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Articoli di riviste sul tema "Pharmacokinetic interactions"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 9 giugno 2025

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1

Taylor, David. "Pharmacokinetic interactions involving clozapine." British Journal of Psychiatry 171, no. 2 (August 1997): 109–12. http://dx.doi.org/10.1192/bjp.171.2.109.

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BackgroundMetabolism of clozapine is complex and not fully understood. Pharmacokinetic interactions with other drugs have been described but, in some cases, their mechanism is unknown.MethodPublished trials and case reports relevant to the human metabolism of clozapine and to suspected pharmacokinetic interactions were reviewed.ResultsMetabolism of clozapine appears to be largely controlled by the function of the hepatic cytochrome p4501A2 (CYPIA2). Compounds which induce CYPIA2 activity (carbamazepine, tobacco smoke) may reduce plasma clozapine levels. Inhibitors of CYPIA2 (caffeine, erythromycin) have the opposite effect. Drugs which inhibit the hepatic cytochrome p4502D6 (CYP2D6) have also been reported to elevate plasma clozapine levels. The mechanism of this interaction is unclear.ConclusionsThe co-administration of clozapine and compounds reported to alter its metabolism should be avoided where possible. A host of other interactions can be predicted and so caution should be exercised when co-administering drugs which affect the function of CYPIA2 and CYP2D6. The pharmacokinetics of clozapine require further investigation so that its safe use can be assured.

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Keirns, J., T. Sawamoto, M. Holum, D. Buell, W. Wisemandle, and A. Alak. "Steady-State Pharmacokinetics of Micafungin and Voriconazole after Separate and Concomitant Dosing in Healthy Adults." Antimicrobial Agents and Chemotherapy 51, no. 2 (November 20, 2006): 787–90. http://dx.doi.org/10.1128/aac.00673-06.

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ABSTRACT We assessed the pharmacokinetics and interactions of steady-state micafungin (Mycamine) or placebo with steady-state voriconazole in 35 volunteers. The 90% confidence intervals around the least-squares mean ratios for micafungin pharmacokinetic parameters and placebo-corrected voriconazole pharmacokinetic parameters were within the 80%-to-125% limits, indicating an absence of drug interaction.

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Soyata, Amelia, Aliya Nur Hasanah, and Taofik Rusdiana. "Interaction of Warfarin with Herbs Based on Pharmacokinetic and Pharmacodynamic Parameters." Indonesian Journal of Pharmaceutics 2, no. 2 (June 5, 2020): 69. http://dx.doi.org/10.24198/idjp.v2i2.27289.

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Warfarin is an oral anticoagulant that has been widely used and has strong efficacy, but the use of warfarin is still a concern because of its narrow therapeutic index which cause interactions when co-administration with drugs, herbs or food. This interaction can affect the pharmacokinetics and pharmacodynamics of warfarin and the most fatal effect from warfarin interactions is bleeding. In this review article data on warfarin-herbs interactions were collected based on pharmacokinetic parameters (AUC0-∞, Cmax, T1/2, Cl/F, and V/F), while pharmacodynamic parameters (International normalized ratio (INR), platelet aggregation, AUC INR and Protombine Time). As a result some herbs had significant interactions with warfarin. Herbs that affect warfarin pharmacokinetic were Danshen gegen, echinacea, St. John's wort and caffeine and herbs that affect pharmacodynamic were policosanol, Ginkgo biloba, cranberry, St. John's wort, ginseng, pomegranate, Psidium guajava and curcumin, so co-administration warfarin with herbs need to be considered.Keywords: Warfarin, Interactions, Herbs, Pharmacokinetics, Pharmacodynamics

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Costache, Irina-Iuliana, Anca Miron, Monica Hăncianu, Viviana Aursulesei, Alexandru Dan Costache, and Ana Clara Aprotosoaie. "Pharmacokinetic Interactions between Cardiovascular Medicines and Plant Products." Cardiovascular Therapeutics 2019 (September 2, 2019): 1–19. http://dx.doi.org/10.1155/2019/9402781.

