R García-Grávalos

Hospital Universitario de La Princesa, Madrid, Madrid, Spain

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Publications (9)61.16 Total impact

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    ABSTRACT: To evaluate the effect of Helicobacter pylori (H. pylori) eradication on ulcer bleeding recurrence in a prospective, long-term study including 1,000 patients. Patients with peptic ulcer bleeding were prospectively included. Prior non-steroidal anti-inflammatory drug (NSAID) use was not considered exclusion criteria. H. pylori infection was confirmed by rapid urease test, histology, or (13)C-urea breath test. Several eradication therapies were used. Subsequently, ranitidine 150 mg o.d. was administered until eradication was confirmed by (13)C-urea breath test 8 weeks after completing therapy. Patients with therapy failure received a second, third, or fourth course of eradication therapy. Patients with eradication success did not receive maintenance anti-ulcer therapy and were controlled yearly with a repeat breath test. NSAID use was not permitted during follow-up. Thousand patients were followed up for at least 12 months, with a total of 3,253 patient-years of follow-up. Mean age 56 years, 75% males, 41% previous NSAID users. In all, 69% had duodenal ulcer, 27% gastric ulcer, and 4% pyloric ulcer. Recurrence of bleeding was demonstrated in three patients at 1 year (which occurred after NSAID use in two cases, and after H. pylori reinfection in another one), and in two more patients at 2 years (one after NSAID use and another after H. pylori reinfection). The cumulative incidence of rebleeding was 0.5% (95% confidence interval, 0.16-1.16%), and the incidence rate of rebleeding was 0.15% (0.05-0.36%) per patient-year of follow up. Peptic ulcer rebleeding virtually does not occur in patients with complicated ulcers after H. pylori eradication. Maintenance anti-ulcer (antisecretory) therapy is not necessary if eradication is achieved. However, NSAID intake or H. pylori reinfection may exceptionally cause rebleeding in H. pylori-eradicated patients.
    The American Journal of Gastroenterology 05/2012; 107(8):1197-204. · 9.21 Impact Factor
  • Gastroenterology 01/2011; 140(5). · 12.82 Impact Factor
  • Gastroenterology 01/2010; 138(5). · 12.82 Impact Factor
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    Alimentary Pharmacology & Therapeutics 09/2008; 28(4):499-500; author reply 500-1. · 4.55 Impact Factor
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    ABSTRACT: To evaluate the effect of Helicobacter pylori eradication on ulcer bleeding recurrence in a prospective, long-term study including more than 400 patients. Patients with peptic ulcer bleeding were prospectively included. H. pylori infection was confirmed by rapid urease test, histology or (13)C-urea breath test. Several eradication regimens were used. Ranitidine 150 mg was administered daily until eradication was confirmed by breath test 8 weeks after completing eradication therapy. Patients with therapy failure received a second or third course of therapy. Patients with eradication success did not receive maintenance anti-ulcer therapy, and were controlled yearly with a repeated breath test. Four hundred and twenty-two patients were followed up for at least 12 months, with a total of 906 patient-years of follow up. Mean age was 59 years, and 35% were previous nonsteroidal anti-inflammatory drug (NSAID) users. Sixty-nine percent had duodenal, 24% gastric, and 7% pyloric ulcer. Recurrence of bleeding was demonstrated in two patients at 1 year (incidence: 0.22% per patient-year of follow up), which occurred after NSAID use in both cases. Peptic ulcer rebleeding does not occur in patients with complicated ulcers after H. pylori eradication. Maintenance anti-ulcer (antisecretory) therapy is not necessary if eradication is achieved.
