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Background : Eradication therapy with omeprazole (O), amoxycillin (A) and clarithromycin (C) is used extensively, although it often fails. A ‘rescue’ therapy with a quadruple combination of O, bismuth (B), tetracycline (T) and metronidazole (M) has been recommended. Aim : To assess ranitidine bismuth citrate (Rbc) instead of O and B for treatment failure. Methods : Sixty consecutive patients (13 duodenal ulcer, 47 non-ulcer dyspepsia) in whom a previous eradication trial with O, A and C had failed were randomized to receive one of two regimens for 7 days: O (20 mg b.d.), B (120 mg q.d.s.), T (500 mg q.d.s.) and M (250 mg q.d.s.) (group OBTM, n=30); or Rbc (400 mg b.d.), T (500 mg q.d.s.) and M (250 mg q.d.s.) (group RbcTM, n=30). Eradication was defined as a negative 13C-urea breath test 1 month after completing therapy. Results : Mean age ± s.d. was 45 ± 12 years, 47% were males. Distribution of studied variables (age, sex, smoking, duodenal ulcer/non-ulcer dyspepsia) was similar in both therapeutic groups. Per protocol eradication was achieved in 17 out of 29 patients (59%) in group OBTM and in 25 out of 29 patients (86%) in group RbcTM (P

The prevalence of H. pylori infection has beenreported to be very high in duodenal ulcer (DU) disease,but the precise frequency and causes of H.pylori-negative DU are not well known. In somegeographical regions, however, a relatively low prevalenceof the infection has been described. Our aim was tostudy the frequency and causes of H. pylori-negative DUand to evaluate whether empirical H. pylori eradication therapy without confirmation of the infectionis justified. In all 774 consecutive patients with anendoscopic diagnosis of DU were studied prospectively.Exclusion criteria were associated diseases and previous gastric surgery. The use of NSAIDs,antibiotics (during the last month), and proton pumpinhibitors (during the last month) was evaluated bymeans of a specific questionnaire. At endoscopy, two biopsies from both antrum and corpus wereobtained in all 774 patients for histologic study(HE χ2) with regard to NSAIDintake (7% vs 58%; P < 0.0001) and previousantibiotic use (5% vs 28%; P < 0.0001). In themultivariate analysis (logistic regression), NSAID use(OR: 0.06; CI: 0.03- 0.13; P < 0.001) andantibiotic use (OR: 0.23; CI: 0.09-0.59; P < 0.01)were the only variables that correlated with H. pyloriinfection. The most important factors associated with H. pylori-negative DU are NSAIDs and priorantibiotic use, and if these agents are excluded, theprevalence of infection in our area is as high as 99%.Therefore, in DU patients not taking NSAIDs and living in areas where previous studies haveshown the prevalence of the infection in DU disease tobe very close to 100%, empirical H. pylori eradicationtherapy without confirmation of the infection may be justified.

An immune response occurring in Helicobacter pylori-infected gastric mucosa could have a direct implication for associated pathologies. In the present study we analyzed the expression of the immune activation, proliferation, and phenotype markers by immune cell subpopulations in H. pylori-infected and uninfected gastric samples.Antral gastric biopsies from both H. pylori-positive and -negative patients were processed by immunohistochemistry; gastric epithelial cells were isolated from biopsy tissue and analyzed by flow cytometry.Ten of the 13 biopsies that contained follicles were H. pylori positive. Follicular CD69 was expressed mainly by CD4+ T cells and the central core of follicles showed double immunopositivity for the B-cell marker CD19 and transferrin receptor. Also detected was an increase in the percentage of epithelial cells from H. pylori-positive samples expressing HLA-DR and beta2 microglobulin, compared to negative samples (61 +/- 15% vs 9 +/- 9%, p = 0.003 and 93 +/- 7% vs 52 +/- 18%, p = 0.002, respectively), whereas no variation on class I HLA was detected.These results suggest that chronic H. pylori infection could facilitate the persistence of follicles on which continuous follicular helper T-cell activation could lead to uncontrolled follicular B-cell proliferation. Furthermore, beta2 microglobulin expression by epithelial cells in a nonparallel way to class I HLA may indicate the possibility of nonclassical class I MHC expression on the basal surface of the epithelium.

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 patients40 years old and only 0.85% (0.2%-3.1%) in thoseor =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 eradicationor =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 oror =40 years; P = 0.0054), breath test value (delta) 1 month after therapy (3 oror =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.

We retrospectively investigated the annual incidence and prevalence of inflammatory bowel disease (IBD) from 1981 to 1988 in an urban and a rural area of central Spain. Two hundred and eighty-one patients presented with IBD; 193 ulcerative colitis (UC) and 88 Crohn's disease (CD) (prevalence 43.4/100,000 and 19.8/100,000, respectively). Of these patients, 168 were diagnosed for the first time during the study period. One hundred and eleven UC and 57 CD (incidence 3.16/100,000 and 1.61/100,000 respectively). Within the urban area, the UC incidence was 3.15/100,000 and the CD 1.87/100,000. In the rural area, the incidence for the UC was 3.25/100,000 and 0.86/100,000 for the CD. No sex differences were found. The incidence rates have increased significantly (p0.05) for CD in the study period. However, for UC rates did not change. During 1986-1988, the patient's age at the time of diagnosis was significantly lower than that of 1981-1983 (p0.05).

Summary Background In patients with a first eradication failure, a second (rescue) therapy still fails in > 20% of cases. Aim To compare rifabutin and levofloxacin rescue regimens in patients with two consecutive Helicobacter pylori eradication failures. Methods Patients, in whom first treatment with omeprazole–clarithromycin–amoxicillin and a second trial with omeprazole–bismuth–tetracycline–metronidazole (or ranitidine bismuth citrate with these antibiotics) had failed, received 10 days of treatment with either rifabutin (150 mg b.d.) or levofloxacin (500 mg b.d.), plus amoxicillin (1 g b.d.) and omeprazole (20 mg b.d.). Cure rates were evaluated by the 13C-urea breath test. Results Twenty patients received rifabutin, and 20 levofloxacin. All the patients returned for follow-up. Compliance in the rifabutin group was 100%. Four patients in the levofloxacin group did not take the medication correctly (in two cases due to adverse effects: myalgia and rash). Side effects in the rifabutin and levofloxacin groups were reported in 60% and 50% of the cases, respectively. Five patients (25%) treated with rifabutin presented with leucopenia, and six (30%) treated with levofloxacin presented with myalgias. Per-protocol cure rates were 45% (95% confidence interval, 26–66%) in the rifabutin group, and 81% (57–93%) in the levofloxacin group (P

