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study aims to compare the efficacy and safety of capecitabine plus oxaliplatin (XELOX) with 5-fluorouracil\u002Fleucovorin plus oxaliplatin (FOLFOXs) in patients with advanced gastric cancer. Five databases were searched up to June 2014, without language restrictions. The outcomes included overall response rate (ORR), clinical benefit rate (CBR), and toxicity. Twenty-six eligible trials were selected from 178 studies that initially were identified. All trials were published in Chinese journals between 2005 and 2014 and included 1585 patients (787 in XELOX group and 798 in FOLFOXs group). The pooled results failed to show statistical significance of XELOX regimen on ORR (OR 1.18, 95 % CIs 1.00–1.41, P = 0.057) and CBR (OR 1.10, 95 % CIs 0.95–1.28, P = 0.191) as compared with FOLFOXs regimen. None of the 26 clinical trials reported progression-free survival, and only one reported overall survival rate. The meta-analysis demonstrated that XELOX regimen was associated with a significant lower risk with nausea, stomatitis, diarrhea and alopecia, and a significant higher risk of hand-foot syndrome. The evidence is limited to suggest that XELOX may share similar efficacy as FOLFOXs and reduce toxicities of chemotherapy in advanced gastric cancer therapy. However, owing to limited data and potential bias of the included studies, further rigorously controlled trials are required.",{"EN":288,"VI":289},"Capecitabine plus oxaliplatin (XELOX) compared with 5-fluorouracil\u002Fleucovorin plus oxaliplatin (FOLFOXs) in advanced gastric cancer: meta-analysis of randomized controlled trials","Capecitabine phối hợp oxaliplatin (XELOX) so với 5-fluorouracil\u002Fleucovorin phối hợp oxaliplatin (FOLFOXs) trong ung thư dạ dày tiến triển: phân tích gộp các thử nghiệm ngẫu nhiên có đối chứng",{"VOID":291},"Bittoni A, Maccaroni E, Scartozzi M, Berardi R, Cascinu S (2010) Chemotherapy for locally advanced and metastatic gastric cancer: state of the art and future perspectives. Eur Rev Med Pharmacol Sci 14:309–314\nSchoffski P (2004) The modulated oral fluoropyrimidine prodrug S-1, and its use in gastrointestinal cancer and other solid tumors. Anticancer Drugs 15:85–106\nOkines AF, Norman AR, McCloud P, Kang YK, Cunningham D (2009) Meta-analysis of the REAL-2 and ML17032 trials: evaluating capecitabine-based combination chemotherapy and infused 5-fluorouracil-based combination chemotherapy for the treatment of advanced oesophago-gastric cancer. Ann Oncol 20:1529–1534\nJadad AR, Moore RA, Carroll D, Jenkinson C, Reynolds DJ, Gavaqhan DJ, McQuay HJ (1996) Assessing the quality of reports of randomized clinical trials: is blinding necessary? Control Clin Trials 17:1–12\nDerSimonian R, Laird N (1986) Meta-analysis in clinical trials. Control Clin Trials 7:177–188\nSun Q, Mao YJ, Zhao W, Cao L, Hang XS, Chang SJ, Wang Q (2005) A randomized clinical study of capecitabine plus oxaliplatin in the treatment of advanced gastric cancer. Cancer Res Prev Treat 32:729–730\nCai DY, Tao M, Duan WM, Wang ZX, Xie Q, Feng J, Wang QC (2007) Capecitabine plus oxaliplatin and 5-fluorouracil\u002Fleucovorin plus oxaliplatin combination chemotherapy for advanced gastric cancer. J Clin Exp Med 16:45–46\nChen SJ, Huang HX, Li GS (2007) A randomized clinical study of XELOX compared with FOLFOX-4 in the treatment of advanced gastric cancer. China Oncol 17:483–486\nQu ZF, Feng XS, Gao SG, Wang ZH, Shan TY, Zhang L, Han J (2007) Clinical study of capecitabine plus oxaliplatin in the treatment of advanced gastric cancer. Fujian Med J 29:41–43\nXue FQ, Li WH, Lin MB, Huang LL (2008) Comparative study of continuous intravenous infusional 5-flnorouracil or capecitabine combined with oxaliplatin in the treatment of advanced gastric cancer: analysis of 67 cases. Fujian Med J 30:114–116\nShi M, Li LB, Liao WJ, Zheng H, Luo RC (2008) A randomized clinical study of XELOX compared with FOLFOX-4 in the treatment of advanced gastric cancer. J South Med Univ 28:1490–1491\nGao X, Cai DY, Hang XS (2008) Comparison of combination chemotherapy with XELOX and FOLFOX in the treatment of advanced gastric cancer. Mod Med J China 10:35–37\nWang HM, Cheng XM, Zhang ML (2009) Clinical efficacy of oxaliplatin plus capecitabine in the treatment of patients with advanced gastric cancer. Eval Anal Drug-Use Hosp China 9:856–857\nHu JB, Wang F, Weng J (2009) A randomized clinical study of XELOX compared with FOLFOX in the treatment of advanced gastric cancer. China Pract Med 4:25–26\nZhao WY, Ji ZN (2009) Comparison of XELOX (oxaliplatin plus capecitabine) and FOLFOX-4 (oxaliplatin plus 5-fluororacil\u002Fcalcium folinate) in the treatment of advanced gastric cancer. Chin J Clin Oncol 36:1044–1046\nLei JH, Hong T, Zeng JZ, He ZH (2009) Clinical observation of XELOX regimen in progressive gastric cancer. Med J Natl Defending Forces N China 21:10–12\nCui WF, Li Y, Lin HZ (2009) Therapeutic effects and side effects of FOLFOX-4 and XELOX on patients with advanced gastric cancer. Chin J Curr Adv Gen Surg 12:869–871\nWang HZ, Wang XH, Lv ZC (2010) A randomized clinical study of XELOX compared with FOLFOX-4 in the treatment of advanced gastric cancer. Mod Oncol 18:947–950\nDu C, Chen CH (2010) A clinical study of capecitabine plus oxaliplatin and 5-fluororacil\u002Fcalcium folinate plus oxaliplatin in the treatment of advanced gastric cancer. Inn Mong Med J 42:260–263\nLiu C, Mao WZ, Song YQ, Li LH, Lin HZ, Li Y (2010) Clinical report of neoadjuvant chemotherapy of FOLFOX-4 and XELOX for the preoperative patients with advanced gastric cancer. Chin J Curr Adv Gen Surg 13:960–963\nLiu FL, Zheng YL (2010) Clinical study comparing capecitabine plus oxaliplatin with 5-fluororacil\u002Fcalcium folinate plus oxaliplatin in the treatment of advanced gastric cancer. J Clin Med Pract 14:50–51\nWu F, Yang YG, Hu JH, Zhang SJ, Pan DF, Lu GX (2011) Clinical study of oxaliplatin (L-OHP) plus xeloda (capecitabine) in treatment of gastric carcinoma in senile patients. Chin J Clin Gastroenterol 23:330–331\nLu HL, Li Y, Nin ZQ, Cao YH (2011) Clinical study of XELOX compared with FOLFOX-4 in the treatment of advanced gastric cancer. J Clin Med Pract 15:112–113\nWang L, Hu B, Ji CS, Hu CL, He YF, Shan BJ (2011) Combination chemotherapy with capecitabine plus oxaliplatin and 5-fluororacil\u002Fcalcium folinate plus oxaliplatin: a comparison in the treatment of advanced gastric cancer. Anhui Med Pharm J 15:329–330\nYang J (2011) The observation of clinical and nurse effect of capecitabine combined with oxaliplatin in the patients with advanced gastric cancer. Pract J Card Cereb Pneumal Vasc Dis 19:369–370\nJiang ZH (2012) Clinical study of XELOX compared with FOLFOX-6 in the treatment of advanced gastric cancer. Guide China Med 10:118–119\nZhou JH, Wei R (2012) Clinical observation of curative effect and side effects of XELOX regimen and FOLFOX-4 regimen on advanced gastric carcinoma. Chin Foreign Med Res 10:11–12\nWang AY, Zhang MJ (2012) Clinical observation of chemotherapy of capecitabine combined with oxaliplatin in treatment of advanced gastric cancer. China Med Her 9:58–59\nHu ZH, Mao SR (2013) Clinical observation of XELOX chemotherapeutic scheme in treatment of elderly patients with advanced gastric