    Helicobacter 09/2007; 12(4):279-86. · 3.51 Impact Factor
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    ABSTRACT: Several authors have reported low prevalence of Helicobacter pylori infection in patients with upper gastrointestinal bleeding (UGIB). Our aim was to study the prevalence of H. pylori in bleeding duodenal ulcer (DU), with both invasive and non-invasive methods, and to assess the role of non-steroidal anti-inflammatory drugs (NSAIDs). Ninety-two patients with bleeding DU were prospectively studied. The use of NSAIDs was evaluated by specific questionnaire. As a control group, 428 patients undergoing outpatient evaluation for the investigation of dyspepsia and found to have a DU at endoscopy were included. At endoscopy, two antral biopsies were obtained (H&E stain). A 13C-urea breath test was carried out in all patients. Breath test was repeated in patients treated with omeprazole during the hospitalization if H. pylori was not detected with the first test. Gastric biopsies could be obtained in 39 patients with UGIB. Three patients with UGIB treated with omeprazole and being H. pylori-negative with the first breath test were finally considered infected with the second test. Overall, 92.4% (95% CI, 85%-96%) of the patients with UGIB were infected (89.7% with histology and 92.4% with breath test (P = 0.15)). Concordance kappa value for both diagnostic tests was 0.64. NSAID intake was more frequent in patients with UGIB (34%) than in those without UGIB (5.6%) (P < 0.001), while H. pylori infection was less frequent in patients with UGIB (92.4% (85%-96%)) than in those without UGIB (99.1% (98%-100%); P < 0.001). Even in patients with UGIB, NSAID intake was the only risk factor in 5% of cases. The proportion of cases without H. pylori infection and without NSAID intake was very low in both bleeding and non-bleeding ulcers (2% and 0.5%, respectively; P = 0.146). H. pylori prevalence in bleeding ulcers was of 84% (67%-93%) in patients with NSAID intake, and 96.7% (89%-99%) when patients taking NSAIDs were excluded. In the multivariate analysis, NSAID intake (odds ratio, 9.8 (5.2-18.4)) correlated with UGIB; however, neither H. pylori status nor the interaction between H. pylori infection and NSAID intake correlated with UGIB. In the multivariate analysis in the subgroup of patients with UGIB, NSAID use was the only variable which correlated with H. pylori prevalence (odds ratio, 0.18 (0.03-0.97)). The most important factor associated with H. pylori-negative bleeding DU is NSAID use, and if this factor is excluded prevalence of infection is almost 100% (97%), similar to that found in patients with non-bleeding DU (and without NSAID intake). Bleeding DU patients with neither H. pylori infection nor NSAID use are extremely rare (only 2%), which suggests that the pathogenesis of bleeding DU is similar to that of non-complicated DU disease.
    Scandinavian Journal of Gastroenterology 08/2001; 36(7):717-24. · 2.33 Impact Factor
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    ABSTRACT: Our aim was to study the incidence of Helicobacter pylori recurrence in our country and to assess the different variables that might influence it. We studied prospectively 331 duodenal ulcer patients (mean age, 48 +/- 14 years, 71% male) in whom H. pylori had been eradicated. Several therapies were used, classified as low-efficacy (omeprazole + amoxycillin, 32% eradication rate; omeprazole + amoxycillin + metronidazole, 56%) and high-efficacy therapies (omeprazole + clarithromycin + amoxycillin or metronidazole, 88%; bismuth triple therapy, 77%). One month after completion of therapy an endoscopy with biopsies and/or 13C-urea breath test was performed. A breath test was carried out again at 6 months, 1 year, and 2 years, to study H. pylori recurrences. Endoscopy (with biopsies) was performed only to confirm recurrences. Multiple logistic regression analysis was used. Differences between Kaplan-Meier curves were evaluated with the log-rank test. Sixty-seven patients were followed up for 6 months, 136 for 1 year, and 128 for 2 years, giving 425 patient-years of follow-up. A total of 18 H. pylori recurrences was observed (12 at 6 months, 4 at 1 year, and 2 after 2 years), yielding a yearly recurrence of 4.2% patient-years(-1). The respective risk of H. pylori recurrence for each period was 3.6% (95% confidence interval (CI), 2.1%-6.2%), 1.5% (0.6%-3.8%), and 