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PubMed2000

[Application of serology to confirm the eradication of Helicobacter pylori in peptic ulcer patients].

BACKGROUND: Measurement of changes in serum antibodies is an excellent predictor of Helicobacter pylori eradication after antibiotic treatment. AIM: To measure the changes in serum antibody titers to Helicobacter pylori, before and after treatment. MATERIAL AND METHODS: IgG antibodies to H. pylori were prospectively evaluated in 107 duodenal ulcer patients treated either with antibiotics (amoxicillin, metronidazole and bismuth subsalicylate) plus omeprazole or omeprazole alone. IgG antibody levels were determined using an "in house" ELISA in sera from 49 eradicated patients that received quadruple therapy and 58 non-eradicated patients (12 in whom antibiotic therapy failed and 46 that received omeprazole alone). Endoscopy, urease test, microscopy, and culture of gastric biopsies confirmed H. pylori eradication. RESULTS: Patients in whom H. pylori was eradicated, showed a maintained drop in serum antibody titers that ranged from 15%, 62%, 74% to 76% at 28 days, 4, 8 and 12 months respectively. Such reduction was not observed in patients treated with omeprazole. Patients, in whom quadruple therapy failed to eradicate H. pylori, showed a discrete and transient decrease in antibody titers. By the fourth month, patients in whom eradication with quadruple therapy was not achieved, irrespective of whether they received quadruple therapy or omeprazole alone. CONCLUSIONS: A 45% decrease in IgG titer after 4 months is indicative of therapeutic success in H. pylori eradication. Therefore, serology may be useful to monitor the outcome of antibiotic therapy (Rev Méd Chile 2000; 128: 1119-26).

Adult↗
PubMed2001

Follow-up of Helicobacter pylori status by using 13C-urea breath test in nonulcer dyspeptic patients after eradication therapy.

BACKGROUND: The role of eradication therapy is still controversial in H. pylori-related nonulcer dyspepsia (NUD). The aim of this study was to follow up the H. pylori status after eradication therapy in patients with NUD by using l3C-urea breath test (UBT). METHODS: Patients with a clinical and endoscopic diagnosis of NUD were included. H. pylori infection was established by endoscopic biopsies and 13C-UBT. Patients with H. pylori infection then received a quadruple therapy with colloidal bismuth subcitrate, metronidazole, tetracycline and lansoprazole. Two months after completion of therapy, endoscopic biopsies and 13C-UBT were performed again to confirm eradication. A follow-up 13C-UBT was carried out again in one year to detect recurrence of H. pylori infection. RESULTS: Eighty-eight of the 148 patients (59.5%) were found to have H. pylori infection by both endoscopic biopsies and 13C-UBT. Anti-H. pylori therapy was given for 55 patients and proved successful in 33 of them two months after the end of therapy. However, recurrence was found one year later in three of these 33 cases, making a recurrence rate of 9.1% (3/33). Three of the 22 cases with unsuccessful eradication were found to have H. pylori eradication at one year by follow-up 13C-UBT. One of the 33 H. pylori-positive patients without anti-H. pylori therapy, who had negative 13C-UBT in one year follow-up, was found taking a high dose and long period of antibiotics. CONCLUSIONS: The recurrence rate of H. pylori infection in our study was higher than that in the Western population. Delayed eradication of H. pylori may occur after anti-H. pylori therapy. Spontaneous eradication is rare in patients not receiving anti-H. pylori eradication.

Breath Tests↗
PubMed2001

Helicobacter pylori (H. pylori) infection in coronary artery disease: influence of H. pylori eradication on coronary artery lumen after percutaneous transluminal coronary angioplasty. The detection of H. pylori specific DNA in human coronary atherosclerotic plaque.