cancer. Chongqing Med 42:156–159\nFan ZM, He HG, Huang CH, Chen LQ, Li YH, Chen W, Xiao FX, Yin ZM (2013) Clinical effects of FOLFOX-4 and XELOX on patients with advanced gastric cancer. Pract J Cancer 28:396–398\nZhang D (2014) The short-term clinical efficacy and adverse reactions of XELOX chemotherapy for the treatment of elderly patients with advanced gastric cancer. Chin J Med Guid 16:129–130\nKang YK, Kang WK, Shin DB, Chen J, Xiong J, Wang J, Lichinitser M, Guan Z, Khasanov R, Zheng L, Philco-Salas M, Suarez T, Santamaria J, Forster G, McCloud PI (2009) Capecitabine\u002Fcisplatin versus 5-fluorouracil\u002Fcisplatin as first-line therapy in patients with advanced gastric cancer: a randomised phase III noninferiority trial. Ann Oncol 20:666–673\nCassidy J, Twelves C, Van Cutsem E, Hoff P, Bajetta E, Boyer M, Bugat R, Burger U, Garin A, Graeven U, McKendric J, Maroun J, Marshall J, Osterwalder B, Pérez-Manga G, Rosso R, Rougier P, Schilsky RL (2002) First-line oral capecitabine therapy in metastatic colorectal cancer: a favorable safety profile compared with intravenous 5-fluorouracil\u002Fleucovorin. Ann Oncol 13:566–575\nBiljana M, Jelena M, Branislav J, Milorad R (1999) Bias in meta-analysis and funnel plot asymmetry. Stud Health Technol Inform 68:323–328\nSterne JA, Sutton AJ, Ioannidis JP, Terrin N, Jones DR, Lau J, Carpenter J, Rücker G, Harbord RM, Schmid CH, Tetzlaff J, Deeks JJ, Peters J, Macaskill P, Schwarzer G, Duval S, Altman DG, Moher D, Higgins JP (2011) Recommendations for examining and interpreting funnel plot asymmetry in meta-analyses of randomised controlled trials. 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biliary secretion of [14C]felodipine in 4 healthy human subjects was studied by use of the multiple marker dilution principle with double lumen tubes placed in the stomach and intestine. Insignificant amounts of14C activity were recovered from gastric aspirates. The individual recovery from intestinal aspirates varied from 2.9 to 8.5% of the dose of radioactivity over the period of 4.5 h after dosing. Less than 0.1% was identified as unchanged felodipine. The results show that biliary secretion is a minor route of elimination of felodipine or its metabolites. Bile collection for 4.5 h had no significant effect on the pharmacokinetics of felodipine, although the 72 h urinary recovery of radioactivity tended to be lower when bile was collected (59%) than in the control experiment (66%).",{"EN":453,"VI":454},"Biliary secretion of felodipine metabolites in man after intravenous [14C]felodipine","Bài tiết qua mật của các chất chuyển hóa felodipine ở người sau khi tiêm tĩnh mạch [14C]felodipine",{"VOID":456},"Weidolf L, Borg KO, Hoffmann K-J (1984) Urinary metabolites of felodipine, a new vasodilator drug, in man, dog, rat and mouse. Xenobiotica 14: 657–666\nEdgar B, Reg»rdh CG, Johnsson G, Johansson L, Lundborg P, Löfberg I, Rönn O (1985) Pharmacokinetics of felodipine in healthy male subjects. Clin Pharmacol Ther 38: 205–211\nSutfin TA, Gabrielsson M, Reg»rdh CG (1987) Effects of biliary excretion on the disposition of felodipine and metabolites in the rat. Xenobiotica 17: 1203–1214\nLind T, Andersson T, Sk»nberg I, Olbe L (1987) Biliary excretion of intravenous14C omeprazole in man. Clin Pharmacol Ther 42: 504–508\nAngelin A, Arvidsson A, Dahlqvist R, Hedman A, Schenck-Gustafsson K (1987) Quinidine reduces biliary clearance of digoxin in man. Eur J Clin Invest 17: 262–265\nAhnoff M (1984) Determination of felodipine in plasma by capillary gas chromatography with electron capture detection. J Pharm Biomed Anal 2: 519–526\nSheiner LB, Beal SL (1985) Pharmacokinetic parameter estimates from several least squares procedures: superiority of extended least squares. J Pharmacokinet Biopharm 13: 185–201\nYamaoka K, Nakagawa T, Uno T (1978) Statistical moments in pharmacokinetics. J Pharmacokinet Biopharm 6: 547–558\nBäärnhielm C, Sk»nberg I, Borg KO (1984) Cytochrome P-450-dependent oxidation of felodipine — a 1,4-dihydropyridine — to the corresponding pyridine. Xenobiotica 14: 719–726\nBäärnhielm C, Dahlbäck H, Sk»nberg I (1986) In vivo pharmacokinetics of felodipine predicted from in vitro studies in rat, dog and man. Acta Pharmacol Toxicol 59: 113–122\nHoffmann K-J, Weidolf L (1985) Identification of felodipine metabolites in rat urine. Biomed Mass Spec 12: 414–423\nHirom PC, Millburn P, Smith RL (1976) Bile and urine as complementary pathways for the excretion of foreign organic compounds. Xenobiotica 6: 55–64\nRollins DE, Klaassen CD (1979) Biliary excretion of drugs in man. 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Methods: Six extensive (mephenytoin S\u002FR ratio \u003C0.3; EM) and six poor (mephenytoin S\u002FR ratio >0.8; PM) hydroxylators of S-mephenytoin ingested a single 10-mg oral dose of selegiline hydrochloride. Serum concentrations of selegiline, desmethylselegiline and l-methamphetamine were measured by gas chromatography – mass spectrometry for up to 48 h. In addition, the platelet monoamine oxidase type B (MAO-B) activity was measured for 14 days to describe possible differences in the pharmacodynamics of selegiline and its metabolites between EM and PM. Results: The CYP2C19 phenotype had no significant effects on the pharmacokinetic variables of selegiline. PM of S-mephenytoin had 68% higher mean AUC of desmethylselegiline (P=0.0017) than EM, but no significant differences were observed in other pharmacokinetic parameters of desmethylselegiline. Contrary to desmethylselegiline, the serum l-methamphetamine concentrations were slightly lower in PM, but no statistically significant differences were observed in l-methamphetamine pharmacokinetics between the two CYP2C19 phenotypes. Accordingly, the magnitude of MAO-B inhibition showed no significant differences between the study groups. 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Six subjects with normal renal function and 20 patients with various degrees of renal impairment participated. The mean areas under the plasma concentration-time curves of oxcarbazepine and its monohydroxy-metabolite were 2–2.5-times higher in patients with severe renal impairment (CLCR\u003C10 ml·min−1) than in healthy subjects. The apparent elimination half-life of the monohydroxy-metabolite [19 (SD 3) h] in these patients was about twice that in healthy subjects. The effect of renal impairment on the plasma concentrations of glucuronides was more marked. The renal clearances of the unconjugated monohydroxy-metabolite and its glucuronides (the main compounds recovered in urine) correlated well with creatinine clearance. The maximum target dose in patients with slight renal impairment (CLCR>30 ml·min−1) should not be changed. In patients with moderate renal impairment (CLCR10–30 ml·min−1) it should be reduced by 50%. In patients with severe renal impairment (CLCR\u003C10 ml·min−1), the glucuronides of oxcarbazepine and its monohydroxy-metabolite are likely to accumulate during repeated administration, and dosage adjustment of oxcarbazepine in these patients could not be proposed from this single administration study.",{"EN":733,"VI":734},"The effect of renal impairment on the pharmacokinetics of oxcarbazepine and its metabolites","Ảnh hưởng của suy giảm chức năng thận