Bibliografías temáticas / Rabeprazole

Literatura académica sobre el tema "Rabeprazole"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 20 de febrero de 2023

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Artículos de revistas sobre el tema "Rabeprazole"

1

Cusimano, Joseph. "Rabeprazole". WikiJournal of Medicine 9, n.º 1 (2022): 6. http://dx.doi.org/10.15347/wjm/2022.006.

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Rabeprazole is a proton pump inhibitor that suppresses gastric acid production in the stomach. Available under different brand name products as well as in a variety of combination products, rabeprazole has several medical uses concerning the management of problems of pathological gastric acid. Rabeprazole's adverse effects tend to be mild but can be serious, including deficiencies in essential nutrients, rare incidences of liver damage, and immune-mediated reactions. As a class effect, rabeprazole can increase the risk for osteoporosis, serious infections (including Clostridium difficile infections), and kidney damage. Rabeprazole can theoretically contribute to numerous drug interactions, mediated both through its metabolic properties and its direct effect on acid in the stomach, though its potential for clinically meaningful drug interactions is low. Like other medications in the proton pump inhibitor class, rabeprazole's mechanism of action involves the irreversible inhibition of proton pumps in the stomach, which are responsible for gastric acid production. Rabeprazole has a number of chemical metabolites, though it is primarily degraded by non-enzymatic metabolism and excreted in the urine. Genetic differences in a person's drug-metabolizing enzymes may theoretically affect individual responses to rabeprazole therapy, though the clinical significance of this interaction is unlikely in comparison to other proton pump inhibitors. The purpose of this review is to provide an up-to-date monograph on rabeprazole.
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&NA;. "Rabeprazole". Reactions Weekly &NA;, n.º 1394 (marzo de 2012): 35. http://dx.doi.org/10.2165/00128415-201213940-00129.

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&NA;. "Rabeprazole". Reactions Weekly &NA;, n.º 1159 (julio de 2007): 25. http://dx.doi.org/10.2165/00128415-200711590-00075.

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&NA;. "Rabeprazole". Reactions Weekly &NA;, n.º 1373 (octubre de 2011): 27. http://dx.doi.org/10.2165/00128415-201113730-00091.

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Prakash, Amitabh y Diana Faulds. "Rabeprazole". Drugs 55, n.º 2 (1998): 261–67. http://dx.doi.org/10.2165/00003495-199855020-00009.

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Bank, Simmy. "Rabeprazole". Drugs 55, n.º 2 (1998): 268. http://dx.doi.org/10.2165/00003495-199855020-00010.

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Takeguchi, Noriaki. "Rabeprazole". Drugs 55, n.º 2 (1998): 268. http://dx.doi.org/10.2165/00003495-199855020-00011.

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Langtry, Heather D. y Anthony Markham. "Rabeprazole". Drugs 58, n.º 4 (1999): 725–42. http://dx.doi.org/10.2165/00003495-199958040-00014.

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Carswell, Christopher I. y Karen L. Goa. "Rabeprazole". Drugs 61, n.º 15 (2001): 2327–56. http://dx.doi.org/10.2165/00003495-200161150-00016.

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Baldwin, Claudine M. y Susan J. Keam. "Rabeprazole". Drugs 69, n.º 10 (julio de 2009): 1373–401. http://dx.doi.org/10.2165/00003495-200969100-00007.

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Tesis sobre el tema "Rabeprazole"

1

Garcia, Cassia Virginia. "Validação de métodos analíticos e estudo da estabilidade de rabeprazol sódico". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2007. http://hdl.handle.net/10183/10382.

