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Javier P. Gisberta,∗,1, Xavier Calvetb,1, Fernando Bermejoc, Daniel Boixedad, Felipe Borye, Luis Bujandaf, Manuel Castro-Fernandezg, Enrique Dominguez-Munozh, Juan Ignasi Elizalde i, Montserrat Fornej, Emili Genek, Fernando Gomollon l, Angel Lanasm, Carlos Martin de Argilad, Adrian G. McNicholl a, Fermin Mearinm, Javier Molina-Infanten, Miguel Montoroo, Jose Maria Pajaresa, Angeles Perez-Aisap, Emilio Perez-Tralleroq y Jordi Sanchez-Delgadob

Summary Background Several ‘rescue’ therapies have been recommended to eradicate Helicobacter pylori, but they still fail in >20% of the cases, and these patients constitute a therapeutic dilemma. Aim To evaluate the efficacy of different ‘rescue’ therapies empirically prescribed during 10 years to 500 patients in whom at least one eradication regimen had failed to cure H. pylori infection. Methods Design: Prospective single-centre study. Patients: Consecutive patients in whom at least one eradication regimen had failed. Intervention: Rescue regimens included: (i) quadruple therapy with omeprazole–bismuth–tetracycline–metronidazole; (ii) ranitidine bismuth citrate–tetracycline–metronidazole; (iii) omeprazole–amoxicillin–levofloxacin; and (iv) omeprazole–amoxicillin-rifabutin. Antibiotic susceptibility was unknown (rescue regimens were chosen empirically). Outcome: Eradication was defined as a negative 13C-urea breath test 4–8 weeks after completing therapy. Results Five hundred patients were included (76% functional dyspepsia, 24% peptic ulcer). Compliance rates with first-, second- and third-line regimens were 92%, 92%, and 95%, respectively. Adverse effects were reported by 30%, 37%, and 55% of the patients receiving second-, third-, and fourth-line regimens. Overall, H. pylori cure rates with the second-, third-, and fourth-line rescue regimens were 70%, 74%, and 76%, respectively. Cumulative H. pylori eradication rate with four successive treatments was 99.5%. Conclusion It is possible to construct an overall treatment strategy to maximize H. pylori eradication, on the basis of administration of four consecutive empirical regimens; thus, performing bacterial culture even after a second or third eradication failure may not be necessary.

Even before the discovery of Helicobacter pylori as their cause, chronic gastritis and peptic ulcer disease were empirically treated with anti-infectious agents. However, it was not until that finding that an antibiotic approach began to be used systematically. The main aim of this article is to review the evolution of H. pylori therapy from a meta-analytical perspective. Initially, antibiotic monotherapy had a minor efficacy on H. pylori. Dual therapy including either bismuth compounds or proton-pump inhibitors (PPI) and one antibiotic also resulted in insufficient cure rates. Bismuth-based triple therapy (the first used) and PPI-based triple therapies (combined with two antibiotics, including amoxicillin, nitroimidazole, or clarithromycin) have been the most widely recommended. PPI-based regimens are superior to H2-antagonist-based ones. The influence of the type of PPI, the dose and the duration of the treatment will be discussed. Among the factors influencing the efficacy of therapy, resistance to clarithromycin and metronidazole are the most important risk factors for eradication failure. Several rescue therapies can be used. Bismuth-based quadruple therapy is effective, but the complexity of the regimen and the associated adverse effects limit the compliance. PPI-based triple therapy with amoxicillin and levofloxacin is at least equally effective and better tolerated.

Aim: Ranitidine bismuth citrate and levofloxacin-based regimen may be an alternative to quadruple therapy after Helicobacter pylori eradication failure. Our aim was to compare two 7-day triple second-line regimens containing ranitidine bismuth citrate or levofloxacin. Methods: Patients in whom a first eradication trial with omeprazole-clarithromycin-amoxicillin had failed were randomized to receive 7-day treatment with: 1, ranitidine bismuth citrate (400 mg b.i.d.), tetracycline (500 mg q.i.d.), and metronidazole (250 mg q.i.d.), or 2, levofloxacin (500 mg b.i.d.), amoxicillin (1 g b.i.d.), and omeprazole (20 mg b.i.d.). Cure rates were evaluated by 13C-urea breath test. Results: One-hundred patients were included: 50 received the ranitidine bismuth citrate regimen, and 50 the levofloxacin one. Groups were comparable in terms of demographic variables. Two percent of the patients (one in each group) did not return for follow up. Compliance was similar in both groups (90% took all the medications correctly). Side-effects (only mild/moderate) in the two groups were also comparable (38% with ranitidine bismuth citrate and 36% with levofloxacin). Per-protocol cure rates were 69% (95% CI = 54–80%) in the ranitidine bismuth citrate group, and 71% (57–82%) in the levofloxacin one. Intention-to-treat cure rates were, respectively, 68% (59–79%) and 68% (59–79%) (nonstatistically significant differences). Conclusions: Both 7-day ranitidine bismuth citrate- and levofloxacin-containing second-line regimens represent alternatives to quadruple therapy in patients with previous omeprazole-clarithromycin-amoxicillin failure.

Aims: 1) To review clinical and endoscopic variables in patients hospitalized for upper gastrointestinal bleeding (UGIB) due to peptic gastroduodenal lesions over a period of 3 years; 2) to identify factors associated with unfavorable evolution; and 3) to evaluate characteristics of patients discharged immediately after endoscopy. Methods: A 3-year retrospective analysis of all UGIB episodes was performed. Patients with gastroduodenal ulcer or erosive gastritis/duodenitis at endoscopy were included. The prognostic value of several clinical, endoscopic, and analytical variables was assessed. Persistence or recurrence of bleeding, surgery, and mortality were considered as outcome variables (evolution was classified as “unfavorable” when any of these was observed). Results: A total of 341 patients were identified, with a mean age of 62 years. Melena was the most frequent UGIB presentation (70%). Forty-five percent had associated diseases, and 45% were taking gastroerosive drugs. Duodenal ulcer was the most frequent cause of UGIB (48%), followed by gastric ulcer (32%). The evolution of UGIB was unfavorable in 7% of cases. Variables associated with unfavorable evolution in the multivariate analysis were: systolic blood pressure ≤ 100 mm Hg, heart rate ≥ 100 bpm, and a Forrest endoscopic classification of severe. Only 10% of patients were immediately discharged, with no subsequent complications. However, if predictive variables obtained in the multivariate analysis had been used, hospitalization could have been prevented in 115 patients (34%) without subsequent complications. Conclusions: A number of clinical and endoscopic variables (blood pressure, heart rate, and endoscopic stigmata of bleeding) with prognostic value have been identified. These are easy to obtain and apply in clinical practice and allow an accurate estimation of the evolution of UGIB. This diagnostic strategy identifies a relatively high proportion of UGIB patients who can be managed on an outpatient basis.

