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Eradication therapy for peptic ulcer disease in Helicobacter pylori positive patients
Abstract
Background:
Peptic ulcer disease is the cause for dyspepsia in about 10% of patients. 95% of duodenal and 70% of gastric ulcers are associated with Helicobacter pylori. Eradication of H pylori reduces the relapse rate of ulcers but the magnitude of this effect is uncertain.
Objectives:
The primary outcomes were the proportion of peptic ulcers healed initially and proportion of patients free from relapse following successful healing. Eradication therapy was compared to placebo or pharmacological therapies in H. pylori positive patients. Secondary aims included symptom relief and adverse effects.
Search strategy:
Searches were conducted on the Cochrane Central register of Controlled Trials - CENTRAL (which includes the Cochrane Upper Gastrointestinal and Pancreatic Diseases Group Trials Register) on The Cochrane Library (Issue 3 2002) MEDLINE (1966 to July 2002) and EMBASE (1980 to July 2002). Reference lists from trials selected by electronic searching were handsearched to identify further relevant trials. Published abstracts from conference proceedings from the United European Gastroenterology Week (published in Gut) and Digestive Disease Week (published in Gastroenterology) were handsearched. The search was updated in September 2003, November 2004 and November 2005. Members of the Cochrane UGPD Group, and experts in the field were contacted and asked to provide details of outstanding clinical trials and any relevant unpublished materials
Selection criteria:
Randomised controlled trials of short and long-term treatment of peptic ulcer disease in H. pylori positive adults were analysed. Patients received at least one week of H pylori eradication compared with ulcer healing drug, placebo or not treatment. Trials were included if they reported assessment from 2 weeks onwards.
Data collection and analysis:
Data were collected on ulcer healing, recurrence, relief of symptoms and adverse effects.
Main results:
63 trials were eligible. Data extraction was not possible in 7 trials, and 56 trials were included. In duodenal ulcer healing, eradication therapy was superior to ulcer healing drug (UHD) (34 trials, 3910 patients, relative risk [RR] of ulcer persisting = 0.66; 95% confidence interval [CI] = 0.58, 0.76) and no treatment (2 trials, 207 patients, RR = 0.37; 95% CI 0.26, 0.53). In gastric ulcer healing, no significant differences were detected between eradication therapy and UHD (14 trials, 1572 patients, RR = 1.25; 95% CI = 0.88, 1.76). In preventing duodenal ulcer recurrence no significant differences were detected between eradication therapy and maintenance therapy with UHD (4 trials, 319 patients, relative risk [RR] of ulcer recurring = 0.73; 95% CI = 0.42, 1.25), but eradication therapy was superior to no treatment (27 trials 2509 patients, RR = 0.20; 95% CI = 0.15, 0.26). In preventing gastric ulcer recurrence, eradication therapy was superior to no treatment (11 trials, 1104 patients, RR = 0.29; 95% CI 0.20, 0.42).
Authors' conclusions:
A 1 to 2 weeks course of H. pylori eradication therapy is an effective treatment for H. pylori positive peptic ulcer disease.
... In meta-analyses in adults with H. pylori-associated gastric or duodenal ulcers, 13,14 patients with successful eradication significantly increased healing rates and decreased relapse rates compared with those with failed eradication or without eradication therapy. 13,14 In a randomized controlled trial, 15 H. pylori eradication has accelerated rates of ulcer healing in children with H. pylori-associated peptic ulcer disease. ...
... In meta-analyses in adults with H. pylori-associated gastric or duodenal ulcers, 13,14 patients with successful eradication significantly increased healing rates and decreased relapse rates compared with those with failed eradication or without eradication therapy. 13,14 In a randomized controlled trial, 15 H. pylori eradication has accelerated rates of ulcer healing in children with H. pylori-associated peptic ulcer disease. In a cohort study of children with duodenal ulcers, 16 ulcer recurrence rates after H. pylori were successfully eradicated were low with rates of 9% per year at, on average, 2 years' follow up. ...
... For example, there are numerous studies that demonstrate very low positive predictive values for the antibody test(s) when employed in the geographic areas of decreasing prevalence of H. pylori infection. 104 66-100% 94-100% 100% 96% Noninvasive tests 13 C-UBT (meta-analysis) 107 95.9% [Clinical Question 11] What do we need to do to increase the diagnostic accuracy for H. pylori infection? Statement 11: We recommend more than two H. pylori tests such as two non-invasive tests, i.e. breath test and stool test, or a biopsy-based and non-invasive test (i.e. ...
About childhood Helicobacter pylori infection, the Japan Pediatric H. pylori Study Group published the first guidelines in 1997. These guidelines were later revised by the Japanese Society for Pediatric Gastroenterology, Hepatology and Nutrition (JSPGHAN). H. pylori eradication rates when employing triple therapy with amoxicillin and clarithromycin, currently recommended as the first‐line therapy of H. pylori infection in Japan have substantially decreased creating an important clinical problem worldwide. In Japanese adults, the “test and treat” strategy for H. pylori infection is under consideration as an approach for gastric cancer prevention. On the contrary, the combined North American and European pediatric guidelines have recommended against such strategy in asymptomatic children. Since risk for gastric cancer development is high in Japan, it has been an urgent issue to determine whether the “test and treat” strategy can be recommended in children. Accordingly, the JSPGHAN has done the second revision of the H. pylori guidelines, which includes discussion about the issues mentioned above, consisting of nineteen clinical questions and 34 statements. H. pylori culture from gastric biopsies is recommended not only as a diagnostic test for active infection but for antimicrobial susceptibility testing to optimize eradication therapy. Based upon antimicrobial (especially clarithromycin) susceptibility testing of H. pylori strains, an eradication regimen including the susceptible antibiotics is recommended as the first‐line therapy of H. pylori‐associated diseases. The guidelines recommend against a “test and treat” strategy for H. pylori infection for asymptomatic children to protect gastric cancer development, because there has been no evidence supporting such strategy.
... Studies from various parts of the country have shown a strong association of this bacteria with duodenal and gastric ulcers [24][25] . Many papers from the West showed that treatment of this infection not only caused ulcer healing, but also prevented ulcer recurrenc [26][27] . However peptic ulcer can occur again if there was recurrence (either recrudescence or re-infection). ...
... pylori eradication resulted in greater peptic ulcer healing rate (92% vs. 61%) and lower 12-month relapse rate (21% vs. 84%) than non-eradication" 26 . A meta-analysis which included thirty four studies involving around four thousand patients, eradication therapy with antibiotics was superior to proton pump inhibitors alone in healing duodenal ulcer and better to placebo in avoidance of ulcer recurrence 27 . ...
Helicobacter pylori (H. pylori) is a very common infection In India. Nevertheless there remain a lot of
challenges with relation to this infection in this country. The lack of good clinical studies and absence
of guidelines pertaining to the Indian sub continent makes dealing with this infection difficult. There
is a lot of confusion whether to “test and treat” for H. pylori even in patients of peptic ulcer disease
(PUD), un investigated dyspepsia, and those with high risk for gastric malignancy. Invasive and costly
methods such as gastroscopy, rapid urease test (RUT) and biopsy are used to test H. pylori. The noninvasive and cheap diagnostic tools such as breath tests and stool tests are not easily available in
India. Once the diagnosis of H. pylori infection is made, the next challenge is to determine the most
effective antibiotic regimen in Indian context. Issues of antibiotic resistance and re infection make
the management even more difficult. The Indian enigma of high H. pylori infection and low gastric
cancer(GC) rates makes the case against eradication even more strong. It is also important to consider
the genetic diversity of H. pylori in India. More long term prospective studies are required from India
before we can take the eradication at community levels. Improvement of hygiene and sanitation and
providing proper drinking water is a challenge that needs to be taken up by the health administration
to deal with the H. pylori problem.
... 1 H. pylori eradication accelerates the healing of peptic ulcers and prevents their recurrence. 2 Despite many efforts to achieve a proper H. pylori eradication regimen in recent decades, up to 15% to 20% treatment failure is seen in H. pylori eradication regimens. [3][4][5] Thus, the need for new clinical trials to determine an appropriate treatment is obvious. ...
... The relevant organism plays an important role in the development of upper gastrointestinal tract diseases, such as peptic ulcer disease, gastric adenocarcinoma, and MALT lymphoma (1). H. pylori eradication accelerates the healing of peptic ulcers and prevents their recurrence (2). Despite many efforts to achieve a proper H. pylori eradication regimen in recent decades, successful ones are few (3- . ...
Aim: We compared the efficacy of two different regimens for H. pylori eradication in areas with high antibiotic resistance. Background: Helicobacter pylori (H. pylori) is a gram-negative bacillus that has a strong association with chronic gastritis and peptic ulcer disease. Different regimens with varying degrees of effectiveness have been used for H. pylori eradication. Methods: The current randomized controlled trial (RCT) randomly assigned 217 patients who had indications for H. pylori eradication therapy to two groups. One group were administered concomitant quadruple therapy (pantoprazole 40 mg, amoxicillin 1 gr, clarithromycin 500 mg, and metronidazole 500 mg every 12 hours) for 14 days, and the second group received 14 days of high-dose dual therapy, consisting of esomeprazole 40 mg BID and amoxicillin 1g TDS. H. pylori eradication was assessed eight weeks after the end of treatment. Results: H. pylori eradication rates by PP analysis for 14 days concomitant quadruple therapy and high-dose dual therapy were 88.6% (95% CI, 80.3-92.8) and 82.2% (95% CI, 74.8-89.5), respectively (p = 0.19). According to intention-to-treat (ITT) analysis, the eradication rates were 81.6% (95% CI, 74.5-88.6) and 80.6% (95% CI, 73-88.1), respectively (p = 0.58). Overall drug side effects were 20.8% in high-dose dual therapy and 49.6% in concomitant quadruple therapy (p < 0.001). Conclusion: Fourteen days concomitant quadruple therapy can be considered as a relatively acceptable regimen for H. pylori eradication in areas with high clarithromycin and metronidazole resistance. It seems that high-dose dual therapy could be a promising alternative regimen in these areas
... The conventional approach for addressing H. pylori infection is eradication therapy, typically involving combinations of two to three antibiotics in conjunction with a proton-pump inhibitor (3,4). This therapeutic regimen not only fosters the healing of peptic ulcers and prevents their recurrence but also reduces the risk of gastric cancer (5). ...
Background
Helicobacter pylori infection is a global health concern, contributing to gastritis, peptic ulcer disease, and gastric cancer. However, knowledge about H. pylori epidemiology in Somalia is limited. This scoping review aims to synthesize evidence on H. pylori prevalence in Somalia and associated factors.
Methods
We systematically retrieved six scholarly investigations on H. pylori prevalence in Somalia published until 2023 from academic databases. We extracted data on prevalence, demographics, and covariate factors.
Results
H. pylori infection varied (32.4–56.5%) across studies, with higher rates in adults and outpatient settings. Temporal variability was observed. Gastritis symptoms and female gender showed an association with H. pylori infection, while age, family history, diet, lifestyle, and comorbidities had inconclusive associations.
Conclusions
Somalia faces a substantial H. pylori burden, reaching 56.5% in symptomatic adults seeking outpatient care. Temporal prevalence fluctuations require further investigation. These findings inform research and clinical management. Population-based studies are essential to establish a national prevalence profile. This research addresses a critical knowledge gap in Somalia's H. pylori epidemiology, guiding public health strategies. Journals in gastroenterology, infectious diseases, and public health may consider this for publication.
... Helicobacter pylori is a causal risk factor for peptic ulcer disease; its eradication therapy is effective in treating and preventing the recurrence of both gastric and duodenal ulcers. 27,28 There is a potential causal link between H pylori infection and dyspeptic symptoms. Helicobacter pylori eradication had a small but statistically significant effect on the relief of dyspeptic symptoms in H pylori-positive patients. ...
Helicobacter pylori infection causes chronic gastric inflammation that contributes to various gastroduodenal diseases, including peptic ulcer and gastric cancer. Despite broad regional variations, the prevalence of resistance to antibiotics used to manage H pylori infection is increasing worldwide; this trend could hinder the success of eradication therapy. To increase awareness of H pylori and improve the diagnosis and treatment of its infection in Hong Kong, our consensus panel proposed a set of guidance statements for disease management. We conducted a comprehensive review of literature published during 2011 and 2021, with a focus on articles from Hong Kong or other regions of China. We evaluated the evidence using the Oxford Centre for Evidence-Based Medicine's 2011 Levels of Evidence and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system and sought consensus through online voting and a subsequent face-to-face meeting, which enabled us to develop and refine the guidance statements. This report consists of 24 statements regarding the epidemiology and burden, screening and diagnosis, and treatment of H pylori. Key guidance statements include a recommendation to use the test-and-treat approach for high-risk individuals, as well as the confirmation that triple therapy with a proton pump inhibitor, amoxicillin, and clarithromycin remains a valid first-line option for adults and children in Hong Kong.
... Es liegen mehrere homogene Metaanalysen vor, die den Nutzen einer Eradikationsbehandlung bei peptischen Ulzera des Magens und Duodenums mit und ohne Komplikationen eindeutig belegen [237][238][239][240][241][242][243]. ...
... Most of the patients affected with H. Pylori have no symptoms, but the infection can lead to peptic ulcers, MALToma and adenocarcinoma of the stomach [2]. Chronic untreated reflux diseases can cause a variety of conditions including esophagitis, Barrett's esophagus, esophageal carcinoma, gastric ulcers, and even life-threatening esophageal and gastric perforation [3][4][5][6][7]. Studies have shown that these complications can be avoided or minimized by agents that work by neutralizing the acidic pH of the stomach [8] (see Fig. 1) Different classes of medications are used to decrease the gastric pH including Proton pump inhibitors (PPIs), H2 Histamine blockers, antacids etc. ...
Gastroesophageal reflux disease (GERD) is one of the most prevalent conditions worldwide and is conventionally treated by proton pump inhibitor therapy. However, around 40% of people have reported some form of resistance to this therapy. Vonoprazan has recently been approved for the treatment of GERD. Literature was searched on PubMed, Google Scholar, Embase and Medline. Inclusion criteria were 1) Human subjects; 2) papers published in English language; 3) study types that are RCTs.
In pre-clinical studies, VPZ was unaffected by changes in pH, making it 1.2–2 times more potent than PPI, both in-vivo and in-vitro. In studies involving GERD, several RCTs proved higher efficacy of VPZ than conventional PPI. RCTs on patients affected by H. Pylori showed a higher efficacy than VPZ (95.8%) as compared to PPI (69.6%). In another RCT, adverse effects including diarrhea, nausea and body rash were observed in 32.7% of the people taking VPZ as compared to 40.5% of the people taking PPI. VPZ was shown to be much more cost effective as compared to PPI.
This article concludes that VPZ is superior to PPI in terms of efficacy, safety and cost-effectiveness in reflux disorders and H. pylori eradication. Hence, use of vonoprazan should be preferred over conventional PPIs in these disorders. As most of the research was conducted in Japan, studies should be carried out in different regions of the world to explore if these results are extrapolated in those regions. Research is also needed to explore the efficiency of VPZ in scenarios of PPI resistance.
... The relevant organism plays an important role in the development of upper gastrointestinal tract diseases, such as peptic ulcer disease, gastric adenocarcinoma, and MALT lymphoma (1). H. pylori eradication accelerates the healing of peptic ulcers and prevents their recurrence (2). Despite many efforts to achieve a proper H. pylori eradication regimen in recent decades, successful ones are few (3- . ...
Aim:
We compared the efficacy of two different regimens for H. pylori eradication in areas with high antibiotic resistance.
Background:
Helicobacter pylori (H. pylori) is a gram-negative bacillus that has a strong association with chronic gastritis and peptic ulcer disease. Different regimens with varying degrees of effectiveness have been used for H. pylori eradication.
Methods:
The current randomized controlled trial (RCT) randomly assigned 217 patients who had indications for H. pylori eradication therapy to two groups. One group were administered concomitant quadruple therapy (pantoprazole 40 mg, amoxicillin 1 gr, clarithromycin 500 mg, and metronidazole 500 mg every 12 hours) for 14 days, and the second group received 14 days of high-dose dual therapy, consisting of esomeprazole 40 mg BID and amoxicillin 1g TDS. H. pylori eradication was assessed eight weeks after the end of treatment.
