scholarly journals Helicobacter pyloriManagement: How to Improve the Therapeutic Confusion in Practice

2003 ◽  
Vol 17 (suppl b) ◽  
pp. 21B-24B ◽  
Author(s):  
Nicholas J Talley

There appears to be a disconnect between current guidelines forHelicobacter pyloritesting and treatment, and clinical practice, including physician beliefs and actual prescribing patterns. In particular, there are markedly different approaches in primary and secondary care, and country- specific differences in eradication therapy forH pyloriinfection. Although most physicians do not believe thatH pyloricauses nonulcer dyspepsia, the majority appear to prescribe eradication. Less information is available on the management ofH pyloriinfection and gastroesophageal reflux disease, and more marked differences in attitudes and practice occur in this condition. Even in peptic ulcer disease, where most clinicians both in primary and in secondary care believeH pylorishould be eradicated, there is often a breakdown in the translation of this belief into practice. There is also confusion in terms of treatment regimens applied forH pylorieradication. Eradication regimens are less successful in practice than in clinical trials. Furthermore, a sizable proportion of patients with peptic ulcer remain symptomatic despite cure of the ulcer diathesis, which may undermine confidence. Therapeutic confusion about what to prescribe, side effects limiting compliance, bacterial resistance, and socioeconomic factors may all impair therapeutic success with eradication therapy in practice. Unfortunately, it has been well documented that guidelines alone are likely to have little or no impact in practice. Publication in a journal is unlikely to lead to effective implementation in primary care. On the basis of available evidence, clinical behaviour is most likely changed when guidelines are developed by the peer group of clinicians for whom they were intended, are disseminated through a specific educational program, and are implemented by applying, preferably during the consultation, specific reminders.

2020 ◽  
Vol 15 ◽  
Author(s):  
Nasr Alrabadi ◽  
Iyad S. Albustami ◽  
Husam A. Abuhayyeh ◽  
Khaled M. El-Muwalla ◽  
Rama J. Alawneh ◽  
...  

Background: Helicobacter pylori (H.pylori) infection is the most common cause of peptic ulcer disease and it can be associated with many complications including malignancies. In clinical practice, some clinicians may use clavulanic acid (CA) in combination with amoxicillin or other beta-lactams as an addition to the standard treatment regimens. This practice may be made by habitual mistake, non-evidence based hypothetical assumptions, or by prescribing it as an alternative treatment. This review aims to expose the effect of CA against H.pylori infection and to review the possible mechanisms that may contribute to that effect. Methods: A PubMed and Google Scholar literature search was obtained on both pre-clinical and clinical studies related to CA and H.pylori infection. Results: Available clinical studies showed improvement in the eradication of H. pylori by about 10-20% when CA was added to the treatment regimens. This effect for CA could be related to several mechanisms including inhibition of H. pylori growth by binding to penicillin-binding proteins (PBPs), the transformation of H. pylori from the active filamentous form into coccoidal form, induction of the release of dopamine, modulation of immunological response towards H. pylori infection and its relationship with other microbiota. Randomized-controlled studies on patients with resistance H. pylori are needed. Moreover, In_vitro studies to evaluate the mechanisms by which CA may influence H. pylori are warranted. Conclusion: The presented literature suggests potential avenues for the use of CA in the management of peptic ulcer disease and H.pylori infection.


Author(s):  
Tomoari Kamada ◽  
Kiichi Satoh ◽  
Toshiyuki Itoh ◽  
Masanori Ito ◽  
Junichi Iwamoto ◽  
...  