Aim: It has been suggested that enhancement of amoxicillin or clarithromycin concentration at the gastric tissue may improve the anti-Helicohacter pylori effect of these drugs. This could be achieved by allowing the drug to remain longer in the stomach using dried hydrogels. Our aim was to evaluate the efficacy of an H. pylori eradication regimen including both amoxicillin and clarithromycin hydrogels. Methods: Design: prospective clinical trial. Patients: with peptic ulcer or functional dyspepsia. Intervention: 7-day rabeprazoleamoxicillin-clarithromycin regimen. In addition, amoxicillin and clarithromycin hydrogels were administered twice daily during the 7 days. The polyionic complex hydrogel was prepared with Chitosan and polyacrylic acid. Outcome: H. pylori eradication was defined as a negative 13 C-urea breath test 8 weeks after completing therapy. Results: Forty patients were included. One patient did not return for follow-up. Ninety percent of the patients took all the medications correctly. Per-protocol and intention-to-treat eradication rates were 74% (95% CI = 58%-86%) and 70% (55%-82%). Mild adverse effects were reported in 4 (10%) patients (diarrhea in 3, and nausea/heartburn in 1). Conclusions: Although dried polyionic complexes could serve as suitable candidates for amoxicillin and clarithromycin site-specific delivery in the stomach, its addition does not increase the eradication efficacy of the generally prescribed proton pump inhibitor plus amoxicillin and clarithromycin regimen.

To prospectively evaluate whether, in patients with inflammatory bowel disease, the choice of azathioprine (AZA) or 6-mercaptopurine (6-MP) dose based on thiopurine methyltransferase (TPMT) activity prevents myelotoxicity.TPMT activity in red blood cells was measured in 99 patients with Crohn's disease and 32 with ulcerative colitis prior to initiating AZA/6-MP treatment. AZA/6-MP dose was chosen based on TPMT activity, which was again determined one month after starting therapy. Incidence of adverse effects was evaluated for at least 6 months of follow-up.Mean basal TPMT value was 21.6 +/- 5 U/mL. No patient had low levels (5 U/mL), 6.9% had intermediate levels (5-13.7 U/mL), and 93.1% had high levels (13.8 U/mL). In patients with Crohn's disease, mean TPMT activity significantly decreased after AZA/6-MP therapy, while in patients with ulcerative colitis this activity did not change. Among the 4 patients having myelotoxicity, one had intermediate basal TPMT levels, and 3 even had high levels, but no patient had low levels.In this prospective study we could not confirm that the choice of AZA/6-MP dose based on TPMT activity prevents myelotoxicity in patients with inflammatory bowel disease. Routine analytical controls should be performed in these patients independently of TPMT activity.

Objectives: to analyze scientific output from Spanish hospitals in relation to Helicobacter pylori infection. Methods: papers collected from the Medline database between January 1988 and December 2003 were selected. Our search strategy was: "Helicobacter pylori" [MeSH] AND ((Spain [AD] OR Espana [AD] OR Spanien [AD] OR Espagne [AD] OR Espanha [AD]) OR (Spanish [LA]) OR Spain). The following was analyzed: geographic area, Spanish or foreign publication, topic, and year of publication. Output and impact bibliometric markers were evaluated. Results: in all, 691 papers were identified, of which 241 were excluded. Number of papers went from 2 in 1988 to 47 in 2002 and 13 in 2003. There were more reports in Spanish versus foreign journals (58 vs. 42%). In the first 5 years the areas with greater output were associated with diagnosis and microbiology (33 and 20%), whereas therapy was the predominating subject during the last 5 years (27%). Original papers were most common among publications (69%). Hospitals with highest output included La Princesa (24%) and Ramon y Cajal (17.6%) in Madrid, and Parc Tauli in Barcelona (6.4%). Mean impact factor progressively increased from 1.826 in 1988 to 2.142 in 2002 and 2.493 in 2003. Conclusions: the production and impact of documents published by Spanish scientists regarding H. pylori infection considerably increased during the past two decades.

Summary Aim To study the incidence of Helicobacter pylori recurrence, its chronological aspects, and the variables that might influence it. Methods A total of 1000 patients in whom H. pylori had been eradicated were prospectively studied. Therapies were classified as low and high efficacy regimens. Four to eight weeks after completion of therapy, 13C-urea-breath-test was performed, and it was repeated yearly up to 5 years. In some patients, endoscopy with biopsies was also performed to confirm H. pylori eradication. Results A total of 1000 patients were included, giving 2744 patient-years of follow-up. Seventy-one H. pylori recurrences were observed (2.6% per patient-year). Probability of being H. pylori-negative at 1 year was 94.7%, and at 5 years 90.7%. In the multivariate analysis, low age (OR: 1.84; 95% CI: 1.04–3.26) and low efficacy therapies (OR: 2.5; 1.23–5.04) correlated with 1-year H. pylori recurrence. Differences were observed when Kaplan–Meier curves were compared depending on age and therapy regimen. Conclusion Risk of posteradication H. pylori recurrence is higher during the first year, which suggests that most recurrences during this period are recrudescence and not true reinfections. H. pylori recurrence is more frequent in younger patients and in those treated with low efficacy therapies, but is exceptional if high efficacy therapies are used, in which case post-therapy eradication can be safely confirmed at 4 weeks with 13C-urea-breath-test.

Introduction Recently, several new diagnostic methods aimed to detect Helicobacter pylori stool antigens have been developed. Our aim was to evaluate the accuracy of 3 different stool tests to confirm H. pylori eradication. Patients and methods Twenty-six patients received H. pylori eradication treatment. Eradication was confirmed with 13C-urea breath test 6-8 weeks later, when stool samples were analyzed by polyclonal (Premier-Platinum-HpSA™), monoclonal (Amplified-IDEIA™-HpStAR™), and rapid test (ImmunoCard-STAT-HpSA™). Results H. pylori was eradicated in 85% of the cases. Sensitivity, specificity, positive predictive value and negative predictive value with the polyclonal test were: 25%, 91%, 33% and 87%. Corresponding results with the monoclonal test, using the cut-off point recommended by the manufacturer, were 100%, 46%, 25% and 100%. However, the best cut-off point in our study had 100% sensitivity and 91% specificity. The area under ROC curve for the polyclonal and the monoclonal tests was 0.65 and 0.95. Diagnostic accuracy with the rapid test was 75%, 90%, 60% and 95%. Conclusion Neither the polyclonal stool antigen test nor the rapid stool antigen test can be recommended to confirm H. pylori eradication after treatment. The monoclonal test has better diagnostic accuracy, although more studies are necessary to definitively recommend its use for the confirmation of H. pylori eradication success.

NF-κB: nuclear factor κB; TNF-α: tumor necrosis factor α; DD: death domain; FADD: Fas-associated death domain; FasL: Fas receptor ligand; TNFR: TNF receptor; TRADD: TNFR-associated death domain; TRAF: TNFR-associated factor; COX: cyclooxygenase; PG: prostaglandin; iNOS: inducible nitric oxide synthase; NO: nitric oxide; MDR-1: multiple drug resistance gene; IL: interleukin; EGF: epithelial growth factor; IGF: insulin-like growth factor; HGF: hepatocyte growth factor; PI-3 kinase: phosphoinositol-3 kinase, RIP: receptor interactive protein, SOD: superoxide dismutase, MTP: mitochondrial transition pore, Apaf-1: apoptotic protease activation factor, MHC: major histocompatibility complex, TGF-α: transforming growth factor α, ROS: reactive oxygen species, MAPK: mitogen-activated protein kinase, NSAID: non-steroidal anti-inflammatory drug.