lên dược động học của oxcarbazepine và các chất chuyển hóa của nó",{"VOID":736},"Dam M (1990) Oxcarbazepine in monotherapy. Behav Neurol 3:31–34\nHoutkooper NA, Lammertsma A, Meyer JWA, Goedhart DM, Meinardi H, Oorschot CAEH van, Blom GF, Höppener RJEA, Hulsman JARJ (1987). Oxcarbazepine (GP 47 680): a possible alternative to carbamazepine? Epilepsia 28:693–698\nFaigle JW, Menge GP (1990) Pharmacokinetic and metabolic features of oxcarbazepine and their clinical significance: comparison with carbamazepine. Int Clin Psychopharmacol 5:73–82\nFeldmann KF, Brechbühler S, Faigle JW, Imhof P (1978) Pharmacokinetics and metabolism of GP 47 680, a compound related to carbamazepine, in animals and man. In: Advances in Epileptology. Proceedings of the Thirteenth Congress of the International League Against Epilepsy, and Ninth Symposium of the International Bureau for Epilepsy, Amsterdam, September 1977, pp 290–293\nDickinson RG, Hooper WD, Dunstan PR, Eadie MJ (1989) First dose and steady-state pharmacokinetics of oxcarbazepine and its 10-hydroxy metabolite. Eur J Clin Pharmacol 37:69–74\nTheisohn M, Heimann G (1982) Disposition of the antiepileptic oxcarbazepine and its metabolites in healthy volunteers. Eur J Clin Pharmacol 22:545–551\nSchütz H, Feldmann KF, Faigle JW, Kriemler HP, Winkler T (1986) The metabolism of 14C-oxcarbazepine in man. Xenobiotica 16: 769–778\nRouan MC, Decherf M., Le Clanche V, Lecaillon JB, Godbillon J (1994) Automated microanalysis of oxcarbazepine and its monohydroxy and transdiol metabolites in plasma by liquid chromatography. J Chromatogr (in press)\nBennett WM (1988) Guide to drug dosage in renal failure. Clin Pharmacokinet 15:326–354\nGrant SM, Faulds D (1992) Oxcarbazepine. A review of its pharmacology and therapeutic potential in epilepsy, trigeminal neuralgia and affective disorders. 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this pilot study, we attempted to determine the optimal dosage regimens of esomeprazole for treatment of GERD with minimal influence of the CYP2C19 polymorphism through a study of the pharmacokinetics and pharmacodynamics of esomeprazole given at 3 different dosage regimens with the same total daily dose. Each of the 3genotypes of CYP2C19, homozygous extensive metabolizers (homEMs), heterozygous EMS (hetEMs), and poor metabolizers (PMs) were recruited in this clinical trial. Subjects were given a placebo followed by the administration of esomeprazole, at a dose of 40 mg once daily (40QD), 20 mg twice daily (20TD), or 10 mg 4 times daily (10Q4D) for 7 days. Twenty-four-hour and nocturnal intragastric pH and plasma esomeprazole concentrations were all determined on day 7. The pharmacokinetic parameters and dynamic characteristics differed among the 3 CYP2C19 genotype groups. With esomeprazole 40QD, gastric acid suppression was insufficient to achieve a therapeutic effect, while 20TD and 10Q4D were found to be effective in controlling both daytime and nocturnal gastric acidity for all 3 genotype groups. It was confirmed that intragastric pH values and plasma esomeprazole concentrations potentially depended on the CYP2C19 genotype status for treatment with esomeprazole. Dosage regimens of divided doses of 20TD or 10Q4D esomeprazole yielded improved antisecretory effects with a minimal influence of CYP2C19 polymorphisms.",{"EN":957,"VI":958},"Optimal dose regimens of esomeprazole for gastric acid suppression with minimal influence of the CYP2C19 polymorphism","Các chế độ liều tối ưu của esomeprazole để ức chế acid dạ dày với ảnh hưởng tối thiểu từ đa hình CYP2C19",{"VOID":960},"Orr WC (2005) Night-time gastro-oesophageal reflux disease: prevalence, hazards, and management. Eur J Gastroenterol Hepatol 17:113–120\nLindberg P, Keeling D, Fryklund J, Andersson T, Lundborg P, Carlsson E (2003) Esomeprazole - enhanced bio-availability, specificity for the proton pump and inhibition of acid secretion. Aliment Pharmacol Ther 17:481–488\nBell NJV, Burget D, Howden CW, Wilkinson J, Hunt RH (1992) Appropriate acid suppression for the management of gastro-oesophageal reflux disease. Digestion 51(Suppl. 1):59–67\nAdachi K, Fujishiro H, Katsube T, Yuki M, Ono M, Kawamura A et al (2001) Predominant nocturnal acid reflux in patients with Los Angeles grade C and D reflux esophagitis. J Gastroenterol Hepatol 16:1191–6\nPeghini PL, Katz PO, Castell DO (1998) Ranitidine controls nocturnal gastric acid breakthrough on omeprazole: a controlled study in normal subjects. Gastroenterology 115:1335–1339\nMiner P Jr, Katz PO, Chen Y, Sostek M (2003) Gastric acid control with esomeprazole, lansoprazole, omeprazole, pantoprazole, and rabeprazole: a five-way crossover study. Am J Gastroenterol 98:2616–2620\nThomson A, Claar-Nilsson C, Hasselgren G, Niazi M, Rohss K, Nyman L (2000) Esomeprazole 40 mg provides more effective acid control than lansoprazole 30 mg during single and repeated administration. Gut 47(Suppl. 3):A63 (Abstract)\nLind T, Rydberg L, Kyleback A et al (2000) Esomeprazole provides improved acid control vs. omeprazole in patients with symptoms of gastro-oesophageal reflux disease. Aliment Pharmacol Ther 14:861–867\nRöhss K, Hasselgren G, Hedenström H (2002) Effect of esomeprazole 40 mg vs. omeprazole 40 mg on 24-hour intragastric pH in patients with symptoms of gastroesophageal reflux disease. Dig Dis Sci 47:954–958\nWilder-Smith C, Röhss K, Lundin C, Rydholm H (2000) Esomeprazole (E) 40 mg provides more effective acid control than pantoprazole (P) 40 mg. Gastroenterology 118:A22–23\nWilder-Smith C, Claar-Nilsson C, Hasselgren G, Röhss K (2002) Esomeprazole 40 mg provides faster and more effective acid control than rabeprazole 20 mg in patients with symptoms of GORD. J Gastroenterol Hepatol 17(Suppl.):A612 (Abstract)\nKatz PO, Castell DO, Chen Y, Andersson T, Sostek MB (2004) Intragastric acid suppression and pharmacokinelics of twice-daily esomeprazole: a randomized, three-way crossover study. Aliment Pharmacol Ther 20:399–406\nGalmiche JP, Bruley S, Varannes DES, Ducrotte P, Sacher-Huvelin S, Vavasseur F et al (2004) Tenatoprazole, a novel proton pump inhibitor with a prolonged plasma half-life: effects on intragastric pH and comparison with esomeprazole in healthy volunteers. Aliment Pharmacol Ther 19:655–662\nPeghini PL, Katz PO, Bracy NA, Castell DO (1998) Nocturnal recovery of gastric acid secretion with twice-daily dosing of proton pump inhibitors. Am J Gastroenterol 93:763–767\nKatz PO, Anderson C, Khoury R, Castell DO (1998) Gastro-oesophageal reflux associated with nocturnal gastric acid breakthrough on proton pump inhibitors. Aliment Pharmacol Ther 12:1231–1234\nKatsube T, Adachi K, Kawamura A, Amano K, Uchida Y, Watanabe M, Kinoshita Y (2000) Helicobacter pylori infection influences nocturnal gastric acid breakthrough. Aliment Pharmacol Ther 14:1049–1056\nStedman CAM, Barclay ML (2000) Review article: comparison of the pharmacokinetics, acid suppression and efficacy of proton pump inhibitors. Aliment Pharmacol Ther 14:963–978\nHassan-Alin M, Andersson T, Niazi M, Röhss K (2005) A pharmacokinetic study comparing single and repeated oral doses of 20 mg and 40 mg omeprazole and its two optical isomers, S-omeprazole (esomeprazole) and R-omeprazole, in healthy subjects. Eur J Clin Pharmacol 60:779–784\nShimatani