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Neste trabalho, foram desenvolvidos e validados métodos qualitativos e quantitativos para o controle de qualidade de rabeprazol sódico, um inibidor da bomba de prótons. O fármaco apresenta eficácia comprovada na cicatrização, alívio de sintomas e prevenção de recidivas de úlceras pépticas e doença do refluxo gastroesofágico. A substância química de referência utilizada nas análises foi caracterizada por espectrofotometria no infravermelho e por espectroscopia de ressonância magnética nuclear. A análise qualitativa foi realizada por cromatografia em camada delgada, espectrofotometria no ultravioleta (UV), cromatografia líquida de alta eficiência (CLAE) e eletroforese capilar (EC), possibilitando a identificação das amostras. Os métodos quantitativos validados foram: UV, espectrofotometria ultravioleta derivada de primeira ordem, CLAE e EC. Todos demonstraram ser específicos, lineares, precisos, exatos e sensíveis. Além disso, o teste de dissolução para os comprimidos revestidos contendo rabeprazol foi desenvolvido e validado, obtendo-se um perfil de dissolução satisfatório. Outro objetivo deste trabalho foi o estudo da estabilidade de rabeprazol. Os fatores de degradação avaliados foram a temperatura (50 e 80 ºC), a hidrólise em meio ácido (HCl 0,01-0,1M), a oxidação por peróxido de hidrogênio e a luz (UVC-254 nm e metal haleto). De modo geral, o fármaco demonstrou ser sensível a todos os fatores, principalmente quando em solução, mas de forma mais intensa frente à acidez e luz. A cinética de fotodegradação em metanol frente à lâmpada UVC foi determinada, indicando tratar-se de uma reação de ordem zero. Três produtos da fotodegradação foram isolados e identificados por ressonância magnética nuclear: 1H-benzimidazol, 1,3-diidro-benzimidazol-2-ona e [4-(3-metoxipropoxi)- 3-metil-piridina-2-il]metanol. Alguns resultados sugerem que o 1,3-diidrobenzimidazol- 2-ona também é formado na degradação em meio ácido.
In this work, qualitative and quantitative methods were developed and validated for the quality control of rabeprazole sodium, a proton pump inhibitor. The drug has proven efficacy in healing, symptoms relief and prevention of relapse of gastric ulcer and gastro-oesophageal reflux disease. The substance used as reference standard in the analysis was characterized by infrared spectroscopy and nuclear magnetic resonance. The qualitative analysis was performed by thin layer chromatography, UV spectrophotometry, high performance liquid chromatography (HPLC) and capillary electrophoresis (CE), allowing the identification of samples. The quantitative methods validated were: UV, first-order derivative spectrophotometry, HPLC and CE. All of them demonstrated to be specific, linear, precise, accurate and sensitive. Besides, the dissolution test for rabeprazole coated tablets was developed and validate, obtaining a satisfactory dissolution profile. Another objective of this work was the study of rabeprazole stability. The degradation factors evaluated were the temperature (50 and 80 ºC), the acid (HCl 0.01-0.1 M), the oxidation by hydrogen peroxide and light (UVC-254 and metal halide). In general, the drug demonstrated to be sensitive to all factors studied, mainly in solution, but in a more intensive way front to acid and light. The photodegradation kinetics in methanol, front to UVC light was determined, indicating a zero-order reaction. Three photodegradation products were isolated and identified by nuclear magnetic resonance: 1H-benzimidazole, 1,3-diidro-benzimidazole-2-one and [4-(3-methoxypropoxy)- 3-methyl-pyridin-2-yl]methanol. Some results suggest that the 1,3-diidrobenzimiazole- 2-one is also formed in the acidic degradation.
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2

Naghmeh, Jabarizadekivi. "A Comparison of the Effect of Omeprazole and Rabeprazole on Clozapine Serum Concentrations". University of Sydney, 2008. http://hdl.handle.net/2123/2471.