Results:
H. pylori eradication rates by PP analysis for 14 days concomitant quadruple therapy and high-dose dual therapy were 88.6% (95% CI, 80.3-92.8) and 82.2% (95% CI, 74.8-89.5), respectively (p = 0.19). According to intention-to-treat (ITT) analysis, the eradication rates were 81.6% (95% CI, 74.5-88.6) and 80.6% (95% CI, 73-88.1), respectively (p = 0.58). Overall drug side effects were 20.8% in high-dose dual therapy and 49.6% in concomitant quadruple therapy (p < 0.001).
Conclusion:
Fourteen days concomitant quadruple therapy can be considered as a relatively acceptable regimen for H. pylori eradication in areas with high clarithromycin and metronidazole resistance. It seems that high-dose dual therapy could be a promising alternative regimen in these areas.
... Только такая тактика позволяет избежать рецидива ЯБ в долгосрочной перспективе после рубцевания язвенного дефекта [39]. Согласно Кокрейновскому обзору и метаанализу, эрадикационная терапия инфекции H. pylori у инфицированных пациентов снижает риск рецидива ЯБ двенадцатиперстной кишки (относительный риск (ОР) 0,20; 95% ДИ: 0,15-0,26) и желудка (ОР 0,31; 95% ДИ 0,22-0,45) в сравнении с плацебо [41]. В другом метаанализе, обобщившем результаты 5 рандомизированных контролируемых исследований в популяции пациентов с ЯБ, осложненной перфорацией, было продемонстрировано, что эрадика-ционная терапия значительно снижает риск рецидива заболевания в течение года после ушивания дефекта (ОР 1,49; 95% ДИ: 1,10-2,03) [42]. ...
Peptic ulcer disease (PUD) is a chronic polyetiological recurrent disease of gastroduodenal region. In most cases, the pathogenesis of PU is caused by imbalance between the aggressive factors and protective factors of the gastric or duodenal mucosa. Helicobacter pylori (H. pylori ) infection and the use of non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin, are the major causative factors leading to PUD development. 65% of gastric ulcers and 80% of duodenal ulcers were found to be associated with H. pylori infection. In turn, NSAIDs account for 30% of gastric ulcers and 15% of duodenal ulcers. About 0.1–1% of all PUs are caused by Zollinger-Ellison syndrome. Abdominal pain is the leading symptom in the clinical findings of patients with exacerbation of PUD. Dyspeptic syndrome (vomiting, nausea, belching, abnormal bowel pattern) is much less common in patients with PUD. Endoscopic examination of the upper gastrointestinal tract is currently the gold standard test used in the diagnosis of PUD and is recommended for all patients suspected of having this disease (unless contraindicated). Antisecretory therapy including proton pump inhibitors is the main approach to the treatment of PUD, as well as the prevention of its complications. Integral to the treatment of patients with H. pylori -associated PU is the eradication therapy of the infection. It is reasonable to use a cytoprotector rebamipide, which accelerates ulcer healing and improves the resulting scar quality, as part of the pharmacotherapy of PUD. In addition, the use of rebamipide in H. pylori eradication therapy regimens contributes to increased efficiency of elimination of the microorganisms.
... In fact, treatment effects in other medical conditions often have similar absolute risk reduction rates between 2 and 10 out of 100. So for example 2 patients out of 100 have a benefit from antibiotic treatment of Helicobacter-associated peptic ulcer disease (Ford et al., 2006). This fits with our earlier work showing that framing critical risk information in a patient-centred way and communicating especially scientific uncertainties is bearable for pwMS (Heesen et al., 2004, Köpke et al., 2018. ...
Background
Multiple sclerosis treatment options are increasing. Evidence-based patient information (EBPI) are therefore crucial to enable patient involvement in decision making. Based on earlier work on decision support, patient information handbooks on 8 MS immunotherapies were developed, piloted and evaluated with support from the German Clinical Competence Network MS and the German MS Society.
Methods
Handbooks were structured according to EBPI concepts. Drafts were commented by patient representatives and neurologists with an MS expertise. Executive boards of the German MS Society and the Competence Network as well as pharmaceutical companies’ feedback was included. Handbooks were distributed among MS neurologists by the German MS Society. Evaluation followed applying a mixed methods approach with interviews, focus groups and surveys. One survey addressed persons with MS (pwMS) based on a questionnaire included in each handbook. Neurologists who received printed patient handbooks were invited to give feedback in a second survey.
Results
Eight handbooks were developed providing absolute and relative risk information in numbers and figures as well as monitoring needs and drug fact boxes. Despite the high amount of information and the display of low absolute risk reduction rates of treatments, handbooks were overall appreciated by pwMS (n=107) and mostly also by physicians (n=24). For more than 70% of the pwMS the information was new, understandable and supportive for decision making. But patients felt uncomfortable with relative risk information. However, response rates in the evaluation were low, exposing the challenges when implementing EBPI into clinical care. Therefore, conclusions must be considered preliminarily.
Conclusion
EBPI on immunotherapies for MS seem feasible and are appreciated by patients and treating neurologists but more implementation research is needed.
... Eradication of H. pylori can promote ulcer healing, significantly reduce the ulcer recurrence rate, and benefit some patients with functional dyspepsia. [4,26,27] PPIs are a vital part of the H. pylori eradication program, making antibiotics more stable in gastric acid and improving the eradication rate by increasing the PH value of gastric juice. [28] However, some studies have found that PPI alone can induce the sphericity of H. pylori, [24] which reduces the sensitivity of H. pylori to antibiotics and reduces the eradication rate. ...
Background:
In this meta-analysis, we aimed to comprehensively investigate the impact of pretreatment with proton pump inhibitor (PPI) on Helicobacter pylori (H. pylori) eradication and provide novel inspiration to clinical practice.
Methods:
Relevant studies were selected through PubMed, Embase, and Cochrane Library from inception to March 2021. Two reviewers performed the selection independently. The primary outcome of the meta-analysis was the eradication rate. A modified Jadad scale was used to evaluate literature quality quantitatively.
Results:
Ten studies were included in this research. The results showed no significant difference between PPI pretreatment and standard treatment on eradication of H. pylori [relative risk (RR): 1.17, 95% confidence interval (95% CI): 0.0.73-1.88]. There was no significant difference between the PPI pretreatment group and the standard therapy group for conventional triple therapy, PPI and amoxicillin and clarithromycin (RR: 1.29, 95% CI: 0.60-2.77). Similar results were obtained in the therapy strategy of PPI and amoxicillin and metronidazole (RR: 3.01, 95% CI: 0.62-14.74). Interestingly, for the therapy regimen of PPI and clarithromycin and metronidazole, PPI pretreatment indicated superiority on H. pylori eradication rate (RR: 0.48, 95% CI: 0.23-0.97, P < .05).
Conclusion:
PPI pretreatment did not affect the H. pylori eradication rates, regardless of the various types of bacteriostatic antibiotic, except the therapy regimen of PPI and clarithromycin and metronidazole.
... La infección por H. pylori está asociada con diferentes patologías serias de carácter benigno y maligno como la dispepsia refractaria al tratamiento, la úlcera péptica, el linfoma y el cáncer gástrico; su erradicación se ha relacionado con una disminución del riesgo para presentarlas (19)(20)(21). La pérdida de eficacia de los tratamientos antibióticos se ha convertido en preocupación creciente, sobre todo en Latinoamérica, donde el cáncer gástrico es una de las neoplasias con índices altos de mortalidad (22,23). ...
Introducción: el Helicobacter pylori (H. pylori) es una bacteria gram negativa y es considerado como el principal agente etiológico de diversas patologías gastrointestinales como gastritis, úlceras pépticas, cáncer gástrico y linfoma MALT. Las guías de la Asociación Colombiana de Gastroenterología para el diagnóstico y tratamiento del H. pylori recomiendan el uso de la triple terapia estándar con claritromicina, amoxicilina y un inhibidor de la bomba de protones como la terapia de primera línea cuando la resistencia a la claritromicina es inferior al 15%.Objetivo: determinar la eficacia del tratamiento con claritromicina, amoxicilina y esomeprazol, durante diez días para el tratamiento de la infección por H. pylori e identificar factores asociados a la respuesta del tratamiento.Materiales y métodos: se estudiaron pacientes remitidos para esofagogastroduodenoscopia, que consultaron los centros Soluciones Integrales en Gastroenterología/Hepatología y a la Clínica Crecer en Cartagena - Colombia, en el período comprendido entre marzo de 2013 y agosto de 2015. Se ordenó evitar consumo de inhibidores de bombade protones y antibióticos entre 15-30 días previos a la realización del procedimiento endoscópico; en biopsia gástrica previa se demostró la presencia de H.pylori. Se administró el tratamiento indicado por 10 días, por lo que se realizó un seguimiento diario de los medicamentos y, después de 30 días, se realizó estudio endoscópico de control.Resultados: 190 pacientes fueron incluidos en el estudio. 67 fueron excluidos por no presentar el diario de medicamentos en la cita de control para confirmar la adherencia al tratamiento, y otros 83 por diversas razones. 50 de ellos fueron estudiados, se observó mejoría en 32 (64%), mientras que 18 pacientes no mostraron mejoría alguna.Ninguno de los factores valorados fue estadísticamente significativo con respecto al resultado terapéutico.Conclusión: la eficacia estimada fue 60%; y ninguno de los factores evaluados fue significativamente asociado a la respuesta al tratamiento. Rev.cienc.biomed. 2016;7(2)258-264.
... Комментарии: В метаанализе, обобщившем результаты 5 рандомизированных контролируемых исследований в популяции пациентов с язвенной болезнью, осложненной перфорацией, было продемонстрировано, что эрадикационная терапия значительно снижает риск рецидива заболевания в течение года после ушивания дефекта (ОР 1,49; 95 % ДИ: 1,10-2,03) [28]. Согласно Кокрейновскому обзору и другому метаанализу, эрадикационная терапия инфекции H. pylori у инфицированных пациентов с снижает риск рецидива язвенной болезни двенадцатиперстной кишки (ОР = 0,20; 95 % ДИ: 0,15-0,26) и желудка (ОР = 0,29; 95 % ДИ 0,20-0,42) в сравнении с плацебо [29]. ...
Aim. These clinical recommendations present up-to-date methods for the diagnosis and treatment of peptic ulcer. The recommendations are intended for gastroenterologists and general practitioners.General provisions. Peptic ulcer (PU) represents a chronic relapsing disease occurring with alternating periods of exacerbation and remission. The main manifestation of the disease is the formation of a defect (ulcer) in the wall of the stomach and duodenum. Most cases of peptic ulcer are pathogenetically associated with the infection of H. pylori. PU can be an independent disease or represent symptomatic ulcers of the stomach and duodenum (medicinal, as a result of stress or endocrine pathologies, associated with chronic diseases of internal organs). In the absence of contraindications, esophagogastroduodenoscopy is recommended for all patients with suspected ulcer with the purpose of confirming the diagnosis. In order to determine indications for eradication therapy, all ulcer patients should be tested for the presence of H. pylori using a 13C-breath test or a stool antigen test. In the case of simultaneous endoscopy, rapid urease test can be used. For the prevention of subsequent relapses of ulcer, all PU patients with confirmed H. pylori should undergo eradication therapy. In addition, in order to achieve ulcer healing, 4–6 week antisecretory therapy with proton pump inhibitors is recommended. Clinical recommendations contain criteria for assessing the quality of medical care, an algorithm of the doctor’s actions, as well as information for patients.Conclusions. These clinical recommendations present modern ideas about the etiology and pathogenesis of peptic ulcer disease, its clinical manifestations, methods of laboratory and instrumental diagnostics and basic approaches to conservative and surgical treatment.
... Helicobacter pylori (H. pylori) infection is a major cause of DU and the eradication of H. pylori is essential to prevent the development of DU (1). In the duodenal bulb, anterior ulcers are common, with Kang et al. reporting that recurrent DUs were more likely to occur in the anterior region (2). ...
Objective: To evaluate the diagnostic utility of wall hypertrophy of the duodenal bulb with a hyperechoic lumen, designated as the “HH sign,” using ultrasound sonography (US) in pediatric duodenal ulcer (DU) patients.
Study design: We performed a US for five pediatric subjects diagnosed with DU by upper gastroscopy to determine the presence of the potentially diagnostic HH sign. The sonographic images were analyzed before and after DU treatment. Computed tomography was performed in three cases and fecal occult blood test (FOBT) in all five cases.
Results: Upper gastroscopy confirmed DU in all patients. While the HH sign was observed using US in four cases, with the DU located in the anterior bulb, the FOBT was positive in only one case. In these four cases, the HH sign diminished in response to treatment, as visualized by US. This was observed for both the initial as well as recurrent episodes. A mass-like region was observed in only one case, with the ulcer located in the proximity of the inferior duodenal wall.
Conclusion: The HH sign is useful for the follow-up of DU, and US may be a suitable modality for the follow-up. We believe that this diagnostic marker can aid in following up a greater number of DU cases.
... 15 If the patient is treated when no testing is available, serology can show if infection was present when samples are taken at the first convenient point. 12,14 If symptoms persist despite treatment and if there are any worrying symptoms such as progressive, unintentional weight loss, progressive difficulty with swallowing, persistent vomiting or an epigastric mass, the patient should be referred for urgent specialist input. These symptoms would require a patient to be repatriated to the UK when possible. ...
Peptic ulcer disease (PUD) is decreasing in incidence but is still prevalent within the military population. This article describes the epidemiology, pathophysiology and key clinical manifestations as well as outlining the diagnosis, treatment and complications of this disease. McKnight G, Powell C.
... Endoscopically confirmed peptic ulcers without H pylori infection are treated with a PPI until healed, along with elimination of any other known risk factors. Systematic reviews have shown that PPIs accelerate the healing process and facilitate eradication of H pylori. [50][51][52] The odds of ulcer healing were three times higher with PPIs compared with control group (odds ratio 3.49, 95% confidence interval 3.28 to 3.72) in a recent meta-analysis (847 randomised trials, 142 485 participants). 50 For duodenal ulcers, when H pylori is the predominant cause, acid suppression included in the eradication therapy for 7-14 days is usually sufficient for healing. ...
... Treatment for H. pylori-positive gastric and duodenal ulcers has been demonstrated to prevent recurrence and decrease ulcer-related complications (eg, bleeding) according to high-level evidence, including multiple published meta-analyses conducted in Japan and other countries. [21][22][23][24][25] Eradication therapy should be the first-choice treatment for H. pylori-positive peptic ulcers (including ulcer scars) unless the patient is allergic to the drug used for eradication or has a severe complication that hinders eradication treatment. ...
Background
Since “Helicobacter pylori (H. pylori) infection” was set as the indication in the Japanese Society for Helicobacter Research (JSHR) Guidelines 2009, eradication treatment for H. pylori gastritis is covered under insurance since 2013 in Japan, and the number of H. pylori eradication has rapidly increased. Under such circumstances, JSHR has made the third revision to the “Guidelines for diagnosis and treatment of H. pylori infection” for the first time in 7 years.
Methods
The Guideline Committee held 10 meetings. Articles published between the establishment of the 2009 Guidelines and March 2016 were reviewed and classified according to the evidence level; the statements were revised on the basis of this review. After inviting public comments, the revised statements were finalized using the Delphi method.
Results
There was no change in the basic policy that H. pylori infectious disease is an indication for eradication. Other diseases presumed to be associated with H. pylori infection were added as indications. Serum pepsinogen level, endoscopic examination, and X‐ray examination were added to the diagnostic methods. The effects of 1‐week triple therapy consisting of potassium‐competitive acid blocker (P‐CAB), amoxicillin, and clarithromycin have improved, and high eradication rates can also be expected with proton pump inhibitors (PPI) or P‐CAB combined with amoxicillin and metronidazole. If the susceptibility test is not performed, the triple PPI or P‐CAB/amoxicillin/metronidazole therapy should be chosen, because the PPI/amoxicillin/metronidazole combination demonstrated a significantly higher eradication rate than PPI/amoxicillin/clarithromycin. In the proposal for gastric cancer prevention, we divided gastric cancer prevention measures by age from adolescent to elderly, who are at an increased gastric cancer risk, and presented measures for gastric cancer prevention primarily based on H. pylori eradication.
Conclusion
We expect the revised guidelines to facilitate appropriate interventions for patients with H. pylori infection and accomplish its eradication and prevention of gastric cancer.