T, Inoue M, Kuroiwa T, Xu J, Mieno H, Nakamura M, Tazuma S (2006) Acid-suppressive effects of rabeprazole, omeprazole, and lansoprazole at reduced and standard doses: a crossover comparative study in homozygous extensive metabolizers of cytochrome P450 2C19. Clin Pharmacol Therapeutics 79:144–1452\nRobinson M (2004) The pharmacodynamics and pharmacokinetics of proton pump inhibitors – overview and clinical implications. Aliment Pharmacol Ther 20:1–10\nSugimoto M, Furuta T, Shirai N, Kajimura M, Hishida A, Sakurai MO, Ishizaki T (2004) Different dosage regimens of rabeprazole for nocturnal gastric acid inhibition in relation to cytochrome P450 2C19 genotype status. Clin Pharmacol Ther 76:290–301\nSheu B-S, Kao A-W, Cheng H-C, Hunag S-F, Chen T-W, Lu C-C, Wu J-J (2005) Esomeprazole 40 mg twice daily in triple therapy and the efficacy of Helicobacter pylori eradication related to CYP2C19 metabolism. Aliment Pharmacol Ther 21:283–288\nSchwab M, Klotz U, Hofmann U, Schaeffeler E, Leodolter A, Malfertheiner P, Treiber G (2005) Esomeprazole-induced healing of gastroesophageal reflux disease is unrelated to the genotype of CYP2C19: evidence from clinical and pharmacokinetic data. Clin Pharmacol Ther 78:627–634\nDe Morais SMF, Wilkinson GR, Blaisdell J, Nakamura K, Meyer UA, Goldstein JA (1994) The major genetic defect responsible for the polymorphism of S- mephenytoin metabolism in humans. J Biol Chem 269:15419–15422\nAdachi K, Komazawa Y, Fujishiro H, Mihara T, Ono M, Yuki M et al (2003) Nocturnal gastric acid breakthrough during the administration of rabeprazole and ranitidine in Helicobacter pylori-negative subject: effects of different regimens. J Gastroenterol 38:830–835\nWagner JG (1979) Fundamentals of Clinical Pharmacokinetics, 2nd edn. Drug Intelligence Publications, Inc., Hamilton, IL, pp 36–7",{"VOID":962},"10.1007\u002Fs00228-008-0552-0",[299],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs00228-008-0552-0",[966,981,994,1009,1022],{"id":967,"sortIndex":21,"researcher":20,"roles":968,"affiliations":969,"properties":978,"displayName":980,"givenName":20,"familyName":20},"cd5933b0-c115-4692-a0b2-ac16a9861602",[305],[970],{"id":971,"sortIndex":21,"affiliation":972,"properties":20},"b8e24978-3b39-4c26-bca4-d39e5c89325e",{"id":971,"createTime":20,"updateTime":20,"relativeEntities":973,"slug":20,"properties":974,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":977,"statistic":20},[],{"title":975},{"VI":976},"Division of Gastroenterology, Department of Internal Medicine, Taipei Medical University and Hospital, Taipei, Taiwan",[],{"title":979},{"VI":980},"Horng-Yuan 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Chang",{"id":995,"sortIndex":215,"researcher":20,"roles":996,"affiliations":997,"properties":1006,"displayName":1008,"givenName":20,"familyName":20},"44d32bc3-5507-4ab9-9ba5-b95be073a72b",[305],[998],{"id":999,"sortIndex":21,"affiliation":1000,"properties":20},"9b2129f9-e351-43fe-ab92-5a9abb841a00",{"id":999,"createTime":20,"updateTime":20,"relativeEntities":1001,"slug":20,"properties":1002,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1005,"statistic":20},[],{"title":1003},{"VI":1004},"College of Pharmacy, Taipei Medical University, Taipei, Taiwan",[],{"title":1007},{"VI":1008},"Ming-Thau 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ishDate":1282,"publishYear":1274,"citationAnalyzeStatus":1283,"lastCitationAnalyze":1284,"indexDatabases":1285,"openAccess":20,"references":20,"isForceReanalyzing":442},"d9044cc9-1325-4391-8103-2f82814d88b5","2023-12-28T08:33:21.727+00:00","2026-08-25T00:41:50.677+00:00",[],"Synergy-of-fosfomycin-with-other-antibiotics-for-Gram-positive-and-Gram-negative-bacteria",{"abstract":1110,"title":1112,"gsPaper":1114,"references":1116,"doi":1118},{"EN":1111},"The alarming increase in drug resistance and decreased production of new antibiotics necessitate the evaluation of combinations of existing antibiotics. Fosfomycin shows no cross-resistance to other antibiotic classes. Thus, its combination with other antibiotics may potentially show synergy against resistant bacteria. To evaluate the available published evidence regarding the in vitro synergistic activity of fosfomycin with other antibiotic agents against Gram-positive and Gram-negative bacteria. PubMed and the Cochrane Library were searched. Forty-one studies, including 34 (82.9%) conducted\u002Fpublished before 2000, were eligible for inclusion. The relatively limited number of isolates examined and the considerable heterogeneity of the retrieved studies regarding the definitions of synergy and the methodologies used hamper conclusive remarks for specific combinations of fosfomycin with other antibiotics. Yet, in the 27 studies providing data for Gram-positive strains (16 for Staphylococcus aureus, 3 for coagulase-negative staphylococci, 5 for Streptococcus pneumoniae, and 3 for Enterococcus spp.), fosfomycin showed synergy against methicillin-resistant Staphylococcus aureus when combined with cefamandole, cephazolin, ceftriaxone, ciprofloxacin, imipenem, and rifampicin. Data regarding Gram-negative strains reported from 15 studies (12 exclusively for P. aeruginosa, 2 exclusively for Enterobacteriaceae, 1 for both, and 1 for Acinetobacter baumannii) suggested that fosfomycin showed an estimable synergistic effect with gentamicin, amikacin, ceftazidime, cefepime, ciprofloxacin, levofloxacin, and aztreonam against P. aeruginosa. The synergistic combination of fosfomycin with other antibiotics may be a useful alternative treatment option for Gram-negative and Gram-positive infections. Additional studies using more stringent definitions of synergy, and studies reporting on the clinical efficacy of fosfomycin combinations in the current era of high antimicrobial resistance are needed.",{"EN":1113},"Synergy of fosfomycin with other antibiotics for Gram-positive and Gram-negative bacteria",{"VOID":1115},"[\"1248544735987504716\"]",{"VOID":1117},"Falagas ME, Grammatikos AP, Michalopoulos A (2008) Potential of old-generation antibiotics to address current need for new antibiotics. Expert Rev Anti Infect Ther 6:593–600\nFalagas ME, Kasiakou SK (2005) Colistin: the revival of polymyxins for the management of multidrug-resistant gram-negative bacterial infections. Clin Infect Dis 40:1333–1341\nKnottnerus BJ, Nys S, Ter Riet G, Donker G, Geerlings SE, Stobberingh E (2008) Fosfomycin tromethamine as second agent for the treatment of acute, uncomplicated urinary tract infections in adult female patients in the Netherlands? J Antimicrob Chemother 62:356–359\nPatel SS, Balfour JA, Bryson HM (1997) Fosfomycin tromethamine. A review of its antibacterial activity, pharmacokinetic properties and therapeutic efficacy as a single-dose oral treatment for acute uncomplicated lower urinary tract infections. Drugs 53:637–656\nFalagas ME, Giannopoulou KP, Kokolakis GN, Rafailidis PI (2008) Fosfomycin: use beyond urinary tract and gastrointestinal infections. Clin Infect Dis 46:1069–1077\nFalagas ME, Kastoris AC, Karageorgopoulos DE, Rafailidis PI (2009) Fosfomycin for the treatment of infections caused by multidrug-resistant non-fermenting Gram-negative bacilli: a systematic review of microbiological, animal and clinical studies. Int J Antimicrob Agents 