Drugs online research references
Gut. 2001 Nov;49(5):624-8.
Duodenal fat intensifies the perception of heartburn.
Meyer JH, Lembo A, Elashoff JD, Fass R, Mayer EA.
Department of Medicine, Division of Gastroenterology, West Los Angeles Healthcare Center, VA Greater Los Angeles Healthcare System, UCLA School of Medicine, Los Angeles, CA, USA.
BACKGROUND: Patients with gastro-oesophageal reflux disease (GORD) frequently report that meals high in fat worsen heartburn. Nevertheless, studies to determine whether high fat meals promote gastro-oesophageal reflux have produced conflicting and equivocal conclusions. PATIENTS AND METHODS: To determine, alternatively, whether fat in the small intestinal lumen intensifies the perception of heartburn, we studied 11 patients with typical heartburn from GORD. After being placed on omeprazole to suppress endogenous acid, these fasting subjects underwent oesophageal perfusions with graded doses of HCl at pH values of 1.0, 1.5, 2.0, and 2.5. Oesophageal perfusions were conducted while the duodenum was perfused with saline (control) and again with fat at 8 g/h. RESULTS: Time to onset, intensity, and severity of heartburn varied with dose of oesophageal acid (p<0.01). Time to onset was significantly (p<0.01) shorter, and intensity and severity of heartburn significantly (p<0.05) greater, during duodenal perfusion with fat. CONCLUSION: We conclude that duodenal fat intensifies the perception of heartburn.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11600463&dopt=Abstract
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Gastroenterology. 2001 Oct;121(4):792-8.
Recrudescence and reinfection with Helicobacter pylori after eradication therapy in Bangladeshi adults.
Hildebrand P, Bardhan P, Rossi L, Parvin S, Rahman A, Arefin MS, Hasan M, Ahmad MM, Glatz-Krieger K, Terracciano L, Bauerfeind P, Beglinger C, Gyr N, Khan AK.
Department of Research, University Hospital, Basel, Switzerland.
BACKGROUND & AIMS: In developing countries where Helicobacter pylori infection is widespread, posttherapeutic recurrence rates may be high. Many of the limited studies available have methodological problems and show varied recurrence rates. We determined late recrudescence rates, true reinfection, and ulcer recurrence. METHODS: One hundred five Bangladeshi patients with H. pylori infection and duodenal ulcer disease were treated with a triple therapy. Follow-up included 13C-urea breath tests, endoscopy, and biopsy-based tests. In reinfected patients, genomic typing compared pretherapeutic and posttherapeutic strains. RESULTS: Recrudescence, associated with nitroimidazole-based treatment, occurred in 15 of 105 patients (14%) within the first 3 months, but only 8 of 105 patients tested positive 4 weeks after therapy ended. True reinfection was diagnosed in 11 of 105 patients between 3 and 18 months after therapy. The annual reinfection rate was 13%, based on a total follow-up of 84.7 patient years. Ulcer relapse occurred in 2 of 15 (13%) recrudescence cases and in 6 of 11 (55%) reinfection cases, but also in 4 of 73 (5%) H. pylori-negative patients. CONCLUSIONS: In Bangladesh, late recrudescence of H. pylori after eradication therapy occurs within the first 3 months. The reinfection rate is high and might influence cost-benefit analyses for determining diagnostic and therapeutic procedures.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11606492&dopt=Abstract
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sat.ap-hop-paris.fr
Clarithromycin resistance of Helicobacter pylori is relatively frequent in France and is assumed to be the main cause of failure of the proton pump inhibitor-amoxicillin-clarithromycin (PPI-AC) therapy, which is the first-line regimen in our country. We determined the respective effects of clarithromycin primary and secondary resistances on efficacy of the PPI-AC regimen and examined whether failures were associated with persistence of the same strain or with emergence of a new one. Hundred and twenty three H. pylori-infected patients were treated for seven days with omeprazole 20 mg b.d., amoxicillin 1 g b.d., and clarithromycin 500 mg b.d. Eradication was assessed by breath test in 102 patients. MICs of clarithromycin were determined by E-test. Strain genotyping was performed by random amplified polymorphic DNA. The pre-treatment and post-treatment prevalences of clarithromycin resistance were 18.7% (23/123) and 69.2% (9/13), respectively. The rates of eradication were 67.6% (69/102), 78.8% (67/85), and 11.8% (2/17) for all, susceptible and resistant strains, respectively. The post-treatment isolate was available for six patients with a susceptible pre-treatment isolate and a persistent infection; resistance emerged in two patients and was associated with persistence of the pre-treatment strain in one and with selection of a new strain in the other. In conclusion, in our hospital, failures of the PPI-AC therapy are related to both clarithromycin primary and secondary resistances but emergence of secondary resistance does not explain all failures in the initial clarithromycin-susceptible group. In that group a new strain can emerge after failure.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11642014&dopt=Abstract
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