... versus 2.67%, respectively) (23,24). Failure of H. pylori eradication is associated with diverse clinical outcomes, including chronic gastritis, hypergastrinemia, ulcer formation, intestinal metaplasia, atrophy, dystrophy, obesity, insulin resistance and cancer in the infected patients (25)(26)(27)(28)(29)(30)(31)(32). The prolonged inflammatory reaction is believed to be one of the main factors contributing to the malignant transformation of the gastric epithelium in these patients. ...
... Different therapeutic schemes have been proposed over time and many of them include two antibiotics and a PPI given in two standard daily doses for 7-14 days [48]. So, PPIs represent a key component of any currently adopted regimen for H. pylori eradication and many clinical trials have shown that it is possible to obtain rates of success as high as 80-90% [49]. As these rates tended to diminish in the last years, mainly due to the development of clarithomycin resistance, recent Consensus statements suggest the use of quadruple regimens containing also bismuth as powerful drug against H. pylori [50]. ...
Introduction: The introduction of proton pump inhibitors (PPIs) into clinical practice has greatly improved our therapeutic approach to acid-related diseases for their efficacy and safety.
Areas Covered:The following evidence-based indications for PPI use are acknowledged by many scientific societies: treatment of the various forms and complications of gastroesophageal reflux disease, eradication of H. pylori infection in combination with two or more antibiotics, short- and long-term therapy of H. pylori-negative peptic ulcers, healing and prevention of NSAID/COXIB-associated gastric ulcers, co-therapy with endoscopic procedures to control upper digestive bleeding and medical treatment of Zollinger Ellison syndrome.
Expert Commentary:Despite the above well defined indications, however, the use of PPIs continues to grow every year in both western and eastern countries and the endless expansion of PPI market has created important problems for many regulatory authorities for two relevant features: the progressive increase of the costs of therapy and the greater potential harms for the patients. The major reasons for the misuse of PPIs are the prevention of gastro-duodenal ulcers in patients without risk factors and the stress ulcer prophylaxis in non-intensive care units, steroid therapy alone, anti-platelet or anti-coagulant treatment in patients without risk of gastric injury and the overtreatment of functional dyspepsia.
... H. pylori is gram-negative, helical, rod-shaped bacterium, colonizes the mucosa of stomach approximately one-half of population [2] . H. pylori is found in 95% of patient of duodenal ulcer and 70% of cases with gastric ulcers [3] . It is typically transmitted via the fecal-oral route during early childhood and persists for decades. ...
Introduction: Peptic ulcer disease (PUD) is very common problem encountered by physicians in day-today practice. Prevalence of this disease varies from country to country and Previous concept regarding PUD was that “no acid, no ulcer”. Now, it is certain that H. pylori is the main agent causing peptic ulcer.H. pylori is found in 95% of patients with duodenal ulcers and 70% of cases with gastric ulcers. H. pylori infection is chronic and once acquired remains life long, unless eradicated by antibiotics given for some other conditions.
Methods and Materials: This study was conducted on 100 acid PUD patients at Internal Medicine Department of Index Medical College Hospital and Research Centre, Indore from October 2017 to April
2018.Patients who were suffering from symptoms related to PUD who gave consent for upper gastrointestinal endoscopy, those patients were selected for this study and the H. pylori infection was
detected by rapid urease test (RUT) kit test.
Results: Among the 100 patients of PUD who were studied in this study, 75 patients had RUT positive result and 25 patients had RUT negative result. It was also observed that amongst the RUT positive
patients, those who had strongly positive RUT status, they had more severe form of peptic ulcer disease, whereas weakly positive RUT patients had moderately severe form of the disease, and those who had negative RUT report, they had very minor form of the disease.
Conclusion: High prevalence of H. pylori infection is found in patients suffering from PUD in rural India hence its treatment can help in preventing significant morbidity as well as recurrence in these patients. Patients with various complaints, where UGI endoscopy is done, they should routinely have their H. pylori status checked, regardless of indication.
Keywords: Peptic ulcer disease, H. pylori, Upper gastrointestinal endoscopy, Rapid Urease Test.
... Different therapeutic schemes have been proposed over time and many of them include two antibiotics and a PPI given in two standard daily doses for 7-14 days [51]. So, PPIs represent a key component of any currently adopted regimen for H. pylori eradication and many clinical trials have shown that it is possible to obtain rates of success as high as 80%-90% [52]. As these rates tended to diminish in last years, mainly due to the development of clarithomycin resistance, recent Consensus statements suggest the use of quadruple regimens containing also bismuth as powerful drug against H. pylori [53]. ...
The introduction of proton pump inhibitors (PPIs) into clinical practice about thirty years ago has greatly improved our therapeutic approach to acid-related diseases for their well-recognized efficacy and safety.
Despite the well-defined indications, however, the use of PPIs continues to grow every year in both western and eastern countries and this phenomenon poses serious queries that include the onset of potential adverse effects and the increase in health care costs. The major reason explaining this worrying market expansion is the inappropriate use of PPIs. In order to re-establish a correct use of these effective drugs in daily clinical practice, the Italian Society of Gastroenterology (SIGE), nominated a panel of experts who reviewed the available clinical literature and produced a series of updated position statements on the use of PPIs in clinical practice.
... 56 So, PPIs represent a key component of any currently adopted regimen for H. pylori eradication and many clinical trials have shown that it is possible to obtain rates of success as high as 80%-90%. 57 as these rates tended to diminish in last years, mainly due to the development of clarithomycin resistance, recent consensus statements suggest the use of quadruple regimens containing also bismuth as powerful drug against H. pylori. 58 However, PPis remain the mainstay of anti-Helicobacter therapy also in these more complex regimens. ...
The introduction of proton pump inhibitors (PPIs) into clinical practice since about thirty years has greatly improved our therapeutic approach to acid-related diseases for their well recognized efficacy and safety. Accordingly, the role of surgery has been enormously reduced in this field. The main indications for PPI use are universally acknowledged by many scientific societies and are the following: treatment of gastroesophageal reflux disease in its various forms and complications, eradication of H. pylori infection in combination with two or more antibiotics, therapy of H. pylori-negative peptic ulcers, healing and prevention of NSAID-associated gastric ulcers, co-therapy with endoscopic procedures to control upper digestive bleeding and medical treatment of Zollinger Ellison syndrome. Despite the above well defined indications, however, the use of PPIs continues to grow every year in both western and eastern countries and this phenomenon poses serious queries about the appropriate prescription of these drugs worldwide. In fact, the endless expansion of PPI market has created important problems for many regulatory authorities for two relevant features : the progressive and irreversible increase of the costs of therapy with this class of drugs and the greater potential harms for the patients. So, there is the need for a reappraisal of PPI correct indications for both general practitioners and various specialists in order to re-establish a correct use of these effective drugs in daily clinical practice, according to the best evidence-based guidelines.
... Along with rats, Guinea pigs are used when histamine is used to induce ulcers. [17][18][19][20] Anti-secretory activity screening ...
Ulcers are caused by imbalance between the gastro duodenal mucosal defensive factors such as bicarbonate, mucus versus aggressive factors like acid and pepsin secretion. The drug treatment of peptic ulcer has significantly brought down the morbidity and mortality and need of surgical interventions which may be attributed to the advent of H2 blockers and proton pump inhibitors. These symptoms frequently occur several hours following a meal, after the food leaves the stomach but while acid production is still high. Instead of pain, some patients experience intense hunger or bloating. Many animal models are using to induce ulcer to identify the antiulcer property of many new and existed drugs such as Pyloras ligated rat, Stress ulcers, Histamine induced gastric ulcers, Cysteamine induced duodenal ulcers and Dulcerozine induced duodenal ulcers.
... In some cases, these lesions penetrate the muscularis mucosa and as such may be called ulcers. It is suggested that the above mentioned all types of induced models procedure meets the established criteria for a useful experimental ulcer model and thus represents a viable research tool [22,23]. ...
Peptic ulcers are caused by imbalance between the gastro duodenal mucosal defensive factors such as
bicarbonate, mucus versus aggressive factors like acid and pepsin secretion. The drug treatment of peptic
ulcer has significantly brought down the morbidity and mortality and need of surgical interventions which
may be attributed to the advent of H2 blockers and proton pump inhibitors. These symptoms frequently
occur several hours following a meal, after the food leaves the stomach but while acid production is still
high. Instead of pain, some patients experience intense hunger or bloating. Many animal models are using to
induce ulcer to identify the antiulcer property of many new and existed drugs such as Pyloras ligated rat,
Stress ulcers, Histamine induced gastric ulcers, Cysteamine induced duodenal ulcers, Dulcerozine induced
duodenal ulcers, Duodenal ulcers following Infusion of pentagastrin and carbacol, Indomethacin and
histamine induced duodenal ulcers, MPTP induced duodenal ulcers. The above all induced types are useful
experimental model for the research.
... showed that eradication therapy significantly reduced the risk of gastric ulcer by 69% compared to no eradication therapy. 22 In two meta-analyses including five and seven RCTs, significant reductions of 57% and 50% were found, respectively, in the prevention of peptic ulcers among NSAID users following H. pylori eradication. 23,24 NSAIDs can also cause peptic ulcers through direct ulcerogenic effects as well as the inhibition of cyclooxygenase and depletion of endogenous prostaglandins, which impair mucosal defense mechanism. ...
Helicobacter pylori (H. pylori) infection remains to be the major cause of important upper gastrointestinal diseases such as chronic gastritis, peptic ulcer, gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma. H. pylori management in ASEAN: the Bangkok consensus report gathered key opinion leaders for the region to review and evaluate clinical aspects of H. pylori infection and to develop consensus statements, rationales and grades of recommendation for the management of H. pylori infection in clinical practice in ASEAN countries. This ASEAN Consensus consisted of 34 international experts from 10 ASEAN countries, Japan, Taiwan and the United States. The meeting mainly focused on four issues: 1) Epidemiology and Disease Association; 2) Diagnostic tests; 3) Management; and 4) Follow-up after eradication. The final results of each workshop were presented for consensus voting by all participants. Statements, rationale and recommendations were developed from the available current evidence to help clinicians in the diagnosis and treatment of H. pylori and its clinical diseases.
Background: Helicobacter pylori infection is a global health concern, contributing to gastritis, peptic ulcer disease, and gastric cancer. However, knowledge about H. pylori epidemiology in Somalia is limited. This scoping review aims to synthesize evidence on H. pylori prevalence in Somalia and associated factors. Methods: We systematically retrieved six scholarly investigations on H. pylori prevalence in Somalia published until 2023 from academic databases. We extracted data on prevalence, demographics, and covariate factors. Results: H. pylori infection varied (32.4% to 56.5%) across studies, with higher rates in adults and outpatient settings. Temporal variability was observed. Gastritis symptoms and female gender showed an association with H. pylori infection, while age, family history, diet, lifestyle, and comorbidities had inconclusive associations. Conclusions: Somalia faces a substantial H. pylori burden, reaching 56.5% in symptomatic adults seeking outpatient care. Temporal prevalence fluctuations require further investigation. These findings inform research and clinical management. Population-based studies are essential to establish a national prevalence profile. This research addresses a critical knowledge gap in Somalia's H. pylori epidemiology, guiding public health strategies. Journals in gastroenterology, infectious diseases, and public health may consider this for publication.
Zusammenfassung
Unangenehmes Völlegefühl nach den Mahlzeiten, Schmerzen im Oberbauch, Übelkeit und andere dyspeptische Symptome sind in der Allgemeinbevölkerung weit verbreitet, beeinträchtigen die Lebensqualität und verursachen erhebliche Kosten im Gesundheitswesen. In dieser Übersichtsarbeit wird die Rom-IV-Definition der funktionellen Dyspepsie und verwandter „Störungen der Gehirn-Darm-Interaktion“ (früher als funktionelle gastrointestinale Erkrankungen bezeichnet) beschrieben. Die pathophysiologischen Ursachen der Symptome werden erörtert und ein strukturierter Ansatz für die Behandlung von funktioneller Dyspepsie wird vorgestellt. Insbesondere wird die Stellung der klinischen Untersuchung der gastrischen Funktion thematisiert. Es wird vorgeschlagen, dass die Identifizierung spezifischer Phänotypen auf der Grundlage der klinischen Präsentation und der Ergebnisse physiologischer Messungen eine spezifischere und effektivere Behandlung von Patienten mit dyspeptischen Beschwerden ermöglichen kann.
Background
Helicobacter pylori ( H. pylori ), a bacterium implicated in the development of peptic ulcer and gastric cancer, is estimated to infect around half the world’s population. Its prevalence in Australia is unclear. This scoping review aimed to evaluate all Australian literature providing estimates of the prevalence of H. pylori .
Methods
Australian studies examining H. pylori prevalence from 1982 onwards were eligible for inclusion. Medline, Embase and Scopus databases, and grey literature sources, were searched. Two independent reviewers undertook a two-stage screening process. Data were extracted by two independent reviewers using a pre-specified template.
Results
Of 444 identified studies, 75 were included in the review. H. pylori prevalence in Australian population-based studies ( n = 8) ranged from 38.0% in 1991 to 15.1% in 2002; however, estimated prevalence across all non-clinical population studies in diverse sub-groups ( n = 29) has varied dramatically. Decreased prevalence has been more marked in populations with gastrointestinal symptoms and conditions compared to non-clinical populations. Data on H. pylori prevalence in vulnerable populations are lacking.
Conclusions
This is the first scoping review of Australian studies reporting H. pylori prevalence. A wide range of study designs, population groups, geographic regions, and diagnostic methods was included, involving data collected over a 50-year period (1969 to 2018). The summary of H. pylori prevalence estimates over time in this review points to a decrease in prevalence in Australia, particularly among populations with gastrointestinal symptoms and illnesses; however, it is unknown whether there is inequity in prevalence trends across vulnerable sub-groups of the Australian population. Future research and interventions supporting the health and wellbeing of vulnerable populations is required to ensure equitable health gains are made for all.
Introduction:
This article summarizes the evidence-based recommendations of the clinical practice guide (CPG) for the diagnosis and management of Helicobacter pylori infection in gastroduodenal diseases.
Methods:
For the provision of these recommendations, a guideline development group (local GDG) was established, including medical specialists andmethodologists that formulated seven clinical questions. Systematic searches of systematic reviews and -when it was considered pertinent- primary studies were conducted in PubMed and CENTRAL during December 2017 and July 2019. The evidence to answer each of the posed clinical questions was selected. The quality of the evidence was evaluated using the Grading ofRecommendations Assessment, Development, and Evaluation (GRADE) methodology. In periodic work meetings, the local GDG used the GRADE methodology to review the evidence and formulate the recommendations, points of good clinical practice, and flowcharts. Finally, the CPG was approved with Resolution N° 104-IETSI-ESSALUD-2020.
Results:
This CPG addressed seven clinical questions, divided into four topics. Based on these questions, 12 recommendations (3 strong and 9 weak), 17 points of good clinical practice, and two flowcharts (one for diagnosis and another for management) were formulated.
Conclusion:
This article summarizes the methodology and evidence-based conclusions from the CPG for for the diagnosis and management of Helicobacter pylori infection in gastroduodenal diseases.
Upper gastrointestinal symptoms are among the most common reasons for medical consultation and represent a challenge for general practitioners in the outpatient care setting. History taking, symptom evaluation and physical examination are the crucial steps toward establishing an initial working diagnosis. The subsequent abdominal ultrasound and laboratory analyses are essential tools for the differential diagnosis.
Introduction
In a previous study we demonstrated that a simple training programme improved quality indicators of Oesophagogastroduodenoscopy (OGD) achieving the recommended benchmarks. However, the long-term effect of this intervention is unknown. The aim of this study was to assess the quality of OGDs performed 3 years after of having completed a training programme.
Material and methods
A comparative study of 2 cohorts was designed as follows: Group A included OGDs performed in 2016 promptly after a training programme and Group B with OGDs performed from January to March 2019, this group was also divided into 2 subgroups: subgroup B1 of Endoscopists who had participated in the previous training programme and subgroup B2 of Endoscopists who had not. The intra-procedure quality indicators proposed by ASGE-ACG were used.