34:111–120\nPrakash V, Lewis JS 2nd, Herrera ML, Wickes BL, Jorgensen JH (2009) Oral and parenteral therapeutic options for outpatient urinary infections caused by enterobacteriaceae producing CTX-M extended-spectrum beta-lactamases. Antimicrob Agents Chemother 53:1278–1280\nRodriguez-Bano J, Alcala JC, Cisneros JM et al (2008) Community infections caused by extended-spectrum beta-lactamase-producing Escherichia coli. Arch Intern Med 168:1897–1902\nYamada S, Hyo Y, Ohmori S, Ohuchi M (2007) Role of ciprofloxacin in its synergistic effect with fosfomycin on drug-resistant strains of Pseudomonas aeruginosa. Chemotherapy 53:202–209\nSahuquillo Arce JM, Colombo Gainza E, Gil Brusola A, Ortiz Estevez R, Canton E, Gobernado M (2006) In vitro activity of linezolid in combination with doxycycline, fosfomycin, levofloxacin, rifampicin and vancomycin against methicillin-susceptible Staphylococcus aureus. Rev Esp Quimioter 19:252–257\nMikuniya T, Kato Y, Kariyama R, Monden K, Hikida M, Kumon H (2005) Synergistic effect of fosfomycin and fluoroquinolones against Pseudomonas aeruginosa growing in a biofilm. Acta Med Okayama 59:209–216\nPruekprasert P, Tunyapanit W (2005) In vitro activity of fosfomycin-gentamicin, fosfomycin-ceftazidime, fosfomycin-imipenem and ceftazidime-gentamicin combinations against ceftazidime-resistant Pseudomonas aeruginosa. SE Asian J Trop Med Public Health 36:1239–1242\nNakazawa H, Kikuchi Y, Honda T, Isago T, Nozaki M (2003) Enhancement of antimicrobial effects of various antibiotics against methicillin-resistant Staphylococcus aureus (MRSA) by combination with fosfomycin. J Infect Chemother 9:304–309\nOkazaki M, Suzuki K, Asano N et al (2002) Effectiveness of fosfomycin combined with other antimicrobial agents against multidrug-resistant Pseudomonas aeruginosa isolates using the efficacy time index assay. J Infect Chemother 8:37–42\nGrif K, Dierich MP, Pfaller K, Miglioli PA, Allerberger F (2001) In vitro activity of fosfomycin in combination with various antistaphylococcal substances. J Antimicrob Chemother 48:209–217\nHayami H, Goto T, Kawahara M, Ohi Y (1999) Activities of beta-lactams, fluoroquinolones, amikacin and fosfomycin alone and in combination against Pseudomonas aeruginosa isolated from complicated urinary tract infections. J Infect Chemother 5:130–138\nTraub WH, Scheidhauer R, Leonhard B, Bauer D (1998) Surveillance of Pseudomonas aeruginosa in intensive care units: clusters of nosocomial cross-infection and encounter of a multiple-antibiotic resistant strain. Chemotherapy 44:243–259\nDubrous P, Cavallo JD, Buisson Y (1997) Sensitivity to fosfomycin of multiresistant serotype 012 Pseudomonas aeruginosa. Multicenter study. Pathol Biol (Paris) 45:472–478\nFerrara A, Dos Santos C, Cimbro M, Gialdroni Grassi G (1997) Effect of different combinations of sparfloxacin, oxacillin, and fosfomycin against methicillin-resistant staphylococci. Eur J Clin Microbiol Infect Dis 16:535–537\nTessier F, Quentin C (1997) In vitro activity of fosfomycin combined with ceftazidime, imipenem, amikacin, and ciprofloxacin against Pseudomonas aeruginosa. Eur J Clin Microbiol Infect Dis 16:159–162\nTotsuka K, Uchiyama T, Shimizu K, Kanno Y, Takata T, Yoshida T (1997) In vitro combined effects of fosfomycin and β-lactam antibiotics against penicillin-resistant Streptococcus pneumoniae. J Infect Chemother 3:49–54\nMartinez-Martinez L, Rodriguez G, Pascual A, Suarez AI, Perea EJ (1996) In-vitro activity of antimicrobial agent combinations against multiresistant Acinetobacter baumannii. J Antimicrob Chemother 38:1107–1108\nKikuchi K, Totsuka K, Shimizu K, Ishii T, Yoshida T, Orikasa Y (1995) Effects of combination of benzylpenicillin and fosfomycin on penicillin-resistant Streptococcus pneumoniae. Microb Drug Resist 1:185–189\nPestel M, Martin E, Aucouturier C, Lemeland JF, Caron F (1995) In vitro interactions between different beta-lactam antibiotics and fosfomycin against bloodstream isolates of enterococci. Antimicrob Agents Chemother 39:2341–2344\nDoit CP, Bonacorsi SP, Fremaux AJ et al (1994) In vitro killing activities of antibiotics at clinically achievable concentrations in cerebrospinal fluid against penicillin-resistant Streptococcus pneumoniae isolated from children with meningitis. Antimicrob Agents Chemother 38:2655–2659\nDrugeon HB, Caillon J, Juvin ME (1994) In-vitro antibacterial activity of fusidic acid alone and in combination with other antibiotics against methicillin-sensitive and -resistant Staphylococcus aureus. J Antimicrob Chemother 34:899–907\nWatine J, Bourrel C, Dubourdieu B et al (1994) Susceptibility of multiresistant serotype 012 Pseudomonas aeruginosa to fosfomycin in combination with other antibiotics. Pathol Biol (Paris) 42:293–295\nBarakett V, Lesage D, Delisle F et al (1992) Bacteriostatic activity and killing curves of eight antibiotics against seven strains of penicillin G-resistant pneumococci. Pathol Biol (Paris) 40:483–491\nHamilton-Miller JM (1992) In vitro activity of fosfomycin against ‘problem’ gram-positive cocci. Microbios 71:95–103\nMatsuda K, Asahi Y, Sanada M, Nakagawa S, Tanaka N, Inoue M (1991) In-vitro activity of imipenem combined with beta-lactam antibiotics for methicillin-resistant Staphylococcus aureus. J Antimicrob Chemother 27:809–815\nChang SC, Hsieh WC, Luh KT, Ho SW (1989) Effects of antibiotic combinations on methicillin-resistant Staphylococcus aureus in vitro. Taiwan Yi Xue Hui Za Zhi 88:488–492\nGatermann S, Schulz E, Marre R (1989) The microbiological efficacy of the combination of fosfomycin and vancomycin against clinically relevant staphylococci. Infection 17:35–37\nRice LB, Eliopoulos GM, Moellering RC Jr (1989) In vitro synergism between daptomycin and fosfomycin against Enterococcus faecalis isolates with high-level gentamicin resistance. Antimicrob Agents Chemother 33:470–473\nFigueredo VM, Neu HC (1988) Synergy of ciprofloxacin with fosfomycin in vitro against Pseudomonas isolates from patients with cystic fibrosis. J Antimicrob Chemother 22:41–50\nCourcol RJ, Martin GR (1987) In-vitro activity of the combination of ceftriaxone and fosfomycin against staphylococci. J Antimicrob Chemother 19:276–278\nDavid C, Combremont AG (1987) In vitro study of a ceftriaxone-fosfomycin combination on 55 strains of methicillin-sensitive and heterogeneous methicillin-resistant Staphylococcus aureus. Pathol Biol (Paris) 35:507–509\nMay T, Weber M, Gerard A et al (1987) Treatment of post-traumatic and post-neurosurgical bacterial meningitis with ceftriaxone alone or in combination with fosfomycin. Pathol Biol (Paris) 35:839–842\nUllmann U (1987) Synergism between ciprofloxacin and fosfomycin in vitro. Infection 15:264\nDebbia E, Varaldo PE, Schito GC (1986) In vitro activity of imipenem against enterococci and staphylococci and evidence for high rates of synergism with teicoplanin, fosfomycin, and rifampin. Antimicrob Agents Chemother 30:813–815\nStahl JP, Croize J, Baud A et al (1986) Treatment of neurosurgical bacterial meningitis using the combination of ceftriaxone-fosfomycin. Pathol Biol (Paris) 34:479–482\nUtsui Y, Ohya S, Magaribuchi T, Tajima M, Yokota T (1986) Antibacterial activity of cefmetazole alone and in combination with fosfomycin against methicillin- and cephem-resistant Staphylococcus