Effect of omeprazole-induced achlorhydria on trefoil peptide expression in the rat stomach. A comparative study on the activity of lansoprazole, omeprazole and PD-136450 on acidified ethanol- and indomethacin-induced gastric lesions in the rat. [Acquisition of secondary resistance after failure of a first treatment of Helicobacter pylori infection in children] Rx drugs

Drugs online research references

J Gastroenterol Hepatol. 2001 Nov;16(11):1222-7.
Effect of omeprazole-induced achlorhydria on trefoil peptide expression in the rat stomach.

Kang B, Alderman BM, Nicoll AJ, Cook GA, Giraud AS.

Department of Medicine, University of Melbourne, Western Hospital, Footscray, Australia.

BACKGROUND: Omeprazole is an inhibitor of the H+K+ ATPase of the gastric parietal cell, which is used clinically to suppress gastric acid secretion. It has also been found to inhibit gastric mucin production; however, its effects on the synthesis and secretion of the trefoil peptides, which are also expressed by mucus cells, and which play a key role in cytoprotection and epithelial repair, are unknown. METHODS: Rats (n=8) were given either omeprazole (30 mg/kg per day; p.o.) or inert carrier for 1 week, and the effects on synthesis and peptide expression of the gastric trefoil peptides, TFF1/pS2 and TFF2/SP, were compared. RESULTS: As expected, omeprazole treatment abolished H+ ion production with a mean gastric juice pH of 7.2 compared with 2.4 for controls. The omeprazole group had elevated total protein levels of 35-fold and TFF1/pS2 peptide levels elevated fourfold, respectively, but not TFF2/SP peptide in gastric juice, suggesting that the increased pH reduced the viscosity of adherent mucus, thereby increasing gastric juice concentrations by dissolution of adherent TFF1/pS2 and increased secretion. Concomitant with increased TFF1/pS2 secretion was a fall in predominantly antral mucosal trefoil peptide concentrations. In contrast to trefoil secretory rates, the steady-state synthesis of both TFF1/pS2 and TFF2/SP was unchanged after omeprazole treatment, implying both a large cellular pool of processed peptide and rapid secretion. CONCLUSION: The increase in the concentration of TFF1/pS2 in gastric secretions during chronic omeprazole-induced achlorhydria may be important in preventing tissue injury and promoting repair in response to an increased luminal bacterial population.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11903739&dopt=Abstract

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Clin Exp Pharmacol Physiol. 2002 Mar;29(3):173-80.
A comparative study on the activity of lansoprazole, omeprazole and PD-136450 on acidified ethanol- and indomethacin-induced gastric lesions in the rat.

Chandranath SI, Bastaki SM, Singh J.

Department of Pharmacology, Faculty of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates.