BACKGROUND: The role of infections in pathogenesis of atherosclerosis has been a point of extensive discussion and research. Chronic infection has been proposed to account for the formation and progression of atherosclerotic plaques. Gastric mucosal damage caused by Helicobacter pylori (H. pylori) involves various bacterial and host-dependent toxic substances that have been recently associated with increased risk of coronary artery disease (CAD). AIMS: This study was designed to: 1) to determine the seroprevalence of H. pylori and its cytotoxin associated gene A (CagA) in patients with and without CAD (group A), 2) to evaluate the influence of infection with H. pylori expressing CagA (Cytotoxin associated gene A--as a determinant of high virulence) on coronary arterial lumen reduction in patients after percutaneous transluminal coronary angioplasty (PTCA) with stent (group B), 3) to assess the effect of H. pylori eradication on coronary artery lumen reduction after PTCA (group C), 4) to determine the influence of the H. pylori eradication on plasma levels of cytokines, lipids and coagulation factors in the same patients before and after PTCA (group C) and 5) to analyse coronary specimens in patients with severe CAD for the presence of H. pylori originated specific DNA (Group D). PATIENTS AND METHODS: Group A included 96 patients with CAD (subgroup I) and 96 patients without CAD (subgroup II). For H. pylori seroprevalence, plasma anti-H. pylori and anti-CagA IgG were examined by ELISA and Western blot. Group B included 135 patients (86 male, 49 female, mean age 67 +/- 12 years) who had underwent PTCA with stent implantation initially and recoronaro-angiography about 6 months afterwards. All patients were tested for H. pylori--specific antibodies (IgG and CagA). Patients were divided into three subgroup "a": 34 patients with H. pylori IgG and CagA seropositivity, subgroup "b": 37 patients infected with H. pylori positive and CagA negative germs and subgroup "c": 64 patients with H. pylori IgG sero-negativity serving as control group. For all patients coronary lumen loss (percentage) in the dilated segment was measured at the end of PTCA and during re-coronaro-angiography and obtained values were considered taking into account the major risk factors of CAD (hypertension, hyperlipidemia, diabetes, obesity and smoking). Group C included 40 patients with significant single-vessel CAD and H. pylori infection confirmed by 13C-urea breath test (UBT) and serologically using anti-H. pylori and anti-CagA IgG. In addition, plasma interleukin (IL)-1beta and IL-8 and tumor necrosis factor alpha (TNFalpha) levels were measured by ELISA. Plasma total triglycerides, cholesterol, low (LDL) and high density lipoproteins (HDL), homocysteine levels, as well as some clotting factors such as thromboplastin and fibrinogen levels, thrombin time and platelet count were determined. All patients of group B undergoing PTCA were divided into two matched subgroups I and II used in exploratory study; subgroup I (20 patients) received H. pylori eradication triple-therapy for one week (Clarithromycin, Amoxicillin and Omeprazole), while subgroup II (20 patients) received similarly prepared placebo for the same time period starting immediately after PTCA. Six months after PTCA, the H. pylori status was re-assessed by UBT and found to be negative in all but two patients of subgroup I subjected to H. pylori therapy. Coronary angiography and laboratory tests were repeated in both subgroups of group B included into the trial and the reduction in coronary artery lumen in these subgroups was compared to baseline after PTCA considered as 100%. Large atherosclerotic plaques from coronary endatherectomy were obtained in 46 consecutive patients (9 female, 37 male, mean age 63 +/- 9 years) during coronary bypass procedures (group D). Serum was analysed for positive IgG antibodies specific for H. pylori by enzyme-linked-immunosorbent assay (ELISA). Antibodies specific for the CagA were detected by immunoblot analysis. Polymerase chain reaction (PCR) was used to identify bacterial DNA with primers encoding for the 16 S ribosomal RNA of H. pylori. Sequence analysis of PCR-products confirmed the specificity of the gene products for H. pylori. Coronary artery biopsies from 19 autopsies from a Forensic Medicine Department without coronary atherosclerosis were examined as a control group. RESULTS: The H. pylori seropositivity reached 69.79% (67 pts) of CAD (subgroup I of group A) and it was significantly higher than that in controls without CAD (subgroup II)--40.62% (39 pts), the odds ratio (OR) being 3.38 95% CI: 1.8598-6.1306 for H. pylori in CAD. CagA IgG detection was also significantly higher (58.20%) in CAD group than in controls (35.89%) giving the OR about 2.49 (95% CI: 1.1012-5.6175). Mean lumen loss in group B in H. pylori-positive subjects was 37.0% +/- 17.3%, whereas for H. pylori negative patients 29.9 +/- 13.8% were measured compared to initial values following PTCA (p = 0.0196). Even subgroup analysis and analysis regarding risk factors show significantly higher lumen loss for H. pylori-positive patients (especially CagA positive) compared to H. pylori negative patients. Mean coronary artery lumen reduction in patients undergoing PTCA + H. pylori eradication therapy (subgroup I of group C) was found to be significantly (P < 0.05) smaller compared to PTCA + placebo-treated subgroup II (22% vs 41%). The plasma cytokines such as TNFalpha, IL-1beta and IL-8 were significantly lower after the H. pylori-eradication in PTCA patients, while changes in plasma lipids, homocysteine and clotting factors were not significantly affected by H. pylori eradication. In group D thirty two patients (69.5%) were H. pylori-seropositive, 14 patients out of 32 H. pylori-positive were CagA positive. Eighteen of these patients showed positive results for H. pylori DNA, whereas 4 patients of the seronegative group also showed positive DNA results, but all 4 had undergone eradication therapy within the past two years. A total of 22 patients (47.8%) of the CAD group and none of the 19 controls revealed positive DNA assessed by PCR. Out of 14 anti-Cag A positive patients 11 showed positive detection of H. pylori DNA (p = 0.015) CONCLUSIONS: 1) There is a significant link between CAD and infection with H. pylori, especially expressing CagA proteins; 2) Patients infected with CagA-positive H. pylori show significantly greater coronary artery lumen loss and arterial re-stenosis after PTCA with stent implantation; 3) H. pylori eradication significantly attenuates the reduction in coronary artery lumen in CAD patients after PTCA possibly due to the elimination of chronic inflammation and the decline in proinflammatory cytokine release and 4) The identification of DNA in atherosclerotic plaques of patients with severe CAD supports the hypothesis that infection with H. pylori (especially CagA positive) may influence the development of atherosclerosis.