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The growing use of plant products among patients with cardiovascular pharmacotherapy raises the concerns about their potential interactions with conventional cardiovascular medicines. Plant products can influence pharmacokinetics or/and pharmacological activity of coadministered drugs and some of these interactions may lead to unexpected clinical outcomes. Numerous studies and case reports showed various pharmacokinetic interactions that are characterized by a high degree of unpredictability. This review highlights the pharmacokinetic clinically relevant interactions between major conventional cardiovascular medicines and plant products with an emphasis on their putative mechanisms, drawbacks of herbal products use, and the perspectives for further well-designed studies.

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Cohen, Lawrence J., and C. Lindsay DeVane. "Clinical Implications of Antidepressant Pharmacokinetics and Pharmacogenetics." Annals of Pharmacotherapy 30, no. 12 (December 1996): 1471–80. http://dx.doi.org/10.1177/106002809603001216.

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OBJECTIVE: To review available data on pharmacokinetic and pharmacogenetic influences on the response to antidepressant therapy, analyze the mechanisms for and clinical significance of pharmacokinetic and pharmacogenetic differences, and explain the implications of pharmacokinetics and pharmacogenetics for patient care. DATA SOURCES: A MEDLINE search of English-language clinical studies, abstracts, and review articles on antidepressant pharmacokinetics, pharmacogenetics, and drug interactions was used to identify pertinent literature. DATA SYNTHESIS: The pharmacokinetic profiles of selected antidepressants are reviewed and the impact of hepatic microsomal enzymes on antidepressant metabolism is considered. How phenotypic differences influence the metabolism of antidepressant drug therapy is addressed. To evaluate the clinical implications of these pharmacokinetic and pharmacogenetic considerations, the findings of studies designed to elucidate drug interactions involving antidepressant agents are discussed. CONCLUSIONS: Differences in antidepressant plasma concentrations, and possibly safety, are caused by polymorphism in the genes that encode some of the cytochrome P450 isoenzymes that metabolize antidepressants. The isoenzymes 1A2, 2C9/19, 2D6, and 3A4 are the major enzymes that catalyze antidepressant metabolic reactions. Antidepressants can be either substrates or inhibitors of these enzymes, which also metabolize many other pharmacologic agents. Although the cytochrome enzymes that metabolize antidepressants have not been fully characterized, interaction profiles of the newer antidepressants are becoming more clearly defined. Determining patient phenotypes is not practical in the clinical setting, but an awareness of the possibility of genetic polymorphism in antidepressant metabolism may help explain therapeutic failure or toxicity, help predict the likelihood of drug interactions, and help clinicians better manage antidepressant drug therapy.

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ERESHEFSKY, LARRY, STEPHEN R. SAKLAD, MARK D. WATANABE, CHESTER M. DAVIS, and MICHAEL W. JANN. "Thiothixene Pharmacokinetic Interactions." Journal of Clinical Psychopharmacology 11, no. 5 (October 1991): 296???301. http://dx.doi.org/10.1097/00004714-199110000-00004.

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7

Hartshorn, Edward A. "Pharmacokinetic Drug Interactions." Journal of Pharmacy Technology 1, no. 5 (September 1985): 193–99. http://dx.doi.org/10.1177/875512258500100505.

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8

Eichelbaum, Michel. "Pharmacokinetic Drug Interactions." Journal of Clinical Pharmacology 26, no. 6 (July 8, 1986): 469–73. http://dx.doi.org/10.1002/j.1552-4604.1986.tb03560.x.

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9

Pukrittayakamee, Sasithon, Joel Tarning, Podjanee Jittamala, Prakaykaew Charunwatthana, Saranath Lawpoolsri, Sue J. Lee, Warunee Hanpithakpong, et al. "Pharmacokinetic Interactions between Primaquine and Chloroquine." Antimicrobial Agents and Chemotherapy 58, no. 6 (March 31, 2014): 3354–59. http://dx.doi.org/10.1128/aac.02794-13.