Our objective was to assess the activity of thiopurine methyltransferase (TPMT) in a very large number of Spanish patients with inflammatory bowel disease (IBD), to evaluate the influence of several variables (including azathioprine or 6-mercaptopurine) on that activity, and to know the proportion of patients with low TPMT activity and therefore high risk of myelotoxicity when treated with these drugs.TPMT activity in red blood cells (RBCs) was measured by a radiochemical method. The association between several variables and TPMT values was assessed by multiple lineal regression.7046 patients were included (mean age: 37 years; 53% males): 70% with Crohn's disease, 22% with ulcerative colitis, and 8% with indeterminate colitis. Mean TPMT value was 20 (6) U/ml RBCs (minimum 0 and maximum 46). TPMT activity distribution was as follows: low levels (5 U/ml), 0.5%; intermediate (5-13.7), 11.1%; and high (or = 13.8), 88.4%. TPMT values did not follow a normal distribution (p0.001). In the univariate study, statistically significant differences (p0.001), yet of doubtly clinical significance because its minimal magnitude, were demonstrated in TPMT values depending on age, sex, type of disease, and treatment with azathioprine/6-mercaptopurine. In the multivariate study, the variables associated with TPMT activity were: sex, treatment with 5-aminosalicylates, steroids and azathioprine/6-mercaptopurine.This study shows that 0.5% of the Spanish patients with IBD have low TPMT activity (5 U/ml RBCs), a figure similar to that reported in other countries, these patients being at higher risk of myelotoxicity when treated with azathioprine or 6-mercaptopurine. The drugs usually prescribed for the treatment of IBD, including 5-aminosalicylates and azathioprine/6-mercaptopurine, do not seem to modify in a clinically relevant manner TPMT activity.

We sought to assess the activity of thiopurine methyltransferase (TPMT) in 14,545 Spanish patients with different diseases amenable to treatment with azathioprine/6-mercaptopurine (6-MP), and to evaluate the proportion of patients with low TPMT activity and therefore a higher risk of myelotoxicity with these drugs. TPMT activity in red blood cells (RBCs) was measured by a radiochemical method. The association between several clinical variables and TPMT activity was assessed by multiple linear regression. We included 14,545 patients: autoimmune hepatitis (n=359 patients), inflammatory bowel disease (n=7,046), multiple sclerosis (n = 814), myasthenia gravis (n=344), pemphigus (n=133), and other diseases (n=5,849). Mean TPMT activity was 20.1 ± 6 U/mL, but differed depending on the disease (P < .001). TPMT distribution was low (

Aim To study if there is a correlation between 13C-urea breath test values prior to treatment and the response to first-line and rescue Helicobacter pylori eradication therapies. Methods Six-hundred patients with peptic ulcer or functional dyspepsia infected by H. pylori were prospectively studied. Pre-treatment H. pylori infection was established by 13C-urea breath test. Three-hundred and twelve patients were treated with first-line eradication regimen, and 288 received a rescue regimen. H. pylori eradication was defined as a negative 13C-urea breath test, 8 weeks after completion of treatment. Results H. pylori eradication was achieved in 444 patients. No statistically significant differences were demonstrated when mean δ13C-urea breath test values were compared between patients with eradication success and failure (49.4 ± 33 versus 49.2 ± 31). Differences in mean pre-treatment δ13CO2 between patients with eradication success/failure were not demonstrated either when first-line or rescue regimens were prescribed. With the cut-off point of pre-treatment δ13CO2 set at 35 units, sensitivity and specificity for the prediction of H. pylori eradication success was 43 and 60%. The area under the receiver operating characteristic curve evaluating all the cut-off points of the pre-treatment δ13CO2 for the diagnosis of H. pylori eradication was 0.5. Finally, δ13CO2 values did not influence the eradication in the logistic regression model. Conclusion No correlation was observed between 13C-urea breath test values before treatment and the response to first-line and rescue H. pylori eradication therapies. Therefore, we conclude that the quantification of δ13CO2 prior to treatment is not useful to predict the success or failure of eradicating therapy.

Summary Aims : To systematically review the efficacy on ulcer healing of 1-week combination of a proton pump inhibitor plus two antibiotics and to perform a meta-analysis of randomized clinical trials to evaluate whether 7 days of proton pump inhibitor-based triple therapy is sufficient to heal peptic ulcer. Methods : Studies where 1-week proton pump inhibitor-based triple therapy was administered to heal peptic ulcer were included. Randomized clinical trials comparing the efficacy on ulcer healing of 7-day proton pump inhibitor-based triple therapy versus this same regimen but prolonging the proton pump inhibitor for several more weeks were included in the meta-analysis. Electronic and manual bibliographical searches were conducted. Meta-analysis was performed combining the odds ratios of the individual studies. Results : Twenty-four studies (2342 patients) assessed ulcer healing with 1-week proton pump inhibitor-based triple therapy. Mean healing rate was 86%, and 95% in Helicobacter pylori-eradicated patients. Six studies (862 patients), were included in the meta-analysis. Mean ulcer healing rate with a 7-day treatment was 91% versus 92% when proton pump inhibitor was prolonged for 2–4 more weeks (odds ratio = 1.11; 95% confidence interval = 0.71–1.74). Conclusion : In patients with peptic ulcer and H. pylori infection, prolonging therapy with proton pump inhibitor after a triple therapy for 7 days with a proton pump inhibitor and two antibiotics is not necessary to induce ulcer healing.

Summary Aim: To systematically review the experience of therapeutic studies where α-interferon with or without ribavirin was administered to patients with lymphoproliferative disorders, in order to evaluate whether eradication of hepatitis C virus may induce regression of lymphoproliferative disorders. Methods: We used bibliographical searches in electronic databases and in the Cochrane Library to determine our results. Results: Sixteen studies where an anti-viral regimen was administered to 65 hepatitis C virus-infected patients with lymphoproliferative disorders were identified. Complete remission of the lymphoproliferative disorder was achieved in 75% of the cases. In contrast, hepatitis C virus-negative subjects did not respond to interferon, indicating that the response in the hepatitis C virus-infected patients is not merely due to the antiproliferative effect of interferon. Remission after HCV eradication was maintained, provided that infection did not reappear. In hepatitis C virus-infected patients with non-Hodgkin's lymphoma treated with corticosteroids/chemotherapy liver function tests deterioration did not occur. The addition of interferon to standard chemotherapy may decrease hepatic side-effects of chemotherapy. Conclusions: Although it is evident that larger therapeutical trials of anti-viral therapy are needed to determine the role of this strategy in hepatitis C virus-infected patients with lymphoproliferative disorders, encouraging data emerge from recent studies showing that interferon (plus ribavirin) is an attractive therapeutic option for some hepatitis C virus-related low-grade lymphomas.