The precise choice of cut-off point for the 13C-urea breath test to define whether it is positive or negative represents a controversial issue.To quantify the 13C-urea breath test result for several years following Helicobacter pylori eradication, and to evaluate the frequency and the significance of borderline delta13CO2 values.Two-hundred H. pylori eradicated patients confirmed by 13C-urea breath test (100 mg of urea, citric acid), and having had repeated this test yearly up to 5 years, were studied. Delta13CO2 values between 2 and 5/1000 were considered as borderline results.Eight H. pylori recurrences were observed during 406 patient-years of follow-up (1.97% yearly). In two of eight reinfected patients, the reinfection was preceded by a negative delta13CO2 value2/1000. Borderline delta13CO2 values were detected in 4% of the 606 urea breath tests performed, and in 25% when only patients in whom H. pylori recurrence was detected in subsequent urea breath tests were included (P0.05). The negative-predictive value of a post-treatment delta13CO22/1000 for the diagnosis of H. pylori recurrence was 99%.Positive and negative urea breath test results tend to cluster outside the range between 2/1000 and 5/1000. Nevertheless, a borderline urea breath test delta value (e.g. very close to the selected cut-off point) should be interpreted cautiously, and the result should probably be confirmed either by repeating the urea breath test or by other diagnostic methods. On the contrary, a delta13CO2 value2/1000 very confidently confirms H. pylori eradication.

Summary Background : Helicobacter pylori eradication is a challenge in patients allergic to penicillin, especially those who have failed a first-eradication trial. Aim : To assess the efficacy and tolerability of H. pylori first-line treatment and rescue options in patients allergic to penicillin. Methods : Prospective single centre study including 40 consecutive treatments administered to patients allergic to penicillin. Therapy regimens: First-line (12 patients) omeprazole, clarithromycin and metronidazole for 7 days; second-line (17 patients) ranitidine bismuth citrate, tetracycline and metronidazole for 7 days; third-line (nine patients) rifabutin, clarithromycin and omeprazole for 10 days; and fourth-line (two patients) levofloxacin, clarithromycin and omeprazole for 10 days. Outcome variable: a negative 13C-urea breath test 8 weeks after completion of treatment. Results : Per-protocol/intention-to-treat eradication rates were: first-line (64/58%); second-line (ranitidine bismuth citrate; 53/47%); third-line (rifabutin; 17/11%) and fourth-line regimen (levofloxacin; 100/100%). Compliance with treatment was generally good, except with the rifabutin-based regimen, which presented adverse effects in 89% of the patients, including four cases of myelotoxicity. Conclusions : H. pylori-infected patients who are allergic to penicillin may be treated with a first-line treatment combining a proton-pump inhibitor, clarithromycin and metronidazole. Rescue options may include a regimen with ranitidine bismuth citrate, tetracycline and metronidazole. A levofloxacin-based rescue regimen (with proton-pump inhibitor and clarithromycin) may also represent an alternative, even when two or more consecutive eradication treatments have previously failed. However, rifabutin + clarithromycin + proton-pump inhibitor regimen is ineffective and poorly tolerated.

Nowadays, apart from having to know well first-line eradication regimens, we must also be prepared to face Helicobacter pylori treatment failures. Therefore, in designing a treatment strategy we should not focus on the results of primary therapy alone, but also on the final--overall--eradication rate. After failure of a combination of proton pump inhibitor (PPI), amoxicillin, and clarithromycin, the use of empirical quadruple therapy (PPI-bismuth-tetracycline-metronidazole), has been generally used as the optimal second-line therapy. Even after two consecutive failures, several studies have demonstrated that H. pylori eradication can finally be achieved in almost all patients if several "rescue" therapies are consecutively given. It seems that performing culture even after a second eradication failure may not be necessary, as it is possible to construct an overall strategy to maximize H. pylori eradication, based on the different possibilities of empirical treatment (when antibiotic susceptibilities are unknown). Thus, if one does not want to perform culture before the administration of the third treatment after failure of the first two, different empirical treatments exist, including regimens based on: 1, amoxicillin (amoxicillin-PPI at high doses); 2, amoxicillin plus tetracycline (PPI-bismuth-tetracycline-amoxicillin, or ranitidine-bismuth-citrate-tetracyline-amoxicillin); 3, rifabutin (rifabutin-amoxicillin-PPI); 4, levofloxacin (levofloxacin-amoxicillin-PPI); and 5, furazolidone (furazolidone-bismuth-tetracycline-PPI).

Fundamento y objetivo El objetivo del presente estudio es describir la actividad enzimatica de la tiopurina metiltransferasa (TPMT) en un grupo muy numeroso de pacientes espanoles con enfermedad inflamatoria intestinal (EII), evaluar el efecto de algunas variables sobre dicha actividad y conocer la proporcion de pacientes con baja actividad y, por tanto, mayor riesgo de mielotoxicidad por azatioprina/6-mercaptopurina. Pacientes y metodo Se determino la actividad de TPMT mediante un metodo radioquimico en pacientes con EII. La asociacion entre diversas variables y la actividad de TPMT se estudio mediante regresion lineal multiple. Resultados Se incluyo a 7.046 pacientes, el 70% con enfermedad de Crohn, el 22% con colitis ulcerosa y un 8% con colitis indeterminada. El valor medio de TPMT fue de 20 U/ml (extremos: 0-46). La distribucion de actividad de TPMT fue: un 0,5% con valores bajos ( Conclusiones El 0,5% de los pacientes espanoles con EII tiene una baja actividad enzimatica de TPMT (

Summary The urea breath test is a non-invasive, simple and safe test which provides excellent accuracy both for the initial diagnosis of Helicobacter pylori infection and for the confirmation of its eradication after treatment. Some studies have found no differences between urea breath test performed under non-fasting conditions. The simplicity, good tolerance and economy of the citric acid test meal probably make its systematic use advisable. The urea breath test protocol may be performed with relatively low doses (

The aim of this study was to evaluate the effect of ibuprofen on gastric mucosa and enzymes involved in gastroprotection in healthy volunteers. Twenty-four Helicobacter pylori-negative subjects were randomized to treatment with ibuprofen or ibuprofen-arginate (each 600 mg/6 hr during 3 days). Endoscopies were performed 1 week before and after treatment. Biopsies were taken from the gastric antrum and corpus for determination of prostaglandin E2 (PGE2) by ELISA and cyclooxygenase (COX-1 and COX-2) and nitric oxide synthase (eNOS and iNOS) by western blot. All subjects had at least one gastric lesion except for two individuals taking ibuprofen-arginate. Ibuprofen-arginate caused a lower rate of clinical adverse reactions than ibuprofen. Subjects with gastric lesions or adverse reactions had lower PGE2 levels. COX-1, COX-2, eNOS, and iNOS were detectable in all subjects. The constitutive enzymes (COX-1 and eNOS) did not change after treatment. COX-2 was higher in corpus than antrum and it increased after ibuprofen treatment. iNOS tended to increase mildly in the corpus in subjects with adverse reactions or endoscopic lesions. There were no significant differences between ibuprofen and ibuprofen-arginate in PGE2, or enzymes.