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ABSTRACTChloroquine combined with primaquine has been the standard radical curative regimen forPlasmodium vivaxandPlasmodium ovalemalaria for over half a century. In an open-label crossover pharmacokinetic study, 16 healthy volunteers (4 males and 12 females) aged 20 to 47 years were randomized into two groups of three sequential hospital admissions to receive a single oral dose of 30 mg (base) primaquine, 600 mg (base) chloroquine, and the two drugs together. The coadministration of the two drugs did not affect chloroquine or desethylchloroquine pharmacokinetics but increased plasma primaquine concentrations significantly (P≤ 0.005); the geometric mean (90% confidence interval [CI]) increases were 63% (47 to 81%) in maximum concentration and 24% (13 to 35%) in total exposure. There were also corresponding increases in plasma carboxyprimaquine concentrations (P≤ 0.020). There were no significant electrocardiographic changes following primaquine administration, but there was slight corrected QT (QTc) (Fridericia) interval lengthening following chloroquine administration (median [range] = 6.32 [−1.45 to 12.3] ms;P< 0.001), which was not affected by the addition of primaquine (5.58 [1.74 to 11.4] ms;P= 0.642). This pharmacokinetic interaction may explain previous observations of synergy in preventingP. vivaxrelapse. This trial was registered at ClinicalTrials.gov under reference number NCT01218932.

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Marvanova, Marketa. "Pharmacokinetic characteristics of antiepileptic drugs (AEDs)." Mental Health Clinician 6, no. 1 (January 1, 2016): 8–20. http://dx.doi.org/10.9740/mhc.2015.01.008.

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Abstract Antiepileptic drugs (AEDs) are routinely prescribed for the management of a variety of neurologic and psychiatric conditions, including epilepsy and epilepsy syndromes. Physiologic changes due to aging, pregnancy, nutritional status, drug interactions, and diseases (ie, those involving liver and kidney function) can affect pharmacokinetics of AEDs. This review discusses foundational pharmacokinetic characteristics of AEDs currently available in the United States, including clobazam but excluding the other benzodiazepines. Commonalities of pharmacokinetic properties of AEDs are discussed in detail. Important differences among AEDs and clinically relevant pharmacokinetic interactions in absorption, distribution, metabolism, and/or elimination associated with AEDs are highlighted. In general, newer AEDs have more predictable kinetics and lower risks for drug interactions. This is because many are minimally or not bound to serum proteins, are primarily renally cleared or metabolized by non–cytochrome P450 isoenzymes, and/or have lower potential to induce/inhibit various hepatic enzyme systems. A clear understanding of the pharmacokinetic properties of individual AEDs is essential in creating a safe and effective treatment plan for a patient.

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Kalam, Muhammad Nasir, Muhammad Fawad Rasool, Asim Ur Rehman, and Naveed Ahmed. "Clinical Pharmacokinetics of Propranolol Hydrochloride: A Review." Current Drug Metabolism 21, no. 2 (June 11, 2020): 89–105. http://dx.doi.org/10.2174/1389200221666200414094644.

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Background: Nobel laureate Sir James Black’s molecule, propranolol, still has broad potential in cardiovascular diseases, infantile haemangiomas and anxiety. A comprehensive and systematic review of the literature for the summarization of pharmacokinetic parameters would be effective to explore the new safe uses of propranolol in different scenarios, without exposing humans and using virtual-human modeling approaches. Objective: This review encompasses physicochemical properties, pharmacokinetics and drug-drug interaction data of propranolol collected from various studies. Methods: Clinical pharmacokinetic studies on propranolol were screened using Medline and Google Scholar databases. Eighty-three clinical trials, in which pharmacokinetic profiles and plasma time concentration were available after oral or IV administration, were included in the review. Results: The study depicts that propranolol is well absorbed after oral administration. It has dose-dependent bioavailability, and a 2-fold increase in dose results in a 2.5-fold increase in the area under the curve, a 1.3-fold increase in the time to reach maximum plasma concentration and finally, 2.2 and 1.8-fold increase in maximum plasma concentration in both immediate and long-acting formulations, respectively. Propranolol is a substrate of CYP2D6, CYP1A2 and CYP2C19, retaining potential pharmacokinetic interactions with co-administered drugs. Age, gender, race and ethnicity do not alter its pharmacokinetics. However, in renal and hepatic impairment, it needs a dose adjustment. Conclusion: Physiochemical and pooled pharmacokinetic parameters of propranolol are beneficial to establish physiologically based pharmacokinetic modeling among the diseased population.