Our aim was to review systematically the diagnostic accuracy of the Helicobacter pylori stool antigen test. Bibliographical searches were performed in several electronic databases and abstracts from congresses up to May 2003. Eighty-nine studies (10,858 patients) evaluated the stool antigen test in untreated patients. Mean sensitivity, specificity, positive predictive value and negative predictive value were 91%, 93%, 92% and 87%, respectively. Analysis of the eight studies (1399 patients) in which pretreatment evaluation of the monoclonal stool antigen test was performed showed better (p

Aim It has been suggested that patients with porphyria cutanea tarda (PCT) are at high risk of developing hepatocellular carcinoma (HCC); however, this has not been confirmed by other workers. The aim of our study was to evaluate the incidence of HCC in patients with PCT, and to assess the possible co-factors associated with cancer development. Methods Thirty-nine consecutive patients with a diagnosis of PCT were included. Hepatitis B virus and hepatitis C virus (HCV) infection was investigated, and a percutaneous liver biopsy was performed. Patients were treated with phlebotomies, which resulted in a clinical remission in all. These patients were included in a surveillance programme for the detection of HCC, with ultrasonography and serum alpha-fetoprotein every 6 months. Results Thirty-nine patients (92% male; mean age, 55 +/- 16 years) with PCT were included. Alcohol abuse was reported in 87% of the cases. The mean follow-up time since the initial diagnosis of PCT was 9.7 years (378 patient-years of follow-up). Serological markers of past infection with hepatitis B virus were found in 20% of the patients, while HCV infection was diagnosed in 56%. The stage of fibrosis in patients having liver biopsy was: 0 (32%), 1 (32%), 2 (9%), 3 (18%), and 4 (9%). HCC was diagnosed in 1/39 patients with PCT (cumulative incidence, 2.6%), giving a yearly incidence of 0.26% per patient-year. This patient was a 69-year-old male, alcohol abuser, with HCV infection, with a 12-year period between diagnosis of PCT and HCC, and with liver biopsy (3 years before) showing fibrosis stage 3. Conclusion The risk of developing HCC in patients with PCT in our area is relatively low (a yearly incidence of less than 1% per patient-year of follow-up), and perhaps attributable, at least in part, to concomitant HCV infection. Patients presenting with PCT should undergo both HCV infection determination and liver biopsy, and those with concomitant HCV infection or advanced fibrosis/cirrhosis should probably be included in a standard surveillance programme in order to achieve early diagnosis of HCC.

Aim. To perform a systematic review on the efficacy of esomeprazole-based therapies in Helicobacter pylori eradication, and to conduct a meta-analysis comparing the efficacy of esomeprazole and other proton pump inhibitors when co-prescribed with antibiotics. Methods. Studies evaluating esomeprazole plus antibiotics were considered. Only randomised trials comparing esomeprazole and other proton pump inhibitors with antibiotics, and differing only in the proton pump inhibitor, were included in the meta-analysis. Electronic and manual bibliographical searches were conducted. The percentage (weighted mean) of eradication success was calculated. Meta-analysis was performed combining the odd ratios of the individual studies. Results. Mean cure rates with dual regimens (esomeprazole plus clarithromycin) were 51 and 54%, respectively, by intention-to-treat and by per-protocol. Corresponding figures with triple regimens (esomeprazole plus clarithromycin and either amoxicillin or metronidazole) were 82% (intention-to-treat) and 86% (per-protocol). Four studies were included in the meta-analysis: mean H. pylori eradication rates (intention-to-treat) with esomeprazole plus antibiotics was 85 and 82% when omeprazole was used ( odds ratio =1.19 ; 95% confidence interval =0.81 –1.74), results being statistically homogeneous. When subanalysis included only high quality studies, the odds ratio for this comparison was closer to one (1.08; 95% confidence interval =0.4 –1.47) and results were more homogeneous. Conclusions. Esomeprazole-based triple therapy is highly effective for the eradication of H. pylori infection and offers comparable efficacy to omeprazole-based therapy.

To perform a systematic review on the efficacy of pantoprazole based therapies in Helicobacter pylori eradication, and to conduct a meta-analysis comparing the efficacy of pantoprazole and other proton pump inhibitors (PPIs) when co-prescribed with antibiotics.Studies evaluating pantoprazole combined with antibiotics were considered. Only randomized clinical trials comparing pantoprazole and other PPIs when co-prescribed with antibiotics, and differing only in the PPI (pantoprazole vs other), were eligible for inclusion in the meta-analysis. Bibliographical searches in several electronic databases, and manual search of abstracts from congresses, were conducted. The percentage (weighted mean) of patients with eradication success was calculated. Meta-analysis was performed combining the odds ratios (ORs) of the individual studies in a global OR.The mean eradication rate with pantoprazole plus clarithromycin for 14 days was 60%. Cure rates with 7 day pantoprazole based triple regimens were higher: pantoprazole, amoxicillin and clarithromycin (78%); pantoprazole, clarithromycin and nitroimidazole (84%); and pantoprazole, amoxicillin and nitroimidazole (74%). Twelve studies comparing pantoprazole and other PPIs were selected for the meta-analysis, including 534 and 603 patients, respectively. The mean eradication rate for H. pylori using pantoprazole plus antibiotics was 83%, and 81% when other PPIs were used (OR = 1; 95% confidence interval (CI) from 0.61 to 1.64). When sub-analysis was performed, including only studies comparing pantoprazole with omeprazole, or pantoprazole with lansoprazole, differences were also statistically non-significant. The meta-analysis of the six studies prescribing equivalent doses of all PPIs demonstrated similar results with pantoprazole and with other PPIs (OR = 1.07; 95% CI from 0.71 to 1.62), the results being statistically homogeneous.Pantoprazole achieves similar cure rates to those of omeprazole and lansoprazole when co-prescribed with antibiotics for the eradication of H. pylori infection.

We assessed the prevalence and diagnostic value of antineutrophil cytoplasmic antibodies (ANCA) with a perinuclear pattern (pANCA) in patients with Crohn's disease (CD) and ulcerative colitis (UC).pANCA were determined by indirect immunofluorescence and positive results were confirmed by ELISA.We included 117 patients with CD, 72 with UC and 2 with indeterminate colitis. One CD patient (0.9%) and 6 with UC (8.3%) had a positive pANCA result. Sensitivity, specificity, positive and negative predictive value, and positive and negative likehood ratio of pANCA for a diagnosis of UC (vs CD) were 8%, 99%, 86%, 64%, 8 and 0.9, respectively, thus indicating the need to standardize the methodology. No differences were observed with regard to age, tobacco consumption, localization and extension of UC and need of immunosuppressive agents according to pANCA.In our setting, the prevalence of pANCA is very low (8%) in UC and exceptional (1%) in CD. As a result, pANCA sensitivity for a diagnosis of UC in patients with inflammatory bowel disease is also very low, yet the specificity is very high.