Results
A total of 1236 OGDs were analysed, 600 from Group A and 636 from Group B (439 subgroup B1 and 197 subgroup B2). The number of complete examinations was lower in Group B (566 [94.3%] vs. 551 [86.6%]; P < .001). A significant decrease was observed in nearly all quality indicators and they did not reach the recommended benchmarks: retroflexion in the stomach (96% vs. 81%; P < .001); Seattle biopsy protocol (86% vs. 50%; P = .03), description of the upper GI bleeding lesion (100% vs. 62%; P < .01), sufficient intestinal biopsy specimens (at least 4) in suspected coeliac disease (92.5% vs. 18%; P < .001), photo documentation of the lesion (94% vs. 90%; P < .05). Regarding the overall assessment of the procedure (including correct performance and adequate photo documentation), a significant decrease was also observed (90.5% vs. 62%; P < .001). There were no differences between subgroups B1 and B2.
Conclusions
The improvement observed in 2016 after a training programme did not prevail after 3 years. In order to keep the quality of OGDs above the recommended benchmarks, it is necessary to implement continuous training programmes.
Resumen
Introducción
En un estudio previo demostramos que un pequeño programa de formación mejoraba los indicadores de calidad de la esofagogastroduodenoscopia (EGD) que llegaban a los estándares recomendados. Sin embargo, desconocemos el efecto de esta formación a largo plazo. El objetivo de este estudio fue valorar la calidad de las EGD después de 3 años de haber realizado un programa de mejora.
Material y métodos
Estudio comparativo de 2 cohortes: EGD posteriores a un programa de formación realizado en 2016 (grupo A) y EGD en enero-marzo de 2019 (grupo B). El grupo B se dividió en 2 subgrupos: endoscopistas que habían participado en el programa de formación previo (B1) y los que no (B2). Se utilizaron los indicadores de calidad intraprocedimiento recomendados por la ASGE-ACG.
Resultados
Se analizaron un total de 1.236 EGD, 600 en el grupo A y 636 en el B (439 subgrupo B1 y 197 subgrupo B2). El número de exploraciones completas fue inferior en el grupo B (566 [94,3%] vs. 551 [86,6%]; p < 0,001). Se observó una disminución significativa en prácticamente todos los indicadores de calidad que, además, no alcanzaron los estándares recomendados: retroversión gástrica (96% vs. 81%; p < 0,001); protocolo de biopsias de Seattle (86% vs. 50%; p = 0,03), descripción de la lesión en la hemorragia (100% vs. 62%; p < 0,01), toma de ≥ 4 biopsias en sospecha de celiaquía (92,5% vs. 18%; p < 0,001), fotodocumentación de lesión (94% vs. 90%; p < 0,05). Cuando consideramos el global de la prueba (incluyendo la actuación correcta y la fotodocumentación adecuada), también se observó una disminución significativa (90,5% vs. 62%; p < 0,001). No hubo diferencias entre los subgrupos B1 y B2.
Conclusiones
La mejora observada en 2016 tras un programa de formación no perdura a los 3 años. Es necesario hacer programas de formación continuados para mantener la calidad de la EGD por encima de los estándares recomendados.
Background/aims:
Serologic tests are commonly used for screening Helicobacter pylori infection because they not only provide quick results but also are inexpensive. A new latex agglutination serum antibody assay (LZ test) has been developed and it is expected to be as effective as conventional assays. This study aimed to calculate a reliable cutoff value for the LZ test and to estimate the sensitivity and specificity of the cutoff value in screening adolescents for H. pylori infection in Japan.
Methods:
We screened junior high school students in Akita Prefecture, Japan, for H. pylori infection. We used the data of 213 such students who underwent H. pylori stool antigen (HpSA) tests in 2016. The students who had positive results with HpSA tests were diagnosed with H. pylori infection. Of the 213 students, 209 underwent the LZ test.
Results:
The prevalence rate of H. pylori infection was 3.8% (8/209). The area under the curve for the LZ test was 0.88. The cutoff value of the LZ test was determined to be 3.1 U/mL. At this value, the sensitivity and specificity were 87.5 and 91.5%, respectively.
Conclusion:
The accuracy of the LZ test in adolescents was well balanced for sensitivity and specificity as well as for tolerable results.
Vonoprazan-based regimens have improved the rate of successful Helicobacter pylori (H. pylori) eradication, but it has not reached 100%. The aim of this study is to clarify significant predictors of successful H. pylori eradication using a vonoprazan-based regimen. In this retrospective cohort study, 174 patients who underwent primary H. pylori eradication therapy were included. All patients underwent esophagogastroduodenoscopy before treatment. The vonoprazan-based regimen includes amoxicillin 750 mg, clarithromycin 200 mg and vonoprazan 20 mg twice daily for one week. Pre-treatment with a proton pump inhibitor (PPI) was defined as continued PPI use for more than four weeks prior to eradication therapy. The rates of successful eradication were 83% (145/174) in intention-to-treat analysis and 85% (145/171) in per-protocol analysis. Predictors of successful eradication among 171 patients were evaluated in per-protocol analysis. In univariate analysis, male gender was a significant positive predictor of successful eradication (odds ratio [OR] 3.813, 95% confidence interval [CI] 1.363–10.663, p = 0.010) and pre-treatment with PPIs was a negative predictor (OR 0.193, 95%CI 0.076–0.485, p < 0.001). In multivariate analysis, male gender remained a positive predictor (OR 3.826, 95%CI 1.317–11.116, p = 0.013), and pre-treatment with PPIs (OR 0.232, 95%CI 0.087–0.615, p = 0.003) remained a negative predictor. In conclusion, pre-treatment with PPIs before eradication therapy decreases the rate of successful eradication. Therefore, it may be desirable to discontinue pre-treatment with PPIs prior to eradication therapy, because of the potential to improve the rate of successful eradication.
INTRODUCTION: L’application en soins primaires des recommandations nationales etinternationales semble insuffisante. Leur pertinence en soins primaires est discutable en raison de la faible participation d’experts de médecine générale aux groupes de travail et de rédaction. L’objectif de cette étude était de proposer des recommandations applicables en soins primaires sur les indications de prescription d’un test de dépistage non invasif de Helicobacter pylori.MÉTHODE : Une revue de la littérature respectant les standards prisma a été réalisée. Les résultats ont été présentés à un groupe composé de 7 médecins dont 4 généralistes, 1 hépato gastroentérologue, 1 biologiste et 1 interniste, ce qui a permis de réaliser la méthode du groupe nominal.RÉSULTATS : Indications en respectant les conditions d’emploi des tests: contrôled’éradication, avant prescription d’aspirine ou d’AINS à faible dose au long cours, antécédent familial du premier degré de cancer gastrique et âge #lt# 50 ans, récidive d’une symptomatologie ulcéreuse, anémie chronique par carence martiale, traitement par IPP au long cours en vue de son arrêt, dyspepsie sans signe d’alarme ou persistante à plus de 6 mois de traitement symptomatique. Non-indications: patient asymptomatique, pas de test non invasif après 55 ans mais endoscopie indiquée. Le test respiratoire à l’urée marquée est le plus approprié.CONCLUSION : Les recommandations jugées applicables en soins primaires sont voisines des recommandations nationales ou internationales, mais organisées de manière différente
Quality improvement in healthcare has emerged as an increasingly central focus of public discourse. The death of Libby Zion in 1984 introduced the fallibility of healthcare providers and potential for error inherent in the practice of medicine into the public consciousness. The Institute of Medicine’s 1999 landmark report “To Err is Human” crystallized awareness of the widespread prevalence of medical errors, capturing the attention of lawmakers and the general public with its estimate of up to 98,000 deaths attributable to medical errors annually (Kohn LT, Corrigan J, Donaldson MS. To err is human: building a safer health system. Washington, D.C.: National Academy Press; 2000.) and serving as a call to action to advance the cause of patient safety. The report prompted legislation such as the “Healthcare Research and Quality Act of 1999”, which renamed the Agency for Health Care Policy and Research to the Agency for Healthcare Research and Quality and funded agency projects to address these new priorities. The Institute of Medicine followed up with its 2001 report “Crossing the Quality Chasm” which expanded its focus from error and patient safety to the health system organization and more explicitly emphasized aligning payment methods with quality improvement goals and empowerment of consumers and payers (Institute of Medicine. Crossing the quality chasm: a new health system for the 21st century. Washington, D.C.: National Academy Press; 2001). The Medicare Prescription Drug, Improvement, and Modernization Act in 2003 enacted these recommendations and linked hospital payment to quality. The combined forces of public interest, regulatory emphasis, and financial inducements have contributed to the burgeoning attention to quality improvement.
Dyspepsia is one of the most common gastrointestinal conditions seen in both primary and specialist care. The most prevalent organic causes of dyspeptic symptoms are peptic ulcer disease and gastroesophageal reflux disease (GERD). The key investigation in patients with (chronic) dyspeptic symptoms is upper gastrointestinal endoscopy, which can identify erosive esophagitis, peptic ulcer, or gastric or esophageal cancer. In patients presenting with dyspeptic symptoms, clinical history should identify the major complaint, and determine whether symptoms are related to meal ingestion, and whether they are intermittent or continuous. The differential diagnosis of dyspepsia is extremely broad, including virtually all upper gastrointestinal tract diseases. Management of uninvestigated dyspepsia includes prompt diagnostic endoscopy, noninvasive testing for Helicobacter pylori infection followed by eradication therapy if positive (test and treat) and initial empirical acid-suppressive therapy. In refractory patients, psychological therapies such as cognitive behavioral therapy or hypnotherapy can be considered.
Peptic ulcer disease – chiefly gastric and duodenal ulcers – remains of global importance to human health. The majority of peptic ulcers are caused by Helicobacter pylori (Hp) infection or nonsteroidal anti-inflammatory drug (NSAID) use, including aspirin. However non-Hp, non-NSAID ulcers are becoming more common. Healthcare practitioners from different countries face different diagnostic and therapeutic challenges, at both the patient and population level. These arise from the changing epidemiology of the major causes, differences in Hp antibiotic resistance, and other temporal and geographical trends. Fundamental considerations in management are however constant: firstly treatment to achieve ulcer healing; and secondly the identification and management of specific causes – particularly eradication therapy for Hp and preventative strategies for drug-induced ulcers.
Helicobacter pylori infection can lead to the occurrence of many diseases of the upper gastrointestinal tract and is one of the most common causes of peptic ulcer disease (PUD). This discovery of H. pylori made possible not only to understand the origin of the disease, but also to use an appropriate treatment and prevent PUD recurrence.
The first Canadian Helicobacter pylori Consensus Conference took place in April 1997. The initial recommendations of the conference were published in early 1998. An update meeting was held in June 1998, and the present paper updates and complements the earlier recommendations. Key changes included the following: the recommendation for testing and treating H pylori infection in patients with known peptic ulcer disease was extended to testing and treating patients with ulcer-like dyspepsia; it was decided that the urea breath test (not serology) should be used for routine diagnosis of H pylori infection unless endoscopy is indicated for another reason; and recommended therapies were a twice daily, seven-day regimen of a proton pump inhibitor (omeprazole 20 mg, lansoprazole 30 mg, pantoprazole 40 mg) or ranitidine bismuth citrate 400 mg, plus clarithromycin 500 mg and amoxicillin 1000 mg, or plus clarithromycin 500 or 250 mg and metronidazole 500 mg. The need was reiterated to have funding for readily accessible, accurate testing for H pylori infection with the urea breath test. It was strongly recommended that regional centres be established to monitor the prevalence of antibiotic resistant H pylori infections. The initial consensus document referred to pediatric issues that were not addressed in this update but were the subject of a subsequent Canadian Helicobacter Study Group meeting, and will be published later in 1999.
Background
We hypothesized that treatment of duodenal ulcer disease with antibiotic therapy directed toward Helicobacter pylori infection is more cost-effective than therapy with antisecretory agents.Methods
A randomized, double-blind, multicenter clinical trial of adult patients with active duodenal ulcer and H pylori infection was conducted. Patients were randomized to receive 500 mg of clarithromycin 3 times a day plus 40 mg of omeprazole daily for 14 days followed by 20 mg of omeprazole daily for an additional 14 days (group 1), 20 mg of omeprazole daily for 28 days (group 2), or 150 mg of ranitidine hydrochloride twice a day for 28 days (group 3). The use of ulcer-related health care resources was documented during monthly interviews for 1 year after the initial therapy. Clinical success was evaluated 4 to 6 weeks and 1 year after the end of therapy.Results
Of the 819 patients enrolled, 727 completed the study. Group 1 included 243 patients; group 2, 248 patients; and group 3, 236 patients. Patients in group 1 used fewer ulcer-related health care resources during the 1 year after therapy compared with groups 2 and 3 (comparisons are given as group 1 vs group 2 and group 1 vs group 3, respectively): the number of endoscopies performed, 28 vs 76 (P<.001) and vs 71 (P<.001); patients receiving drugs to treat an ulcer, 118 vs 180 (P<.001) and vs 168 (P<.001); clinic visits, 83 vs 135 (P=.05) and vs 161 (P<.001); hospitalizations, 0 vs 5 (P=.045) and vs 6 (P=.02); and length of hospital stay, 0 vs 24 days (P=.04) and vs 37 (P=.04). When ulcer-related costs were defined as the outcome variable in a multivariate linear regression analysis, therapy was determined to have a significant influence on costs (group 1 vs group 2, P<.001; group 1 vs group 3, P=.008). Clinical success rates at the end of the study and cure of H pylori infection were significantly greater in group 1 compared with groups 2 and 3 (P<.001). Therapy with clarithromycin plus omeprazole provided savings of $1.94 and $2.96 (compared with therapy with omeprazole and with ranitidine hydrochloride, respectively) per dollar spent within the first year after therapy. This incremental cost-benefit translates to savings of $547 or $835 per patient in group 1 (compared with patients in group 2 or group 3, respectively) during the first year after therapy.Conclusions
Combination therapy with clarithromycin and omeprazole resulted in significantly fewer uses of ulcer-related health care resources than conventional antisecretory therapy during a 1-year follow-up and significant savings in associated costs during the same period. Patients who received clarithromycin plus omeprazole also showed a significantly improved clinical outcome compared with patients who received only omeprazole or ranitidine.
Figures in this Article
HELICOBACTER PYLORI infection is present in approximately 90% of patients with duodenal ulcer disease, and the causal relationship between H pylori infection and duodenal ulcers is supported by the observation that ulcer recurrence is significantly decreased after the cure of infection.1 Based on these findings, a comprehensive economic analysis of the treatment of H pylori infection was recommended by the National Institutes of Health Consensus Development Conference.1 Studies using simulated economic models to compare the cost-effectiveness of various therapies for the treatment of duodenal ulcer disease2- 9 suggest that eradication of H pylori infection is cost-effective compared with intermittent or maintenance therapy with antisecretory agents such as omeprazole or ranitidine hydrochloride. However, no prospective, randomized clinical trials have assessed this hypothesis.
In previous studies, the treatment of duodenal ulcer with clarithromycin plus omeprazole resulted in decreased ulcer recurrence compared with omeprazole monotherapy.10- 13 We hypothesized that this improved clinical outcome would be associated with savings in the use of ulcer-related health care resources and associated health care costs. The present study was designed to assess the clinical effectiveness, the use of health care resources, and the economic costs of therapy with clarithromycin plus omeprazole compared with therapy with only omeprazole or ranitidine for 1 year in a setting that approximated usual clinical practice.
Objective: To evaluate, prospectively, whether omeprazole and amoxycillin eradicate Helicobacter pylori and prevent duodenal ulcer relapse. Patients and methods: This prospective multicentre trial included 53 patients. Twenty-nine H. pylori-positive patients were treated with omeprazole for 4 weeks (group A) and the remaining 24 received amoxycillin 'plus' omeprazole for 2 weeks. Eradication of H. pylori was evaluated using the rapid urease test and histological examination. Results: Six months after the end of therapy, H. pylori was eradicated in two out of 23 patients (9%) from group A and 10 out of 21 (48%) from group B. The ulcer relapse rate was 68% (n = 15) for patients from group A and 17% (n = 3) for those from group B. Conclusions: Our regimen eradicated H. pylori in half of our patients and is effective in preventing ulcer relapse with few adverse events.
To determine whether one week's drug treatment is sufficient to eradicate Helicobacter pylori in patients with duodenal ulcer.
Single blind, randomised controlled trial.
Specialised ulcer clinic in a teaching hospital.
155 patients with H pylori and a duodenal ulcer verified endoscopically which had either bled within the previous 24 hours or was causing dyspepsia.