aureus. Antimicrob Agents Chemother 30:917–922\nAlvarez S, Jones M, Berk SL (1985) In vitro activity of fosfomycin, alone and in combination, against methicillin-resistant Staphylococcus aureus. Antimicrob Agents Chemother 28:689–690\nPortier H, Kazmierczak A, Lucht F, Tremeaux JC, Chavanet P, Duez JM (1985) Cefotaxime in combination with other antibiotics for the treatment of severe methicillin-resistant staphylococcal infections. Infection 13(Suppl 1):S123–S128\nFosse T, David MF, Duluc F, Darmusey D, Tamalet C, Toga B (1984) In vitro study of the cefamandole-fosfomycin combination against methicillin-resistant staphylococci. Pathol Biol (Paris) 32:528–531\nTakahashi K, Kanno H (1984) Synergistic activities of combinations of beta-lactams, fosfomycin, and tobramycin against Pseudomonas aeruginosa. Antimicrob Agents Chemother 26:789–791\nTremeaux JC, Duez JM, Pechinot A, Sautreaux JL, Thierry A, Kazmierczak A (1983) [Importance of the cefotaxime-fosfomycin combination. Apropos of a case of meningitis due to heterogeneously resistant Staphylococcus aureus]. Agressologie 24:169–171\nOlay T, Rodriguez A, Oliver LE, Vicente MV, Quecedo MC (1978) Interaction of fosfomycin with other antimicrobial agents: in vitro and in vivo studies. J Antimicrob Chemother 4:569–576\nPerea EJ, Torres MA, Borobio MV (1978) Synergism of fosfomycin-ampicillin and fosfomycin-chloramphenicol against Salmonella and Shigella. Antimicrob Agents Chemother 13:705–709\nBaquero F, Hortelano JG, Navarro M et al (1977) Antibiotherapy of Serratia marcescens septicemia in children. Chemotherapy 23(Suppl 1):416–422\nWarren JW, Abrutyn E, Hebel JR, Johnson JR, Schaeffer AJ, Stamm WE (1999) Guidelines for antimicrobial treatment of uncomplicated acute bacterial cystitis and acute pyelonephritis in women. Infectious Diseases Society of America (IDSA). Clin Infect Dis 29:745–758\nHernandez M, Garcia J, Munoz J (2009) [In vitro activity of fosfomycin against ESBL-producing enterobacteria of urinary origin.]. Rev Esp Quimioter 22:25–29\nZahar JR, Lortholary O, Martin C, Potel G, Plesiat P, Nordmann P (2009) Addressing the challenge of extended-spectrum beta-lactamases. Curr Opin Investig Drugs 10:172–180\nEllington MJ, Livermore DM, Pitt TL, Hall LM, Woodford N (2006) Mutators among CTX-M beta-lactamase-producing Escherichia coli and risk for the emergence of fosfomycin resistance. J Antimicrob Chemother 58:848–852\nHorii T, Kimura T, Sato K, Shibayama K, Ohta M (1999) Emergence of fosfomycin-resistant isolates of Shiga-like toxin-producing Escherichia coli O26. Antimicrob Agents Chemother 43:789–793\nNilsson AI, Berg OG, Aspevall O, Kahlmeter G, Andersson DI (2003) Biological costs and mechanisms of fosfomycin resistance in Escherichia coli. Antimicrob Agents Chemother 47:2850–2858\nRoussos N, Karageorgopoulos DE, Samonis G, Falagas ME (2009) Clinical significance of the pharmacokinetic and pharmacodynamic characteristics of fosfomycin for the treatment of patients with systemic infections. Int J Antimicrob Agents 34:506–515\nMonden K, Ando E, Iida M, Kumon H (2002) Role of fosfomycin in a synergistic combination with ofloxacin against Pseudomonas aeruginosa growing in a biofilm. J Infect Chemother 8:218–226\nMarchese A, Bozzolasco M, Gualco L, Debbia EA, Schito GC, Schito AM (2003) Effect of fosfomycin alone and in combination with N-acetylcysteine on E. coli biofilms. Int J Antimicrob Agents 22(Suppl 2):95–100\nInouye S, Niizato T, Komiya I, Yuda Y, Yamada Y (1982) Mode of protective action of fosfomycin against dibekacin-induced nephrotoxicity in the dehydrated rats. J Pharmacobiodyn 5:941–950\nYoshiyama Y, Yazaki T, Wong PC, Beauchamp D, Kanke M (2001) The effect of fosfomycin on glycopeptide antibiotic-induced nephrotoxicity in rats. J Infect Chemother 7:243–246\nLeach JL, Wright CG, Edwards LB, Meyerhoff WL (1990) Effect of topical fosfomycin on polymyxin B ototoxicity. Arch Otolaryngol Head Neck Surg 116:49–53\nBlacky A, Makristathis A, Apfalter P, Willinger B, Rotter ML, Hirschl AM (2005) In vitro activity of fosfomycin alone and in combination with amoxicillin, clarithromycin and metronidazole against Helicobacter pylori compared with combined clarithromycin and metronidazole. Eur J Clin Microbiol Infect Dis 24:276–279",{"VOID":1119},"10.1007\u002Fs00228-010-0794-5","2024-05-16T02:08:58.117+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs00228-010-0794-5",[1123,1138,1161,1174,1187],{"id":1124,"sortIndex":21,"researcher":20,"roles":1125,"affiliations":1126,"properties":1135,"displayName":1137,"givenName":20,"familyName":20},"e0ff973d-dcf0-4030-88be-aa360c3db3e2",[305],[1127],{"id":1128,"sortIndex":21,"affiliation":1129,"properties":20},"151a3be8-f043-4e37-9f20-a6966cae961f",{"id":1128,"createTime":20,"updateTime":20,"relativeEntities":1130,"slug":20,"properties":1131,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1134,"statistic":20},[],{"title":1132},{"VI":1133},"Alfa Institute of Biomedical Sciences (AIBS), Athens, Greece",[],{"title":1136},{"VI":1137},"Antonia C. 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"relativeEntities":1290,"slug":1291,"properties":1292,"entityType":294,"verifyStatus":295,"verifyTime":1303,"verifyNote":297,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1304,"fullTextUrl":20,"authors":1305,"publicationType":382,"publisherRelationship":1356,"citationCount":21,"citationInfo":1412,"publishDate":1415,"publishYear":1413,"citationAnalyzeStatus":1416,"lastCitationAnalyze":1417,"indexDatabases":1418,"openAccess":20,"references":20,"isForceReanalyzing":442},"68291a87-2a43-4328-8135-18fe40881f35","2024-02-06T23:26:17.578+00:00","2026-08-24T23:16:14.938+00:00",[],"Immediate-haemodynamic-effects-of-prenalterol-a-new-adrenergic-beta-1-receptor-agonist-in-healthy-volunteers",{"abstract":1293,"title":1295,"gsPaper":1297,"references":1299,"doi":1301},{"EN":1294},"The acute haemodynamic effects of prenalterol, a selective adrenergic beta-1-receptor agonist, were studied in eight healthy male volunteers. Prenalterol was administered i.v. in five increasing doses to a cumulative dose of 5.55 mg. After the last dose of prenalterol, three doses of the selective adrenergic beta-1-receptor antagonist metoprolol were administered i.v. to a cumulative dose of 17.5 mg. After each dose, cardiac output (CO), stroke volume (SV), blood pressure (BP), heart rate (HR), systolic time intervals (STI) and forearm blood flow (FBF) were determined. Prenalterol had the following effects: CO was significantly increased by 21.0% after the fourth dose, but the fifth dose did not further change CO. SV was unchanged after the first four doses, but after the fifth dose a significant decrease in SV of 7.0% was seen. Mean BP was increased significantly by 7.7%, but diastolic BP remained unchanged. HR was increased by 28.4%. Total peripheral resistance was reduced by 8.8%. STI were reduced significantly after the second dose, which indicates that prenalterol has a positive inotropic action. FBF was increased significantly after the fourth dose. After the third dose of metoprolol, the CO, SV, mean BP, HR, STI and FBF had returned to their control values. It is concluded that prenalterol has positive inotropic and chronotropic effects on the myocardium, and that metoprolol is a specific