Aims. To study the prevalence of Helicobacter pylori infection in patients with perforated peptic ulcer, to compare it with the prevalence in patients with uncomplicated ulcer, and to assess the role of non-steroidal anti-inflammatory drugs in this prevalence. Methods. Consecutive patients with perforated peptic ulcer were included in this retrospective study. As a control group, patients undergoing elective outpatient evaluation for the investigation of dyspepsia during the same time period and found to have a peptic ulcer at endoscopy were included. A 13 C -urea breath test was carried out in all patients to diagnose H. pylori infection. Results. Sixteen patients with perforated peptic ulcer and 160 with non-complicated peptic ulcer were included. Sixty-two percent of the patients with perforated peptic ulcer were infected by H. pylori , while the microorganism was detected in 87% of the patients without this complication ( P =0.01). Non-steroidal anti-inflammatory drugs intake was more frequent ( P =0.012) in patients with perforated peptic ulcers (56%) than in those without perforation (26%). H. pylori prevalence in perforated peptic ulcers was of 44% in patients with non-steroidal anti-inflammatory drugs intake, but this figure increased up to 86% when only patients not taking non-steroidal anti-inflammatory drugs were considered ( P =0.09). In the multivariate analysis, non-steroidal anti-inflammatory drugs intake was the only variable that correlated with peptic ulcer perforation [odds ratio, 3.6 (95% confidence interval, 1.3–10); P =0.016]. Conclusion. The mean prevalence of H. pylori infection in patients with perforated peptic ulcer is, overall, of only about 60%, which contrasts with the 90–100% figure usually reported in non-complicated ulcer disease. However, the most important factor associated with H. pylori -negative perforated peptic ulcer is non-steroidal anti-inflammatory drugs use, and if this factor is excluded, prevalence of infection is almost 90%, similar to that found in patients with non-perforating ulcer disease.

Lymphomagenesis is a multifactorial process in which genetic, environmental and infectious factors can be involved. The aim of the present study was to assess the prevalence of hepatitis C virus (HCV) infection among patients with non-Hodgkin's lymphoma (NHL), and to compare it with that of a control group of voluntary blood donors.All consecutive patients with a histological diagnosis of NHL from January 1996 to December 2001 were included in this prospective study. As control group for HCV infection, voluntary blood donors recruited over the same time period from the same geographical area were considered. The presence of anti-HCV antibodies was investigated by ELISA-II and RIBA-II, and viraemia (HCV RNA) was tested by using a polymerase chain reaction (PCR). HCV genotyping was also performed.Ninety-nine patients (mean age 48 years) with NHL were diagnosed during the study period. Histological classification of NHL was high-intermediate grade (63 patients), and low grade (36 patients). Immunophenotype distribution was type B (86 patients) and type T (13 patients). Seven of the 99 NHL patients (7%) were infected with HCV (both using serology and PCR), five of them with immunophenotype B and two with immunophenotype T. The prevalence of HCV infection according to NHL phenotype was 5.8% in B-cell NHL and 15.4% in T-cell NHL. The HCV genotype was 1b in six cases, and 3a in one. In voluntary blood donors (mean age 45 years), HCV infection was detected in 517/55 587 (0.93%). Therefore, HCV infection was more frequent in NHL patients than in controls (odds ratio = 8.1; 95% CI = 3.7-17.6). The odds ratio for the association of HCV and B-cell NHL was 6.2 (95% CI = 2.5-15.3), and for T-cell NHL 16.4 (95% CI = 3.7-72.8).The prevalence of HCV infection in patients with NHL (both B- and T-type) is higher than that observed in controls, suggesting a role of HCV in lymphoma aetiopathogenesis.

Aims. To prospectively evaluate the effectiveness of the test-and-treat strategy in a large group of dyspeptic patients in clinical practice. Methods. Patients with ulcer-like dyspepsia

Aim. Even with the current most effective Helicobacter pylori treatment regimens, approximately 20% of patients do not eradicate the infection. Several “rescue” therapies have been recommended, but they still fail to eradicate H. pylori in approximately 20–30% of the cases. Our aim was to evaluate the efficacy of different rescue therapies prescribed to patients in whom two consecutive H. pylori eradication regimens had failed. Methods. Design. Prospective single-centre study. Patients. Consecutive patients in whom two eradication regimens had failed to eradicate H. pylori. Intervention. Third eradication regimens included: (1) omeprazole–amoxicillin–clarithromycin for 7 days; (2) quadruple therapy with omeprazole–bismuth–tetracycline–metronidazole for 7 days; (3) omeprazole–amoxicillin–clarithromycin–bismuth for 14 days; and (4) omeprazole–amoxicillin–rifabutin for 14 days. H. pylori antibiotic susceptibility was unknown and, therefore, rescue regimens were chosen empirically. In no case, was the same regimen repeated. Outcome. H. pylori eradication was defined as a negative in 13 C -urea breath test 8 weeks after completing the therapy. Results. Forty-eight patients were included (mean age 45 years, 44% males, 82% with peptic ulcer and 18% with functional dyspepsia). No patient was lost from follow-up. Adverse effects were described in 21% of the patients. One patient receiving omeprazole, amoxicillin and rifabutin was removed from medication due to adverse effects (vomiting). Overall, mean H. pylori eradication with third therapy after failure of two eradication treatments was 34/48 (71%; 95% confidence interval 57–82%) by intention-to-treat and 34/47 (72%; 95% confidence interval 58–83%) by per-protocol. Conclusion. It seems that performing culture even after a second eradication failure may not be necessary, as it is possible to construct an overall strategy to maximise H. pylori eradication, based on the different possibilities of empirical treatment.

Background/Aims : To conduct a systematic review and meta-analysis on the prevalence of hepatitis C virus (HCV) infection in porphyria cutanea tarda (PCT). Methods : Studies evaluating prevalence of HCV infection in patients with PCT were considered. Bibliographical searches were conducted in several electronic databases. Studies comparing HCV prevalence in PCT (cases) and in a reference group (controls) were included in the meta-analysis, combining the Odds Ratios (OR) of the individual studies. Results : Fifty studies including 2,167 patients were identified. Mean HCV prevalence by serology was 47%, and 50% with polymerase chain reaction (PCR). HCV prevalence markedly varied depending on the country and the type of PCT (57% in the sporadic and 26% in the familial form). Eight case-contol studies were identified. Seven studies compared HCV prevalence in PCT vs. healthy controls: 40% vs. 0.24%, respectively (OR=275; 95% confidence interval=104-725). Heterogeneity disappeared when only studies evaluating HCV infection by PCR were included. Conclusions : HCV prevalence in patients with PCT is approximately 50%, much higher than that reported in general population, suggesting a possible etiopathogenic role of HCV in PCT. The striking geographical variation in this association suggests that genetic and/or environmental factors may also be involved in the pathogenesis of this disorder.