1. The proton pump inhibitors lansoprazole (LP) and omeprazole (OP) and the cholecystokinin (CCK)-receptor antagonist PD-136450 (PD) provide a broad spectrum of activities in their ability to inhibit gastric acid secretion and protect the stomach against ulcerogens. In the present study, we investigated the protective effects of these compounds against gastric ulcers induced by acidified ethanol (AE) and indomethacin. 2. Both AE (60% ethanol in 150 mmol/L HCl, 1 mL/rat) and indomethacin (30 mg/kg) produced gastric haemorrhagic lesions in the rat 1 and 6 h after oral administration, respectively. 3. The gastric mucosal protective effects of LP (1-20 mg/kg), OP (0.5-10 mg/kg) and PD (1-20 mg/kg), administered either orally or subcutaneously (s.c.) 30 min before the administration of AE or indomethacin, were dose dependent against both models of ulcer induction. 4. To determine whether the cytoprotective effect of LP, OP and PD (each 10 mg/kg) was mediated by endogenous prostaglandins (PG), indomethacin (10 mg/kg, s.c.) was administered 15 min before AE to inhibit prostanoids biosynthesis. Indomethacin reduced the cytoprotective effects of OP, but not LP, administered either orally or s.c. Indomethacin reduced the cytoprotective effect of PD administered orally, although the effect was much less significant than when PD was administered s.c. The results exclude the role of PG in mediating the protective effects of LP, whereas the possibility exists for PG to have a role in mediating the protective effects of OP and PD. 5. To investigate the possible involvement of endogenous nitric oxide (NO) in the cytoprotective action of LP, OP and PD, we treated rats with a selective inhibitor of NO synthesis, namely NG-nitro-L-arginine methyl ester (L-NAME; 25 mg/kg, s.c.). Administration of L-NAME 15 min prior to LP, OP or PD (each 10 mg/kg) orally or s.c. and challenge with AE or indomethacin did not significantly increase the degree of the ulcer index and L-NAME was not able to antagonize the protective effects of LP, OP and PD, thus excluding the role of NO in mediating the protective effects of these drugs. However, the effects of PD in reducing the indomethacin-induced ulcer index were less significant in the presence than the absence of L-NAME (P < 0.05 vs P < 0.001, respectively), suggesting a role for NO. 6. In conclusion, the results of the present study suggest that LP and OP are equally effective against AE- as well as indomethacin-induced gastric ulcers and were more potent than PD in protecting the stomach against ulcer formation. Lansoprazole, OP and PD bring about their cytoprotective action through the reduction of acid secretion and some other unknown mechanisms. However, OP and PD may exert their cytoprotective action through PG and NO pathways.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11906479&dopt=Abstract

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Arch Pediatr. 2002 Feb;9(2):130-5.
[Acquisition of secondary resistance after failure of a first treatment of Helicobacter pylori infection in children]

[Article in French]

Kalach N, Benhamou PH, Bergeret M, Gottrand F, Husson MO, Barbier C, Dupont C, Raymond J.

Service de pediatrie, hopital Saint-Vincent-de-Paul, 82, avenue Denfert-Rochereau, 75674 Paris, France.

AIMS: To assess the frequency of acquisition of secondary Helicobacter pylori resistant-strains after a first course of antimicrobial treatment. PATIENTS AND METHODS: A retrospective study was performed during the 1994-2000 period, in 15 girls and eight boys, mean age 10.9 +/- 4.8 years (1.4-17 years), with Helicobacter pylori gastritis (culture and antimicrobial susceptibility) presenting a failure of first course treatment, with during one week a proton pump inhibitor and amoxicillin together with either clarithromycin (n = 14) or metronidazole (n = 9). Two endoscopies were performed, the first at the time of diagnosis and the second after the failure of bacterial eradication demonstrated by a positive 13C urea breath test six weeks after the end of treatment. Antimicrobial susceptibility of all Helicobacter pylori strains was tested after each endoscopy and before starting a second course of the treatment. RESULTS: Comparison of antimicrobial susceptibility before and after the first course of treatment showed that Helicobacter pylori strains were all sensitive to amoxicillin, clarithromycin-resistant in eight children (34.7%) before treatment vs 12 (52.1%) after treatment, p = 0.42, ns, metronidazole-resistant in 13 (56.5%) vs 12 (52.1%), p = 0.80, ns, and both clarithromycin and metronidazole-resistant in four (17.3%) vs seven (30.4%), p = 0.63, ns. Among the 14 children treated by a triple therapy including clarithromycin, three (21.4%) developed a secondary resistance to clarithromycin and in one metronidazole resistance was no more detected. Among the nine children treated with a triple therapy including metronidazole, none developed a secondary resistance to metronidazole and one developed a secondary resistance to clarithromycin. CONCLUSION: This study shows the absence of amoxicillin-resistant strains, a high initial clarithromycin-resistant strains level (primary resistance), increasing after a first course of treatment, and for metronidazole a high initial level of resistance not influenced by treatment. Secondary clarithromycin-resistance of Helicobacter pylori strains following the first course of treatment could account for failure of bacterial eradication and suggests the importance of antimicrobial susceptibility.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11915493&dopt=Abstract

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