1,721,238 research outputs found
What is the role of Helicobacter pylori in complicated ulcer disease?
No full textThe role of Helicobacter pylori in the pathogenesis of duodenal and gastric ulcer and ulcer recurrence is widely known. Bleeding, perforation, and obstruction represent the most serious, potentially life-threatening manifestations of ulcer disease (hemorrhage in 15%-20%). The lifetime prevalence of perforation and obstruction is much lower (approximately 5% and 2%, respectively). Despite improved diagnostic and therapeutic options, bleeding-related mortality rates remain at 6%-7% in the United States and between 4% and 14% in Europe. H. pylori and nonsteroidal anti-inflammatory drugs are now recognized as the two primary causes of ulcer disease. Eradication of H. pylori in patients with uncomplicated ulcers results in recurrance rates of < 10%, suggesting that eradication of H. pylori in patients with bleeding ulcers may virtually prevent recurrence of both the disease and its complications. Although the prevalence of H. pylori infection is almost 100% in duodenal and 80%-90% in gastric ulcer patients not using nonsteroidal anti-inflammatory drugs, the prevalence of the organism in bleeding duodenal and gastric ulcers does not reach 70% and 60%, respectively, which may be due to false-negative test results
Combination antiviral therapy with ribavirin and interferon alfa in interferon alfa relapsers and non-responders: Italian experience
No full textBackground/Aims: A sustained biochemical and virologic response to standard interferon therapy for chronic hepatitis C is seen in no more than 25% of patients, and the efficacy of re-treatment or of higher doses in non-responders and relapsers has not been established. A more effective therapy for interferon alfa-resistant hepatitis C is needed. Methods: A study of ribavirin plus interferon alfa combination therapy was conducted in 30 patients with chronic hepatitis C resistant to a previous standard course of interferon alfa (14 interferon non-responders, 16 interferon relapsers). Patients were randomly assigned to receive either ribavirin, 800 mg daily, and interferon alfa, 3 MU thrice weekly (n=15), or interferon alfa alone, 3 MU thrice weekly (n=15), for 6 months. Results: At the end of treatment, normal alanine aminotransferase levels were observed in eight patients in the combination therapy group: one (14%) interferon non-responder and seven (87%) interferon relapsers (p=0.01). Six months post-therapy, sustained normalization of alanine aminotransferase was achieved in seven (87%) interferon alfa relapsers, but not in any of the interferon alfa non-responders (p=0.001). In the group of patients treated with interferon alfa alone, sustained normalization of alanine aminotransferase was observed in one interferon relapser only. Serum HCV RNA became negative in eight patients receiving combination therapy - two (28%) interferon non-responders and six (75%) interferon relapsers. Six months later, circulating HCV RNA remained negative in seven patients: one (14%) interferon non-responder and six (75%) interferon relapsers (p=0.04). Sustained clearance of HCV RNA was not observed in patients re-treated with interferon alone. The sustained response to combination therapy was accompanied by reduced hepatic necroinflammatory activity on liver biopsy. Hepatitis C virus genotype was not significantly associated with response to combination therapy. Side effects were mild and well tolerated. Conclusions: Our experience indicates that combination therapy of ribavirin plus interferon alfa induces sustained biochemical, virologic, and histologic responses in most patients who are interferon relapsers
Anti-cagA reactivity in Helicobacter pylory negative subjects: a comparison of three different methodsFusconi M, Vaira D, Menegatti M, Farinelli S, Figura N, Holton J, Ricci C, Corinaldesi R,Miglioli M
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Treatment of symptom-free Helicobacter pylori-positive subjects
