The presence of DupA and clarithromycin resistance in H. pylori among patients with peptic ulcer disease; a rational connection

Gene Reports ◽  
2022 ◽  
pp. 101508
Author(s):  
Masoud Keikha ◽  
Ali Beheshti Namdar
2018 ◽  
Vol 24 (18) ◽  
pp. 2034-2040 ◽  
Author(s):  
Berrak C. Yegen

The risk of developing Peptic Ulcer Disease (PUD) was shown to be associated with genetic inheritance, lifestyle and social status of the patients. Unhealthy lifestyle habits and failure in coping with stress have been closely associated with the occurrence of PUD. In contrary, limiting the use of analgesic drugs and glucocorticoids, controlling environmental and socioeconomic factors that predispose to H. Pylori infection, having a balanced diet, exercising regularly, coping successfully with stress, avoiding smoking, limiting alcohol intake and getting sufficient night sleep are essential in prevention and healing of PUD.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mi Hong Yim ◽  
Keun Ho Kim ◽  
Bum Ju Lee

AbstractPeptic ulcer disease (PUD) is caused by many sociodemographic and economic risk factors other than H. pylori infection. However, no studies reported an association between PUD and the number of household members. We showed the number of family members affected by PUD based on sex in a Korean population. This cross-sectional study used 1998–2009 data from the Korea National Health and Nutrition Examination Survey of the Korea Centers for Disease Control and Prevention. Multiple binary logistic regression models adjusted for confounders were constructed to analyze the association of PUD with the number of household members. The number of household members was associated with PUD, age, body mass index (BMI), waist circumference, systolic blood pressure, hemoglobin, glucose, location (urban/rural), income, education level, stress, current drinking, and smoking in both sexes. Men with other household members had a higher PUD risk compared to men or women living alone (reference), and the opposite was observed for women. Men with 4 household members had a higher PUD risk than men living alone in the model adjusted for age, BMI, income, location, education, and stress (OR = 2.04 [95% CI 1.28–3.27], p value = .003). Women with more than 6 household members had a lower PUD risk than women living alone in the adjusted model (OR = 0.50 [0.33–0.75], p value = .001). Women with more household members had a lower PUD risk. However, more men had PUD than women regardless of the number of household members.


2006 ◽  
Vol 74 (7) ◽  
pp. 4064-4074 ◽  
Author(s):  
Mónica Oleastro ◽  
Lurdes Monteiro ◽  
Philippe Lehours ◽  
Francis Mégraud ◽  
Armelle Ménard

ABSTRACT Peptic ulcer disease (PUD) occurs after a long-term Helicobacter pylori infection. However, the disease can develop earlier, and rare cases have been observed in children, suggesting that these H. pylori strains may be more virulent. We used suppressive subtractive hybridization for comparative genomics between H. pylori strains isolated from a 5-year-old child with duodenal ulcer and from a sex- and age-matched child with gastritis only. The prevalence of the 30 tester-specific subtracted sequences was determined on a collection of H. pylori strains from children (15 ulcers and 30 gastritis) and from adults (46 ulcers and 44 gastritis). Two of these sequences, jhp0562 (80.0% versus 33.3%, P = 0.008) and jhp0870 (80.0% versus 36.7%, P = 0.015), were highly associated with PUD in children and a third sequence, jhp0828, was less associated (40.0% versus 10.0%, P = 0.048). Among adult strains, none of the 30 sequences was associated with PUD. However, both jhp0562 and jhp0870 were less prevalent in adenocarcinoma strains than in PUD strains from children and adults, the difference being statistically significant for jhp0870. In conclusion, two H. pylori genes were identified as being strongly associated with PUD in children, and their putative roles as an outer membrane protein for jhp0870 and in lipopolysaccharide biosynthesis for jhp0562, suggest that they may be novel virulence factors of H. pylori.


2021 ◽  
Author(s):  
Aaron Oh ◽  
Han Truong ◽  
Judith Kim ◽  
Sheila D. Rustgi ◽  
Julian A. Abrams ◽  
...  