Aged↗
PubMedDate not supplied

Long-term effect of Helicobacter pylori eradication on quality of life, body mass index, and newly developed diseases in Japanese patients with peptic ulcer disease.

BACKGROUND/AIMS: Eradication of Helicobacter pylori is known to reduce ulcer recurrence in patients with peptic ulcer disease, however, other long-term effects after eradication therapy are not well known. The aim of this study is to examine the long-term effect of H. pylori eradication on clinical symptoms, quality of life, body mass index, newly emerging symptoms, and newly developed diseases. METHODOLOGY: One hundred and ninety-two Japanese patients with peptic ulcer disease who received H. pylori eradication therapy at Department of Gastroenterology, Osaka City University Hospital between 1993 and 1995 were asked to fill in specially a prepared questionnaire. RESULTS: One hundred and fourteen patients returned the questionnaires; out of them 98 could be analyzed in this study. Successful eradication (n = 88) resulted in alleviation of symptoms, improvement of quality of life and increase of body mass index while failure of eradication (n = 10) had much less or no effects. A relatively high incidence of hyperlipidemia (25.0%) was observed in patients with successful H. pylori eradication. Development of hyperlipidemia was associated with significant improvement of quality of life especially the item concerning eating and drinking habits but not with increased body mass index. In the elderly, no significant change in body mass index was observed, however, post-eradication body mass index was significantly higher in patients with hyperlipidemia than those without. CONCLUSIONS: Cure of H. pylori infection alleviates symptoms and improves quality of life of treated patients, but might be associated with an increased incidence of hyperlipidemia.

Body Mass Index↗
PubMed2003

The efficacy of furazolidone-based quadruple therapy for eradication of Helicobacter pylori infection in Iranian patients resistant to metronidazole-based quadruple therapy.

BACKGROUND: Furazolidone has recently shown promising efficacy in H. pylori eradication and has replaced metronidazole in different eradication regimens especially in countries, like Iran, with high prevalence of metronidazole resistance and where clarithromycin is expensive and hardly available. This study tries to determine the efficacy of a quadruple therapy based on furazolidone as a second line treatment. MATERIAL/METHODS: 90 consecutive patients with a prior history of H. pylori infection who had failed to respond to a 14 day course of metronidazole-based quadruple therapy were included to take a two week quadruple therapy consisting of furazolidone, bismuth subcitrate, amoxicillin and omeprazole. Eradication was described as negative 14C-urea breath test, 4 to 6 weeks after end of the treatment. RESULTS: 89 of 90 patients completed the treatment course. The total eradication rate was 70/89 (78.7%). 35/49 (71.4%) of male patients and 35/40 (87.5%) of female patients had successful eradication. Eradication rate did not have any significant relationship with patient's sex (p>0.05). All patients had at least one upper GI endoscopy before the treatment by which they were categorised into three groups: duodenal ulcer (DU, 78.9%), gastric ulcer(GU, 11.1%) and non-ulcer dyspepsia (NUD, 10%). Eradication rates was different in these groups, but not significantly (p>0.05). Eradication rate was significantly lower in smokers (p<0.05, OR=3.12). CONCLUSIONS: Furazolidone can replace metronidazole successfully in those patients who have failed to respond to metronidazole-based quadruple therapy and it is well tolerated. We recommend it, especially in countries where clarithromycin is expensive or not available.