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Master of Philosophy
Clozapine is a drug of choice for treatment of refractory schizophrenia, which is primarily metabolized by Cytochrome P450 1A2 (CYP1A2). Norclozapine is its main metabolite. There are reports of wide ranging gastrointestinal side effects associated with clozapine therapy, that result in concomitant administration of proton pump inhibitors to treat acid-related disorders. Omeprazole is an established CYP1A2 inducer, while an in vitro study has shown that rabeprazole is much less potent in this regard. There is no available information about the impact of rabeprazole on CYP1A2 activity in patients. Firstly, this information is essential when prescriptions are changed from omeprazole to rabeprazole to reduce medication costs. Therefore, the aim of this study was to compare the effects of rabeprazole and omeprazole on CYP1A2-mediated clearance (CL/F) of clozapine. Secondly, the effective dosage of clozapine varies widely among patients, making it necessary to individualize drug therapy with clozapine. The reason for dosage variation could be due to the influence of patient-related variables on clozapine plasma concentrations. Therefore, another aim of this study was to investigate the relationship between patient variables, such as age, gender, cigarette smoke, weight and body mass index and clozapine clearance (CL/F). A cross-over study design was used for this study. Twenty patients from Macquarie hospital who were receiving clozapine and rabeprazole (with no other interacting medications) were recruited in this study. Blood samples were taken at 30 min, 1 hr, 2 hr and 12 hr after a dose of clozapine. Rabeprazole was then replaced with omeprazole. After at least 1 month blood samples were again collected at the above corresponding intervals after clozapine. The plasma concentrations of clozapine and norclozapine were determined by high performance liquid chromatography. Abbottbase Pharmacokinetic Systems Software, which utilizes Bayesian forecasting, was used to estimate pharmacokinetic parameters of clozapine. The ratio of plasma norclozapine/clozapine concentrations at trough level was used to reflect CYP1A2 activity. No difference was observed in clozapine clearance (CL/F) and CYP1A2 activity during concurrent therapy with either rabeprazole or omeprazole. According to some studies CYP1A2 induction by omeprazole is dose dependent. Furthermore, since rabeprazole is a weak CYP1A2 inducer in vitro, we conclude that omeprazole and rabeprazole may not induce CYP1A2 activity when used at conventional therapeutic dosage (<40 mg/day). Hence, replacement of omeprazole with rabeprazole at conventional therapeutic dosages (20 or 40 mg daily) offers no advantages in the management of patients with schizophrenia on clozapine and no dose adjustment is required. Consistent with previous studies, clozapine concentrations were found to be significantly lower in cigarette smokers due to CYP1A2 induction. No relationship was found between age, gender, or weight and clozapine clearance (CL/F). However, body mass index showed a significant negative correlation with clozapine clearance (CL/F). Since weight gain and lipid accumulation are common side effects of clozapine they may be associated with a reduction of CYP1A2 activity and clozapine clearance (CL/F). Moreover, high lipoprotein levels may decrease the unbound fraction of clozapine and decrease the availability of clozapine for oxidation by cytochrome P450 enzymes. Therefore, it is concluded that omeprazole and rabeprazole may not induce CYP1A2 activity when used at conventional therapeutic dosage (<40mg/day). Hence, replacement of omeprazole with rabeprazole does not require the dose of clozapine to be adjusted. Moreover, the negative correlation between clozapine clearance (CL/F) and BMI is informative. Further studies are now required to clarify the relationship between BMI, lipoprotein levels and clozapine clearance in patients with schizophrenia.
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3

Naghmeh, Jabarizadekivi. "A Comparison of the Effect of Omeprazole and Rabeprazole on Clozapine Serum Concentrations". Thesis, The University of Sydney, 2007. http://hdl.handle.net/2123/2471.