1.5% (0.4%-5.5%). The probability of being H. pylori-negative at 6 months, 1 year, and 2 years was, respectively, 96.4% (94.4%-98.4%), 94.9% (92.5%-97.4%), and 93.4% (90.3%-96.6%). Duodenal ulcer was found in half of the reinfected patients. The recurrence rate at 6 months was 10.3% (5.7%-18%) in patients <40 years old and only 0.85% (0.2%-3.1%) in those > or =40 years old (P = 0.0002). Of the patients who became reinfected at 6 months 27% (6%-61%) had delta breath test values between 3 per thousand and 5 per thousand 1 month after therapy, whereas only 4.6% (2.7%-7.7%) of non-reinfected patients had delta after eradication > or =3 per thousand (P = 0.0097). H. pylori recurrence at 6 months was 8.2% (4.5%-15%) in patients previously treated with low-efficacy therapies and only 1.7% (0.7%-4.3%) when high efficacy therapies were used (P = 0.0098). In the multivariate analysis age (odds ratio (OR), 0.9; 95% CI, 0.8-0.96; P = 0.0008), the delta breath test value after therapy (OR, 2.2; CI, 1.2-4.1; P = 0.0076), and therapy regimen (OR, 6.4; CI, 1.5-27; P = 0.0109) were the only variables that correlated with H. pylori recurrence at 6 months. Differences were observed when Kaplan-Meier curves were compared, depending on age (<40 or > or =40 years; P = 0.0054), breath test value (delta) 1 month after therapy (<3 or > or =3 per thousand; P = 0.0089), and therapy regimen (high or low efficacy; P = 0.0006). Risk of post-eradication H. pylori recurrence is higher during the first 6 months, which suggests that most recurrences during this period are recrudescences and not true reinfections. Patients who have H. pylori recurrence tend to be younger and have higher delta 13C-urea breath test values after therapy, which suggests that a 'negative' value between 3 per thousand and 5 per thousand needs to be confirmed. Recurrence of H. pylori is more frequent in patients treated with low-efficacy therapies but is exceptional when high-efficacy therapies are used, in which case post-therapy eradication can be safely confirmed at 4 weeks. Finally, recurrence of H. pylori is clinically relevant, as ulcer recurrence is observed in a considerable proportion of these patients.
    Scandinavian Journal of Gastroenterology 11/1998; 33(11):1144-51. · 2.33 Impact Factor
  • R. García-Grávalos, J. M. Pajares, A. Gracia, R. Lozano, J. Mercadal
    Gastroenterology 01/1998; 114. · 12.82 Impact Factor
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    ABSTRACT: To assess whether H. pylori therapy is significantly better than control therapy in patients with functional dyspepsia, and to assess whether curing the infection relieves symptoms of dyspepsia. We prospectively included consecutive H. pylori-positive patients in whom a gastroscopy was carried out and who were diagnosed of functional dyspepsia. At endoscopy, biopsies were obtained (histology and rapid urease test), and a 13C-urea breath test was carried out. Patients were randomly assigned to 10 days of treatment with either eradication therapy (omeprazole, amoxicillin and clarithromycin) or with ranitidine. No antisecretory therapy was prescribed thereafter. Breath test was repeated four weeks after completing eradication treatment. A validated five-point Likert scale was used to measure severity of symptoms, both at the beginning of the study and 6 and 12 months after treatment. Fifty patients were included in the study. Sixteen patients were randomized to ranitidine and 34 to eradication treatment. The two groups were well balanced for base-line characteristics. One patient in each treatment arm was lost to follow-up at 12 months. Differences between ranitidine and eradication groups were not demonstrated in any of the symptom comparisons, either initially or at 12 months. The rates of treatment success for each symptom were similar in both groups. H. pylori was eradicated in 76% of the patients receiving antibiotics. Differences between groups of patients with eradication success and failure were not demonstrated in any of the symptom comparisons, either initially or at 12 months. Among the groups given eradication regimen, the rates of treatment success for each symptom were similar in the group with H. pylori eradication success and failure. H. pylori eradication is not likely to play a major role in the treatment of symptoms in patients with functional dyspepsia.
    Hepato-gastroenterology 51(55):303-8. · 0.77 Impact Factor