Background & Aims: The aim of our study was to conduct a systematic review of studies evaluating prevalence of hepatitis C virus (HCV) infection in B-cell non-Hodgkin's lymphoma (B-NHL) and to perform a meta-analysis of case-control studies comparing this prevalence with that of a reference group.Methods: Data sources: Electronic databases and the Cochrane Controlled Trials Register. Study selection: Studies evaluating prevalence of HCV infection in patients with B-NHL. Studies comparing HCV prevalence in B-NHL (cases) and in a reference group (controls) were included in the meta-analysis. Data extraction: Author/country, diagnostic method (serology/PCR), control type, matching/design, and VHC prevalence. Data synthesis: Prevalence of HCV infection and meta-analysis combining the odds ratios (OR).Results: Forty-eight studies (5542 patients) were identified. Mean HCV infection prevalence was 13% (95% CI: 12%–14%), which was higher in Italy (20%) and Japan (14%). Ten studies compared HCV prevalence in B-NHL (17%) and healthy controls (1.5%) (OR: 10.8; 95% CI: 7.4–16), results being homogeneous; OR increased up to 14.1 when only Italian studies were considered. Sixteen studies compared HCV prevalence in B-NHL (13%) and in other hematologic malignancies (2.9%) (OR: 4.2; 95% CI: 2.5–7), also with homogeneous results; OR increased up to 7.8 when subanalysis included only Italian studies.Conclusions: HCV prevalence in patients with B-NHL is approximately 15%, higher than that reported not only in general population (1.5%) but also in patients with other hematologic malignancies (2.9%), suggesting a role of HCV in the etiology of B-NHL. The striking geographic variation in this association suggests that genetic and/or environmental factors are also involved in the pathogenesis of this disorder.

The measurement of the activity of thiopurine methyltransferase (TPMT) is useful to monitor, on an individual basis, the dose of azathioprine in order to identify patients at risk of myelotoxicity. However, the distribution of the enzymatic activity in patients with autoimmune hepatitis is unknown. Our objective was to analyze the activity of TPMT in a group of 200 patients with autoimmune hepatitis and to evaluate the possible effect of some variables such as the treatment with azathioprine on this activity.The activity of TPMT was determined by a radiochemical method; the activity was determined in the erythrocytes of patients with autoimmune hepatitis from 31 Spanish hospitals. We studied the relationship between TPMT levels and several demographic variables as well as its correlation with azathioprine treatment.We included 209 patients (80% females, mean age 50 years, 39% on azathioprine). The mean value of TPMT was 20.7 U/ml erythrocytes (from 0 to 39). TPMT levels were adjusted to a normal distribution. 1%, 9% and 90% patients had low (5 U/ml), intermediate (5-13.7 U/ml) and high (= 13.8 U/ml) TPMT levels, respectively. In the multivariate analysis, there were no differences when comparing the mean TPMT values according to age, gender or previous azathioprine treatment.TPMT activity in patients with autoimmune hepatitis displays a similar distribution to that reported in other populations (approximately 1% of patients have low levels and 9% have intermediate levels) and it does not depend on the age, gender or simultaneous azathioprine treatment.

Achalasia is a disease of unknown origin in which there is a denervation of the myenteric plexus on the smooth muscle of the lower oesophageal sphincter, causing a cardial stenosis and a loss of efficacy of oesophageal peristalsis. The predominant symptoms are dysphagia for solids and liquids and regurgitation of the retained food. Occasionally, there may be oesophageal haemorrhage as a consequence of oesophagitis and stasis ulcers. An important but uncommon complication is the development of oesophageal cancer, which is typically squamous cell carcinoma. We report an exceptional case of a 77-year-old woman with a long-term achalasia and mega-oesophagus who presented four episodes of upper gastrointestinal bleeding in a 2 month period. The patient underwent surgical resection of the 10 cm of distal oesophagus, performing a partial fundoplication, and the pathological study revealed an oesophageal infiltration by a low-grade non-Hodgkin's lymphoma. After an insidious outcome, she died on the 47th day after admission.

Even with the current most effective treatment regimens, about 10% to 20% of patients will fail to eradicate Helicobacter pylori infection. 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. The choice of a second-line treatment depends on which treatment was used initially, because retreatment with the same regimen is not recommended. Therefore, it seems that performing culture after a first eradication failure is not necessary and assessing H. pylori sensitivity to antibiotics only after failure of the second treatment is suggested in clinical practice. Different possibilities of empirical treatment are suggested. After failure of proton pump inhibitor (PPI)-amoxicillin-clarithromycin, quadruple therapy has been generally used. More recently, replacing the PPI and the bismuth compound by ranitidine bismuth citrate has also achieved good results. After PPI-amoxicillin-nitroimidazole failure, retreatment with PPI-amoxicillin-clarithromycin has proved to be effective. Finally, the first therapy should not combine clarithromycin and metronidazole in the same regimen because of the problem of resistance against both antibiotics. Recently, rifabutin-based rescue therapies have been shown to constitute an encouraging strategy for eradication failures because they are effective for H. pylori strains resistant to antibiotics.

Background: The 13 C-urea breath test is an accurate, noninvasive method for the diagnosis of Helicobacter pylori in adults. A dose of 75 to 100 mg of urea is generally used, especially in adults, but the optimal dose in children is still unknown. Our aim was to determine whether urea breath test performed with a single 50-mg dose of 13 C-urea was sufficient and accurate for diagnosing H. pylori infection in children. Methods: Consecutive children 4 to 14 years of age undergoing upper intestinal endoscopy to evaluate symptoms of recurrent abdominal pain were prospectively included. Exclusion criteria included use of antibiotics or proton pump inhibitors during the last month, gastric surgery, and previous H. pylori eradication therapy. Reference criteria for diagnosis of infection were based on histology, culture, and serology. Urea breath test (TAU-KIT; Isomed, S.L., Madrid, Spain) was performed as follows: citric acid (Citral pylori) dissolved in 100 mL of water was initially given. Ten minutes later, a baseline exhaled breath sample was collected, and thereafter 50 mg of 13 C-urea dissolved in 50 mL of water was given. A second breath sample was obtained 30 minutes later. Breath samples were analyzed by isotope ratio mass spectrometry. The endoscopist, the pathologist, the microbiologist, and the person responsible for reading the serology and the urea breath test were all unaware of H. pylori status by the other diagnostic methods. Results: One hundred children were included (40% males; mean age, 9.2 ± 2 years; mean weight, 33.9 ± 12 kg). Based on the reference criteria, 45% were infected, 37% were not infected, and 18% were indeterminate. Sensitivity, specificity, positive predictive value, and negative predictive value were, respectively, 91% (95% confidence interval [CI], 79%-96%), 97% (95% CI, 86%-99%), 98% (95% CI, 87%-91%), and 90% (95% CI, 76%-96%). Positive and negative likelihood ratios were of 33 and 0.09. Any cutoff point between 2 and 14 8 units had the same high diagnostic accuracy. The area under the receiver operating characteristic curve was 0.94. No adverse effects were reported. Conclusion: Urea breath test using 50 mg of urea is sufficient and accurate for the diagnosis of H. pylori infection in children. Use of a small test dose significantly lowers the cost of the test.