Patients were allocated randomly to receive either omeprazole for four weeks plus bismuth 120 mg, tetracycline 500 mg, and metronidazole 400 mg (all four times a day) for the first week (n = 78), or omeprazole alone for four weeks (n = 77). Further endoscopy was performed four weeks after cessation of all drugs.
Presence or absence of H pylori (by urease testing, microscopy, and culture of antral biopsy specimens), duodenal ulcer, and side effects.
Eradication of H pylori occurred in 70 (95%) patients taking the four drugs (95% confidence interval 86% to 97%) compared with three (4%) patients taking omeprazole alone (1% to 11%). Duodenal ulcers were found in four (5%) patients taking the four drugs (2% to 12%) and in 16 (22%) patients taking omeprazole alone (14% to 32%). Mild dizziness was the only reported side effect (six patients in each group) and did not affect compliance.
A one week regimen of bismuth, tetracycline, and metronidazole is safe and effective in eradicating H pylori and reduces the number of duodenal ulcers four weeks after completing treatment.
Persistence of Helicobacter pylori after duodenal ulcer healing is associated with high rates of ulcer relapse. We compared colloidal bismuth subcitrate alone with CBS combined with one of four antibiotic regimens in the treatment of duodenal ulcers. Endoscopy and antral biopsies were performed before treatment and four weeks afterwards. Biopsy specimens were examined for histological evidence of gastritis and by Gram stain and culture for H pylori infection. Altogether 141 patients were allocated to one of five treatment groups. Giving CBS and metronidazole (400 mg tid for 7 days) with and without amoxycillin (500 mg tid) achieved higher clearance rates of H pylori than treatment with CBS alone (p less than 0.01). These two combinations also achieved higher rates of antral gastritis healing than CBS alone (p less than 0.01 and p less than 0.05 respectively). Susceptibility to metronidazole was tested in 29 isolates before and in seven isolates after treatment with metronidazole by disc diffusion test and minimum inhibitory concentration assay. Twenty seven (93%) of the isolates were sensitive before treatment while six of seven (86%) were resistant afterwards. Four of the six resistant strains had acquired resistance during treatment and one of these had acquired metronidazole resistance despite concomitant treatment with amoxycillin, to which it remained sensitive. CBS with adjuvant metronidazole at a dose of 400 mg tid for seven days significantly improves the eradication of H pylori compared with CBS alone. Acquired metronidazole resistance, however, seems to be an important cause of failure to eradicate H pylori.
To determine the 12-month posttherapy recurrence (recrudescence) of Helicobacter pylori in patients with healed duodenal ulcer after apparent eradication of the organism with anti-H. pylori treatment. The influence of original anti-H. pylori treatment regimens on the recrudescence was also evaluated.
One hundred and ninety patients who had duodenal ulcer healed and H. pylori eradicated (as assessed by four routine techniques 4 wk after the end of anti-H. pylori therapy) with one of five regimens were studied. The five regimens were: 1) colloidal bismuth subcitrate (CBS) 120 mg; 2) CBS plus amoxicillin (500 mg); 3) CBS plus metronidazole (400 mg); 4) CBS plus metronidazole and amoxicillin; and 5) CBS plus metronidazole and tetracycline (500 mg). CBS was taken four times daily for 4 wk, and antibiotics were taken three times daily for the first week. The patients were re-endoscoped, and the status of H. pylori, duodenal ulcer, and gastritis was assessed after a period of follow-up (mean 14 months after commencement of treatment).
H. pylori infection recurred in 36 (18.9%) of these patients. Recrudescence rate with monotherapy was 47.1%, with dual therapy 29.2-35% and with triple therapy 9.2-14.3%. Nineteen (52.7%) of the 36 patients with recrudescent infection had ulcer relapse, and the rate for H. pylori-negative patients was 3.2% (5/154).
Recrudescence of H. pylori infection after apparent eradication can occur, but it could be that the treatment was only suppressing the organism. The definition of eradication of H. pylori infection may need to be revised, and more sensitive techniques to assess eradication of H. pylori are required.
Persistent infection with Helicobacter pylori is associated with the recurrence of duodenal ulcer. Whether the efficacy of bismuth therapy in reducing the rate of recurrence of duodenal ulcer is due to its antimicrobial effects on H. pylori or to a direct protective action on the mucosa is still a matter of debate.
To study the effect of the eradication of H. pylori on the recurrence of duodenal ulcer, we treated 104 patients with H. pylori infection and recurrent duodenal ulcer with either amoxicillin (750 mg three times daily) plus metronidazole (500 mg three times daily) or identical-appearing placebos, given orally for 12 days. All patients also received ranitidine (300 mg each night) for 6 or 10 weeks. Endoscopy was performed before treatment and periodically during follow-up for up to 12 months after healing.
Among the 52 patients given antibiotics, H. pylori was eradicated in 46, as compared with 1 of the 52 given placebo (89 percent vs. 2 percent, P < 0.001). After six weeks, the ulcers were healed in 48 patients given antibiotics and 39 given placebo (92 percent vs. 75 percent, P = 0.011). Side effects, mainly diarrhea, occurred in 15 percent of the patients given antibiotics. Among the patients followed up for 12 months, duodenal ulcers recurred in 4 of 50 patients given antibiotics and 42 of 49 given placebo (8 percent vs. 86 percent, P < 0.001). Ulcers recurred in 1 of 46 patients in whom H. pylori had been eradicated, as compared with 45 of 53 in whom H. pylori persisted (2 percent vs. 85 percent, P < 0.001).
In patients with recurrent duodenal ulcer, eradication of H. pylori by a regimen that does not have any direct action on the mucosa is followed by a marked reduction in the rate of recurrence, suggesting a causal role for H. pylori in recurrent duodenal ulcer.
Helicobacter pylori is presently considered a major factor predisposing to the development of duodenal ulceration. Long-term remission of duodenal ulcer after initial healing is closely related to eradication of H. pylori. But, H. pylori is difficult to eradicate, and successful treatment requires the concurrent administration of two or more antimicrobial drugs. The aim of this study is to compare different therapeutic regimens in the treatment of duodenal ulcer and H. pylori infection. 125 patients with duodenal ulcer were studied. Multiple endoscopic biopsies were obtained from the corpus, antrum and the duodenal bulb of each patient. Sections of biopsy tissue were stained with hematoxylen-eosin and Warthin-Starry to examine for mucosal inflammation and H. pylori, respectively. The patients were randomised to receive one of the five different therapeutic regimens; (1) famotidine, (2) omeprazole plus amoxicillin (OA), (3) bismuth (De-Nol, 480 mg/d, 1 month), metronidazole and amoxicillin (DMA), (4) omeprazole plus clarithromycin (OC), (5) omeprazole, amoxicillin and clarithromycin (OAC).(omeprazole 40 mg/d, amoxicillin 2 g/d, and clarithromycin 1 g/d were given for two weeks.) Investigations were repeated at the end of treatment, after two and six months. Rates of ulcer healing were higher in the DMA (76%) and OAC (81%) groups than others (p<0.001). Eradication of H. pylori was similar in DMA (53%), OC (55%) and OAC (62%) groups (p > 0.05). The patients in OA group had the lowest eradication rate (21%). Continuous suppression of acid secretion with famotidine was not successful, because of low healing (47%) and high relapse (50%) rates of duodenal ulcer.
Objective: To test the hypothesis that omeprazole facilitates the eradication of Helicobacter pylori. This paper seeks to continue this hypothesis and to search for treatment with a low incidence of side effects. Design and patients: Sixty patients with a duodenal ulcer and H. pylori colonization were randomly assigned to either omeprazole (OME) 40 mg twice daily for 10 days followed by 20 mg for a total duration of 6 weeks (n = 30), or omeprazole 40 mg twice daily with amoxicillin (AMO) 1000 mg (OME + AMO) for the first 10 days followed by 20 mg OME only for a similar 6-week period (n = 30). Results: Four patients on OME monotherapy and three patients on OME + AMO had to be withdrawn because of lack of compliance (0/1; OME/OME + AMO), missing follow-up control examinations (2/1; OME/OME + AMO), side effects (1/0; OME/OME + AMO), or negative H. pylori status at the time of recruitment (1/1; OME/OME + AMO). All duodenal ulcers healed in patients on OME + AMO and 25 out of 26 (96%) duodenal ulcers healed in patients on OME monotherapy. H. pylori was eradicated in 22 out of 27 patients (82%) receiving OME + AMO; no ulcer relapses occurred within 9 months in these 22 patients. In the five patients who remained H. pylori-positive after OME + AMO therapy relapse was not detected during a 9-month follow-up. In the OME group all patients remained H. pylori positive and duodenal ulcers relapsed in 12 out of 25 patients (48%) within a median follow-up of 9 months. Side effects were absent in the OME + AMO group; one patient with OME had severe headaches. Conclusions: The results further support preliminary data that H. pylori eradication may heal duodenal ulcer disease. The well tolerated OME + AMO regimen which carried a high H. pylori eradication rate makes it a potential therapeutic agent for the healing of duodenal ulcer disease.
Background: Trials evaluating long-term management of duodenal ulcer disease have mainly been focused on recurrence of ulcers, disregarding effects on dyspeptic and reflux symptoms. Profound acid inhibition with a proton pump inhibitor is the gold standard therapy in acid-related diseases. We aimed to compare the symptomatic effects of eradication therapy with those of long-term omeprazole treatment in a design with periods both with and without acid inhibition. Methods: Patients with active duodenal ulcer were randomized either to omeprazole, 20 mg twice daily until healing, followed by omeprazole, 20 mg/day for 1 year, or to eradication therapy (metronidazole, amoxicillin, and omeprazole for 2 weeks) followed by placebo for 1 year. All patients were followed up passively for an additional year. Clinical controls were performed every 2 months the 1st year (maintenance phase) and every 6 months during the passive follow-up phase. The study was multicentric and double-blind. The primary end-point was disco...
▪ Objective: To determine whether antimicrobial therapy for Helicobacter pylori infection accelerates the healing of duodenal ulcers.
▪ Design: Single-blind, randomized, controlled trial.
▪ Setting: Veterans Affairs hospital.
▪ Participants: One hundred and five patients with endoscopically verified duodenal ulcers.
▪ Intervention: Patients received either ranitidine, 300 mg/d, or ranitidine, 300 mg/d, plus "triple therapy" (2 g/d of tetracycline, 750 mg/d of metronidazole, and 5 or 8 bismuth subsalicylate tablets per day). Triple therapy was administered for only the first 2 weeks of ulcer treatment.
▪ Measurements: Videoendoscopic assessment of ulcer status was done until ulcer healing was complete. Evaluations were done after 2, 4, 8, 12, and 16 weeks of therapy.
▪ Main Results: Ulcer healing was more rapid in patients receiving ranitidine plus triple therapy than in patients receiving ranitidine alone (P < 0. 01). The cumulative percentages of patients with healed ulcers in the group receiving ranitidine plus triple therapy and in the group receiving ranitidine alone were as follows: 37% and 18% after week 2; 74% and 53% after week 4; 84% and 68% after week 8; 96% and 80% after week 12; and 98% and 84% after week 16.
▪ Conclusion: Combined therapy with anti-H. pylori agents and ranitidine was superior to ranitidine alone for duodenal ulcer healing. Our results indicate that H. pylori plays a role in duodenal ulcer disease.
▪ Objective: To determine the effect of treating Helicobacter pylori infection on the recurrence of gastric and duodenal ulcer disease.
▪ Design: Follow-up of up to 2 years in patients with healed ulcers who had participated in randomized, controlled trials.
▪ Setting: A Veterans Affairs hospital.
▪ Participants: A total of 109 patients infected with H. pylori who had a recently healed duodenal (83 patients) or gastric ulcer (26 patients) as confirmed by endoscopy.
▪ Intervention: Patients received ranitidine, 300 mg, or ranitidine plus triple therapy. Triple therapy consisted of tetracycline, 2 g; metronidazole, 750 mg; and bismuth subsalicylate, 5 or 8 tablets (151 mg bismuth per tablet) and was administered for the first 2 weeks of treatment; ranitidine therapy was continued until the ulcer had healed or 16 weeks had elapsed. After ulcer healing, no maintenance antiulcer therapy was given.
▪ Measurements: Endoscopy to assess ulcer recurrence was done at 3-month intervals or when a patient developed symptoms, for a maximum of 2 years.
▪ Results: The probability of recurrence for patients who received triple therapy plus ranitidine was significantly lower than that for patients who received ranitidine alone: for patients with duodenal ulcer, 12% (95% Cl, 1% to 24%) compared with 95% (Cl, 84% to 100%); for patients with gastric ulcer, 13% (Cl, 4% to 31%) compared with 74% (44% to 100%). Fifty percent of patients who received ranitidine alone for healing of duodenal or gastric ulcer had a relapse within 12 weeks of healing. Ulcer recurrence in the triple therapy group was related to the failure to eradicate H. pylori and to the use of nonsteroidal anti-inflammatory drugs.
▪ Conclusions: Eradication of H. pylori infection markedly changes the natural history of peptic ulcer in patients with duodenal or gastric ulcer. Most peptic ulcers associated with H. pylori infection are curable.
. Objective : To compare the costs of alternative strategies for the treatment of duodenal ulcer. . Design : A cost comparison using decision analysis. . Methods : A decision model was used to compare the costs per cure of an endoscopically documented duodenal ulcer for three initial treatment strategies : 1) H 2 -receptor antagonist therapy for 8 weeks, 2) antibiotic therapy for Helicobacter pylori infection plus H 2 -receptor antagonist therapy, and 3) urease test-based treatment. For symptomatic recurrences, secondary treatment strategies included empiric retreatment with the same or other regimen, and treatment based on repeat endoscopy-guided urease test or biopsy, with an assumption of subsequent cure. The cohort modeled for this analysis consisted of patients at low risk for a malignant ulcer. Probability estimates were derived from published clinical trials, cohort studies, and expert opinion. Side effects from combination therapy with antibiotics and H 2 -receptor antagonists and resulting costs were included from the perspective of a group practice model health maintenance organization. . Results : For all secondary treatment strategies, initial therapy with antibiotics for H. pylori infection plus an H 2 -receptor antagonist resulted in the lowest average costs per symptomatic cure when the prevalence or likelihood of H. pylori infection exceeded 66% to 76% ; the costs ranged from $284 for secondary (re)treatment with empiric antibiotic and H 2 -receptor antagonist therapy to $398 for endoscopy-guided secondary treatment. Initial treatment with an H 2 -receptor antagonist resulted in the highest costs, ranging from $372 for secondary treatment with empiric antibiotic and H 2 -receptor antagonist therapy to $679 for endoscopy-guided secondary treatment. The results were not sensitive to the rates of duodenal ulcer recurrence after either treatment, to the cost of either treatment, or to prevalence of H. pylori. . Conclusions : This cost analysis indicates that, regardless of the secondary treatment used for ulcer recurrence, initial therapy with antibiotics for H. pylori infection plus an H 2 -receptor antagonist provides the lowest costs per symptomatic cure. These cost savings and the lower recurrence rates associated with this treatment favor eradication of H. pylori as part of the initial treatment of duodenal ulcer.
Background and aims:
Although the role of H. pylori in peptic ulcer disease is no longer in dispute, certain aspects of eradication therapy in this condition have yet to be settled. Uncertainties still surround the relationship between Helicobacter pylori status and ulcer healing, the efficacy of eradication therapy in alleviating acute symptoms and healing ulcers, and the prognosis after eradication with respect to recurrence of symptoms, ulcers and complications. The present literature review, encompassing studies published up to October 1995, specifically addresses these issues.
Results:
Pooled data show that eradication therapy heals > or = 90% of duodenal ulcers and > or = 85% of gastric ulcers, while individual studies repeatedly confirm that it is more effective at healing ulcers than conventional treatment with anti-secretory drugs. Recent reports indicate that triple therapy regimens for 1 week, provided they include an anti-secretory drug, are sufficient to achieve high rates of healing and rapid symptom relief. A detailed analysis of the data, particularly those from studies reporting healing rates in relation to H. pylori status after eradication therapy, provides strong evidence that eradication of H. pylori produces ulcer healing. Follow-up studies show that ulcer recurrence and complications are rare after eradication treatment in patients with either gastric or duodenal ulcer disease. However, while ulcer symptoms are infrequent during follow-up, a proportion of patients appear to develop gastrooesophageal reflux after eradication.