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Sumartin, Yunita, and Elin Yulinah Sukandar. "STUDI INTERAKSI OBAT-OBAT JANTUNG YANG DILAKUKAN TERHADAP ORANG SEHAT: TINJAUAN SISTEMATIS." Kartika : Jurnal Ilmiah Farmasi 9, no. 2 (August 14, 2024): 128–46. http://dx.doi.org/10.26874/kjif.v9i2.669.

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Pasien dengan penyakit kardiovaskular memiliki prevalensi interaksi obat yang lebih tinggi dibandingkan kelompok pasien lain karena jumlah dan penggunaan obat yang komplek. Interaksi obat merupakan perubahan efek kerja dari suatu obat karena adanya obat lain ketika diberikan bersamaan. Jenis interaksi obat terdiri dari interaksi farmakokinetik, farmakodinamik, dan farmasetik. Studi ini berupa tinjauan sistematis yang bertujuan untuk mengidentifikasi interaksi obat yang berkaitan dengan obat-obat jantung. Proses penelusuran artikel dilakukan pada database PubMed dan ScienceDirect untuk mengidentifikasi semua artikel mengenai studi interaksi obat-obat jantung. Penelusuran artikel dibatasi pada tahun 2013 hingga 2023. Kata kunci yang digunakan dalam penelusuran artikel sebagai berikut: drug-drug interactions, cardiac patient, cardiac drug, cardiovascular drug, pharmacokinetics interaction, pharmacodynamic interaction dikombinasikan dengan boolean operator yaitu AND. Studi artikel yang telah memenuhi syarat, dimasukkan ke dalam penelitian untuk ditinjau. Jumlah keseluruhan artikel yang telah teridentifikasi dari database yang digunakan yaitu sebanyak 805 artikel, 7 artikel duplikasi dikeluarkan, 82 artikel tersedia teks lengkap, namun hanya 20 artikel sesuai dengan inklusi yang dilakukan review. Dari 20 artikel, 18 publikasi mengidentifikasi interaksi obat secara farmakokinetik, sedangkan interaksi secara farmakodinamik dilaporkan dalam 2 publikasi. Interaksi farmakokinetik banyak terjadi pada golongan obat Angiotensin II Reseptor Bloker (ARB). Selain itu terjadi pada golongan obat angiotensin receptor-neprilysin inhibitor (ARNI), calcium channel blocker, penghambat reseptor mineralkortikoid nonsteroid selektif, diuretik, beta-blocker, antikoagulan, dan antiplatelet. Interaksi farmakodinamik terjadi pada golongan obat calcium channel blocker dan beta-blocker. Untuk menghindari terjadinya interaksi obat, perlu pengetahuan mengenai mekanisme terjadinya interaksi obat dan efeknya terhadap pengobatan. Kata kunci : Farmakodinamik, farmakokinetik, interaksi obat, kardiovaskular. Abstract Patients with cardiovascular diseases have a higher prevalence of drug interactions than other patient groups due to the number and complex use of drugs. Drug interactions are changes in the effect of a drug due to the presence of another drug when administered together. Types of drug interactions consist of pharmacokinetic, pharmacodynamic, and pharmaceutical interactions. This study is a systematic review that aims to identify drug interactions related to cardiac drugs. The article search process was conducted on PubMed and ScienceDirect databases to identify all articles on cardiac drug-drug interaction studies. Article searches were limited to the years 2013 to 2023. The keywords used in the article search were as follows: drug-drug interactions, cardiac patient, cardiac drug, cardiovascular drug, pharmacokinetics interaction, pharmacodynamic interaction combined with the boolean operator AND. Eligible study articles were included in the study for review. A total of 805 articles were identified from the database used, 7 duplicate articles were excluded, 82 articles were available in full text, however, only 20 articles that met the inclusion criteria were reviewed. Of the 20 articles, 18 publications identified pharmacokinetic drug interactions, while pharmacodynamic interactions were reported in 2 publications. Pharmacokinetic interactions mostly occurred in the Angiotensin II Receptor Blocker (ARB) drug class. In addition, angiotensin receptor-neprilysin inhibitors (ARNI), calcium channel blockers, selective nonsteroidal mineralocorticoid receptor blockers, diuretics, beta-blockers, anticoagulants, and antiplatelets were also reported. Pharmacodynamic interactions occur with calcium channel blockers and beta-blockers. To avoid drug interactions, it is necessary to know the mechanism of drug interactions and their effects on treatment. Keywords: Pharmacodynamics, pharmacokinetics, drug Interactions, cardiovascular.