A 33-year old female was diagnosed as Graves' disease and started on carbimazole. One month later when she was already euthyroid only on carbimazole therapy, she developed acute pancreatitis associated with mild cholestatic hepatitis and erythema nodosum. Carbimazole therapy was interrupted, pancreatic and liver function gradually improved and became normalized two weeks later. Other potential etiological causes of acute pancreatitis, hepatitis and erythema nodosum were excluded. Rechallenge with a single dose of carbimazole led to a new episode of acute pancreatitis and cholestatic hepatitis one day later. The appearance of different hypersensitivity reactions including pancreatitis, hepatitis and erythema nodosum, together with the observation that the interval between drug intake and onset of symptoms became shorter with repeated exposure to carbimazole, point to an immune-mediated mechanism. Carbimazole has to be added to the list of drugs capable of inducing acute pancreatitis, and should be emphasized the need to discontinue this medication as soon as there is evidence of pancreatic dysfunction.

To evaluate whether the Helicobacter pylori status of the patient's spouse plays a role in reinfection after eradication success, and to assess the possibility of transmission of H. pylori among partners by using molecular methods.We studied prospectively 120 patients in whom H. pylori had been eradicated. Endoscopy with biopsies and a 13C-urea breath test were performed 1 month after completing therapy. The breath test was repeated in all patients at 6 and 12 months. At the 1-year follow-up visit (or before if reinfection occurred), a breath test was also performed on the patient's partner. Samples for the molecular study included gastric biopsies from patients and gastric content obtained by the string test from partners. The heterogeneity of ureC was studied by enzymatic digestion with MseI and HhaI enzymes of a polymerase chain reaction (PCR) product of 1179 bp belonging to the ureC gene, and different band patterns were generated after electrophoresis.Four reinfections were diagnosed at 6 months, and four were diagnosed from 6 to 12 months (incidence 6.8% per patient-year). Seven of eight (87%) of the reinfected patients' spouses were infected, but H. pylori infection of spouses was also frequent (76%) among non-reinfected patients. In the multivariate analysis, age of the patient (odds ratio [OR] 0.93, 95% confidence interval [CI] 0.87 to 0.99, P0.05), delta(13)CO(2) value after therapy (OR 2.51, 95% CI 1.14 to 5, P0.05), and therapy regimen (OR 6.23, 95% CI 1.25 to 31, P0.05) were the only variables that correlated with H. pylori recurrence. However, family variables (H. pylori status of spouse, breath test value of spouse, length of time couple had lived together, number of children living at home, household density) did not correlate with recurrences. Thus, the OR for the H. pylori status of spouse (adjusted by age, delta(13)CO(2) and therapy) was 2.93 (95% CI 0.29 to 29, P0.05). H. pylori recurrence occurred in seven of 92 (7.6%) patients when the spouse was infected (95% CI 3.7% to 15%), and in one of 28 (3.6%) patients when the spouse was H. pylori-negative (95% CI 0.6% to 18%) (P0.05; however, the power of this comparison was20%). Therefore, even if the spouse was infected, 92.4% of patients will remain uninfected 1 year after H. pylori eradication. Three reinfected patients (at 1 year) and their partners (also infected) agreed to have the endoscopy and string test performed, respectively. The molecular study revealed that H. pylori strains involved were different in all cases.Recurrence of H. pylori infection seems to be relatively infrequent, even if the patient's spouse is H. pylori-positive. The molecular study demonstrated that the strains in reinfected patients and their partners are different, suggesting that the patient's partner does not act as a reservoir for H. pylori reinfection.

The main objectives of this study were to review the clinic and endoscopic variables of patients with upper gastrointestinal bleeding (UGB) due to peptic gastroduodenal lesions who were evaluated in our hospital during one year, to identify the characteristics associated with a negative evolution of the UGB and to analyse the characteristics of those patients who were discharged immediately after the endoscopy was performed.A one-year retrospective analysis of all UGB episodes was performed. Patients having gastroduodenal ulcer or erosive gastritis/duodenitis at endoscopy were included. The prognostic value of several clinic, laboratory and endoscopic variables was evaluated. Persistence or recurrence of bleeding, surgery and mortality were considered as outcome variables (the variable evolution was categorized as negative when any of these was observed).156 patients were identified, with a mean (SD) age of 61 (17) years. Melena was the most frequent UGB presentation (79%). 46% patients had associated diseases and 50% were taking gastroerosive drugs. Duodenal ulcer was the commonest cause of UGB (52%), followed by gastric ulcer (30%). The evolution of UGB was negative in 7% cases. Variables associated with a negative evolution in the multivariate analysis were: age, red hematemesis, systolic blood pressure= 100 mmHg, heart rate= 100 b.p.m. and a more severe Forrest endoscopic classification. 11% patients were discharged immediately, without complications afterwards. If predictive variables obtained in the multivariate analysis would have been applied, hospitalization would have been avoided in 59 patients (38%) without subsequent complications.A number of clinic and endoscopic variables (UGB presentation form, blood pressure, heart rate, and Forrest endoscopic classification) with prognostic value have been identified in this study. These variables are easy to obtain and apply in clinical practice, allowing a precise estimate of the UGB evolution. Thus, a relatively high number of patients with UGB susceptible of ambulatory treatment and management can be reliably identified.

Recently, a new diagnostic method based on the detection of Helicobacter pylori antigen in stools (HpSA) has been developed. Our aim was to prospectively evaluate the accuracy of HpSA both in the initial diagnosis of H. pylori infection and in the confirmation of the eradication after treatment.Thirty dyspeptic patients were prospectively evaluated. During endoscopy, biopsies for histology and rapid urease test were obtained, and a 13C-urea breath test was performed. HpSA was determined by radioimmunoassay(Premier Platinum HpSA). Infected patients were administered H.pylori eradication treatment, and breath test and HpSA were performed again 4 weeks after finishing the therapy. Gold standard for H. pylori infection pre-treatment was based on rapid urease test, histology and breath test, whereas 13C-urea breath test was considered the post-treatment gold standard.Pre-treatment H. pylori prevalence was 57%. Eradication was achieved in 85% of patients. The area under ROC curve for HpSA pre-treatment was 0.98. Cut-off points with best pre-treatment diagnostic accuracy were those between 0.10 and 0.12: positive likelihood ratio (LR), negative LR, 0.06; 94% sensitivity (95% CI, 73-99%),100% specificity (75-100%), 100% positive predictive value (81-100%)and 93% negative predictive value (66-100%). After treatment,the area under ROC curve was 1, and all cut-off points between 0.10 and 0.18 had 100% diagnostic accuracy. HpSA levels decreased from 0.94 (0.9) to 0.08 (0.02) (p0.01) in patients withH. pylori eradication success.HpSA test can be considered an accurate, non-invasive method for the diagnosis of H. pylori infection both inuntreated patients and in the confirmation of H. pylori eradication after treatment.