Conclusions:
H. pylori eradication is highly effective in promoting ulcer healing and preventing subsequent ulcer recurrence. These beneficial effects of eradication therapy are observed in patients with either gastric or duodenal ulcers which are associated with H. pylori infection.
Background. Because patients who fail to be cured of H. pylori infection following macrolide or imidazole therapy are difficult to treat, there is a clear need for a reasonably effective and simple second-line treatment regimen. The purpose of these two studies was to evaluate the efficacy of ranitidine bismuth citrate (RBC) plus amoxicillin for the cure of H. pylori infection and for healing duodenal ulcers and preventing ulcer relapse.
Materials and Methods. Two identically designed randomized, double-blind, double-dummy studies were conducted in patients with an H. pylori-associated duodenal ulcer. Patients were treated with either RBC 400 mg bid for 4 weeks plus amoxicillin 500 mg qid for 2 weeks, RBC 400 mg bid for 4 weeks and placebo qid for 2 weeks, placebo bid for 4 weeks and amoxicillin 500 mg qid for 2 weeks, or placebo bid for 4 weeks and placebo qid for 2 weeks. Patients with healed ulcers after 4 weeks of treatment were eligible for entry into a 24-week observation phase for the assessment of H. pylori status (culture, histology, and CLOtestTM) and ulcer relapse.
Results. A total of 229 patients with confirmed H. pylori infection at baseline were evaluated. Of these, 132 whose ulcers had healed entered the 24-week posttreatment observation phase. The combination of RBC plus amoxicillin resulted in higher H. pylori cure rates (55%) and higher duodenal ulcer healing (74%) than did either treatment alone. All treatments were well tolerated.
Conclusions. The combination of ranitidine bismuth citrate plus amoxicillin cures H. pylori infection in more than half of the patients treated. This treatment regimen shows promise as the basis for future non-macrolide, non-imidazole triple therapy regimens for curing H. pylori infection. Such regimens may be appropriate second-line treatment for patients who are resistant to or who are unable to tolerate macrolide- or imidazole-containing therapies.
Significant progress and new insights have been gained in the 4 years since the first Maastricht Consensus Report, necessitating an update of the original guidelines. To achieve this, the European Helicobacter Pylori Study Group organized a meeting of specialists and experts from around the world, representatives from National Gastroenterology Societies and general practitioners from Europe to establish updated guidelines on the current management of Helicobacter pylori infection. The meeting took place on 21–22 September 2000.
A ‘test and treat’ approach is recommended in adult patients under the age of 45 years (the age cut‐off may vary locally) presenting in primary care with persistent dyspepsia, having excluded those with predominantly gastro‐oesophageal reflux disease symptoms, non‐steroidal anti‐inflammatory drug users and those with alarm symptoms. Diagnosis of infection should be by urea breath test or stool antigen test.
As in the previous guidelines, the eradication of H. pylori is strongly recommended in all patients with peptic ulcer, including those with complications, in those with low‐grade gastric mucosa‐associated lymphoid tissue lymphoma, in those with atrophic gastritis and following gastric cancer resection. It is also strongly recommended in patients who are first‐degree relatives of gastric cancer patients and according to patients’ wishes after full consultation.
It is advised that H. pylori eradication is considered to be an appropriate option in infected patients with functional dyspepsia, as it leads to long‐term symptom improvement in a subset of patients. There was consensus that the eradication of H. pylori is not associated with the development of gastro‐oesophageal reflux disease in most cases, and does not exacerbate existing gastro‐oesophageal reflux disease. It was agreed that the eradication of H. pylori prior to the use of non‐steroidal anti‐inflammatory drugs reduces the incidence of peptic ulcer, but does not enhance the healing of gastric or duodenal ulcer in patients receiving antisecretory therapy who continue to take non‐steroidal anti‐inflammatory drugs.
Treatment should be thought of as a package which considers first‐ and second‐line eradication therapies together. First‐line therapy should be with triple therapy using a proton pump inhibitor or ranitidine bismuth citrate, combined with clarithromycin and amoxicillin or metronidazole. Second‐line therapy should use quadruple therapy with a proton pump inhibitor, bismuth, metronidazole and tetracycline. Where bismuth is not available, second‐line therapy should be with proton pump inhibitor‐based triple therapy. If second‐line quadruple therapy fails in primary care, patients should be referred to a specialist. Subsequent failures should be handled on a case‐by‐case basis by the specialist. In patients with uncomplicated duodenal ulcer, eradication therapy does not need to be followed by further antisecretory treatment. Successful eradica‐ tion should always be confirmed by urea breath test or an endoscopy‐based test if endoscopy is clinically indicated. Stool antigen test is the alternative if urea breath test is not available.
The present study evaluated the time in remission during a 2-year follow-up after eradication of Helicobacter pylori (HP) in patients with an HP-associated duodenal ulcer (DU). HP was eradicated by combined treatment with high-dose omeprazole (2 × 40 mg) and amoxicillin (2 × 1,000 mg; n = 27) administered for 10 days (OME + AMX); alternatively, patients were treated with omeprazole monotherapy (OME) using the same dosage (n = 25). During the 2-year follow-up period endoscopy including histological examination was performed after 1 and 2 years or whenever symptoms compatible with ulcer relapse occurred. HP eradication was achieved in 82% of the OME + AMX group, but in 0% of the OME group. The cumulative DU relapse rates were 0% after 1 year and 7% after 2 years in 22 patients who became HP-negative. Both HP-negative patients who relapsed in the 2nd year of follow-up were HP-positive again at the time of relapse. Of the 5 patients who were not eradicated after OME + AMX therapy, 2 relapsed within the 1st year (40%) and another 2 within the 2nd year (80%). In the OME group the cumulative relapse rates within 1 and 2 years of follow-up were 52 and 76%, respectively. The results further confirm that eradication of HP with combined OME + AMX treatment leads to a distinct decrease in DU relapse rates and thus may cure DU disease. Long-term eradication with combined OME + AMX treatment is possible, and the rate of reinfection with HP is low (4.5%/year).
Objective: To evaluate two different therapies, omeprazole/amoxicillin versus omepra-zole alone, in the treatment of duodenal ulcer patients with respect to eradication of Helicobacter pylori and time in remission during a 6-month follow-up after cessation of therapy.
Design: Double-blind, randomized, parallel groups.
Setting: Outpatient referrals in nine Swedish centres.
Patients: This study included 248 patients with active duodenal ulcer.
Main outcome measures: Endoscopic and symptomatic evaluation of time in remission. Culture, histology and serology for determination of H. pylori status.
Results: Eradication of H. pylori was 54 compared with 4% and the proportion of patients in remission at 6 months was 70 compared with 36% in the omeprazole/amoxicillin treated group versus the group treated with omeprazole alone. Of the patients who became H. pylori-negative, 84% were in remission throughout the study.
Conclusion: H. pylori is an almost obligate prerequisite for duodenal ulcer disease. Amoxicillin added to omeprazole nearly doubled the proportion of patients in remission at 6 months follow-up. The eradication rate of H. pylori in patients with excellent compliance was 74%.
(C) Lippincott-Raven Publishers.
The combination of ranitidine bismuth citrate (RBC) and clarithromycin (CLR) was compared with each treatment alone for the eradication of H. pylori and healing of duodenal ulcers in patients infected with H. pylori.
This two-phase, randomized, double-blind, placebo-controlled, multicenter study evaluated 203 patients with an active duodenal ulcer treated with either (1) RBC 400 mg BID for 4 weeks plus CLR 500 mg TID for the first 2 weeks; (2) RBC 400 mg BID for 4 weeks plus placebo TID for the first 2 weeks; (3) placebo BID for 4 weeks plus CLR 500 mg TID for the first 2 weeks; or (4) placebo BID for 4 weeks plus placebo TID for the first 2 weeks. Patients with healed ulcers after treatment entered a 24-week observation phase for the assessment of H. pylori and ulcer relapse.
Four-week ulcer healing rates were higher with RBC + CLR (71%) and RBC alone (66%) compared with placebo (15%;p < 0.05) and CLR alone (49%). H. pylori eradication rates were significantly higher with RBC + CLR (86%) compared with RBC alone (0%, p < .001) or CLR alone (24%, p < .001). Ulcer recurrence rates after 6 months were lower in patients eradicated of H. pylori infection (17%) compared with patients who remained infected (43%). All treatments were well tolerated.
Ranitidine bismuth citrate plus clarithromycin is a simple, convenient, and well-tolerated dual therapy regimen that is effective in eradicating H. pylori and healing duodenal ulcers in patients infected with H. pylori. The eradication of H. pylori in patients with healed ulcers significantly reduces the rate of ulcer relapse.
Helicobacter pylori screening and treatment has been proposed as a cost-effective method of preventing gastric cancer.
To assess, in a randomized controlled trial, the efficacy of therapy in eradicating H. pylori as part of a screening programme, and to report the adverse events associated with this strategy.
Subjects between the ages of 40–49 years were randomly selected from the lists of 36 primary care centres. Participants attended their local practice and H. pylori status was determined by 13C-urea breath test. Infected subjects were randomized to receive omeprazole 20 mg b.d., clarithromycin 250 mg b.d. and tinidazole 500 mg b.d. for 7 days (OCT) or identical placebos. Eradication was determined by a 13C-urea breath test 6 months and 2 years after the first visit. Successful eradication was defined as two negative 13C-urea breath tests or one negative and one missing test. Adverse events and compliance were assessed at the 6-month visit.
A total of 32 929 subjects were invited to attend, 8407 were evaluable, and 2329 (28%) of these were H. pylori-positive. A total of 1161 subjects were randomized to OCT and 1163 to placebo; over 80% returned for a repeat 13C-urea breath test on at least one occasion. The eradication rates in those allocated to OCT were as follows: intention-to-treat, 710 out of 1161 (61%; 95% confidence interval: 58–64%); evaluable 710 out of 967 (73%; 95% CI: 71–76%); took all medication 645 out of 769 (84%; 95% CI: 81–87%). Adverse events occurred in 45% of the treatment group and in 18% of the placebo group (relative risk 2.5; 95% CI: 2.1–2.9). Compliance, male gender, no antibiotic prescription in the subsequent 2 years and experiencing a bitter taste with the medication were independently associated with treatment success.
The OCT regimen has an eradication rate of 61% in intention-to-treat analysis and is therefore less successful in treating H. pylori as part of a screening programme compared with hospital studies in dyspeptic patients.
In this study, 26 patients with duodenal ulcers refractory to treatment with H2-receptor antagonists for 8–12 weeks were randomly assigned to eight weeks of treatment with colloidal bismuth subcitrate (120 mg four times a day) alone (N=12) or in combination with tetracycline hydrochloride (500 mg four times a day, days 0–14) and metronidazole (500 mg three times a day, days 15–28). Symptoms were scored and endoscopy, histology, and CLO tests were performed before, on completion of treatment, and 3, 6, 12, and 18 months after treatment. Treatment was considered successful whenHelicobacter pylori was not detected by CLO tests and Warthin-Starry stains on gastric biopsies taken from antrum, body, and fundus. On triple therapy, ulcers healed in 12/14 patients (85.71%) and 10/14 (71.42%) patients becameHelicobacter pylori-negative. On bismuth, only one patient becameHelicobacter pylori-negative (8.33%,PP=NS). Six patients on bismuth, whose ulcers remained unhealed or relapsed early after healing, were offered triple therapy, which resulted in ulcer healing in three and Helicobacter pylori clearance in two patients. At 18 months, none of theHelicobacter pylori-negative patients had ulcer relapse. On the contrary, ulcers relapsed in all but one patient, who remainedHelicobacter pylori-positive. Smoking and drinking did not influence the therapeutic outcome. The data confirm previous reports that many duodenal ulcers are infectious and therefore curable.
To determine the effect of treating Helicobacter pylori infection on the recurrence of gastric and duodenal ulcer disease.
Follow-up of up to 2 years in patients with healed ulcers who had participated in randomized, controlled trials.
A Veterans Affairs hospital.
A total of 109 patients infected with H. pylori who had a recently healed duodenal (83 patients) or gastric ulcer (26 patients) as confirmed by endoscopy.
Patients received ranitidine, 300 mg, or ranitidine plus triple therapy. Triple therapy consisted of tetracycline, 2 g; metronidazole, 750 mg; and bismuth subsalicylate, 5 or 8 tablets (151 mg bismuth per tablet) and was administered for the first 2 weeks of treatment; ranitidine therapy was continued until the ulcer had healed or 16 weeks had elapsed. After ulcer healing, no maintenance antiulcer therapy was given.
Endoscopy to assess ulcer recurrence was done at 3-month intervals or when a patient developed symptoms, for a maximum of 2 years.
The probability of recurrence for patients who received triple therapy plus ranitidine was significantly lower than that for patients who received ranitidine alone: for patients with duodenal ulcer, 12% (95% CI, 1% to 24%) compared with 95% (CI, 84% to 100%); for patients with gastric ulcer, 13% (CI, 4% to 31%) compared with 74% (44% to 100%). Fifty percent of patients who received ranitidine alone for healing of duodenal or gastric ulcer had a relapse within 12 weeks of healing. Ulcer recurrence in the triple therapy group was related to the failure to eradicate H. pylori and to the use of nonsteroidal anti-inflammatory drugs.
Eradication of H. pylori infection markedly changes the natural history of peptic ulcer in patients with duodenal or gastric ulcer. Most peptic ulcers associated with H. pylori infection are curable.
To determine whether antimicrobial therapy for Helicobacter pylori infection accelerates the healing of duodenal ulcers.
Single-blind, randomized, controlled trial.
Veterans Affairs hospital.
One hundred and five patients with endoscopically verified duodenal ulcers.
Patients received either ranitidine, 300 mg/d, or ranitidine, 300 mg/d, plus "triple therapy" (2 g/d of tetracycline, 750 mg/d of metronidazole, and 5 or 8 bismuth subsalicylate tablets per day). Triple therapy was administered for only the first 2 weeks of ulcer treatment.
Videoendoscopic assessment of ulcer status was done until ulcer healing was complete. Evaluations were done after 2, 4, 8, 12, and 16 weeks of therapy.
Ulcer healing was more rapid in patients receiving ranitidine plus triple therapy than in patients receiving ranitidine alone (P less than 0.01). The cumulative percentages of patients with healed ulcers in the group receiving ranitidine plus triple therapy and in the group receiving ranitidine alone were as follows: 37% and 18% after week 2; 74% and 53% after week 4; 84% and 68% after week 8; 96% and 80% after week 12; and 98% and 84% after week 16.
Combined therapy with anti-H. pylori agents and ranitidine was superior to ranitidine alone for duodenal ulcer healing. Our results indicate that H. pylori plays a role in duodenal ulcer disease.
50 patients with intractable duodenal ulcer were randomly assigned to 4 weeks of treatment with colloidal bismuth subcitrate (CBS) alone (26 patients) or with amoxicillin and metronidazole (24 patients). 5 patients (all on triple therapy) withdrew because of side-effects. In 17 of the 45 patients who completed the treatment, Helicobacter pylori was eradicated, and there was no ulcer relapse during the first 12 months of follow-up. The ulcer relapse rate was significantly higher (17 of 21 [89%]) among patients who remained positive for H pylori. 9 patients who remained positive for H pylori and had ulcer relapses within 6 months of treatment with CBS alone, were subsequently given triple therapy. 7 of the 9 showed H pylori eradication and no relapses within the next 12 months. The 2 patients still H pylori-positive after triple therapy had further ulcer relapses. H pylori eradication, without altering acid output, will become the mainstay of duodenal ulcer treatment because it cures the disease.
