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Efficacy and tolerability of pantoprazole 40 mg versus 80 mg in patients with reflux oesophagitis. 总被引:4,自引:2,他引:2
van Rensburg CJ Honiball PJ Grundling HD van Zyl JH Spies SK Eloff FP Simjee AE Segal I Botha JF Cariem AK Marks IN Theron I Bethke TD 《Alimentary pharmacology & therapeutics》1996,10(3):397-401
BACKGROUND: Pantoprazole is a substituted benzimidazole which is a potent inhibitor of gastric acid secretion by its action upon H+, K+- ATPase. METHODS: Pantoprazole 40 mg and 80 mg were compared in a randomized double-blind study in 192 out-patients with stage II or III (Savary-Miller classification) reflux oesophagitis. Patients received either pantoprazole 40 mg (n = 97) or pantoprazole 80 mg (n = 95), once daily before breakfast for 4 weeks. Treatment was extended for a further 4 weeks if the oesophagitis had not healed. RESULTS: After 4 weeks complete healing of the reflux oesophagitis was seen in 78% of protocol-correct patients given pantoprazole 40 mg daily (n = 86), and in 72% in the 80 mg (n = 87) group. The cumulative healing rates after 8 weeks were 95 and 94%, respectively (P > 0.05, Cochran-Mantel- Haenszel), and time until healing of oesophagitis comparable in both groups. Differences between doses were also not significant in an intention-to-treat analysis. Both dosing schedules were well tolerated and the patients experienced remarkable symptom relief. No adverse event or changes in laboratory values of clinical significance could definitely be ascribed to the trial medication. CONCLUSION: The 40 mg pantoprazole dosage is comparable to 80 mg in reflux oesophagitis, both in efficacy and tolerability. 相似文献
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Plinio Cirillo Salvatore De Rosa Vito Di Palma Roberta De Rosa Paola Maietta Federico Piscione Massimo Chiariello 《Heart and vessels》2009,24(4):313-316
Drug-eluting stents (DES) have become routine therapy in clinical practice because restenosis is significantly reduced in
patients treated with these devices. New generations of DES bearing newer antiproliferative drugs have been developed. Sirolimus
was the first antiproliferative drug eluted by a DES (SES) while Zotarolimus represents a sirolimus-derived, newer antiproliferative
drug borne by a different kind of DES (ZES). This report describes two cases of different vascular response to concurrent
side by side implantation of SES and ZES in the same vessel and highlights significant early restenosis of ZES as compared
with SES. 相似文献
46.
P Barlas TD Hernndez KL McFadden 《Focus on Alternative and Complementary Therapies》2010,15(3):225-226
McFadden KL, Hernández TD. Cardiovascular benefits of acupressure (Jin Shin) following stroke. Complement Ther Med 2010; 18: 42–8. 相似文献
47.
L Moreno SK McMaster T Gatheral LK Bailey LS Harrington N Cartwright PCJ Armstrong TD Warner M Paul-Clark JA Mitchell 《British journal of pharmacology》2010,160(8):1997-2007
Background and purpose:
Gram-negative bacteria contain ligands for Toll-like receptor (TLR) 4 and nucleotide oligomerization domain (NOD) 1 receptors. Lipopolysaccharide (LPS) activates TLR4, while peptidoglycan products activate NOD1. Activation of NOD1 by the specific agonist FK565 results in a profound vascular dysfunction and experimental shock in vivo.Experimental approach:
Here, we have analysed a number of pharmacological inhibitors to characterize the role of key signalling pathways in the induction of NOS2 following TLR4 or NOD1 activation.Key results:
Vascular smooth muscle (VSM) cells expressed NOD1 mRNA and protein, and, after challenge with Escherichia coli or FK565, NOS2 protein and activity were induced. Macrophages had negligible levels of NOD1 and were unaffected by FK565, but responded to E. coli and LPS by releasing increased NO and expression of NOS2 protein. Classic pharmacological inhibitors for NF-κB (SC-514) and mitogen-activated protein kinase (SB203580, PD98059) signalling pathways inhibited responses in both cell types regardless of agonist. While TLR4-mediated responses in macrophages were specifically inhibited by the pan-caspase inhibitor z-VAD-fmk and the PKC inhibitor Gö6976, NOD1-mediated responses in VSM cells were inhibited by the Rip2 inhibitor PP2.Conclusions and implications:
Our findings suggest a selective role for NOD1 in VSM cells, and highlight NOD1 as a potential novel therapeutic target for the treatment of vascular inflammation. 相似文献48.
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