To establish a causal link between Helicobacter pylori infection and functional dyspepsia it is necessary to demonstrate that H. pylori eradication induces an improvement in dyspeptic symptoms. Our aim was to perform a meta-analysis of randomized studies comparing, in functional dyspepsia, the efficacy of H. pylori eradication treatment with that of treatments with no effect on H. pylori infection.PubMed database, Cochrane Controlled Trials Register, and abstracts from congresses until 2001.a) studies including patients with functional dyspepsia and H. pylori infection; b) randomized trials comparing H. pylori eradication treatment with treatment (control) with no effect on H. pylori infection, and c) follow-up of at least 6 months. The quality of studies was assessed by a validated score.the main outcome was the percentage of patients improving in each therapeutic group. A meta-analysis was performed combining the odds ratios (OR) of individual studies in a global OR.Nine studies fulfilled the inclusion criteria and were thus included in the meta-analysis. Overall, 953 patients received an eradication treatment and 958 received a control treatment. The overall percentage of patients with symptomatic improvement in the eradication group was 43% (95% CI, 40-46%), and it was 39% (95% CI, 36-42%) in the control group. The OR for the effect of the eradication treatment vs. the control treatment was 1.20 (95% CI, 0.91-1.58). The number needed to treat (NNT) with eradication therapy to achieve a symptomatic improvement, compared with the control group, was 25. Although heterogeneity was demonstrated, it disappeared when one study showing positive, clearly discordant results was excluded. Thus, the percentage of patients with symptomatic improvement in the eradication treatment group was 47% (95% CI, 43-50%) and it was 45% (95% CI, 41-48%) in the control group (OR: 1.06; 0.85-1.31; NNT: 50).H. pylori eradication treatment is not associated with a statistically significant improvement of symptoms in patients with functional dyspepsia.

Aim. To evaluate outcome of test-and-scope strategy using 13C-urea breath test, Helicobacter pylori IgG serology, and CagA serology. Patients and methods. A series of 100 dyspeptic patients were studied. Biopsies were obtained for histology and rapid urease test (gold standard). Serum samples were obtained for Helicobacter pylori IgG and CagA serology, and 13C-urea breath test was carried out. Results. If endoscopy had n ot been performed in Helicobacter pylori patients based on 13C-urea breath test

To evaluate whether eradication therapy is more effective in peptic ulcer disease (PUD) than in non-ulcer dyspepsia (NUD).We retrospectively studied 481 patients with NUD (183 patients) or PUD (298 patients) infected with Helicobacter pylori included in several prospective clinical trials. Three eradication regimens were given: (1) proton pump inhibitor (PPI) plus clarithromycin, plus either amoxycillin or metronidazole for 7 days (297 patients); (2) ranitidine bismuth citrate (RBC) plus clarithromycin plus amoxycillin for 7 days (79 patients); and (3) RBC plus clarithromycin plus amoxycillin plus metronidazole for 5 days (105 patients). H. pylori eradication was defined as a negative 13C-urea breath test 4 weeks after completing treatment.H. pylori eradication rates were 82% (95% CI 78-87%) with PPI plus two antibiotics for 7 days, 85% (95% CI 75-91%) with RBC plus two antibiotics for 7 days, and 91% (95% CI 86-97%) with RBC plus three antibiotics for 5 days (P0.05 compared with the first regimen). Overall, the H. pylori eradication rate in patients with NUD was 78% (95% CI 71-84%), while in patients with PUD it was 89% (95% CI 86-93%) (P0.001). Both the combination of PPI plus two antibiotics for 7 days and the combination of RBC plus three antibiotics for 5 days were more effective in PUD than in NUD patients. However, RBC plus clarithromycin plus amoxycillin for 7 days was equally effective in both diseases. RBC plus two antibiotics for 7 days achieved better results than the same therapy with PPI only in NUD patients (84% v. 59%, P0.01), but both regimens were similar when prescribed in PUD patients (86% v. 88%). In the multivariate analysis, the type of therapy, the diagnosis (NUD v. PUD), and the product variable of therapy (with RBC plus 2 antibiotics for 7 days) and diagnosis (interaction variable) were the only variables that influenced H. pylori eradication. The odds ratio (OR) for the effect of RBC versus PPI plus two antibiotics for 7 days in patients with NUD was 4 (95% CI 1.7-9.7; P0.01), whereas in patients with PUD no statistical significance was achieved (OR 0.79; 95% CI 0.2-3.9).Overall, H. pylori eradication therapy is more effective in PUD than in NUD patients. This advantage of eradication therapies in PUD patients seems to be observed with 7-day PPI-based triple regimens, and with 5-day RBC-based quadruple therapy, while the 7-day RBC-based triple regimen seems to be equally effective in both diseases.

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 (HE 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%) (P0.001), while H. pylori infection was less frequent in patients with UGIB (92.4% (85%-96%)) than in those without UGIB (99.1% (98%-100%); P0.001). 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.