The epithelial cells of the stomach and duodenum are normally protected from the damaging effects of acid and pepsin by a balancing mechanism of mucosal resistance. If an imbalance occurs, peptic ulcer may result. Traditional teaching has emphasized the importance of acid (and pepsin) as the cause of this imbalance; however, it is clear that acid and pepsin are not the only important factors in the pathogenesis of peptic ulcer. More recent investigative efforts have been directed at what constitutes mucosal resistance and how it can be disrupted to produce, in the presence of gastric acid, a peptic ulcer. Depletion of endogenous prostaglandins and Helicobacter pylori gastritis have emerged as prominent theories. As evidence exists both to support and refute these theories in humans, any definitive conclusions cannot be made at this time. The acute management of peptic ulcer disease is directed at relieving pain, accelerating ulcer healing, and preventing complications. Peptic ulcers can be healed with antisecretory agents (i.e., H2-receptor antagonists, omeprazole), antacids, prostaglandins, and sucralfate. Because they are effective, safe, and convenient, the H2-receptor antagonists are the most widely used agents for the management of peptic ulcer disease. Because the H2-receptor antagonist agents are equally effective in their indicated uses and are equally safe based on scientifically valid data, selection should be based primarily on cost. Omeprazole is the newest antisecretory agent: a single morning dose of 20 mg suppresses acid secretion for 24 h. The agent offers little advantage over H2-receptor antagonists for the majority of patients with peptic ulcer.(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of this study is to assess the relationship between Helicobacter pylori and the relapse of duodenal ulcer, and also to evaluate the differences in efficacy and side effects between 1 week and 2 week triple therapy. Sixty-two patients with active duodenal ulcer, which healed within 8 weeks of nizatidine treatment, were randomly allocated to one of two groups. Group 1 (n = 29) received no drugs, Group II (n = 33) received triple therapy for 1 week (IIa, n = 16) or 2 weeks (IIb, n = 17). Eleven patients whose ulcer did not heal after an 8 week nizatidine treatment period were randomly assigned into Group IIa (n = 5) and IIb (n = 6). Seven patients whose ulcer recurred after discontinuation of nizatidine were allocated to receive 2 weeks of triple therapy. All patients received endoscopy 6 weeks after entry, and again at 3, 6 and 12 months unless both ulcer recurrence and H. pylori infection were found. The frequency of ulcer relapse 6 weeks after the active duodenal ulcer had healed was 83% (24/29 in Group I, 13% in Group 11a and 14% in Group IIb. The cumulative rate of recurrence was significantly higher in Group I than in Group II (90 vs 30% at 12 months, P < 0.01). Ulcer relapse was associated with persistence of H. pylori infection (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
To compare the costs of alternative strategies for the treatment of duodenal ulcer.
A cost comparison using decision analysis.
A decision model was used to compare the costs per cure of an endoscopically documented duodenal ulcer for three initial treatment strategies: 1) H2-receptor antagonist therapy for 8 weeks, 2) antibiotic therapy for Helicobacter pylori infection plus H2-receptor antagonist therapy, and 3) urease test-based treatment. For symptomatic recurrences, secondary treatment strategies included empiric retreatment with the same or other regimen, and treatment based on repeat endoscopy-guided urease test or biopsy, with an assumption of subsequent cure. The cohort modeled for this analysis consisted of patients at low risk for a malignant ulcer. Probability estimates were derived from published clinical trials, cohort studies, and expert opinion. Side effects from combination therapy with antibiotics and H2-receptor antagonists and resulting costs were included from the perspective of a group practice model health maintenance organization.
For all secondary treatment strategies, initial therapy with antibiotics for H. pylori infection plus an H2-receptor antagonist resulted in the lowest average costs per symptomatic cure when the prevalence or likelihood of H. pylori infection exceeded 66% to 76%; the costs ranged from $284 for secondary (re)treatment with empiric antibiotic and H2-receptor antagonist therapy to $398 for endoscopy-guided secondary treatment. Initial treatment with an H2-receptor antagonist resulted in the highest costs, ranging from $372 for secondary treatment with empiric antibiotic and H2-receptor antagonist therapy to $679 for endoscopy-guided secondary treatment. The results were not sensitive to the rates of duodenal ulcer recurrence after either treatment, to the cost of either treatment, or to prevalence of H. pylori.
This cost analysis indicates that, regardless of the secondary treatment used for ulcer recurrence, initial therapy with antibiotics for H. pylori infection plus an H2-receptor antagonist provides the lowest costs per symptomatic cure. These cost savings and the lower recurrence rates associated with this treatment favor eradication of H. pylori as part of the initial treatment of duodenal ulcer.
We investigated the eradication and recurrence rate of Helicobacter pylori-infected gastric ulcer patients by combination therapies. Eighty-six H. pylori-positive gastric ulcer patients were assigned randomly to one of seven groups: I, omeprazole 20 mg (n = 9); II, lansoprazole (LPZ) 30 mg (n = 16); III, LPZ 30 mg plus plaunotol 480 mg (n = 13); IV, LPZ 30 mg plus ecabet sodium 2 g (n = 11); V, LPZ 30 mg plus clarithromycin 600 mg (the first 2 weeks; n = 11); VI, LPZ 30 mg plus plaunotol 480 mg plus clarithromycin 600 mg (the first 2 weeks; n = 13); and VII, LPZ 30 mg plus ecabet sodium 2 g plus amoxicillin 1,500 mg (the first 2 weeks; n = 13). All therapy was for 8 weeks except where otherwise noted. H. pylori eradication rates as diagnosed by culture, histology, urease test, and [13C]urea breath test 4 weeks after stopping therapy were 0, 0, 8, 45, 6, 46, and 62%, respectively, in groups I-VII. No patient achieving H. pylori eradication suffered recurrence. The combination therapies with proton pump inhibitors in addition to antibiotics and antiulcer agents are safe and effective in H. pylori eradication.
This study attempted to determine the efficacy of lansoprazole plus clarithromycin therapy in the eradication of Helicobacter pylori in gastric ulcer patients. The influence of H. pylori eradication on healing and relapse of ulcers was also studied. Thirty-nine patients received either lansoprazole 30 mg daily for 8 weeks (group 1) or clarithromycin 200 mg twice daily for 2 weeks and lansoprazole 30 mg daily for 8 weeks (group 2). Before treatment, H. pylori status was evaluated by a rapid urease test and histologic examination. H. pylori clearance and eradication were evaluated by a rapid urease test, polymerase chain reaction, and a [13C]urea breath test. Clearance of H. pylori was 0% in group 1 and was 33% in group 2. Eradication of H. pylori was 0% in group 1 and 21% in group 2. Although all five ulcers were healed in patients with H. pylori eradication, ulcers were not healed in the five patients without eradication. Relapse of ulcer was observed in three patients in whom eradication had failed. In this study, for H. pylori-positive gastric ulcer patients, better results were obtained when lansoprazole plus clarithromycin therapy was used, and H. pylori eradication was achieved.
Combination therapy with lansoprazole (LPZ) and amoxicillin (AMPC) was administered to eradicate Helicobacter pylori. Changes in eradication rates were monitored and serum antibody titers, levels of pepsinogens I and II (PI and PII), and gastrin were measured. The 40 subjects were divided into two groups: one group received LPZ 30 mg alone, and the other received LPZ 30 mg and AMPC 1,500 mg concomitantly. AMPC was administered for 2 weeks before completion of LPZ treatment. Maintenance therapy was cimetidine 400 mg. The presence of H. pylori was evaluated using the urea breath test (UBT). The clearance rate was 12.5% and the eradication rate was 0% in the LPZ group, and the corresponding rates in the LPZ with AMPC group were 41.6 and 25.0%, respectively. Serum monoclonal H. pylori antibody titers decreased in patients in whom bacterial eradication had been achieved. Serum PI was significantly reduced in those patients in whom eradication had been achieved. Serum PII and gastrin levels also tended to decrease in patients in whom eradication had been achieved, but no such changes were observed in the other patients. Further research into drug treatment and evaluation methods for bacterial eradication is required.
A randomized, single-blind study was designed to assess the effect of lansoprazole alone and lansoprazole plus amoxicillin on the healing and eradication rates in Helicobacter pylori-associated peptic ulcer disease. Seventy-nine patients with gastric ulcers and 54 patients with duodenal ulcers were randomly assigned to two treatment groups. Group 1 received lansoprazole 30 mg daily for 8 weeks for gastric ulcers or 6 weeks for duodenal ulcers. Group 2 received the group 1 regimen plus amoxicillin 2 g daily for 2 weeks. Healing rates at 8 weeks for the gastric ulcer patients were 92 and 84% in groups 1 and 2, respectively (p = not significant). Healing rates at 6 weeks for duodenal ulcers were 96% in group 1 and 100% in group 2 (p = not significant). The eradication rates of H. pylori for gastric ulcer patients were 21 and 54% in groups 1 and 2, respectively (p < 0.05). The H. pylori eradication rates for duodenal ulcer patients were 5 and 73% in groups 1 and 2, respectively (p < 0.001). The H. pylori eradication rates in group 2 were significantly higher than in group 1. Lansoprazole was effective for eradicating H. pylori in this study.
We studied the effects of lansoprazole with or without amoxicillin on the quality of ulcer healing in relation to eradication of Helicobacter pylori. Ulcer healing rates for lansoprazole 30 mg q.d. alone (group A) were 100% for duodenal ulcers (DU; n = 20) and 92% for gastric ulcers (GU; n = 15). The healing rates for lansoprazole 30 mg plus amoxicillin 1-2 g q.d. (group B) were 100% for both DU (n = 20) and GU (n = 12). Endoscopic findings after treatment showed that the red scar/white scar ratio in group A was 16/4 for DU and 12/1 for GU. The red scar/white scar ratio in group B was 4/16 for DU and 6/6 for GU. The numbers of H. pylori in gastric mucus did not change throughout the course of treatment in group A but decreased significantly, without H. pylori relapse, in group B. Changes in ammonia concentration in gastric juice, as well as serum gastrin and pepsinogen I and II levels, differed between group A and group B. Concomitant treatment with lansoprazole and high-dose amoxicillin eradicated H. pylori and modified gastric secretory function, resulting in high-quality ulcer healing.
Helicobacter pylori is a major cause of gastritis and an important factor in duodenal ulcer relapse. Eradication of H. pylori has usually been achieved by triple therapy, a combination of bismuth salts and two antibiotics. The disadvantage of these regimens is the large number of tablets and the high incidence of side effects. A new H+,K(+)-ATPase inhibitor, lansoprazole (LPZ), has a strong acid inhibitory effect and an anti-H. pylori effect in vitro. These dual effects have an advantage for the eradication of H. pylori by LPZ alone or by a combination of LPZ and antibiotics. In this study, we investigated an anti-H. pylori effect of LPZ alone and LPZ plus low-dose amoxicillin and the relation between the status of H. pylori colonization and the endoscopic healing stage. LPZ monotherapy suppressed H. pylori but did not eradicate it. LPZ plus low-dose amoxicillin dual therapy eradicated H. pylori in 45.5% of patients with gastric ulcer disease. However, this rate is not satisfactory for eradication therapy. The optimal dosage and duration of treatment need to be specified. A high rate of healing to the endoscopic S2 stage was achieved by eradication of H. pylori and the recurrence of gastric ulcer was suppressed in patients in whom H. pylori was eradicated. The eradication of H. pylori may change the natural course of gastric ulcer disease as it does in duodenal ulcer disease.
Simpler, effective therapies to treat Helicobacter pylori infection are greatly needed. Omeprazole co-therapy apparently enhances effectiveness of some antimicrobials. Our objective in this study was to determine whether the apparent additional benefit provided by omeprazole to amoxicillin therapy could be equaled by a high dose of ranitidine plus sodium bicarbonate.
In a prospective randomized trial, we tested 1 g amoxicillin b.i.d. with either omeprazole 20 mg b.i.d., or high dose ranitidine (900 and 1800 mg) plus sodium bicarbonate tablets 650 t.i.d. (with meals) for 14 day.
Fifty-two patients with documented H. pylori infection and peptic ulcer completed therapy. The cure rate with omeprazole and amoxicillin was poor (46%), with the 95% confidence interval (CI) = 25-67%. Ranitidine plus sodium bicarbonate was also poor (39% cure) with the 95% CI = 21.5-59% (p > 0.57). Average compliance was more than 92% for all three groups. Side effects were experienced in only two patients (stomatitis and mild diarrhea).
Neither the omeprazole nor ranitidine plus bicarbonate plus amoxicillin therapies used here can be recommended for treatment of H. pylori infection.
Forty-nine patients with Helicobacter pylori (Hp)-positive gastric ulcer (GU) and 39 patients with Hp-positive duodenal ulcer (DU) were studied. Before the trial and every 3 or 4 weeks, phenol red dye spraying endoscopy, the rapid urease test, biopsy specimen histology, and culture were performed to assess the ulcer stage and to detect Hp. Patients were divided into three groups: group I received lansoprazole 30 mg/d; Group II received dual therapy of lansoprazole 30 mg/day and amoxicillin (AMPC) 1 g/day or clarithromycin (CAM) 400 mg/day; and Group III received combination therapy of lansoprazole 30 mg/day, AMPC 1 g/day, or CAM 400 mg/day, and metronidazole 500 mg/day. Patients with GU received lansoprazole for 8 weeks and patients with DU received lansoprazole for 6 weeks. The other agents were administered for 2 weeks at the beginning of the trial. There were no differences in ulcer healing among the three treatment groups in patients with GU or DU, but there were significant differences in the eradication of Hp. No side effects were observed in any of the patients. We conclude that combination therapy is likely to be most effective and is harmless for Hp-persistent patients with peptic ulcer.
Until recently, suppression of gastric acid secretion in patients with peptic ulcer was empirical and of unproven value. Anticholinergic drugs had only modest inhibitory effects on acid secretion, many side effects, and uncertain efficacy. Controlled trials using antacids demonstrated the value of reducing gastric acidity for healing duodenal ulcer. The discovery of histamine-2 (H2) receptor antagonists in the 1970s and the introduction of H+,K(+)-ATPase inhibitors in the 1980s made reduction of acid secretion the first-choice modality for healing and preventing recurrences of duodenal and gastric ulcers. The demonstration in the late 1980s and early 1990s that Helicobacter pylori (Hp) was a major risk factor for duodenal and gastric ulcer recurrences suggested that peptic ulcer could be cured by eradicating this organism from the stomach. However, antibiotic eradication of Hp can be difficult, often requiring simultaneous administration of a drug that suppresses acid secretion. Therefore, H2 and proton pump inhibitors continue to play a role in the management of duodenal and gastric ulcers associated with Hp and also play a primary role in the therapy of other acid-related disorders, such as gastroesophageal reflux diseases, stress ulcers, ulcers associated with nonsteroidal anti-inflammatory drugs, and gastrinoma (Zollinger-Ellison syndrome) and other acid hypersecretory states.
Anti-Helicobacter pylori treatment with combinations of omeprazole and amoxicillin is a promising treatment option. The aim of this study was to investigate whether a daily omeprazole dose of 120 mg combined with amoxicillin would cure H. pylori infection at a rate comparable with that achieved with "triple therapy."
In a double-blind, randomized, controlled, and multicenter trial in Germany, 270 patients with an H. pylori-associated duodenal ulcer were treated with 40 mg omeprazole three times a day and 750 mg amoxicillin three times a day for the first 14 days (n = 139) followed by 20 mg omeprazole once daily until day 42 or with omeprazole plus 750 mg amoxicillin placebo three times a day for the same time period (n = 131).
Cure rates of H. pylori infection were 91% in the omeprazole plus amoxicillin group, 0% in the omeprazole plus placebo group, and 89% and 0%, respectively, performing an intention-to-treat analysis. Cure of H. pylori infection in patients pretreated with omeprazole was only 58% compared with 95% in patients who were not. The cumulative 12-month relapse rates were 11.3% and 44% in the treatment groups and 1.6% in H. pylori-negative and 49% in H. pylori-positive patients.
The combination of 120 mg omeprazole daily and 2.25 g amoxicillin daily with its H. pylori cure rate of around 90% is one of the best tolerated and most effective treatment regimens.
Reduction of gastric acid secretion by maintenance therapy and eradication of Helicobacter pylori by antibiotic treatment have been shown to reduce duodenal ulcer relapse. This study compared the effect of two regimens, a 6-month maintenance on an H2 receptor antagonist versus a one-week antibiotic therapy, on the rate of duodenal ulcer relapse in duodenal ulcer patients with gastric H. pylori infection.
We conducted a 30-week, double-blind, double-dummy, multicentric clinical trial involving 119 patients (97 M, 22 F, mean age 39 +/- 14 years) randomly assigned to a daily dose of 40 mg famotidine for 6 weeks supplemented with, during the first week, either antibiotics (500 mg amoxicillin q.i.d. and 500 mg tinidazole t.i.d.-antibiotic group) or their placebo (maintenance group). Healed patients after 6 weeks entered the 6-month maintenance phase: the maintenance group received 20 mg famotidine at bedtime and the antibiotic group, a placebo. Endoscopy with antral biopsies was performed to allow a rapid urease test, culture and histological examination upon entry, after 6 weeks, 3 months, and 6 months and, whenever symptoms recurred. H. pylori status was regarded as positive if any one of these three tests was positive, and negative if all tests were negative.