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Rodin, Steven M., and Brian F. Johnson. "Pharmacokinetic Interactions with Digoxin." Clinical Pharmacokinetics 15, no. 4 (October 1988): 227–44. http://dx.doi.org/10.2165/00003088-198815040-00003.

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Glue, Paul, Christopher R. Banfield, James L. Perhach, Gary G. Mather, Jagdish K. Racha, and Rene H. Levy. "Pharmacokinetic Interactions with Felbamate." Clinical Pharmacokinetics 33, no. 3 (September 1997): 214–24. http://dx.doi.org/10.2165/00003088-199733030-00004.

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Niemi, Mikko, Janne T. Backman, Martin F. Fromm, Pertti J. Neuvonen, and Kari T. Kivist?? "Pharmacokinetic Interactions with Rifampicin." Clinical Pharmacokinetics 42, no. 9 (2003): 819–50. http://dx.doi.org/10.2165/00003088-200342090-00003.

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Bialer, Meir, Dennis R. Doose, Bindu Murthy, Christopher Curtin, Shean-Sheng Wang, Roy E. Twyman, and Stefan Schwabe. "Pharmacokinetic Interactions of Topiramate." Clinical Pharmacokinetics 43, no. 12 (2004): 763–80. http://dx.doi.org/10.2165/00003088-200443120-00001.

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Scheen, Andr?? J. "Pharmacokinetic Interactions with Thiazolidinediones." Clinical Pharmacokinetics 46, no. 1 (2007): 1–12. http://dx.doi.org/10.2165/00003088-200746010-00001.

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&NA;. "Olanzapine + fluvoxamine: pharmacokinetic interactions." Inpharma Weekly &NA;, no. 1362 (November 2002): 20. http://dx.doi.org/10.2165/00128413-200213620-00050.

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Reinoso, R. F., A. Sánchez Navarro, M. J. García, and J. R. Prous. "Pharmacokinetic interactions of statins." Methods and Findings in Experimental and Clinical Pharmacology 23, no. 10 (2001): 541. http://dx.doi.org/10.1358/mf.2001.23.10.677120.

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Baciewicz, Anne M., and Frank A. Baciewicz. "Cyclosporine pharmacokinetic drug interactions." American Journal of Surgery 157, no. 2 (February 1989): 264–71. http://dx.doi.org/10.1016/0002-9610(89)90541-2.

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Goswami, Suchandra, Shivangi Saxena, Shalini Yadav, Diptendu Goswami, Koushik Brahmachari, Sruti Karmakar, Biswajit Pramanik, and Sunil Brahmachari. "Review of Curcumin and Its Different Formulations: Pharmacokinetics, Pharmacodynamics and Pharmacokinetic-Pharmacodynamic Interactions." OBM Integrative and Complementary Medicine 07, no. 04 (December 27, 2022): 1–35. http://dx.doi.org/10.21926/obm.icm.2204057.