Adult↗
PubMedDate not supplied

Long-term strict monitoring of plasma ghrelin and other serological markers of gastric diseases after Helicobacter pylori eradication.

We report on a case of chronic atrophic gastritis in which the serological markers of gastric diseases were strictly monitored for 2 years after successful Helicobacter pylori (H. pylori) eradication. A 31-year-old man with upper abdominal pain was diagnosed as having H. pylori infection. Laboratory examination revealed low serum levels of pepsinogen (PG) I, low PG I/II ratio, and low plasma levels of ghrelin. Upper gastrointestinal endoscopy revealed severe corpus-dominant atrophic gastritis. H. pylori eradication therapy was performed. Successful eradication was confirmed three months later by the 13C urea breath test. Decreased serum PG II levels and an increased serum PG I/II ratio were detected a week after completion of the eradication therapy. The serum anti-H. pylori IgG titer decreased to less than 75% of the baseline level by 24 weeks after completion of the eradication therapy. On the other hand, the plasma levels of total and active ghrelin showed no marked changes after successful eradication therapy. This is the first report of long-term follow-up of changes of the plasma ghrelin levels after H. pylori eradication therapy, the observations suggesting that reduction of plasma ghrelin levels cannot be achieved merely by H. pylori eradication, without resolution of the gastric atrophy.

Adult↗
PubMedDate not supplied

Efficacy of a triple therapy with rabeprazole, amoxicillin, and faropenem as second-line treatment after failure of initial Helicobacter pylori eradication therapy.

BACKGROUND/AIMS: Triple therapy consisting of lansoprazole, amoxicillin, and clarithromycin (LAC regimen) is widely used to eradicate Helicobacter pylori in Japan. However, the need for appropriate treatment after failure of initial therapy to eradicate H. pylori has been increasing. We therefore assessed the efficacy of a combination of rabeprazole, amoxicillin, and faropenem for second-line eradication therapy. METHODOLOGY: The subjects were 116 patients positive for H. pylori infection. Patients initially received lansoprazole 60 mg/day, amoxicillin 1500 mg/day and clarithromycin 400 mg/day in two divided doses for 7 days. Patients in whom eradication treatment failed were given rabeprazole 20 mg/day and amoxicillin 1500 mg/day in two divided doses, and faropenem 600 mg/day in three divided doses (RAF regimen) for 7 consecutive days. H. pylori status was assessed by the 13C-urea breath test combined with rapid urease test or H. pylori culture method 8 weeks after completion of therapy. Susceptibility to clarithromycin was determined by the agar dilution method, and genetic polymorphism of CYP2C19 was analyzed by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: The initial H. pylori eradication rate with the LAC regimen was 76.4% (84/110). Assessment of the CYP2C19 genotypes of the patients in whom eradication therapy failed revealed that homozygous extensive metabolizers accounted for 70.0% (16/23) and heterozygous extensive metabolizers for 30.0% (7/23), with no poor metabolizers. The acquired resistance rate for clarithromycin was 52.0% (12/23). The success rate of re-eradication with the RAF regimen was 91.3% (21/23) with no serious adverse effects. CONCLUSIONS: Triple therapy comprising rabeprazole, amoxicillin, and faropenem is effective for second-line eradication treatment of H. pylori infection, regardless of the genetic polymorphism of CYP2C19 or the presence of resistance to clarithromycin.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2005

[Global eradication of poliomyelitis. On the 80th anniversary of the founding of the National Institute of Health].

Global eradication of poliomyelitis launched and coordinated by the World Health Organization since 1988 is close to being achieved: the main objective is to discontinue the circulation of the wild, neurovirulent, endemic virus of poliomyelitis. Although this objective has been within the reach, there are two other risks, lower but existing and posing possible threat to the eradication, that need to be controlled: 1) wild polioviruses stored in laboratories should be destroyed or reliably contained and 2) emergence and epidemic role of neurovirulent polioviruses potentially derived from attenuated oral polio vaccine should be prevented. After all these global eradication objectives are met and three years relapse from its certification, under intensive and sensitive surveillance, it will be possible to consider whether or not to stop vaccination against poliomyelitis in the world. The global eradication of poliomyelitis is a complex issue that will require further efforts in the field of both the biomedical research and organizational, economic and political approaches. In the Czech Republic, poliomyelitis has been eradicated since 1960. The former Czechoslovakia was the first country in the world to achieve and to scientifically demonstrate nationwide eradication of poliomyelitis. The current post-eradication surveillance of poliomyelitis in the Czech Republic is managed by the Centre of Epidemiology and Microbiology of the National Institute of Public Health in cooperation with the Ministry of Health of the Czech Republic, WHO Regional Office for Europe in Copenhagen and National Certification Committee for Poliomyelitis Eradication.