Summary Background : It is unknown whether proton pump inhibitors are superior to H2-receptor antagonists in Helicobacter pylori eradication regimens. Aim : To perform a meta-analysis comparing the efficacy of both antisecretors when co-prescribed with antibiotics. Methods : Randomized clinical trials comparing proton pump inhibitors vs. H2-receptor antagonists with the same antibiotics were selected. Data sources included PubMed, the Cochrane Controlled Trials Register and abstracts from congresses up to January 2002. A meta-analysis was performed by combining the odds ratios. Results : Twenty studies fulfilled the inclusion criteria. In the intention-to-treat analysis, the mean eradication rates with proton pump inhibitors and H2-receptor antagonists plus antibiotics were 74% [95% confidence interval (CI), 71–76%] and 69% (95% CI, 66–71%), respectively. The odds ratio for this comparison was 1.31 (95% CI, 1.09–1.58). The number needed to treat with proton pump inhibitors to achieve eradication success, compared with H2-receptor antagonists, was 25. When studies prescribing very high doses of H2-receptor antagonists (two of the outliers) were excluded, the odds ratio (for proton pump inhibitors vs. H2-receptor antagonists) increased to 1.37, the number needed to treat decreased to 20 and the heterogeneity between the studies decreased. Conclusions : Overall, proton pump inhibitors are more effective than H2-receptor antagonists when prescribed at usual doses with antibiotics to eradicate H. pylori infection.

Although the role of Helicobacter pylori infection on noncomplicated peptic ulcer disease has been definitively established, the precise relationship between the organism and complicated ulcer has hardly been studied. The mean prevalence of H. pylori infection in patients with perforated peptic ulcer is of only about 65-70%, which contrasts with the almost 90-100% figure reported in noncomplicated ulcer disease. However, H. pylori infection rates in various studies range markedly from 0% to 100%, suggesting that differences in variables as number and type of diagnostic methods used to diagnose H. pylori infection, or frequency of nonsteroidal anti-inflammatory drug intake, may be responsible for the low prevalence reported in some studies. Recurrent ulcer disease after peptic ulcer perforation mainly occurs in patients with H. pylori infection, which suggests that the microorganism plays an important role in this complication. All patients with perforated peptic ulcer should be treated by simple closure of the perforation and with therapy aimed at healing of the ulcer and eradicating the H. pylori infection, as disappearance of the organism prevents, or at least decreases, ulcer recurrence and ulcer perforation in patients with H. pylori-associated perforated ulcers after simple closure. Therefore, H. pylori eradicating treatment should be started during the immediate postoperative period. The patients with intractable recurrent symptoms of peptic ulcer despite adequate medical treatment, but without H. pylori infection (e.g. a patient using nonsteroidal anti-inflammatory drugs), is probably the only remaining indication for elective definitive surgical treatment of peptic ulcer disease.

Aim. Eradication therapy with proton pump inhibitor, clarithromycin and amoxicillin is extensively used, although it fails in a considerable number of cases. A ‘rescue’ therapy with a quadruple combination of omeprazole, bismuth, tetracycline and metronidazole (or ranitidine bismuth citrate with these same antibiotics) has been recommended, but it still fails in approximately 20% of cases. Our aim was to evaluate the efficacy and tolerability of a rifabutin-based regimen in patients with two consecutive H. pylori eradication failures. Patients and Methods. Design: Prospective multicenter study. Patients: Consecutive patients in whom a first eradication trial with omeprazole, clarithromycin and amoxicillin and a second trial with omeprazole, bismuth, tetracycline and metronidazole (three patients) or ranitidine bismuth citrate with these same antibiotics (11 patients) had failed were included. Intervention: A third eradication regimen with rifabutin (150 mg bid), amoxicillin (1 g bid) and omeprazole (20 mg bid) was prescribed for 14 days. All drugs were administered together after breakfast and dinner. Compliance with therapy was determined from the interrogatory and the recovery of empty envelopes of medications. Outcome: H. pylori eradication was defined as a negative 13C-urea breath test 8 weeks after completing therapy. Results. Fourteen patients have been included. Mean age ± SD was 42 ± 11 years, 41% males, peptic ulcer (57%), functional dyspepsia (43%). All patients took all the medications and completed the study protocol. Per-protocol and intention-to-treat eradication was achieved in 11/14 patients (79%; 95% confidence interval = 49–95%). Adverse effects were reported in five patients (36%), and included: abdominal pain (three patients), nausea and vomiting (one patient), and oral candidiasis (one patient); no patient abandoned the treatment due to adverse effects. Conclusion. Rifabutin-based rescue therapy constitutes an encouraging strategy after multiple previous eradication failures with key antibiotics such as amoxicillin, clarithromycin, metronidazole and tetracycline.

Summary Aim : To perform a systematic review of the efficacy of rabeprazole-based therapies in Helicobacter pylori eradication, and to conduct a meta-analysis comparing the efficacy of rabeprazole and other proton pump inhibitors when co-prescribed with antibiotics. Methods : Studies evaluating rabeprazole plus antibiotics were considered. Only randomized trials comparing rabeprazole and other proton pump inhibitors with antibiotics, and differing only in the proton pump inhibitor, were included in the meta-analysis. Electronic and manual bibliographic searches were conducted. The percentage (weighted mean) of successful eradication was calculated. Meta-analysis was performed by combining the odds ratios (OR) of the individual studies. Results : The eradication rates were as follows: 14-day rabeprazole–amoxicillin, 73%; rabeprazole–amoxicillin–clarithromycin for 3, 5, 7 and 10 days, 44%, 72%, 78% and 75%, respectively; low-dose rabeprazole (20 mg/day), amoxicillin and clarithromycin for 7 days, 81%; high-dose rabeprazole (40 mg/day), amoxicillin and clarithromycin for 7 days, 75%; 7-day rabeprazole–clarithromycin–nitroimidazole, 85%. Twelve comparative studies were included in the meta-analysis. The eradication rate with rabeprazole plus antibiotics was 79%; it was 77% with other proton pump inhibitors (OR = 1.15; 95% confidence interval, 0.93–1.42). Sub-analysis comparing rabeprazole at low doses (10 mg b.d.) with other proton pump inhibitors at standard doses (omeprazole 20 mg b.d. or lansoprazole 30 mg b.d.) showed no differences. Conclusions : Rabeprazole achieves similar H. pylori eradication rates to omeprazole and lansoprazole when co-prescribed with antibiotics. Low doses of rabeprazole (10 mg b.d.), when administered with two antibiotics, may be sufficient to eradicate H. pylori infection.