No full textAim: To investigate the need for treatment in symptom-free Helicobacter pylori-positive subjects. Design: Large-scale ongoing study of seropositive blood donors allocated to six treatment regimens. Methods: Specific immunoglobulin G antibodies to H. pylori were measured by enzyme-linked immunosorbent assay of serum from 1010 Bologna blood donors over 1 year. Out of 442 positive subjects, 298 were endoscoped with infection confirmed in 279. Six treatment regimens were applied, (1) placebo; (2) 240 mg colloidal bismuth subcitrate twice a day plus 500 mg tinidazole three times a day for 2 weeks; (3) 300 mg ranitidine each day for 4 weeks; (4) 120 mg colloidal bismuth subcitrate four times a day plus 500 mg amoxycillin four times a day for 7 days plus 500 mg tinidazole four times a day on days 5-7; (5) standard triple therapy for 2 weeks with amoxycillin; or (6) standard triple therapy for 2 weeks with tetracyclin. Endoscopy was repeated 4 weeks after the end of the treatment. Results: So far, repeat endoscopy has been performed in 162 subjects after the treatment was completed. Of these, 103 had been diagnosed as having active gastritis (determined histologically) and 59 a peptic ulcer (42 duodenal, 17 gastric). The H. pylori eradication rate by treatment group was 0% for group 1, 31% for group 2, 0% for group 3, 59% for group 4, 85% for group 5 and 94% for group 6. Continuation of study: The follow-up of these subjects will provide information on the need for treatment in symptom-free subjects
Three-year follow-up of chronic hepatitis C patients treated with ribavirin plus interferon-alfa combination therapy: Evidence for long-term efficacy and safety
No full textTo date, seven apomucins have been characterized and their expression in malignant and premalignant lesions is under evaluation. In this study, we examined the expression of MUC1, MUC2, MUC3, and MUC5/6 apomucins in cholanglocarcinoma (CC) and biliary epithelial dysplasia. We used 14 liver samples from patients with hepatolithiasis and CC, 11 with hepatolithiasis showing biliary epithelial dysplasia, 31 with CC alone (19 hilar, 10 peripheral, and 2 unclassifiable), and 14 with combined hepatocellular- cholangiocellular carcinoma (HC-CC) and immunohistochemically characterized the expression profiles of apomucins. Noudysplastic biliary epithelial cells in the intrahepatic large bile ducts constantly expressed MUC3 apomucin. MUC5/6 and MUC3 apomucin expression was widespread in dysplastic biliary epithelial cells in hepatolithiasis, although the latter was reduced or absent in dysplastic foci. CC extensively expressed MUC1 apomucin and focally expressed MUC2 apomucin. In addition, CC of the hilar type, including those with hepatolithiasis, frequently expressed MUC3 apomucin (68% and 57%, respectively), whereas those of the peripheral type infrequently expressed MUC3 apomucin (10%) (P < .01). MUC5/6 apomucin was more frequently expressed in well-differentiated (89%), compared with poorly differentiated CC (42%) (P < .01). Cholangiocellular elements of combined HC-CC frequently expressed MUC1 apomucin, although they rarely expressed MUC2 and MUC3 apomucin and infrequently expressed MUC5/6 apomucin. The frequent and aberrant expression of 'gastric type' MUC5/6 apomucin in biliary epithelial dysplasia, as well as in CC, suggests that biliary epithelial cells gain a gastric apomucin phenotype during carcinogenesis. MUC3 apomucin expression in CC is a marker that suggests that CC arises in the intrahepatic large bile ducts
Pathogenic mechanisms of acid-related diseases: Helicobacter and other spiral organisms
No full textColonization by Helicobacter pylori is causally related to duodenal ulceration. There is also suggestive evidence that patients who develop malignancy in the upper gastrointestinal tract are more likely to be colonized by the organisms, although to date there is no suggestion of a causal link. H. pylori possess a number of potential virulence factors that singly or together could contribute to gastric inflammation. Evidence from the past year casts doubt on the production of a mucinase enzyme by H. pylori, but has strengthened the role of the organism's urease enzyme as a virulence factor. The current belief is that the urease, by producing ammonia and altering the pH, affects the quality of the mucus barrier, altering its structure. Also, the ammonia can act as a direct cytotoxin for the gastric cells. Further work has strengthened the possible role of a proteinaceous cytotoxin produced by H. pylori as another possible virulence factor by demonstrating that cytotoxin-producing bacteria are more likely to be isolated from patients with ulceration. Further information has been gained about the surface properties of H. pylori and its production of inflammatory mediators, each of which could be important for colonization and stimulation of inflammation, respectively. Finally, there is an increasing appreciation of other mucosa-associated bacteria both in humans and other animals that may induce inflammation in the stomach
"Further Developments of a Variable Fuel Flow Automatic Mixing Valve for Prescribed Injection Ratio"
No full textLa biologia dell'Helicobacter pylori (epidemiologia, correlazione con il linfoma gastrico)
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