The 2 treatment groups were well balanced for all baseline characteristics. After 6 weeks, H. pylori was eradicated in 25 (45%) patients in the antibiotic group, and in 1 (2%) in the maintenance group (P < 0.01). In term of intention-to-treat, there was no significant difference in the healing rate after 6 weeks (93 and 83% in the antibiotic and maintenance groups, respectively; P = 0.15) or in the relapse rate after 6 months (13 and 28% in the antibiotic and maintenance groups, respectively; P = 0.17 Log-rank test). However, the overall failure rate (absence of healing, relapse) was lower (P = 0.04, Log-rank test) in the antibiotic group in which all relapses but one were observed in H. pylori positive patients. The rate of ulcer relapse (1/20) in patients of antibiotic group who remained free of H. pylori during the study, was significantly (P < 0.01) lower compared with that of H. pylori positive patients in the maintenance group (11/44). During the first 6-week period, more side effects were observed in the antibiotic group than in the maintenance group (4 vs 1 patient, respectively).
Our results indicate no significant difference between ulcer relapse rates after 6 months following a one-week antibiotic therapy or long-term maintenance therapy. Short-term antibiotic therapy should be considered as a valuable alternative to the long-term maintenance therapy.
There is a strong association between infection with Helicobacter pylori and gastric ulcers that are unrelated to the use of nonsteroidal antiinflammatory medications. We studied the efficacy of antibacterial therapy without medication to suppress gastric acid for the treatment of patients with H. pylori infection and gastric ulcers unrelated to the use of nonsteroidal agents.
Patients with gastric ulcers seen on endoscopy and with H. pylori infection confirmed by smear or culture were randomly assigned to receive either a one-week course of antibacterial agents (120 mg of bismuth subcitrate, 500 mg of tetracycline, and 400 mg of metronidazole, each given orally four times a day) or a four-week course of omeprazole (20 mg orally per day). Follow-up endoscopies were performed after five and nine weeks. The patients and their physicians were aware of the treatment assignments, but the endoscopists were not.
A total of 100 patients were randomly assigned to treatment, and 85 completed the trial. At five weeks, H. pylori had been eradicated in 41 of the 45 patients in the antibacterial-treatment group (91.1 percent; 95 percent confidence interval, 82.9 to 99.3) and in 5 of the 40 in the omeprazole group (12.5 percent; 95 percent confidence interval, 2.3 to 22.7; P < 0.001). The gastric ulcers were healed in 38 of the patients treated with antibacterial drugs (84.4 percent; 95 percent confidence interval, 73.9 to 95.0) and in 29 of those treated with omeprazole (72.5 percent; 95 percent confidence interval, 58.6 to 86.4; P = 0.28). At nine weeks, ulcer healing was confirmed in 43 of the patients receiving antibacterial therapy and in 37 of those receiving omeprazole (P = 1.0). The mean (+/- SD) duration of pain during the first week of treatment was 1.9 +/- 2.6 days in the omeprazole group, as compared with 3.6 +/- 3.0 days in the antibacterial-treatment group (P = 0.004). One year after treatment, recurrent gastric ulcers were detected in 1 of 22 patients (4.5 percent) in the antibacterial-treatment group and in 12 of 23 (52.2 percent) in the omeprazole group (P = 0.001). H. pylori was detected in the 1 patient with a recurrent ulcer who had received antibacterial treatment and in 10 of the 12 patients with recurrent ulcers who had received omeprazole.
In patients with H. pylori infection and gastric ulcers unrelated to the use of nonsteroidal antiinflammatory drugs, one week of antibacterial therapy without acid suppression heals the ulcers as well as omeprazole and reduces the rate of their recurrence.
The purpose of this study was to compare the performance of different regimens on Helicobacter pylori (H. pylori) eradication and duodenal ulcer recurrence. During a four-week period, 59 patients with duodenal ulcers who were positive for H. pylori infection were randomly treated with one of three regimens. Seventeen patients were treated with ranitidine, 19 with colloidal bismuth subcitrate (CBS), and 23 with triple therapy (CBS, tetracycline and metronidazole). Forty-six patients with healed ulcers after treatment received follow-up for six months without maintenance therapy. The recurrence rates of duodenal ulcers confirmed by endoscopy in these three groups were 64%, 33% and 0% at the third month, and 73%, 67% and 5% at the sixth month, respectively. In the ranitidine therapy group, H. pylori infection was still present at the final follow-up. In the CBS therapy group, H. pylori was suppressed initially, but recurred in all cases. In the triple therapy group, there was only one case in which H. pylori infection persisted and where ulcer recurrence occurred after 3.5 months. The remaining cases were all H. pylori negative and had no recurrence of duodenal ulcers during the six months of follow-up. Overall, 19/27 (70%) patients positive for H. pylori had a recurrence of duodenal ulcers, while none of the 19 patients who were negative for H. pylori had a recurrence of ulcers at the sixth month. This study shows that triple therapy is more effective than the other two regimens in the eradication of H. pylori and in reducing the recurrence of ulcers. H. pylori may play a role in the recurrence of the duodenal ulcer.
Randomised trials have shown that duodenal ulcers treated by H2 blockers heal faster if Helicobacter pylori is eradicated concurrently. It remains unknown whether eradication of H pylori without suppression of acid-secretion, is sufficient to allow healing. 153 patients with H pylori infection and duodenal ulcer were randomised to receive either a 1-week course of bismuth subcitrate, tetracycline, and metronidazole (76), or omeprazole for 4 weeks with the same three-drug regimen for the first week (77). Endoscopy and antral biopsies were done at entry and 4 weeks after treatment. 132 patients were suitable for analysis. Duodenal ulcers healed in 60 (92%; 95% CI 86-100%) patients taking bismuth, tetracycline, and metronidazole compared with 63 (95%; 88-100%) taking omeprazole in addition to the three other drugs. H pylori was eradicated in 61 (94%; 88-100%) who received only three drugs compared with 66 (98%; 96-100%) who received omeprazole as well. Symptoms were reduced more effectively during the first week in patients who received omeprazole (p = 0.003). We conclude that a 1-week regimen of bismuth, tetracycline, and metronidazole for patients with H pylori and duodenal ulcer eradicates the organism and heals the ulcer in most patients. Concurrent administration of omeprazole reduces ulcer pain more rapidly but has no effect on ulcer healing.
The efficacy of H2-blocker and triple therapy in curing duodenal ulcer was compared and the contribution of the eradication of Helicobacter pylori on ulcer remission was assessed. Forty-two duodenal ulcer patients infected with H. pylori were randomized to receive either H2-blocker therapy with famotidine (n = 21) or triple therapy with bismuth, amoxicillin, and metronidazole (n = 21). All patients received treatment for four weeks. Endoscopic evaluation of ulcer status and bacteriologic identification of H. pylori were performed at two, six and 12 months after therapy. Triple therapy had a similarly high healing rate to H2-blocker therapy (100% vs 90.5%) at two months of follow-up. However, at 12 months of follow-up, the ulcer remission rate in the triple therapy group (94.4%) was significantly higher than that of the H2-blocker therapy group (38.9%) (p < 0.05), resulting in the former therapy having a significantly lower rate of H. pylori infection compared to the latter (5.6% vs 100%, p < 0.005). Patients with persistent H. pylori infection at two months of follow-up had a significantly higher ulcer recurrence rate (64.7%) at 12 months than those without infection (5.3%) (p < 0.05). The success of triple therapy in ulcer remission may be attributed to the high eradication rate of H. pylori.
Patients with peptic ulcer disease are troubled by recurrent episodes of ulcer pain, and remain at risk of developing the serious and occasionally lethal complications of haemorrhage and perforation. As the disease is chronic and persists over many years, a long-term strategy for the management of patients with peptic ulcer is required. Continuous, long-term treatment with H2-receptor antagonists successfully achieves the dual objectives of preventing painful ulcer recurrence and reducing the risk of complications. During nine years of continuous therapy with ranitidine, more than 80% of patients with duodenal ulcers remain free from symptomatic ulcer recurrence, less than 2% suffer from ulcer haemorrhage, and the risk of perforation is 0%. Similar beneficial effects of long-term treatment have been observed in patients with gastric ulcer. Long-term continuous treatment with H2-receptor antagonists may not alter the natural history of ulcer disease. Even after seven years of continuous therapy with ranitidine, ulcers recur in 50% of patients within six months of stopping treatment. Hence, long-term therapy with H2-receptor antagonists may need to be continued beyond 10 years. Patients with peptic ulcer who are elderly, those taking NSAIDs, aspirin or anti-coagulants, those with a previous history of an ulcer complication and those with serious co-existent disease are at increased risk from haemorrhage and perforation. These patients should receive long-term prophylactic therapy with an H2-receptor antagonist.
to study the ulcer recurrence rate of Helicobacter pylori-positive duodenal ulcers at 1 yr after eradication of the bacteria by triple therapy.
Patients with H. pylori-positive duodenal ulcers were randomized to receive either triple therapy for 1 wk plus omeprazole for 4 wk (Triple+OMP) (n = 78), or omeprazole alone (OMP) for 4 wk (N = 77). Patients were followed up every 3 months for symptom enquiry. At 1 yr, all asymptomatic patients were invited to attend for gastroscopy.
At 8 wk, 16 patients in the OMP group and four in the Triple+OMP group had an ulcer. During the 1-yr period, 12 patients in the OMP group and no patient in the Triple+OMP group developed symptomatic ulcers. At follow-up endoscopy at 1 yr, another 10 ulcers were detected in the OMP group and two in the Triple+OMP group. Fifteen patients in the OMP group and 13 in the Triple+OMP group were lost to follow-up. In total, ulcers were detected in 39 of 61 (64%) assessable patients in the OMP group, and in six of 65 (9%) assessable patients in the Triple+OMP group after 1 yr (chi 2 test: p < 0.001). Of the patients whose H. pylori were successfully eradicated by Triple+OMP at 8 wk, 90% remained H. pylori negative at 1 yr.
Triple therapy for 1 wk eradicates H. pylori infection and significantly reduces duodenal ulcer relapses.
Early studies have suggested that omeprazole may facilitate the eradication of Helicobacter pylori. Sixty patients with duodenal ulcer and H. pylori colonization were randomly assigned to receive either omeprazole monotherapy (n = 30) or combination therapy with omeprazole and amoxycillin (n = 30) for a total duration of 6 weeks. Four patients receiving monotherapy and three receiving combination therapy had to be withdrawn from the study. All (100%) duodenal ulcers healed in patients receiving combination therapy, and 25 out of 26 (96%) healed in the group receiving monotherapy. H. pylori was eradicated in 22 out of 27 (82%) patients receiving combination therapy; only two ulcer relapses (9%) occurred within 18 months in these 22 patients. Of the five patients who remained H. pylori-positive after combination therapy, two relapsed during the 18-month follow-up. In the monotherapy group, all patients remained H. pylori-positive after treatment, and duodenal ulcer relapsed in 16 out of 25 (64%) patients within the median follow-up of 18 months. Adverse events were not reported in the group treated with combination therapy; one patient receiving monotherapy reported severe headache. These results lend further support to existing data that H. pylori eradication prevents duodenal ulcer relapse and show that combination therapy with omeprazole and amoxycillin is effective and well tolerated.
Some 10% of the population in Western countries will suffer a duodenal ulcer or gastric ulcer at some time in their lives. Although there has been an improvement in the survival rate of patients with peptic ulcer haemorrhage, the mortality is still approximately 10%. There is evidence to suggest that peptic ulcer disease is a life-long condition and that ulcers remain active with an unchanged potential for complications such as haemorrhage and perforation. Over the past 15 years anti-ulcer drugs with different mechanisms of action have been developed, and their use results in complete healing of an ulcer in four to eight weeks. However, most patients experience recurrence of their peptic ulcer after discontinuation of the healing therapy. Studies of continuous H2-receptor antagonist therapy have shown that recurrence occurs less frequently than in untreated patients, is largely asymptomatic, and is rarely characterized by haemorrhagic complications. Limited data on therapy for the eradication of Helicobacter pylori suggest that this may be an alternative approach for selected patients. As protection afforded by H2-receptor antagonists remains undiminished over the course of several years and is also observed in ulcers which have bled in the past, the implementation of long-term management with these agents constitutes a rational policy.
In five subsequent open clinical studies, 180 patients with Helicobacter pylori (HP)-associated ulcer disease (n = 163) or severe functional dyspepsia (n = 17) requiring therapy were treated with either 40 mg omeprazole plus 4 x 500 mg amoxicillin suspension for 1 wk (group I, n = 35), 2 x 40 mg omeprazole plus 4 x 500 mg amoxicillin for 1 wk (group II, n = 50), 2 x 20 mg omeprazole plus 4 x 500 mg amoxicillin for 2 wk (group III, n = 62), 2 x 20 mg omeprazole (day 1-14) and 4 x 500 mg amoxicillin (day 8-14) (group IV, n = 22) or with 2 x 20 mg omeprazole for 2 wk (group V, n = 11). The HP eradication rates determined with a biopsy urease test, microscopy of a mucosal smear, specific culture, and histology after modified GIEMSA staining in the 5th wk after discontinuation of study medication were 61.3% in group I, 61.7% in group II, 82.8% in group III, 28.6% in group IV, and 0% in group V. Apart from clinical insignificant pharyngeal paresthesias (n = 6), nine patients (5.7%) with combined therapy complained of important side effects (stomatitis: n = 3, diarrhea: n = 3, allergic exanthema: n = 3) that led to termination of amoxicillin treatment in four cases (2.5%). We conclude that omeprazole-enhanced amoxicillin antibiosis is a simple and effective approach to the eradication of HP colonization.
Thirty two patients with Helicobacter pylori positive duodenal ulcers resistant to treatment were randomly assigned to 4 weeks' treatment with sucralphate 4 g/day or colloidal bismuth subcitrate 480 mg/day plus amoxycillin from days 1 to 7 and tinidazole from days 8 to 14. After 4 weeks, patients with unhealed ulcers were crossed over to the other form of treatment for a further 4 week period. Patients with healed ulcers were followed up for 1 year without maintenance therapy with clinical and endoscopic investigations 3, 6, and 12 months after healing. Complete healing rates at 4 weeks were 88% (15 of 17) in the colloidal bismuth subcitrate plus antibiotics group and 40% (six of 15) in the sucralphate group (p < 0.05). After cross over, overall healing rates were 88% (22 of 25) and 47% (eight of 17), respectively (p < 0.05). H pylori eradication occurred in 83% of patients treated with the triple therapy. Cumulative relapse rates at 12 months were 12% (two of 17) in patients in whom H pylori had been eradicated and 100% (10 of 10) in those with persistent infection after short term therapy (p < 0.05). These results show that a colloidal bismuth subcitrate plus antibiotics regimen is highly effective in the short term treatment of resistant duodenal ulcers and that H pylori eradication can change the natural tendency to early recurrence of these ulcers.
In this study, 26 patients with duodenal ulcers refractory to treatment with H2-receptor antagonists for 8-12 weeks were randomly assigned to eight weeks of treatment with colloidal bismuth subcitrate (120 mg four times a day) alone (N = 12) or in combination with tetracycline hydrochloride (500 mg four times a day, days 0-14) and metronidazole (500 mg three times a day, days 15-28). Symptoms were scored and endoscopy, histology, and CLO tests were performed before, on completion of treatment, and 3, 6, 12, and 18 months after treatment. Treatment was considered successful when Helicobacter pylori was not detected by CLO tests and Warthin-Starry stains on gastric biopsies taken from antrum, body, and fundus. On triple therapy, ulcers healed in 12/14 patients (85.71%) and 10/14 (71.42%) patients became Helicobacter pylori-negative. On bismuth, only one patient became Helicobacter pylori-negative (8.33%, P < 0.0001), but ulcers healed in 8/12 patients (67%, P = NS). Six patients on bismuth, whose ulcers remained unhealed or relapsed early after healing, were offered triple therapy, which resulted in ulcer healing in three and Helicobacter pylori clearance in two patients. At 18 months, none of the Helicobacter pylori-negative patients had ulcer relapse. On the contrary, ulcers relapsed in all but one patient, who remained Helicobacter pylori-positive. Smoking and drinking did not influence the therapeutic outcome. The data confirm previous reports that many duodenal ulcers are infectious and therefore curable.