Testing for antimitochondrial antibodies is the most useful laboratory procedure in the diagnosis of primary biliary cirrhosis; nevertheless, 5-10% of patients with typical features of primary biliary cirrhosis do not have detectable antimitochondrial antibodies, their condition being referred to as antimitochondrial antibody-negative primary biliary cirrhosis or "autoimmune cholangitis". Uncertainty exists whether antimitochondrial antibody-positive and -negative primary biliary cirrhosis represent distinct entities. We reviewed studies that compared: (i) the clinical, laboratory and histological characteristics of antimitochondrial antibody-positive and -negative primary biliary cirrhosis; (ii) the response to treatment of both conditions; and (iii) the response of autoimmune cholangitis to ursodeoxycholic acid and immunosuppressive therapy. Antimitochondrial antibody-positive and -negative primary biliary cirrhosis were characterized by similar clinical, laboratory and histological abnormalities, clinical course and survival. Antimitochondrial antibody status did not seem to affect the response to ursodeoxycholic acid. At present, the efficacy of therapies for autoimmune cholangitis has not been established in controlled trials. Of 52 patients with autoimmune cholangitis treated with ursodeoxycholic acid in 13 uncontrolled studies, 83% had serum biochemical improvement. Also, a favourable effect of immunosuppressive drugs occurred in 57% of 54 patients with autoimmune cholangitis in 17 uncontrolled studies. Each of these trials included very few patients and most evaluated the effects of treatment on surrogate markers of disease only. No marker that consistently distinguished patients who would respond favourably to ursodeoxycholic acid or immunosuppression was apparent. Consequently, treatment is, at present, empirical. However, ursodeoxycholic acid may be given when histology reveals bile duct lesions, whereas immunosuppressive therapy should probably be reserved for patients exhibiting interface hepatitis.

The prevalence of Helicobacter pylori infection in peptic ulcer disease complicated by gastric outlet obstruction seems to be, overall, lower than that reported in non-complicated ulcer disease, with a mean value of 69%. However, H. pylori infection rates in various studies range from 33% to 91%, suggesting that differences in variables, such as the number and type of diagnostic methods used or the frequency of non-steroidal anti-inflammatory drug intake, may be responsible for the low prevalence reported in some studies. The resolution of gastric outlet obstruction after the eradication of H. pylori has been demonstrated by several studies. It seems that the beneficial effect of H. pylori eradication on gastric outlet obstruction is observed early, just a few weeks after the administration of antimicrobial treatment. Furthermore, this favourable effect seems to remain during long-term follow-up. Nevertheless, gastric outlet obstruction does not always resolve after H. pylori eradication treatment and an explanation for the failures is not completely clear, non-steroidal anti-inflammatory drug intake perhaps playing a major role in these cases. Treatment should start pharmacologically with the eradication of H. pylori even when stenosis is considered to be fibrotic, or when there is some gastric stasis. In summary, H. pylori eradication therapy should be considered as the first step in the treatment of duodenal or pyloric H. pylori-positive stenosis, whereas dilation or surgery should be reserved for patients who do not respond to such medical therapy.

Fundamento Estudiar la prevalencia de la infeccion por Helicobacter pylori y el fenotipo CagAde la cepa en dos poblaciones (Espana y Cuba), y su relacion con diversas lesiones gastroduodenales,asi como el papel de la estrategia «testar y realizar endoscopia» en la disminucion delnumero de gastroscopias. Pacientes y metodo Se incluyeron 100 pacientes espanoles y 100 cubanos con dispepsia a losque se les realizo una gastroscopia para el estudio de sus sintomas. H. pylori se detecto mediantela prueba de la ureasa rapida. Se determino el fenotipo CagA de la cepa (mediante Westernblot). Se evaluo la estrategia «testar y realizar endoscopia» en funcion de la infeccion porH. pylori y el fenotipo CagA de la cepa. Resultados La edad media (DE) de los pacientes espanoles y cubanos fue de 45 (16) y 46(15) anos, respectivamente. Los sintomas de dispepsia fueron similares en ambos grupos. Laprevalencia de infeccion por H. pylori fue mas alta en Cuba (73%) que en Espana (40%) (p Conclusiones La prevalencia de infeccion por H. pylori es mas alta en los pacientes cubanoscon dispepsia que en los espanoles. Las cepas de H. pylori de Cuba parecen ser mas virulentasque las de Espana. La proteina CagA es un marcador de ulcera peptica en ambas poblaciones.Las diferencias encontradas podrian explicar parcialmente las variaciones en la prevalencia delas diversas enfermedades gastroduodenales entre ambos paises. La estrategia «testar y realizarendoscopia» podria evitar unicamente un reducido numero de endoscopias.

Fundamento Para establecer un nexo de causalidad entre infeccion por Helicobacter pylori y dispepsiafuncional es preciso demostrar que la erradicacion del microorganismo se sigue de una mejoria de lossintomas dispepticos, cuestion que aun no esta aclarada. Nuestro objetivo ha sido realizar un metaanalisisde los estudios aleatorizados que comparan el efecto sobre la dispepsia funcional del tratamientoerradicador de H. pylori frente al tratamiento con farmacos sin efecto alguno sobre la infeccion. Pacientes y metodo Estrategia de busqueda: Internet (PubMed), Registro de Ensayos Clinicos de la ColaboracionCochrane y resumenes de comunicaciones a congresos hasta 2001. Criterios de seleccion:a) estudios en los que se evaluaba a pacientes con dispepsia funcional e infeccion por H. pylori; b)ensayos clinicos aleatorizados que compararan el tratamiento erradicador y el tratamiento control sinefecto sobre H. pylori, y c) seguimiento de al menos 6 meses. La calidad de los estudios se evaluomediante una escala validada. Estudio estadistico: la «variable de resultado» fue el porcentaje de pacientesque mejoraron en cada grupo terapeutico. Se realizo un metaanalisis combinando las odds ratio(OR) de los estudios individuales en una OR global. Resultados Se incluyeron 9 estudios que cumplian los criterios de inclusion. Globalmente, 953 pacientesrecibieron tratamiento erradicador, mientras que 958 correspondian al grupo control. El porcentajeglobal de pacientes con mejoria de los sintomas dispepticos en el grupo de tratamiento erradicadorfue del 43% (intervalo de confianza [IC] del 95%, 40-46%) y del 39% en el grupo control(IC del 95%, 36-42%). La OR para el efecto del tratamiento erradicador frente al control fue de 1,20(IC del 95%, 0,91-1,58). El NNT (numero necesario a tratar) con terapia erradicadora para conseguirla mejoria sintomatica de uno de ellos fue de 25. Se evidencio heterogeneidad en los resultados, quedesaparecio al excluir el unico estudio que comunicaba resultados positivos claramente discordantes,con lo que el porcentaje de pacientes con mejoria sintomatica en el grupo de tratamiento erradicadorfue del 47% (IC del 95%, 43-50%) y del 45% en el grupo control (IC del 95%, 41-48%) (OR =1,06; IC del 95%, 0,85-1,31; NNT = 50). Conclusiones El tratamiento erradicador de H. pylori no se asocia con una mejoria estadisticamentesignificativa de los sintomas en los pacientes con dispepsia funcional.