Czech Republic↗
PubMed2004

Recent success of pantoprazole -or lansoprazole- based clarithromycin plus amoxicillin treatment in the eradication of Helicobacter pylori.

BACKGROUND/AIMS: There are some reports showing that resistance of Helicobacter pylori (H. pylori) to clarithromycin has increased in recent years. We aimed to investigate the current success of a most popular first-line eradication regimen by using two different proton pump inhibitors: lansoprazole and pantoprazole. METHODS: Ninety patients with H. pylori-positive functional dyspepsia were randomized to receive pantoprazole 40 mg b.i.d. or lansoprazole 30 mg b.i.d. in addition to amoxicillin 1,000 mg and clarithromycin 500 mg twice daily for 14 days in a multicenter study. H. pylori infection was determined by histological examination and a rapid urease test. A follow-up endoscopy was performed to assess the H. pylori eradication six weeks after the end of therapy. RESULTS: Seventy-nine patients completed the study protocol properly. The H. pylori eradication rates according to per protocol analysis were 70% in group pantoprazole, amoxicillin and clarithromycin (28/40) and 69.2% in group pantoprazole, amoxicillin and clarithromycin (27/39). The eradication rates according to intention to treat analysis were 62.2% and 60% in lansoprazole, amoxicillin, clarithromycin, pantoprazole, amoxicillin, clarithromycin groups, respectively. The eradication rates were similar in both protocols (p>0.05). CONCLUSIONS: The most popular first-line eradication protocols of H. pylori achieved only a moderate success in the current study. Alternative therapy options are needed instead of clarithromycin-based triple treatment for eradication of H. pylori. The choice of proton pump inhibitor is not important in the eradication rate of H. pylori.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2002

The effect of Helicobacter pylori eradication on symptoms and gastric emptying in patients with nonulcer dyspepsia.

BACKGROUND/AIMS: This study was undertaken to evaluate the effect of eradication therapy on the symptoms of Helicobacter pylori positive non-ulcer dyspepsia patients. METHODS: Twenty-four patients participated in the study and the symptoms of daytime epigastric pain, night or hunger pain, nausea, vomiting, regurgitation, bloating, belching, early satiety and anorexia were scored at the beginning, the 15th day after starting eradication therapy (amoxicillin 2 gr bid, clarithromycin 2 gr bid and omeprazole 40 mg daily for two weeks) and during the third and sixth months. Gastric emptying of radiolabelled solid meal was determined at baseline and during the third month. RESULTS: The Helicobacter pylori eradication rate was 79% and symptom scores significantly decreased during the follow-up period in both of the groups, irrespective of Helicobacter pylori status. The mean symptom scores of the 24 patients at baseline, day 15 and and months three and six were as follows: 1.275, 0.274, 0.496 and 0.238 respectively. Symptom scores for the 19 patients with Helicobacter pylori eradication were 1.084, 0.263, 0.347 and 0.215 respectively while in the five patients in whom Helicobacter pylori eradication therapy failed it was 2.0, 0.314, 1.06 and 0.32 respectively. Of the 16.6% Helicobacter pylori positive non-ulcer dyspepsia patients who had delayed gastric emptying of solids, there was no change after eradication therapy. Nine patients, including all of those in whom eradication therapy failed, required further medication (antacids/prokinetics) for continuing symptoms one month after completion of treatment. CONCLUSIONS: The results of this study suggest that Helicobacter pylori is a causal factor in symptoms of non-ulcer dyspepsia and that eradication therapy improves symptoms and endoscopic findings but has no effect on gastric emptying.

Journal Article↗
PubMed2006

Analysis of the differences in structural chromosomal aberrations of the gastric mucosa between H. pylori positive and negative gastric cancer patients: involvement of H. pylori in the onset of gastric cancer and examination of the mechanism in gastric carcinogenesis following H. pylori eradication.