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Clozapine is a drug of choice for treatment of refractory schizophrenia, which is primarily metabolized by Cytochrome P450 1A2 (CYP1A2). Norclozapine is its main metabolite. There are reports of wide ranging gastrointestinal side effects associated with clozapine therapy, that result in concomitant administration of proton pump inhibitors to treat acid-related disorders. Omeprazole is an established CYP1A2 inducer, while an in vitro study has shown that rabeprazole is much less potent in this regard. There is no available information about the impact of rabeprazole on CYP1A2 activity in patients. Firstly, this information is essential when prescriptions are changed from omeprazole to rabeprazole to reduce medication costs. Therefore, the aim of this study was to compare the effects of rabeprazole and omeprazole on CYP1A2-mediated clearance (CL/F) of clozapine. Secondly, the effective dosage of clozapine varies widely among patients, making it necessary to individualize drug therapy with clozapine. The reason for dosage variation could be due to the influence of patient-related variables on clozapine plasma concentrations. Therefore, another aim of this study was to investigate the relationship between patient variables, such as age, gender, cigarette smoke, weight and body mass index and clozapine clearance (CL/F). A cross-over study design was used for this study. Twenty patients from Macquarie hospital who were receiving clozapine and rabeprazole (with no other interacting medications) were recruited in this study. Blood samples were taken at 30 min, 1 hr, 2 hr and 12 hr after a dose of clozapine. Rabeprazole was then replaced with omeprazole. After at least 1 month blood samples were again collected at the above corresponding intervals after clozapine. The plasma concentrations of clozapine and norclozapine were determined by high performance liquid chromatography. Abbottbase Pharmacokinetic Systems Software, which utilizes Bayesian forecasting, was used to estimate pharmacokinetic parameters of clozapine. The ratio of plasma norclozapine/clozapine concentrations at trough level was used to reflect CYP1A2 activity. No difference was observed in clozapine clearance (CL/F) and CYP1A2 activity during concurrent therapy with either rabeprazole or omeprazole. According to some studies CYP1A2 induction by omeprazole is dose dependent. Furthermore, since rabeprazole is a weak CYP1A2 inducer in vitro, we conclude that omeprazole and rabeprazole may not induce CYP1A2 activity when used at conventional therapeutic dosage (<40 mg/day). Hence, replacement of omeprazole with rabeprazole at conventional therapeutic dosages (20 or 40 mg daily) offers no advantages in the management of patients with schizophrenia on clozapine and no dose adjustment is required. Consistent with previous studies, clozapine concentrations were found to be significantly lower in cigarette smokers due to CYP1A2 induction. No relationship was found between age, gender, or weight and clozapine clearance (CL/F). However, body mass index showed a significant negative correlation with clozapine clearance (CL/F). Since weight gain and lipid accumulation are common side effects of clozapine they may be associated with a reduction of CYP1A2 activity and clozapine clearance (CL/F). Moreover, high lipoprotein levels may decrease the unbound fraction of clozapine and decrease the availability of clozapine for oxidation by cytochrome P450 enzymes. Therefore, it is concluded that omeprazole and rabeprazole may not induce CYP1A2 activity when used at conventional therapeutic dosage (<40mg/day). Hence, replacement of omeprazole with rabeprazole does not require the dose of clozapine to be adjusted. Moreover, the negative correlation between clozapine clearance (CL/F) and BMI is informative. Further studies are now required to clarify the relationship between BMI, lipoprotein levels and clozapine clearance in patients with schizophrenia.
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4

Tu, Cheng-Wen y 杜正文. "Modified Release of Rabeprazole and Oxybutynin Using Enteric Coating System". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/99887508463695080407.

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碩士
嘉南藥理科技大學
藥學系
101
In recent years, scientific and technological advancements have been made in the development of controlled drug delivery system. Controlled drug delivery technology has many advantages, such as improve effectiveness, convenience and reduce side effects. It also helps to improve quality of life. In order to obtain optimum formulation to ensure efficacy and safety profiles, the effect of formulation variables on drug release and stability are crucial. Rabeprazole and oxybutynin are used in the present study as the model drugs. Formulations with different polymer amount and enteric coating ratios were designed to evaluate their effects on drug release as well as chemical stability. The results demonstrate rabeprazole dissolution rates decreased with the increased in inner coating level. As in the acid dissolution media, no significant degradation was observed if enough enteric polymer has been coated. For oxybutynin, the hydrophilic polymer viscosity and amount added can affect the drug release rates. Adjusting the ratios of HPMC and Eudragit L100-55 amounts contributed to different release rates in pH1.2 medium. The study clearly shows that the application of enteric coating systems to obtain optimum release rates of rabeprazole and oxybutynin is feasible.
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Swayze, Emma. "The effects of CTDSP1 on topoI degradation and cellular resistance to topoI inhibitors chemotherapy treatment". Thesis, 2017. https://hdl.handle.net/2144/23723.

