal acid suppression through a proton pump inhibitor (PPI). The patient was given a high-dose PPI and a mucosal protective agent. He was treated for 1 week and had improved complaints.

Peptic Ulcer Disease

2014 ◽  
pp. 710-718
Author(s):  
Tyler M. Berzin ◽  
Kenneth R. Falchuk
Keyword(s):  
Peptic Ulcer ◽  
Peptic Ulcer Disease ◽  
The United States ◽  
Dietary Factors ◽  
Pathogenic Agent ◽  
Ulcer Disease ◽  
History Of ◽  
Ulcer Complications ◽  
H Pylori

Peptic ulcer disease (PUD) involves the stomach or duodenum and is a significant cause of morbidity and mortality both in the United States and worldwide, with a lifetime prevalence estimated at 5–15%. For a good part of the 20th century PUD was felt to be a condition related to stress and dietary factors. More recently, our understanding of PUD has been advanced by research into the role of gastric acid secretion and the benefits of various classes of antisecretory medications and, perhaps most importantly, in 1984, by Warren and Marshall, who identified Helicobacter pylori (H. pylori) as a pathogenic agent in this disease. Proton pump inhibitor (PPI) therapy and H. pylori eradication regimens have altered the natural history of what once was a chronic disease, and they have also reduced peptic ulcer complications, limiting the need for surgery.

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