Gene mutations are essential to carcinogenesis. If an evident difference is observed in gastric mucosal chromosomal structure aberrations between H. pylori (Hp)-negative and Hp-positive gastric cancer patients, it may be interpreted as suggesting the involvement of Hp in gene mutations. This study was undertaken to compare chromosomal structural aberrations between Hp-negative and Hp-positive gastric cancer patients and to evaluate the effects of Hp eradication on chromosomal structures in clinical cases. The subjects of this study were 40 patients with gastric cancer divided into four groups: Group A was composed of 12 patients with Hp-negative gastric cancer (well-differentiated gastric cancer in 5 cases and poorly-differentiated in 7 cases), Group B of 8 patients with Hp-negative gastric cancer following Hp eradication (well-differentiated in 4 case and poorly-differentiated in 4 cases), Group C of 13 patients with Hp-positive gastric cancer (well-differentiated in 7 cases and poorly-differentiated in 6 cases) and Group D of 7 patients with gastric cancer (well-differentiated in 5 cases and poorly-differentiated in 2 cases) undergoing Hp eradication at subtotal gastrectomy. In each of the groups A, B and C, the structural chromosomal aberration such as loss of heterozygosity (LOH) and microsatellite instability (MSI) was analyzed. In Group D, changes in structural chromosomal aberrations after Hp eradication as compared to the pre-eradication structures were also analyzed. LOH and MSI were examined by PCR, using DNA extracted from the cancer-affected and intact gastric mucosal tissue specimens from each patient. In A, B and C groups, structural chromosomal aberrations were noted, and these aberrations tended to be more marked in cases of poorly-differentiated gastric cancer in each group. In terms of structural chromosomal aberrations, there was no marked difference between Group A and either Group B or C. Hp eradication resulted in no change in chromosomal structure as compared to the pre-eradication structure in Group D. These results suggest the possibility that Hp eradication does not affect chromosomal structures and Hp is involved in gastric carcinogenesis as an additive environmental factor rather than as a factor acting at the gene level.

Anti-Bacterial Agents↗
PubMed1994

[Omeprazole/amoxicillin: impaired eradication of Helicobacter pylori in smoking but not in premedication with omeprazole].

The efficacy of high dose omeprazole/amoxicillin (OME/AMOX) for eradication of Helicobacter pylori (HP) is controversial. Reported eradication rates range from 0% to 90%. Different therapy schedules and unknown factors may be crucial; in particular, pretreatment with OME has been thought to endanger HP eradication by subsequent OME/AMOX. Preliminary findings suggested that smoking may impair eradication with OME/AMOX. The aims of this study were (1) to establish whether HP eradication rates differ depending on whether eradication with OME/AMOX was performed before or after ulcer therapy with OME, (2) to determine whether smoking impairs HP eradication by OME/AMOX and (3) to evaluate the efficacy of OME/AMOX in our population. 52 HP positive outpatients with endoscopically documented recurrent duodenal ulcer were included. Exclusion criteria were: alcoholism, previous gastric surgery, or intake of antibiotics, OME, bismuth salts, corticosteroids and NSAIDs within four weeks before study entry. Patients currently smoking > 10 cigarettes/day were classified as smokers. HP infection was confirmed by histology (3 biopsy specimens from the gastric antrum and 2 from the gastric body; H&E, Giemsa) and at least positive rapid urease test (CLO) or culture. Eradication therapy consisted of oral OME (40 mg bid) and AMOX solute (750 mg tid) for 10 days (OME/AMOX). This therapy preceded (group A) or followed (group B) ulcer therapy with OME (20 mg per day for 20 days). In group A 17 patients (2 females, 15 males, mean age 39 [19-70]; 11 smokers, 6 nonsmokers) underwent ulcer therapy with OME (d 1-20) before OME/AMOX d 21-30).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[A trial of modified triple therapy for the eradication of H. pylori in recurrent duodenal ulcer].

In a prospective trial we examined the efficacy and acceptability of a modified triple therapy in H. pylori (HP)-positive patients with recurrent duodenal ulcer disease. Oral administration of amoxicillin for two weeks was substituted for one single injection of intramuscular depot penicillin (benzathine penicillin G). Additionally, patients were given ornidazole 500 mg tid for 14 days and 120 mg colloidal bismuth sub-citrate qid for 28 days. The patients were investigated for H. pylori colonization using a rapid urease test (CLO), histology (H&E-, Giemsa stain), culture (including determination of the minimal inhibitory concentrations for metronidazole, penicillin G and amoxicillin) and H. pylori serology (Cobas Core Anti-H. pylori EIA, F. Hoffmann-La Roche). Control endoscopies using the same methods were performed 1 and 6 months after eradication therapy. The eradication rate was 50% and the ulcer healing rate 90% 1 month after therapy. Ulcers recurred in 2/3 of patients with persistent infection vs 0/5 of HP-eradicated patients after 6 months. Both successfully HP-eradicated patients and patients with treatment failure exhibited comparable decreases in mean serum IgG anti-HP concentration within 2 months. Discrimination between the two groups and hence identification of the eradication success by serology was not possible within a time period of 2 months. After 6 months, serum IgG anti-HP concentrations in non-HP-eradicated patients returned to pre-therapy values, in HP-eradicated patients the concentrations further decreased. The above-described modified triple therapy against HP cannot be recommended as a standard therapy, mainly because of the insufficient eradication effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Sucralfate in Helicobacter pylori eradication strategies.