Fundamento La ulcera peptica representa la causa mas frecuente de hemorragia digestiva alta(HDA). Puesto que en la mayoria de los casos su evolucion es favorable y el episodio hemorragicocede espontaneamente, se ha planteado la posibilidad de reducir el numero de los ingresoshospitalarios en estos pacientes. Nuestro objetivo fue revisar las variables clinicas y endoscopicasde los pacientes con HDA secundaria a lesiones pepticas gastroduodenales evaluadosen nuestro hospital durante un ano, asi como identificar las caracteristicas que se asocian auna evolucion desfavorable de la HDA. Pacientes y metodo Analisis retrospectivo de todos los episodios de HDA de pacientes que acudierona nuestro hospital durante un ano. Se incluyo a aquellos pacientes en los que se identificomediante gastroscopia una ulcera gastroduodenal o una gastritis/duodenitis erosiva comocausa de la HDA. Se evaluo el papel pronostico de diversas variables clinicas, analiticas y endoscopicas.Como variables «resultado» de mala evolucion se incluyeron la persistencia o recidivahemorragica, la cirugia y la mortalidad (la variable «evolucion» se categorizo como «desfavorable» cuando se observaba alguna de las variables mencionadas). Resultados Se identifico a 156 pacientes, con una edad media (DE) de 61 (17) anos. La presentacionmas frecuente fue en forma de melena (79%). El 46% tenia enfermedades asociadas y el50% recibia gastroerosivos. La causa mas frecuente de HDA fue la ulcera duodenal (52%), seguidade la ulcera gastrica (30%). La HDA evoluciono desfavorablemente en el 7% de los casos. Enel analisis multivariante las variables que se asociaron a una evolucion desfavorable fueron laedad, la presentacion como hematemesis de sangre roja, una presion arterial sistolica . 100mmHg, una frecuencia cardiaca . 100 lat/min y una clasificacion endoscopica de Forrest masgrave. El 11% de los pacientes fue dado de alta inmediatamente, sin complicaciones posteriores.Si aplicaran las variables predictivas obtenidas en el modelo multivariante, podria evitarse el ingresoen 59 pacientes (38%) sin complicaciones posteriores. Conclusiones Hemos identificado una serie de variables clinicas y endoscopicas faciles de obtenery de aplicar en la practica clinica, que permiten estimar con relativa seguridad la evolucionde la HDA. De este modo puede identificarse con fiabilidad un subgrupo relativamente numerosode pacientes con HDA susceptible de recibir tratamiento ambulatorio.

Recently a new, noninvasive diagnostic test based on the detection of Helicobacter pylori stool antigen (SA) has been developed. The aim of this study was to systematically review the experience on H. pylori SA test for the diagnosis of H. pylori infection. Bibliographic searches were performed in the PubMed database and abstracts from several congresses. A total of 43 studies fulfilled the inclusion criteria and evaluated H. pylori SA test accuracy for the diagnosis of H. pylori infection in nontreated patients. Overall, 4769 patients were included. The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) (weighted mean) were, respectively: 92.4% (95% CI = 91-93%), 91.9% (91-92%), 92.1% (91-93%), and 90.5% (90-91%). Therefore the SA test can definitively be considered an accurate noninvasive method for the diagnosis of H. pylori infection in untreated patients. A total of 25 studies including 2078 patients evaluated H. pylori SA test for the confirmation of H. pylori eradication > or = 4 wk after completion of therapy. Sensitivity, specificity, PPV and NPV (weighted mean) were: 88.3% (87-90%), 92% (91-93%), 75.1% (73-77%), and 94.8% (94-96%). Although most studies showed that SA test is an accurate method to confirm H. pylori eradication > or = 4 wk after treatment, these favorable results were not confirmed in other studies. Further investigation is necessary to explain these discrepancies, as well as to clarify the precise time for confirmation of eradication after therapy, the appropriate cutoff point for the SA test, and which factors influence it. Proton pump inhibitors seem to affect the accuracy of SA test, but the negative effect disappears 1-2 wk after stopping treatment. The SA test is technically feasible in patients with upper GI bleeding. although the true diagnostic accuracy in this group of patients remains to be more fully assessed. Finally, the SA test seems to be a highly cost-effective method for the diagnosis of H. pylori infection.

Purpose: To evaluate whether proton pump inhibitors are more effective than H2-antagonists (H2-A) for the treatment of bleeding peptic ulcer. Data sources: PubMed database until January 2000. Study selection: Comparative randomized trials of proton pump inhibitors (omeprazole, lansoprazole, or pantoprazole) vs. H2-A (cimetidine, ranitidine or famotidine). Data extraction: Meta-analysis combining the odds ratios (OR) of the individual studies in a global OR (Peto method). Outcomes evaluated: Persistent or recurrent bleeding, need for surgery, or mortality. Data synthesis: Eleven studies fulfilled the inclusion criteria and contained data for at least one of the planned comparisons. Persistent or recurrent bleeding was reported in 6.7% (95% CI: 4.9–8.6%) of the patients treated with proton pump inhibitors, and in 13.4% (95% CI: 10.8–16%) of those treated with H2-A (OR 0.4; 95% CI: 0.27–0.59) (χ2-homogeneity test, 18; P=0.09). Surgery was needed in 5.2% (95% CI: 3.4–6.9%) of the patients treated with proton pump inhibitors, and in 6.9% (95% CI: 4.9–8.9%) of the patients treated with H2-A (OR 0.7; 95% CI: 0.43–1.13). Respective percentages for mortality were 1.6% (95% CI: 0.9–2.9%) and 2.2% (95% CI: 1.3–3.7%) (OR 0.69; 95% CI: 0.31–1.57). Sub-analysis: Five studies evaluated the effect of both therapies given in bolus injections on persistent or recurrent bleeding rate, which was 6% (95% CI: 3.6–8.3%) and 8.1% (95% CI: 5.3–10.9%), respectively (OR, 0.57; 95% CI: 0.31–1.05). Persistent or recurrent bleeding in high risk patients (Forrest Ia, Ib and IIa) occurred in 13.2% (95% CI: 7.9–8%) of the patients treated with proton pump inhibitors and in 34.5% (27–42%) of those treated with H2-A (OR 0.28; 95% CI: 0.16–0.48). In patients not having endoscopic therapy, persistent or recurrent bleeding was reported, respectively, in 4.3% (95% CI: 2.7–6.7%) and in 12% (95% CI: 8.7–15%) (OR 0.24; 95% CI: 0.13–0.43). Less marked differences were observed in patients having adjunct endoscopic therapy: 10.3% (95% CI: 6.7–13.8%) and 15.2% (11.1–19.3%) (OR 0.59; 95% CI: 0.36–0.97). Moreover, the significance disappeared in this group when a single outlier study was excluded. Conclusions: Proton pump inhibitors are more effective than H2-A in preventing persistent or recurrent bleeding from peptic ulcer, although this advantage seems to be more evident in patients not having adjunct sclerosis therapy. This beneficial effect seems to be similar or even more marked in patients with Forrest Ia, Ib or IIa ulcers. However, proton pump inhibitors are not more effective than H2-A for reducing surgery or mortality rates. Nevertheless, the data are too scarce and heterogeneous to draw definitive conclusions, and further comparative trials are clearly warranted.