antidote.",{"EN":1296},"Immediate haemodynamic effects of prenalterol, a new adrenergic beta-1-receptor agonist, in healthy volunteers",{"VOID":1298},"[\"9863996843275999924\"]",{"VOID":1300},"Ariniego R, Waagstein F, Mombay B, Hjalmarson Å (1979) Haemodynamic effects of a new β-1-receptor agonist in acute myocardial infarction. Br Heart J 42: 139–146\nCarlsson E, Dahlöf C, Hedberg A, Persson H, Tångstrand B (1977) Differentiation of cardiac chronotropic and inotropic effects of β-adrenoceptor agonists. Arch Pharmacol 300: 101–105\nHallböök T, Månsson B, Nilsén RA (1970) A strain gauge plethysmograph with electrical calibration. Scand J Clin Lab Invest 25: 413–418\nJohnsson G, Jordö L, Lundborg P, Rönn O, Welin-Fogelberg I, Wikstrand J (1978) Haemodynamic and tolerance studies in man of a new orally active, selective β-1-adrenoceptor agonist H 80\u002F62. Eur. J Clin Pharmacol 13: 163–170\nKnaus M, Pfister B, Dubach UC, Imhof PR (1978) Human Pharmacology studies with a new orally active stimulant of cardiac adrenergic beta-receptors. Am Heart J 95: 602–609\nKubicek WG, Kottke FJ, Ramos MU, Patterson RP, Witsoe DA, Labree JW, Remole W, Layman TE, Schoening H, Garamella JT (1974) The Minnesota impedance cardiograph — theory and applications. Biomed Eng 9: 410–416\nNelson RR, Globel FL, Jorgensen GR, Wang K, Wang Y, Taylor HL (1974) Haemodynamic predictors of myocardial oxygen consumption during static and dynamic exercise. Circulation 50: 1179–1189\nReiz S, Nath S, Pantén N (1979) Prenalterol, a β-1-adrenoceptor agonist in the treatment of hypertension, induced by high thoracic epidural block in man. Acta Anaesthesiol Scand 23: 93–96\nRönn O, Graffner C, Johnsson G, Jordö L, Lundborg P, Wikstrand J (1979) Haemodynamic effects and some pharmacokinetics of a new selective beta-1-adrenoceptor agonist, prenalterol and its interaction with metoprolol in man. Eur J Clin Pharmacol 15: 9–13\nSonnenblick EH, Frishman WH, LeJemtal TH (1979) Dobutamine: a new synthetic cardioactive sympathetic amine N Engl J Med 300: 17–22\nSvendsen TL, Hartling O, Trap-Jensen J (1979) Immediate haemodynamic effects of propranolol, practolol, pindolol, atenolol and ICI 89.406 in healthy volunteers. Eur J Clin Pharmacol 15: 223–228\nScott DHT, Arthur GR, Boyes RN, Scott DB (1979) Cardiovascular effects of prenalterol (H 133\u002F22) in normal man. Br J Clin Pharmacol 7: 365–370\nWeissler AM, Harris WS, Schoenfeld CD (1969) Bedside technics for the evaluation of ventricular function in man. Am J Cardiol 23: 577–583",{"VOID":1302},"10.1007\u002FBF00563002","2024-06-24T03:38:12.010+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00563002",[1306,1330,1343],{"id":1307,"sortIndex":21,"researcher":20,"roles":1308,"affiliations":1309,"properties":1327,"displayName":1329,"givenName":20,"familyName":20},"f628f3c2-cb87-4a90-a148-e16488e82690",[305],[1310,1318],{"id":1311,"sortIndex":21,"affiliation":1312,"properties":20},"4270dfc3-4476-4d7f-9487-573cdf4f0e2b",{"id":1311,"createTime":20,"updateTime":20,"relativeEntities":1313,"slug":20,"properties":1314,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1317,"statistic":20},[],{"title":1315},{"VI":1316},"Department of Clinical Physiology, Frederiksberg Hospital, Copenhagen, Denmark",[],{"id":1319,"sortIndex":317,"affiliation":1320,"properties":1326},"f3fe8fa9-154c-48d9-978a-8ec1bf2455bd",{"id":1319,"createTime":20,"updateTime":20,"relativeEntities":1321,"slug":20,"properties":1322,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1325,"statistic":20},[],{"title":1323},{"VI":1324},"Department of Medicine P, Bispebjerg Hospital Bispebjerg Bakke, Copenhagen NV, Denmark",[],{},{"title":1328},{"VI":1329},"T. 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cytoplasmic antibody (ANCA)–associated vasculitis is a rare autoimmune disease. Mycophenolic acid (MPA) is widely used for ANCA-associated nephritis (AAN) but with large pharmacokinetic variability. This study aims to investigate clinical factors impacting MPA disposition in pediatric AAN. We retrospectively collected 391 MPA concentrations from 25 children diagnosed with AAN. A population pharmacokinetic model was developed to explore the potential effects of demographics and biochemical covariates on MPA. Monte Carlo simulations were performed to optimize dosage regimen. MPA pharmacokinetics best fitted a two-compartment model with first-order absorption and linear elimination. The pharmacokinetic parameters for Ka, CL\u002FF, Vc\u002FF, Vp\u002FF, and Q\u002FF were 0.45 h−1, 9.86 L\u002Fh, 19.69 L, 408.32 L, and 23.01 L\u002Fh. Dosage form significantly affected drug absorption. CL\u002FF significantly decreased with increasing cystatin C, while decreasing with myeloperoxidase. Cystatin C was superior to serum creatinine in predicting apparent clearance of MPA. A dose regimen of 650 mg\u002Fm2 twice daily was required to achieve target exposure in children with normal renal function and no inflammation. The combined effects of myeloperoxidase concentration and renal function resulted in a sixfold range of MPA dose. This was the first study of MPA population pharmacokinetic model in children with AAN. Myeloperoxidase was not only a biomarker of AAN, but also an inflammatory factor to impact drug CL. The influence of renal function and underlying diseases on drug metabolism should be fully considered in personalized medication for AAN.",{"EN":1429},"Population pharmacokinetic and dose optimization of mycophenolic acid in children with anti-neutrophilic cytoplasmic antibody-associated nephritis",{"VOID":1431},"[\"13077296120387028819\"]",{"VOID":1433},"Geetha D, Jefferson JA (2020) ANCA-associated vasculitis: core curriculum. Am J Kidney Dis 75(1):124–137\nHaris Á, Dolgos S, Polner K (2017) Therapy and prognosis of ANCA-associated vasculitis from the clinical nephrologist’s perspective. Int Urol Nephrol 49(1):91–102\nYates M, Watts RA, Bajema IM et al (2016) EULAR\u002FERA-EDTA recommendations for the management of ANCA-associated vasculitis. Ann Rheum Dis 75(9):1583–1594\nJones RB, Hiemstra TF, Ballarin J et al (2019) Mycophenolate mofetil versus cyclophosphamide for remission induction in ANCA-associated vasculitis: a randomised, non-inferiority trial. Ann Rheum Dis 78(3):399–405\nKiang TKL, Ensom MHH (2018) Population pharmacokinetics of mycophenolic acid: an update. Clin Pharmacokinet 57(5):547–558\nJoy MS, Hilliard T, Hu Y, Hogan SL, Wang J, Falk RJ, Smith PC (2009) Influence of clinical and demographic variables on mycophenolic acid pharmacokinetics in antineutrophil cytoplasmic antibody-associated vasculitis. Ann Pharmacother 43(6):1020–1027\nSchaier M, Scholl C, Scharpf D, Schmitt WH, Schwenger V, Zeier M, Sommerer C (2015) High interpatient variability in response to mycophenolic acid maintenance therapy in patients with ANCA-associated vasculitis. Nephrol Dial Transplant 30(Suppl 1):i138-145\nChaigne B, Gatault P, Darrouzain F et al (2014) Mycophenolate mofetil in patients with anti-neutrophil cytoplasmic antibody-associated vasculitis: a prospective pharmacokinetics and clinical study. Clin Exp Immunol 176(2):172–179\nSalvador CL, Tøndel C, Rowe AD, Bjerre A, Brun A, Brackman D, Mørkrid L (2019) Estimating glomerular filtration rate in children: evaluation of creatinine- and