Drugs online research references
Int J Oncol. 2001 Jun;18(6):1207-12.
Helicobacter pylori eradication therapy for high-grade mucosa-associated lymphoid tissue lymphomas of the stomach with analysis of p53 and K-ras alteration and microsatellite instability.
Hiyama T, Haruma K, Kitadai Y, Ito M, Masuda H, Miyamoto M, Tanaka S, Yoshihara M, Sumii K, Shimamoto F, Chayama K.
First Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima 734-8551, Japan.
Recent studies have shown that 70-80% of low-grade mucosa-associated lymphoid tissue (MALT) lymphomas regress in response to eradication of Helicobacter pylori (H. pylori). However, there are no reports on whether gastric high-grade MALT lymphomas regress after H. pylori eradication. We performed H. pylori eradication therapy in 4 patients with stage I, high-grade MALT lymphoma after obtaining their informed consent. H. pylori infection was observed in all 4 patients. The patients were treated with proton-pump inhibitor-based eradication therapy for 1 or 2 weeks, and then underwent endoscopic examination and biopsy sampling. H. pylori eradication was achieved in all 4 patients. Six months after eradication treatment, 2 patients showed complete regression of the lymphoma and 2 patients showed no change. The 2 patients with non-responding lymphoma were then treated with an additional chemotherapy (CHOP regimen), whereupon the tumors completely regressed. These patients, followed-up at least 18 months after eradication treatment, showed no recurrence. We also examined genetic alteration of the p53 and K-ras genes and microsatellite instability in these high-grade MALT lymphomas. One patient with a tumor that showed no change after H. pylori eradication, had a loss of heterozygosity of the p53 gene. No other genetic alterations were detected among the patients. Our results indicate that the eradication of H. pylori may be effective not only for patients with low-grade MALT lymphoma but also for patients with high-grade MALT lymphoma. The treatment may be efficacious as a first-line therapy for patients with high-grade MALT lymphoma. However, our sample size was limited and further studies are needed to clarify the issue.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11351252&dopt=Abstract
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Scand J Gastroenterol Suppl. 2001;(234):3-9.
Relative efficacies of gastric proton-pump inhibitors on a milligram basis: desired and undesired SH reactions. Impact of chirality.
Kromer W.
Dept. of Pharmacology, Byk Gulden, Konstanz, Germany.
Gastric proton-pump inhibitors (PPIs) are prodrugs. Their acid activation at pH 1.0 inside the canaliculus of a parietal cell should be fast relative to their serum elimination rate. Actually, all PPIs display chemical activation half-lives at pH 1.0 of a few minutes at the most, while being eliminated from serum with a half-life of about 1 h. This is the main reason they show similar antisecretory efficacies on a milligram basis. It is in line with about 5% to 15% higher healing rates in GERD, DU and GU when 40 mg is compared to 20 mg of either omeprazole or pantoprazole. The comparably large biological variation between patient samples explains why some studies show statistically significant differences between the two doses, while others do not. However, it would matter to the individual patient if s/he was the one additionally healed by a 40 mg dose within a defined treatment period. Chemical activation of PPI prodrugs is unwanted in weakly acidic tissue compartments such as lysosomes or secretory granules. However, the ratio of the serum elimination half-life (availability at the target) to the chemical activation half-life at a critical pH 5.0 is reversed only with pantoprazole. when compared to pH 1.0 (i.e. the ratio is < 1 at pH 5.0 and > 1.0 at pH 1.0). This is the basis of the high pH selectivity of pantoprazole. In contrast, rabeprazole is activated at pH 5.0 almost as quickly as it is at pH 1.0 and much faster than it is eliminated from serum. This unwanted reactivity of rabeprazole at pH 5.0 does not contribute to the antisecretory action at pH 1.0 and results in poor pH selectivity. Omeprazole and lansoprazole lie in between, as they are activated, at pH 5.0, about as quickly as they are eliminated from serum. The above activation rates refer to room temperature. At 37 degrees C. the activation rates of all PPIs further increase, by about the same factor of between 3 and 4. This renders their differential pH selectivities even more critical for drug safety. Biological consequences have been reported in the literature. It has been claimed that a dose of 40 mg of the S-enantiomer of omeprazole (esomeprazole) results in 10%-15% higher healing rates in GERD patients, compared to 20 mg omeprazole racemate. The same difference is found when the two doses of omeprazole racemate are compared to each other. This is not surprising, as the chiral PPI prodrug is converted by acid into an achiral cyclic sulfenamide which only then reacts with the proton pump. There is therefore no pharmacodynamic argument in favour of any single enantiomer formulation of any PPI. Moreover, potential pharmacokinetic differences between the enantiomers seem to be of little if any importance in the patient.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11768559&dopt=Abstract
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med.va.gov
CONTEXT: Projected cost for lansoprazole, the formulary proton pump inhibitor (PPI) at our institution, was $1.8 million in 1999. While some patients require PPI therapy, many could control their symptoms with a histamine H2-receptor antagonist blocker (H2 blocker) at a much lower cost. OBJECTIVE: To evaluate a practice-based approach to converting patients from PPIs to H2 blockers. DESIGN: Before-after study. SETTING: Portland Veterans Affairs Primary Care Clinics. INTERVENTION: We developed guidelines and educated clinicians about the use of PPIs and H2 blockers. To help physicians convert appropriate patients from PPIs to H2 blockers, we gave them a list of their patients receiving PPIs, form letters for patients explaining the conversion, and structured prescription forms. Patient lists and e-mail reminders, as well as feedback on institutional performance, were sent to clinicians during the intervention period. OUTCOME MEASURES: Number of PPI and H2 prescriptions per enrollee and pharmacy costs. RESULTS: The average number of PPI prescriptions per enrollee at our institution decreased from 0.39 in the 9 months before the intervention to 0.27 in the 9 months after the intervention. The associated pharmacy costs decreased from an average of $43 to $28 per enrollee per quarter, a difference of $15 or a savings of $80,000 per quarter. Accounting for the decrease in medication prices during the study, this difference was $11 per patient per quarter, corresponding to a savings of about $60,000 per quarter. With respect to the conversion process, more than 70% of clinicians felt the intervention had a big impact on how they prescribed PPIs and H2 blockers. Eighty-two percent of clinicians converted patients from PPIs to H2 blockers during clinic time; 56% did so during administrative time. Overall, more clinicians considered the intervention to be helpful rather than a hassle. CONCLUSIONS: The number of PPI prescriptions decreased during the intervention and was sustained at least three quarters afterward. This low-intensity, practice-based intervention may serve as a model for other health care systems.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11769299&dopt=Abstract
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