Abstract Background: Helicobacter pylori is a major risk factor for gastric cancer. Screening and treatment of H. pylori may reduce the risk of gastric cancer and peptic ulcer disease. Polymerase chain reaction (PCR) of gastric biopsies provides superior sensitivity and specificity for the detection of H. pylori. This study explores whether population-based H. pylori screening with PCR is cost-effective in the US.Methods: A Markov cohort state-transition model was developed to compare three strategies: no screening with opportunistic eradication, 13C-UBT population screening and treating of H. pylori, and PCR population screening and treating of H. pylori. Estimates of risks and costs were obtained from published literature. Since the efficacy of H. pylori therapy in gastric cancer prevention is not certain, we broadly varied the benefit 30-100% in sensitivity analysis.Results: PCR screening was cost-effective and had an incremental-cost effectiveness ratio per quality adjusted life-year (QALY) of $38,591.89 when compared to 13C-UBT strategy with an ICER of $2373.43 per QALY. When compared to no screening, PCR population screening reduced cumulative gastric cancer incidence from 0.84% to 0.74% and reduced peptic ulcer disease risk from 14.8% to 6.0%. The cost-effectiveness of PCR screening was robust to most parameters in the model.Conclusion: Our modeling study finds PCR screening and treating of H. pylori to be cost-effective in the prevention of gastric cancer and peptic ulcer disease. However, the potential negative consequences of H. pylori eradication such as antibiotic resistance could change the balance of benefits of population screening.


Author(s):  
Tyler M. Berzin ◽  
Kenneth R. Falchuk

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.


2019 ◽  
Vol 2 (1) ◽  
pp. 4-10
Author(s):  
Sunit Agrawal ◽  
D Thakur ◽  
P Kafle ◽  
A Koirala ◽  
R K Sanjana ◽  
...  

Background: Helicobacter pylori is found in more than 90% cases of peptic ulcer. This study examines the possibility of association of Helicobacter pylori in perforated peptic ulcer disease and its relation to persisting ulcer as well as the influence of other risk factors; namely: smoking, alcohol, current non-steroidal anti inflammatory drugs (NSAIDs) and steroid use. Materials and Methods: In this prospective study, total of 50 cases of peptic ulcer perforation admitted in College of Medical Sciences and Teaching Hospital, Bharatpur, Nepal were selected on the basis of the non-probability (purposive) sampling method. All patients who presented with suspected peptic ulcer perforation were included in the study and the perforations were repaired by Modified Graham’s Patch and were given triple therapy postoperatively. The age, sex, incidence, mode of presentation, precipitating factors, association with the risk factors and postoperative complications were all evaluated and compared. Results: Of 50 patients studied, the age ranged from 17 to 75 years, mean age being 40.1 years with the peak incidence in the 3rd and 5th decades of life showing a male dominance (92%). H. pylori was seen in ulcer edge biopsy in 29 patients (58%). Most common clinical presentation was pain abdomen, the most common signs of perforation were tenderness, rebound tenderness and absent bowel sounds. The mean duration of stay in hospital in H. pylori positive patients was 12.07±8.15 days as compared with 11.1±5.12 days in H. pylori negative patients. The incidence of peptic ulcer perforation was higher in the patients consuming alcohol (64%) than smokers (48%), followed by NSAIDs user(22%). 20% of the patients with delayed presentation developed complications postoperatively. Perforated peptic ulcer was repaired by Modified Graham’s Patch Repair, followed by anti H. pylori therapy in all of them. Conclusion: Peptic ulcer perforation is quite common among the patients with peptic ulcer disease with history of chronic smoking, alcoholism and analgesic intake, more commonly in males. There is association of H. pylori in 58% of patients with peptic ulcer perforation.


2003 ◽  
Vol 66 (7) ◽  
pp. 1292-1303 ◽  
Author(s):  
JAMES L. SMITH

The secretion of hydrochloric acid by the stomach plays an important role in protecting the body against pathogens ingested with food or water. A gastric fluid pH of 1 to 2 is deleterious to many microbial pathogens; however, the neutralization of gastric acid by antacids or the inhibition of acid secretion by various drugs may increase the risk of food- or waterborne illnesses. Peptic ulcer disease is often treated by decreasing or eliminating gastric acid secretion, and such treatment blocks the protective antibacterial action of gastric fluid. The majority of peptic ulcer disease cases originate from Helicobacter pylori infections. Treatment of H. pylori–induced peptic ulcers with antibiotics reduces the need for drugs that inhibit gastric acid secretion and thereby diminishes the risk of food- and waterborne illness for peptic ulcer disease patients. Many bacterial pathogens, such as Escherichia coli, Salmonella Typhimurium, and H. pylori, can circumvent the acid conditions of the stomach by developing adaptive mechanisms that allow these bacteria to survive in acid environments. As a consequence, these bacteria can survive acidic stomach conditions and pass into the intestinal tract, where they can induce gastroenteritis.


Sign in / Sign up

Export Citation Format

Share Document