cystatin C-based equations. Pediatr Nephrol 34(2):301–311\nWoillard JB, Bader-Meunier B, Salomon R et al (2014) Pharmacokinetics of mycophenolate mofetil in children with lupus and clinical findings in favour of therapeutic drug monitoring. Br J Clin Pharmacol 78(4):867–876\nLea-Henry TN, Carland JE, Stocker SL, Sevastos J, Roberts DM (2018) Clinical pharmacokinetics in kidney disease: fundamental principles. Clin J Am Soc Nephrol 13(7):1085–1095\nde Winter BC, van Gelder T, Glander P et al (2008) Population pharmacokinetics of mycophenolic acid: a comparison between enteric-coated mycophenolate sodium and mycophenolate mofetil in renal transplant recipients. Clin Pharmacokinet 47(12):827–838\nRong Y, Jun H, Kiang TKL (2021) Population pharmacokinetics of mycophenolic acid in paediatric patients. Br J Clin Pharmacol 87(4):1730–1757\nShemesh O, Golbetz H, Kriss JP, Myers BD (1985) Limitations of creatinine as a filtration marker in glomerulopathic patients. Kidney Int 28(5):830–838\nKidney Disease: Improving global outcomes KDIGO CKD work group (2013) KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl 3(1):1–150. https:\u002F\u002Fwww.sciencedirect.com\u002Fjournal\u002Fkidney-international-supplements\u002Fvol\u002F3\u002Fissue\u002F1\nBrou NA, Jacqz-Aigrain E, Zhao W (2015) Cystatin C as a potential biomarker for dosing of renally excreted drugs. Br J Clin Pharmacol 80(1):20–27\nBarreto EF, Rule AD, Murad MH et al (2019) Prediction of the renal elimination of drugs with cystatin C vs creatinine: a systematic review. Mayo Clin Proc 94(3):500–514\nDownes KJ, Zane NR, Zuppa AF (2020) Effect of Cystatin C on vancomycin clearance estimation in critically Ill children using a population pharmacokinetic modeling approach. Ther Drug Monit 42(6):848–855\nTan SJ, Cockcroft M, Page-Sharp M, Arendts G, Davis TME, Moore BR, Batty KT, Salman S, Manning L (2020) Population pharmacokinetic study of ceftriaxone in elderly patients, using cystatin C-based estimates of renal function to account for frailty. Antimicrob Agents Chemother 64(10):e00874-e920\nBjörk J, Nyman U, Berg U et al (2019) Validation of standardized creatinine and cystatin C GFR estimating equations in a large multicentre European cohort of children. Pediatr Nephrol 34(6):1087–1098\nCouser WG, Johnson RJ (2015) What is myeloperoxidase doing in ANCA-associated glomerulonephritis? Kidney Int 88(5):938–940\nShah RR, Smith RL (2015) Inflammation-induced phenoconversion of polymorphic drug metabolizing enzymes: hypothesis with implications for personalized medicine. Drug Metab Dispos 43(3):400–410\nLamba V, Sangkuhl K, Sanghavi K, Fish A, Altman RB, Klein TE (2014) PharmGKB summary: mycophenolic acid pathway. Pharmacogenet Genomics 24(1):73–79\nKnights KM, Rowland A, Miners JO (2013) Renal drug metabolism in humans: the potential for drug-endobiotic interactions involving cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT). Br J Clin Pharmacol 76(4):587–602\nde Jong LM, Jiskoot W, Swen JJ, Manson ML (2020) Distinct effects of inflammation on cytochrome P450 regulation and drug metabolism: lessons from experimental models and a potential role for pharmacogenetics. Genes (Basel) 11(12):1509\nRichardson TA, Sherman M, Kalman D, Morgan ET (2006) Expression of UDP-glucuronosyltransferase isoform mRNAs during inflammation and infection in mouse liver and kidney. Drug Metab Dispos 34(3):351–353\nKawase A, Norikane S, Okada A, Adachi M, Kato Y, Iwaki M (2014) Distinct alterations in ATP-binding cassette transporter expression in liver, kidney, small intestine, and brain in adjuvant-induced arthritic rats. J Pharm Sci 103(8):2556–2564\nEvers R, Piquette-Miller M, Polli JW et al (2018) Disease-associated changes in drug transporters may impact the pharmacokinetics and\u002For toxicity of drugs: a white paper from the international transporter consortium. Clin Pharmacol Ther 104(5):900–915\nUdy AA, Roberts JA, Lipman J (2011) Implications of augmented renal clearance in critically ill patients. Nat Rev Nephrol 7(9):539–543\nBarau C, Barrail-Tran A, Hemerziu B, Habes D, Taburet AM, Debray D, Furlan V (2011) Optimization of the dosing regimen of mycophenolate mofetil in pediatric liver transplant recipients. Liver Transpl 17(10):1152–1158\nBarau C, Mellos A, Chhun S, Lacaille F, Furlan V (2017) Pharmacokinetics of mycophenolic acid and dose optimization in children after intestinal transplantation. Ther Drug Monit 39(1):37–42\nWeber LT, Hoecker B, Armstrong VW, Oellerich M, Tönshoff B (2008) Long-term pharmacokinetics of mycophenolic acid in pediatric renal transplant recipients over 3 years posttransplant. Ther Drug Monit 30(5):570–575",{"VOID":1435},"10.1007\u002Fs00228-021-03265-z","2024-06-23T11:38:41.145+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs00228-021-03265-z",[1439,1454,1467,1484],{"id":1440,"sortIndex":21,"researcher":20,"roles":1441,"affiliations":1442,"properties":1451,"displayName":1453,"givenName":20,"familyName":20},"a3876597-c383-423e-9d39-f21aa0021dea",[305],[1443],{"id":1444,"sortIndex":21,"affiliation":1445,"properties":20},"0351bf9d-2b0f-407a-9973-20ee71f8270c",{"id":1444,"createTime":20,"updateTime":20,"relativeEntities":1446,"slug":20,"properties":1447,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1450,"statistic":20},[],{"title":1448},{"VI":1449},"Department of Pharmacy, Children’s Hospital of Fudan University, National Children’s Medical Center, Shanghai, China",[],{"title":1452},{"VI":1453},"Ziwei 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                       Objective: The pharmacokinetics of orally and intravenously administered valsartan were determined in two studies. In a first pilot study, three i.v. doses of valsartan were given in an ascending manner (5, 10 and 20 mg) to evaluate tolerability and basic pharmacokinetics of the i.v. formulation. In a second study, the absolute bioavailability of 80 mg valsartan from a capsule and a buffered solution was compared with a 20 mg i.v. dose. Methods: The concentrations of valsartan in plasma and urine were measured using HPLC. The disposition of valsartan after an i.v. dose was characterized by biphasic decay kinetics, with a distribution phase (half-life 1.0 h), followed by a longer elimination phase (half-life 9.5 h). The volume of distribution at steady state was 16.9 l, and the total body clearance 2.2 l · h−1. 29% of the i.v. dose was recovered unchanged in the urine.  Results: Plasma levels peaked 2 h after oral administration of the 80 mg capsule. Thereafter, plasma levels declined biexponentially with a terminal t1\u002F2 of 7.0 h. Cmax was reached 1 h after administration of the solution, and t1\u002F2 was 7.5 h. On average 7.3% (capsule) and 12.6% (solution) of the dose was excreted in the urine as the unchanged drug. The fraction of dose absorbed and systemically available after oral administration was 0.23 for the capsule and 0.39 for the solution, based on AUC. Absorption appeared to follow two first-order processes. The first phase was rapid, with a half-life of 0.5 h and 0.9 h for solution and capsule, respectively. The slower absorption phase was characterized by a half-life of 6.5 h for the solution and 3.5 h for the capsule. 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