Aim. The combination of a proton pump inhibitor (PPI) or ranitidine-bismuth-citrate (Rbc) and two antibiotics for 7–10 days are, at present, the preferred treatments in Helicobacter pylori eradication. However, therapies for fewer than 7 days have been scarcely evaluated and it is unknown whether the length of treatment can be shortened, without a lost of efficacy, if three instead of two antibiotics are used. The aim of our study was to evaluate the efficacy of Rbc plus three antibiotics for only 5 days in H. pylori eradication. Methods. We prospectively studied 80 patients (34% duodenal ulcer, 66% functional dyspepsia) infected by H. pylori. At endoscopy, biopsies were obtained for histological study and rapid urease test, and a 13C-urea breath test was carried out. Urea breath test was repeated 4 weeks after completing eradication treatment with Rbc [400 mg twice a day (bid)], amoxicillin (1 g bid), clarithromycin (500 mg bid) and metronidazole (500 mg bid). All drugs were administered together after breakfast and dinner for 5 days only, and no treatment was administered thereafter. Compliance with therapy was determined from the interrogatory and the recovery of empty envelopes of medications. Results. In 79 out of the 80 patients, H. pylori eradication success or failure was assessed after therapy (one patient was lost from follow-up). All but one of these 79 patients took all the medications (one patient stopped treatment on the day 3 due to nausea/vomiting). Per protocol eradication was achieved in 72/78 (92%; 95% CI, 84–96%) and in 72/80 (90%; 81–95%) by intention-to-treat. Therapy was more effective in patients with duodenal ulcer than in those with functional dyspepsia [100% (87–100%) vs. 85% (73–92%) by intention-to-treat; p

In the present paper, several points regarding Helicobacter pylori treatment are reviewed, with the following conclusions: (1) all different proton pump inhibitors (PPIs) are equivalent when prescribed with antibiotics; (2) ranitidine bismuth citrate is equal to or, in some cases with antibiotic resistance, more effective than PPI; (3) previous treatment with PPI does not seem to affect the rate of eradication obtained with PPI plus two antibiotics; (4) just 1 week of PPI is enough to obtain duodenal ulcer healing, provided that H. pylori eradication is achieved; (5) the eradication rates seem to be higher in peptic ulcer than in nonulcer dyspepsia; (6) in areas where the prevalence of metronidazole resistance is high, triple therapy including a PPI, clarithromycin, and amoxicillin is the best option, and (7) quadruple therapy (PPI, bismuth, tetracycline, and metronidazole) is the recommended second-line therapy after PPI-clarithromycin-amoxicillin failure, although replacing the PPI and the bismuth compound by ranitidine bismuth citrate achieves also good results.

0953-6205/$ – see front matter © 2010 Euro doi:10.1016/j.ejim.2010.07.009 Helicobacter pylori (H. pylori) is a worldwide infection that affects millions of people. This infection is the main cause of gastritis, gastroduodenal ulcer disease, and gastric cancer. After more than 20 years of experience inH. pylori treatment, however, the ideal regimen to treat this infection has still to be found [1,2]. Themost recommended treatment for the eradication of H. pylori, in all international guidelines, is the so called standard or proton pump inhibitor (PPI) triple therapy, which includes the combination of two antibiotics (clarithromycin plus amoxicillin or metronidazole) with a PPI for at least 7 days [3,4]. However, H. pylori eradication rates with standard triple therapy have fallen from initial heights of N90% to 75–80% in some areas [5–9]. As an example, two recent double-blind, U.S. multicenter studies both found disappointingly low eradication rates with standard therapy: 77% [10,11]. Furthermore, two meta-analyses including more than 53,000 patients showed that the cure rate is, at present, below 80% [12,13]. In summary, eradication rates in most western countries have declined to unacceptable levels [2,14], probably due to increased resistance to antibiotics. In particular, antibiotic resistance to clarithromycin has been identified as one of themajor factors affecting our ability to cureH. pylori infection, and the rate of resistance to this antibiotic seems to be increasing in many geographical areas [15]. The ethics of continued use of standard triple therapy has recently been questioned and the use of alternative therapy has been recommended in its place [16]. Therefore, new strategies in order to improve first-line treatment are still urgently needed. Attempts to increase the duration of triple therapy and therefore prolong exposure to antibiotics have achieved controversial results, but, in general, have

Aim: To perform a meta-analysis of studies comparing twice daily, one-week triple therapy with a proton pump inhibitor, clarithromycin (C) and amoxycillin (A) (PCA) vs. those using proton pump inhibitor, clarithromycin and a nitroimidazole (N) (PCN) for H. pylori eradication. Review methods: Selection criteria: Comparative randomized trials of PCA vs. PCN were included. Data sources: PubMed database and abstracts from congresses until September 1999. Statistics: Meta-analysis was performed combining the Odds Ratios (OR) of the individual studies in a global OR (Peto method) both on an intention-to-treat (ITT) and on a per protocol (PP) basis. Results: Twenty-two studies fulfilled the inclusion criteria. Eighteen studies reported ITT and 20 PP analysis. Mean H. pylori eradication rates were 81% (95% CI: 79–83%) ITT, and 84% (82–86%) PP with PCA, and 81% (78–83%) ITT and 84% (82–86%) PP with PCN; the odds ratio for the effect of PCA vs. PCN was 1 (0.83–1.22) on an ITT, and 0.98 (0.8–1.2) on a PP basis. Subanalysis showed that mean H. pylori eradication efficacy with PC(250 b.d.)A was 81% (78–85%) ITT, vs. 86% (83–89%) with PC(250 b.d.)N. The odds ratio for this comparison was 0.68 (0.48–0.98). Finally, when comparing PC(500 b.d.)A against PC(250 b.d.)N ITT cure rates were 77% (74–80%), and 75% (72–78%) with an odds ratio of 1.18 (0.93–1.5). Conclusion: Overall, one-week combination regimens of PCA and PCN present similar H. pylori eradication efficacy. Nevertheless, the PCN regimen obtains significantly better results when using low doses of C (250 mg b.d.).