BACKGROUND: Sucralfate monotherapy has been shown to suppress but not eradicate Helicobacter pylori. The combination of sucralfate with antibiotic(s) has been evaluated recently in the treatment of H. pylori-positive duodenal ulcer. The aim of this article is to review the efficacy of sucralfate-containing duotherapy and triple therapy in duodenal ulcer healing and H. pylori eradication rates. METHODS: Reports on duotherapy and triple therapy including sucralfate as the mediating agent were analysed to assess the duodenal ulcer healing and H. pylori eradication rates. RESULTS: One study on duotherapy with sucralfate and amoxycillin achieved an ulcer healing rate of 86% and H. pylori eradication rate of 40%, which compared favourably with sucralfate monotherapy that resulted in duodenal ulcer healing and H. pylori eradication rates of 65% and 0% respectively. A total of six studies have examined triple therapy using sucralfate with two antibiotics. The duodenal ulcer healing rates were generally over 90% and the H. pylori eradication rates about 80% (range 59% to 100%). In one comparative study, the 4-week duodenal ulcer healing and H. pylori eradication rates of sucralfate-containing triple therapy were not distinguishable from those of omeprazole-containing triple therapy. CONCLUSIONS: It is concluded that sucralfate is an effective mediating agent for the eradication of H. pylori in patients with duodenal ulcer.

Anti-Bacterial Agents↗
PubMed1996

[Is there a correlation between the values of breath tests and the response to the treatment for the eradication of Helicobacter pylori?].

PURPOSE: To study a possible correlation between the urea breath test values prior to treatment and the response to Helicobacter pylori eradication therapy in patients with duodenal ulcer. METHODS: Seventy-seven patients with duodenal ulcer were retrospectively studied (mean age: 46 +/- 13 years; 71% males). Initially, an endoscopy with biopsy samples (H&E stain) taken from antrum and body was performed, and a 13C-urea breath test (measuring 13C difference: delta 13CO2) was also performed. Both procedures were repeated one month after completing therapy ("classic" triple therapy [n = 25], and omeprazole plus amoxycillin [n = 52]). RESULTS: Eradication was achieved in 40% of cases (n = 32), and it was higher in patients treated with "classic" triple therapy (60%) than in those treated with omeprazole plus amoxycillin (31%) (p = 0.017). Mean delta 13CO2 level was 25 +/- 15. There were no differences when comparing values of patients with successful eradication (24 +/- 18) or therapy failure (25.6 +/- 13). No differences were observed when considering both therapies separately or when comparing eradication rates depending upon breath test levels prior to therapy. Breath test values did not influence the eradication in the logistic regression model. Mean delta 13CO2 values after therapy in patients with eradication failure ran in parallel with those observed previously. CONCLUSION: No correlation was observed between urea breath test values before treatment and the response to H. pylori eradication therapy in patients with duodenal ulcer. Thus, we conclude that quantification of this diagnostic method is not useful to predict the success or failure of eradicating therapy.

Amoxicillin↗
PubMed1997

Omeprazole, amoxicillin and bismuth for peptic ulcer healing and Helicobacter pylori eradication.

A controlled, randomized study was performed in patients with active peptic ulcer disease and positive Helicobacter pylori (Hp) status to assess the clinical efficacy (endoscopic healing and eradication of Hp) of different combined treatments. In the first part of the study a treatment with omeprazole (CAS 73590-58-6) (40 mg once daily) alone (group A) or in combination with tripotassium dicitrato bismuthate (TDB; 240 mg bid, group B) for 4 weeks was evaluated in 20 and 13 patients, respectively. As expected healing rates were high and comparable (75 vs. 85%), however, Hp-eradication was zero in both groups. In the subsequent second part of the trial group A (n = 19) received omeprazole (20 mg bid) for 2 weeks + amoxicillin (CAS 26787-78-0) tablets (1 g bid only 2nd week). Accumulated healing rate increased to 95% but Hp-eradication was 37%. From group B only 8 patients participated in a second 4-week course of monotherapy with TDB. Whereas healing occurred in all individuals, Hp-eradication was still low (12.5%). In addition plasma levels (omeprazole, Bi) and urinary excretion (Bi) were monitored to test whether drug interaction and/or noncompliance of the patients could help to explain the clinical findings. Systemic availability of Bi was increased by the coadministration of omeprazole and plasma levels of omeprazole were in general higher in Hp-positive patients if compared to those of Hp-negative patients. The following conclusions could be drawn from the 4 parts of the study: Treatment of peptic ulcer disease with omeprazole either alone or in combination with TDB is effective for ulcer healing but not for eradicating Hp. Omeprazole seems to decrease the Hp-eradicating potential of Bi probably due to a drug interaction. A second treatment course with TDB is apparently not of much benefit. One week pretreatment with omeprazole does not affect healing but might attenuate Hp-eradication rate of subsequent combined treatment with amoxicillin. One week coadministration of amoxicillin is not sufficient. The magnitude of omeprazole's plasma levels has no effect on Hp-eradication rates. As the numbers of patients in this study was relatively small these conclusions need to be confirmed by larger trials.