AbstractThe Japanese Society of Gastroenterology (JSGE) revised the third edition of evidence-based clinical practice guidelines for peptic ulcer disease in 2020 and created an English version. The revised guidelines consist of nine items: epidemiology, hemorrhagic gastric and duodenal ulcers, Helicobacter pylori (H. pylori) eradication therapy, non-eradication therapy, drug-induced ulcers, non-H. pylori, and nonsteroidal anti-inflammatory drug (NSAID) ulcers, remnant gastric ulcers, surgical treatment, and conservative therapy for perforation and stenosis. Therapeutic algorithms for the treatment of peptic ulcers differ based on ulcer complications. In patients with NSAID-induced ulcers, NSAIDs are discontinued and anti-ulcer therapy is administered. If NSAIDs cannot be discontinued, the ulcer is treated with proton pump inhibitors (PPIs). Vonoprazan (VPZ) with antibiotics is recommended as the first-line treatment for H. pylori eradication, and PPIs or VPZ with antibiotics is recommended as a second-line therapy. Patients who do not use NSAIDs and are H. pylori negative are considered to have idiopathic peptic ulcers. Algorithms for the prevention of NSAID- and low-dose aspirin (LDA)-related ulcers are presented in this guideline. These algorithms differ based on the concomitant use of LDA or NSAIDs and ulcer history or hemorrhagic ulcer history. In patients with a history of ulcers receiving NSAID therapy, PPIs with or without celecoxib are recommended and the administration of VPZ is suggested for the prevention of ulcer recurrence. In patients with a history of ulcers receiving LDA therapy, PPIs or VPZ are recommended and the administration of a histamine 2-receptor antagonist is suggested for the prevention of ulcer recurrence.


2019 ◽  
Vol 8 (10) ◽  
pp. 1722
Author(s):  
Chih-Ming Liang ◽  
Shih-Cheng Yang ◽  
Cheng-Kun Wu ◽  
Yu-Chi Li ◽  
Wen-Shuo Yeh ◽  
...  

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.


2017 ◽  
Vol 6 (80) ◽  
pp. 5661-5663
Author(s):  
Prashant Dorkar S ◽  
Prakash Gurav ◽  
Santosh Dalvi ◽  
Prachi Dharmadhikari ◽  
Anand Devraj H

2003 ◽  
Vol 17 (suppl b) ◽  
pp. 41B-45B ◽  
Author(s):  
Wink A de Boer

Physicians should try to achieve an optimal cure rate with their initialHelicobacter pylorieradication therapy. Most physicians use the same treatment in all their patients.H pyloriinfection in patients with peptic ulcer disease (PUD) is more likely to be cured than that in patients with functional dyspepsia (FD). Differences in cure rates of 5% to 15% are usually reported, which is considered to be clinically relevant. A plausible biological explanation for this finding suggests that different strains (virulent [cagA+,vacAtype s1] compared with nonvirulent strains [cagA–,vacAtype s2]) in PUD and FD induce different changes in the gastric mucosa, and this facilitates or impairs antimicrobial efficacy. Physicians should be aware that most published treatment studies have included only PUD patients. This means that in clinical practice cure rates obtained in patients with FD or perhaps uninvestigated dyspepsia are usually lower than those reported in the literature. This has implications for the choice of treatment. Physicians should consider prolonging the duration of initialHelicobactereradication therapy from seven to 10 to 14 days in patients without ulcers.


2000 ◽  
Vol 14 (11) ◽  
pp. 922-928 ◽  
Author(s):  
Neda Khaghan ◽  
Peter R Holt

The increase in life expectancy demands that more attention be given to gastrointestinal problems, such as peptic ulcer disease, in elderly people. This review summarizes many of the physiological changes that have a role in peptic ulcer disease in elderly patients. HowHelicobacter pyloriinfection modifies the course of peptic disease is also reviewed. The clinical presentation of peptic diseases often differs in elderly people, and atypical symptoms are common. Accurate diagnosis requires aggressive endoscopic evaluation. Treatment regimens using H2receptor antagonists, proton pump inhibitors and regimens to eradicateH pylorimay also need to be altered in elderly patients.


1995 ◽  
Vol 9 (2) ◽  
pp. 91-95 ◽  
Author(s):  
ABR Thomson ◽  
CN Williams

Since its rediscovery 10 years ago,Helicobacter pylorihas reshaped our thinking about the course of peptic ulcer disease. Our approach to the patient with a duodenal ulcer has become one of attempting eradication therapy at the time of first diagnosis, in the hope of curing the ulcer disease. Gastric and duodenal ulceration are only two of the manifestations of this chronic antral infection; other complications ofH pyloriinclude gastritis, gastric cancer and possible maltomas. Therapy ofH pyloriinfection is complicated and involves dual therapy with an antibiotic plus a protein pump inhibitor, such as omeprazole 20 mg bid plus amoxicillin 1 g bid for two weeks, triple or quadruple therapy with bismuth, two antibiotics and an H2-receptor antagonist. Vaccination againstH pyloriis on the far horizon.


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