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The anticancer drug Camptothecin (CPT) specifically targets topoisomerase I (topoI). While this class of drug is used to treat various solid tumors, CPT is only effective in 13-30 percent of the patient population. Although the mechanism of the CPT resistance pathway is not fully understood, we found cancer cells degrade topoisomerase I (topoI) in response to CPT. The observed relationship between higher basal DNA-PKcs mediated phosphorylation of topoI, rapid degradation of topoI, and resistance to CPT suggested that DNA-PKcs is a critical regulator of the phosphorylation status of topoI and the rate of topoI degradation in response to CPT. The data shows CTDSP1 (a dual phosphatase) acts as a negative regulator of DNA-PKcs. Because CTDSP1 functionality plays a role in maintaining higher basal phosphorylation levels of topoI, CTDSP1 impairment contributes to greater CPT resistance. This renders the CPT chemotherapy treatment ineffective. We hypothesized inducing the catalytically inactive form of CTDPS1 via both knockdown and inhibition experiments would increase cancer cell resistance to CPT as a result of an overactive topoI degradation pathway. The function of CTDSP1 was impaired in the two colon cancer cell lines, HCT15 and HCT116, by silencing with siRNA and using Rabeprazole (a pharmacological agent known to inhibit CTDSP1). Inhibition of CTDSP1 phosphatase activity resulted in greater phosphorylation of DNA-PKcs and increased the rate of topoI degradation in the cells in response to CPT. Cellular resistance was also more notable in the sensitive HCT116 cell lines. HCT15 cells degrade topoI rapidly and are resistant to CPT. Thus, the effect of CPT is not as pronounced in this cell line. CTDSP1 knock down cells showed the greatest DNA-PKcs phosphorylation and topoI degradation when treated with CPT. In addition, the present study includes a clonogenic assay that shows a larger cell survival fraction in Rabeprazole treated HCT116 cells in comparison to controls after exposure to CPT. A higher survival fraction after CPT exposure is reflective of greater CPT resistance. This suggests that cell viability is enhanced during CPT chemotherapy treatment in CTDSP1 null colorectal cancer cells. Lastly, An EGFP read out experiment of topoI tagged to EGFP demonstrated CTDSP1 inhibition results in reduced topoI levels in colorectal cancer cells. The present study showed the potential link between lower topoI levels and greater resistance to CPT by showing that both effects are outcomes of silencing CTDSP1.
2018-07-11T00:00:00Z
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6

Yang, Yu-Fan y 楊喻帆. "Role of CYP2C19 polymorphisms in short-term rabeprazole-based triple therapy- Implication of PK/PD correlation". Thesis, 2008. http://ndltd.ncl.edu.tw/handle/12890224878228433172.

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邢惠婷. "The effect of regimen on the pharmacokinetics and pharmacodynamics of Rabeprazole in healthy volunteers:a relation to CTP2C19 genetic polymorphism in Taiwanese". Thesis, 2002. http://ndltd.ncl.edu.tw/handle/13952164826798061242.

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碩士
國立臺灣大學
臨床藥學研究所
90
Abstract Sodium Rabeprazole is a relative new agent in the class of proton pump inhibitors. Rabeprazole is metabolized partially by CYP2C19, and one of its metabolites, thioether-rabeprazole is considered to be metabolized by CYP2C19, too. In addition, CYP2C19 exhibits a genetic polymorphism and there are more PMs in Asians than in Caucasians. Although CYP2C19 is not the major enzyme involved in its metabolism, it has been shown that people with different CYP2C19 genotypes have different abilities to metabolize rabeprazole either after single dose or multiple doses. However, diverse influences of CYP2C19 genotype statuses on pharmacodynamic effect of rabeprazole were observed. Lueth et al. (2001) observed that a four-day triple therapy of rabeprazole (20 mg bid) in combination with clarithromycin and amoxicillin is highly effective in eradication H. pylori. However, Wong et al. (2001) observed that the H. pylori eradication rate of 3-day rabeprazole-based triple therapy is about 72%. This study was a single center, open-label study. It compared the pharmacokinetic and pharmacodynamic properties of rabeprazole after single and multiple dosing between healthy Taiwanese subjects with different genotypes of CYP2C19. Twelve healthy volunteers including 6 CYP2C19 homEMs and 6 CYP2C19 PMs were enrolled in this study. Multiple dose of rabeprazole (20 mg, b.i.d.) were given to volunteers for 4 days. At day-1, aliquots of 10-ml blood samples were drawn 30 minutes before drug administration and 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12 hours after the start of oral administration. At day-4, aliquots of 10-ml blood samples were drawn at 0.5, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, and 24 hours after the seventh dose. Both pharmacokinetic and pharmacodynamic properties were analyzed. After single and repeated dosing of rabeprazole, the plasma concentration of rabeprazole and its thioether metabolite are significantly dependent on CYP2C19 genotype. Plasma gastrin concentration is used as a surrogate marker of intragastric pH. The 12-hrs median plasma gastrin concentrations after the final dose of rabeprazole are different between PMs and homEMs. Otherwise, AUC for rabeprazole and thioether-rabeprazole do not increase with repeated doses. There is no accumulation effect in administrating of rabeprazole with respect to PK properties. However, 12-hrs median plasma gastrin concentrations at day-4 are significant higher than that at day-1 in PMs but not homEMs. In addition, it is also observed that H. pylori infection doesn’t influence gastrin secretion. In conclusion, the CYP2C19-mediated metabolism and the CYP2C19-related pharmacodynamic effect on plasma gastrin concentrations are significant different between the two genotype groups (PMs vs. homEMs). Prior testing of CYP2C19 genotype statuses may be used to optimize drug dosage and H. pylori eradication rate of ultra-short triple therapy in the future.
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Libros sobre el tema "Rabeprazole"