Adult↗
PubMed1997

Helicobacter pylori eradication--comparison of three drug regimens and symptomatic assessment in duodenitis and antral gastritis.

Helicobacter pylori (Hp) eradication in peptic ulcer disease is associated with a greatly reduced recurrence rate. The optimal drug regimen for HP eradication remains uncertain. It is also unclear if eradication of Hp in duodenitis and antral gastritis improves symptoms. The aims of this study were to compare the efficacy of three drug regimens in the eradication of Hp and to assess if Hp eradication improved symptoms in patients with duodenitis and antral gastritis. Patients (n = 79) found to have duodenal ulcer, duodenitis and/or antral gastritis with a positive urease test (CLO) at endoscopy were allocated to one of the three regimens: A. omeprazole 20 mg b.d. and clarithromycin 500 mg t.d.s. for two weeks (n = 27), B. De-Nol 240 mg b.d. for four weeks, metronidazole 400 mg t.d.s. and amoxicillin 500 mg t.d.s. for one week (n = 26), and C. omeprazole 20 mg b.d. and amoxicillin 500 mg t.d.s. for two weeks (n = 26). In conclusion, traditional 'triple' therapy with bismuth and two antibiotics achieved the highest Hp eradication rate and was best tolerated. Recolonisation with Hp was uncommon after eradication. Dyspeptic symptoms improved with Hp eradication in duodenitis and antral gastritis.

Adult↗
PubMed1997

Effect of Helicobacter pylori eradication on gastric histology, serum gastrin and pepsinogen I levels, and gastric emptying in patients with gastric ulcer.

OBJECTIVE: The evolution of gastritis and the behavior of basal and meal-stimulated gastrin release, pepsinogen levels, and gastric emptying of solids were studied in a series of consecutive patients with Helicobacter pylori-positive, uncomplicated, non-NSAID-related type I gastric ulcer over a follow-up period of 3 months after eradication therapy was begun. METHODS: Before starting treatment (consisting of omeprazole 40 mg a day for 1 month and amoxycillin 1 g three times daily for 14 days), and for 3 months after ulcer healing, 16 patients had a series of functional examinations, including basal and meal-stimulated serum gastrin concentration, serum pepsinogen I levels, evaluation of gastric emptying of solids by means of serial ultrasonographic measurement of the gastric antrum area, and histological assessment of antral and corpus gastritis. RESULTS: Double therapy resulted in the successful eradication of H. pylori in eight of 16 evaluable patients. In the group of H. pylori-eradicated patients, the mean scores of gastritis activity and inflammation in the antrum and corpus had fallen, 3 months after eradication. No significant changes in mean gastritis scores were observed in the case and control group with regard to intestinal metaplasia and atrophy in the antrum and corpus. In H. pylori-eradicated patients, the integrated gastrin response to meal, but not fasting gastrin concentration, fell significantly during follow-up, and serum pepsinogen I levels significantly decreased, compared with baseline. In contrast, the fasting and maximal antral area and the gastric emptying of solids remained unchanged over time. In the control group (but not the H. pylori-eradicated group), no significant modifications of any of the above-mentioned parameters were observed during follow-up. CONCLUSION: Our findings suggest that in non-NSAID-related type I gastric ulcers, the eradication of H. pylori significantly reduces gastritis activity and inflammatory scores, but not atrophy and intestinal metaplasia, and modifies gastrin and pepsinogen I release in a short follow-up period. In contrast, H.pylori eradication does not significantly affect gastric emptying of solids, at least within a period of 3 months from therapy.

Amoxicillin↗