The precise role of Helicobacter pylori infection in gastroesophageal reflux disease (GERD) is a matter of intense debate. Twenty-four-hour esophageal pH monitoring has a higher accuracy than endoscopy for the diagnosis of GERD, but the correlation between H. pylori infection and esophageal pH-metric parameters has almost never been assessed. Therefore, we evaluated the relationship between the infection and the presence of disturbances not only in endoscopy but also in 24-hour esophageal pH monitoring. One hundred consecutive patients undergoing 24-hour esophageal pH monitoring because of symptoms suggestive of GERD were included in the study. Esophageal manometry was carried out to study the position and the pressure of the lower esophageal sphincter (LES). Prevalence of H. pylori infection was evaluated by histology (hematoxylin and eosin stain) and rapid urease test. The mean age of the patients was 50 +/- 15 years; 50% were men and 56% had an abnormal pH-metry (DeMeester score more than 14.7). The prevalence of H. pylori in patients with abnormal pH-metry was 57% (95% CI, 42-70%) and was 52% (95% CI, 39-64%) in those with normal pH-metry (nonsignificant differences [NS]). In the multivariate analysis, H. pylori infection did not correlate with an abnormal pH-metry (odds ratio, 0.8; 95% CI, 0.4-1.8; NS). The proportion of cases with abnormal pH-metry among infected patients was 54% (95% CI, 41-66%) and was 59% (95% CI, 44-72%) among uninfected patients (NS). Mean values of pH-metric parameters (+/-SD), respectively for H. pylori-positive and -negative patients, were total score (30 +/- 33 vs. 36 +/- 38), number of reflux episodes (7 +/- 7 vs. 11 +/- 11), number of episodes more than 5 minutes (3.7 +/- 5 vs. 3.8 +/- 5), longest reflux episode (2.4 +/- 2 minutes vs. 3.1 +/- 3 minutes), and fraction time (%) with pH less than 4 (total, 6 +/- 7 vs. 6.8 +/- 8; upright, 3.9 +/- 4 vs. 4.5 +/- 5; supine, 7.4 +/- 12 vs. 7.2 +/- 10) (all findings were NS). Endoscopic findings, respectively for H. pylori-positive and -negative, were hiatus hernia (41% vs. 41%), endoscopic esophagitis (Savary-Miller) (54% vs. 46%), and Barrett's esophagus (15% vs. 11%) (all findings were NS). Finally, differences were not demonstrated in the pressure of the lower esophageal sphincter (12 +/- 8 mmHg vs. 14 +/- 12 mmHg) among H. pylori-positive and -negative patients. H. pylori infection is not associated with gastroesophageal reflux disease, as evaluated endoscopically and with 24-hour esophageal pH monitoring.

Objective To study the prevalence of Helicobacter pylori (H. pylori) infection and gastric metaplasia (GM) in the duodenum a large group of patients with duodenal ulcer was evaluated to determine whether these factors are related to the number of ulcer recurrences. Methods Three hundred and seven patients diagnosed by endoscopy as having active duodenal ulcers were studied. At endoscopy, all patients had gastric biopsies taken for histology, the rapid urease test and culture. Three duodenal biopsies were also taken and processed for histology (haematoxylin & eosin, Giemsa, Warthin-Starry, and PAS stain). Results GM and H. pylori in the duodenum was identified in 73% (68-78%) and 66% (60-71%) of the cases, respectively. All patients with H. pylori in the duodenum also had GM at this location, while areas with GM but without H. pylori were described. The kappa statistic for concordance between GM and H. pylori at the duodenum was 0.82. The prevalence of GM and H. pylori, depending on the number of ulcer recurrences, was: 1 st episode, 34% and 27%, respectively; 2nd episode, 84% and 80%; and ≥3rd episode, 90% and 79% (P< 0.001 when comparing 1 st vs 2nd or ≥3rd episode). In the multivariate analysis, age and number of ulcer recurrences correlated both with GM and with H. pylori in the duodenum. Chronic duodenitis was demonstrated in all duodenal biopsies, 87% being active chronic duodenitis. H. pylori in the duodenum was more frequent in patients with active duodenitis (73%) than in those with inactive duodenitis (13%) (P < 0.001). Conclusions Patients with recurrent ulcer disease have a higher prevalence of both GM and H. pylori infection in the duodenum, suggesting that these two factors are related with the chronicity and recurrence of duodenal ulcer disease. H. pylori infection in the duodenum always appears in areas of GM, although GM is not necessarily colonized by the organism. H. pylori infection cannot be excluded based only on the results of duodenal biopsies, as false negative results at this area are frequent.

Background. To grade liver damage, Child-Pugh classification is used but these tests do not reflect the quantitative functional hepatic reserve. Aims. 13C-Phenylalanine Breath Test and 13C-Methacetin Breath Test are evaluated as possible tools, being both safe and easy to perform, to quantify functional hepatic reserve in chronic liver disease patients. Patients. Both tests were performed in 48 healthy volunteers and 48 chronic liver disease patients. Methods. Breath samples were collected after taking 13C-Phenyl-alanine (100 mg) and 13C-Methacetin (75 mg). 13CO2 enrichment was measured using mass spectrometry. Results. Both tests discriminated the hepatic function, decreasing results of the 13CO2 enrichment agreeing with the increasing severity of the hepatic patient 13C-Phenylalanine Breath Test multiple correlation coefficient: O. 72, global p

Aim A combination of omeprazole plus amoxycillin (Amo) and clarithromycin (Cla) for 7 days has been studied extensively. However, the role of other proton pump inhibitors, such as pantoprazole (Pan), in this therapy is not well known. On the other hand, ranitidine bismuth citrate (RBC) also seems to be effective when combined with Amo and Cla. Our aim was to evaluate and to compare these two novel short-term triple therapies (Pan+Amo+Cla and RBC+Amo+Cla) for treatment of Helicobacter pylori. Methods In a randomized clinical trial 150 consecutive patients (38 with duodenal ulcer, 112 with non-ulcer dyspepsia) infected by H. pylori were studied prospectively. Exclusion criteria were: previous H. pylori eradication therapy, gastroerosive drug use, gastric surgery, and associated diseases. One of two regimens was given for 7 days: Pan (40 mg b.i.d.), Amo (1 g b.i.d.), Cla (500 mg b.i.d.) (group Pan+Amo+Cla, n = 75); or RBC (400 mg b.i.d.), Amo (1 g b.i.d.), Cla (500 mg b.i.d.) (group RBC+Amo+Cla, n = 75). All drugs were administered together after meals. Compliance was evaluated by return tablet count. Data were analysed by univariate (X 2 ) and multivariate (multiple logistic regression) analysis. Eradication was defined as a negative 13 C-urea breath test 1 month after completing therapy. Results The distribution of studied variables (age, gender, smoking, duodenal ulcer/non-ulcer dyspepsia) was similar in both therapy groups. Per-protocol eradication was achieved in 48/71 (68%) in group Pan+Amo+Cla, and in 61/70 (87%) in group RBC+Amo+Cla (P = 0.01). Intention-to-treat (ITT) eradication was achieved in, respectively, 48/ 75 (64%) and in 61/75 (81 %) (P = 0.03). The RBC+ Amo+Cla regimen was more effective than Pan+Amo+Cla in non-ulcer dyspepsia patients (ITT, 84% vs 58%; P= 0.005), but statistically significant differences were not demonstrated in duodenal ulcer patients (72% vs 80%). In the multivariate analysis the odds ratio for the effect of the type of therapy on H. pylori eradication in patients with non-ulcer dyspepsia was 3.8 (95% Cl, 1.6-9.3; P= 0.003). No relevant adverse effects were reported with any regimen. Conclusion A RBC+Amo+Cla regimen for only 1 week is a promising therapy for H. pylori infection, due to its high efficacy, simple posology, and excellent tolerability. Combination of Pan with Amo and Cla, although effective in duodenal ulcer patients, but in non-ulcer dyspepsia has not achieved the favourable results previously reported with other proton pump inhibitors.

(1999). Helicobacter pylori 'Test-and-Treat' Strategy for Dyspeptic Patients. Scandinavian Journal of Gastroenterology: Vol. 34, No. 7, pp. 644-652.