1

Blokdijk, G. J. Rabeprazole Sodium; Complete Self-Assessment Guide. CreateSpace Independent Publishing Platform, 2018.

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Simonis, Kaylin. RabeprazoIe: A Strong Drug Used to Treat Any Gastroesophageal Reflux Disease in Adults and Children. Independently Published, 2019.

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Capítulos de libros sobre el tema "Rabeprazole"

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de Groot, Anton C. "Rabeprazole". En Monographs In Contact Allergy, 850. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003158004-431.

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"Rabeprazole". En Meyler's Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions, 3011–12. Elsevier, 2006. http://dx.doi.org/10.1016/b0-44-451005-2/00604-5.

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"Rabeprazole". En Meyler's Side Effects of Drugs, 43–44. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-444-53717-1.01383-4.

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"RABEPRAZOLE". En Litt's Drug Eruptions and Reactions Manual, 372–74. CRC Press, 2014. http://dx.doi.org/10.1201/b15347-170.

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"Rabeprazole." En Drugs Handbook 2012–2013. Bloomsbury Academic, 2011. http://dx.doi.org/10.5040/9781350363595.art-1483.

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Jewell, Richard. "Rabeprazole". En xPharm: The Comprehensive Pharmacology Reference, 1–5. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.62509-7.

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"RABEPRAZOLE". En Litt's Drug Eruption Reference Manual Including Drug Interactions, 1351–60. CRC Press, 2004. http://dx.doi.org/10.3109/9780203492079-158.

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"Rabeprazole". En PharmacotherapyFirst Drug Information. 2215 Constitution Avenue, N.W. Washington, DC 20037-2985: The American Pharmacists Association, 2017. http://dx.doi.org/10.21019/druginformation.rabeprazole.

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"Rabeprazole". En PharmacotherapyFirst Drug Information. 2215 Constitution Avenue, N.W. Washington, DC 20037-2985: The American Pharmacists Association, 2017. http://dx.doi.org/10.21019/pfdi.rabeprazole.

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"Rabeprazole". En Hale’s Medications & Mothers’ Milk™ 2019. New York, NY: Springer Publishing Company, 2018. http://dx.doi.org/10.1891/9780826150356.0879.

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Actas de conferencias sobre el tema "Rabeprazole"

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Akahoshi, K., S. Nagatomo, S. Osada, E. Yamaguchi, M. Kubokawa, J. Gibo, K. Yodoe, K. Inamura, K. Akahoshi y Y. Shiratsuchi. "ESOMEPRAZOLE VS RABEPRAZOLE IN THE HEALING OF ARTIFICIAL ULCERS AFTER THE ENDOSCOPIC SUBMUCOSAL DISSECTION USING THE CLUTCH CUTTER: A PROSPECTIVE RANDOMIZED CONTROLLED STUDY". En ESGE Days 2018 accepted abstracts. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1637389.

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