Objective: To compare the efficacy of proton pump inhibitor vs. ranitidine bismuth citrate (RBC) with two antibiotics for 1 week in Helicobacter pylori eradication. Methods: Randomized trials comparing 1-week regimens with (i) proton pump inhibitor plus two antibiotics [clarithromycin (C) and amoxycillin (A) or a nitroimidazole (N)]; or (ii) RBC plus the same antibiotics. Eradication was confirmed by histology or 13C-urea breath test at least 4 weeks after therapy. Data sources included PubMed database and abstracts from congresses until October 1999. Statistical analysis was by meta-analysis combining the odds ratios (OR) of the individual studies in a global OR (Peto method). Results: Twelve studies met the selection criteria. Nine compared proton pump inhibitor vs. RBC plus C and A, and five compared proton pump inhibitor vs. RBC plus C and N. With RBC, C and A, mean H. pylori eradication efficacy by intention-to-treat analysis (pooled data) was 76.6% (95% CI: 72–81%) and 73.7% (95% CI: 69–78%) with proton pump inhibitor, C and A. The OR for the effect of RBC vs. proton pump inhibitor (plus C and A) on H. pylori eradication was 1.15 (95% CI: 0.8–1.64%). Mean H. pylori eradication with RBC, C and N was 87.2% (95% CI: 83–91%), and 74.9% (95% CI: 74–84%) with proton pump inhibitor plus these two antibiotics. The OR for the effect of RBC vs. proton pump inhibitor (plus C and N) on H. pylori eradication was 1.76 (95% CI: 1.08–2.85%). Conclusion: RBC and proton pump inhibitor have similar efficacy for H. pylori eradication when given with C and A for 1 week, but RBC seems to have a higher efficacy than proton pump inhibitor when C and N are the co-prescribed antibiotics.

In this study several therapies were administered to 124 H. pylori-positive patients and IgG antibody titers were measured by ELISA at months 0, 2, 3, 6, 12, and 18 months. Serum titers of IgG antibody progressively decreased after H. pylori eradication; at 3 months, the area under the receiver operating characteristic curve for the decrease of IgG antibody titers for confirming H. pylori eradication was 0.99, with 100% sensitivity and 99% specificity (when the cutoff point was set at 3 U/mL). We conclude that a decrease in serum titers of IgG antibody to H. pylori relatively early after completion of therapy (1 month after ranitidine or bismuth therapy is completed and 2.5 months after antibiotic therapy is completed) can be used as a noninvasive, simple, and inexpensive method to confirm H. pylori eradication.

13C-urea breath test is one of the best methods for the diagnosis of Helicobacter pylori infection. Although a citric acid solution is generally used prior to urea intake, the superiority of this strategy has not been sufficiently demonstrated. Thus, our aim was to compare 13C-urea breath test with and without citric acid solution, to evaluate whether 13C-urea breath test can also achieve favourable results when the test meal is omitted.13C-urea breath test with and without citric acid were compared prospectively in 53 subjects without prior Helicobacter pylori eradication therapy prescription. Basal samples and at 15', 30', and 45' after taking 100 mg of 13C-urea were obtained. The gold standard for Helicobacter pylori diagnosis was the 13C-urea breath test result with citric acid at 30', and "Delta Over Baseline" values5 at that time were considered positive.The prevalence of Helicobacter pylori infection was 68%. Mean Delta Over Baseline values with citric acid at 15', 30' and 45' were: 29.6+/-39, 30.8+/-37 and 24.6+/-27; whereas respective values without citric acid were lower: 14.9+/-22, 12.2+/-17 and 10D+/-13 (pO. 001 for all comparisons, Wilcoxon test for paired data). Thus, the area under the curve (constructed with Delta Over Baseline values at different times) with citric acid was 85+/- 102, and 37+/-50 without citric acid [p0.001). Correlation coefficient between Delta Over Baseline values with and without citric acid at 30' was 0.73 (p0.0001). The percentage of subjects achieving the highest Delta Over Baseline value at 15', 30' and 45' with citric acid was 51%, 30% and 19%, whereas without citric acid it was 51%, 26% and 23% (non-significant differences). The area under receiver operating characteristic curve for 13C-urea breath test without citric acid was: 0.98 at 15', 1 at 30' and 0.97 at 45'. The best cut-off point for 13C-urea breath test without citric acid at 30' was anywhere between 3. 3 and 3.9 (that is, a lower value than that usually considered with citric acid), with 100% (95% confidence interval, 90-100%) sensitivity and 100% [82-100%) specificity13C-urea breath test values with citric acid are higher than those obtained without citric acid, although this difference does not imply a diagnostic superiority in untreated patients when considering 13C-urea breath test without citric acid at 30'. Therefore, for the diagnosis of Helicobacter pylori infection in untreated patients, citric acid solution in 13C-urea breath test protocol can be omitted.

Objetivo Evaluar el efecto de la erradicacion de Helicobacter pylori sobre las lesiones anatomopatologicas de la mucosa gastrica a lo largo de un periodo de 18 meses. Metodos Se estudiaron prospectivamente 122 pacientes con ulcera duodenal infectados por H. pylori . Se administro aleatoriamente ranitidina sola, raniditina junto con antibioticos o bismuto junto con antibioticos. Se realizo una endoscopia a los 3, 6, 12 y 18 meses. Se emplearon las tinciones de hematoxilina-eosina, Giemsa y Warthin-Starry. Las lesiones histologicas se clasificaron segun la siguiente puntuacion: normal (0); gastritis cronica (GC) superficial: leve (0,5), moderada (1) y grave (1,5); GC atrofica: leve (2), moderada (3) y grave (4); metaplasia intestinal: ausencia (0), leve (1), moderada (2) y grave (3). La actividad inflamatoria aguda (GC activa) se clasifico de 0 a 3 (ausencia, leve, moderada, grave) con respecto a densidad inflamatoria en la lamina propria, densidad de polimorfonucleares en la lamina propria, densidad de polimorfonucleares intraepiteliales y erosiones superficiales. Resultados Se logro la erradicacion de H. pylori en el 31% de los pacientes (0% en el grupo de ranitidina sola y 48% en aquellos que recibieron antibioticos). La puntuacion correspondiente a la GC descendio progresivamente tras la erradicacion de H. pylori , con unos valores medios, respectivamente, en los meses 0, 3, 6, 12 y 18, de: 2,1 ±1,3, 1,98 ± 1,4, 1,73 ± 1,6, 1,43 ± 1,9 y 1,38 ± 1,9 (p Conclusiones La erradicacion de H. pylori se asocia con una mejoria histologica de la mucosa gastrica que, aunque comienza a producirse ya en un momento precoz, continua a lo largo de 18 meses despues del tratamiento. La mejoria del componente inflamatorio global es lenta y progresiva, mientras que el componente agudo de la gastritis experimenta una mejoria precoz mas acusada, que se objetiva en el periodo inmediatamente posterior a la obtencion de la erradicacion. Sin embargo, la desaparicion de H. pylori no se sigue de una mejoria de la atrofia ni de la metaplasia intestinal.