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Curcumin, the yellow principle of the Indian Turmeric, ‘Haldi’ has recently attracted renewed interest in the field of experimental medicine with pleiotropic activity. This review has emphasized three pharmaceutical studies of interest: the pharmacokinetics, pharmacology, and pharmacodynamics of curcumin. In this review, we attempted to review the general pharmacokinetics profile, pharmacokinetic interactions, and pharmacokinetic-pharmacodynamic interactions of curcumin and its formulations. Different species of turmeric in India, as well as their cultivars, different forms of curcumin, and harvesting methods have also been discussed. Furthermore, pharmacokinetic studies of the interaction of curcumin and its different formulations with efflux transporters such as P-glycoprotein, ABC-transporter protein, multidrug-resistant protein, and cytochrome p450 metabolism enzymes have been broadly explained following data from preclinical and clinical trials reported in the literature. A few interesting chemical interactions between curcumin and its metabolites with the receptor have also been described. The pharmacological activities of curcumin and its related formulations and products have been reviewed in a few targeted disease pathologies of national concern, such as cancer, gastroduodenal disorder, immunodeficiency, liver disease, ophthalmology, diabetes and osteoarthritis among other metabolic diseases, and microbial and viral infections. The pharmacodynamics of curcumin, especially regarding the potassium/calcium ion channel pathway, apoptosis, calcium signaling pathway, endoplasmic reticulum stress, and other intracellular signaling pathways, have been documented. Lastly, the use of curcumin as a cosmetic and the value chain analysis of turmeric products, as well as curcumin, have also been placed appropriately. A total of 174 publications were reviewed and, overall, this review tried to cover various important therapeutic aspects of curcumin, which can generate new research interest in general.

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Sun, Lei, Kun Mi, Yixuan Hou, Tianyi Hui, Lan Zhang, Yanfei Tao, Zhenli Liu, and Lingli Huang. "Pharmacokinetic and Pharmacodynamic Drug–Drug Interactions: Research Methods and Applications." Metabolites 13, no. 8 (July 29, 2023): 897. http://dx.doi.org/10.3390/metabo13080897.

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Because of the high research and development cost of new drugs, the long development process of new drugs, and the high failure rate at later stages, combining past drugs has gradually become a more economical and attractive alternative. However, the ensuing problem of drug–drug interactions (DDIs) urgently need to be solved, and combination has attracted a lot of attention from pharmaceutical researchers. At present, DDI is often evaluated and investigated from two perspectives: pharmacodynamics and pharmacokinetics. However, in some special cases, DDI cannot be accurately evaluated from a single perspective. Therefore, this review describes and compares the current DDI evaluation methods based on two aspects: pharmacokinetic interaction and pharmacodynamic interaction. The methods summarized in this paper mainly include probe drug cocktail methods, liver microsome and hepatocyte models, static models, physiologically based pharmacokinetic models, machine learning models, in vivo comparative efficacy studies, and in vitro static and dynamic tests. This review aims to serve as a useful guide for interested researchers to promote more scientific accuracy and clinical practical use of DDI studies.

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Liang, Liuyi, Xin Jin, Jinjing Li, Rong Li, Xinyi Jiao, Yuanyuan Ma, Rui Liu, and Zheng Li. "A Comprehensive Review of Pharmacokinetics and Pharmacodynamics in Animals: Exploration of Interaction with Antibiotics of Shuang-Huang- Lian Preparations." Current Topics in Medicinal Chemistry 22, no. 2 (February 2022): 83–94. http://dx.doi.org/10.2174/1568026621666211012111442.

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: As a traditional Chinese medicine (TCM), Shuang-Huang-Lian (SHL) has been widely used for treating infectious diseases of the respiratory tract such as encephalitis, pneumonia, and asthma. During the past few decades, considerable research has focused on pharmacological action, pharmacokinetic interaction with antibiotics, and clinical applications of SHL. A huge and more recent body of pharmacokinetic studies support the combination of SHL and antibiotics have different effects such as antagonism and synergism. SHL has been one of the best-selling TCM products. However, there is no systematic review of SHL preparations, ranging from protection against respiratory tract infections to interaction with antibiotics. Since their important significance in clinical therapy, the pharmacodynamics, pharmacokinetics, and interactions with antibiotics of SHL were reviewed and discussed. In addition, this review attempts to explore the possible potential mechanism of SHL preparations in the prevention and treatment of COVID-19. We are concerned about the effects of SHL against viruses and bacteria, as well as its interactions with antibiotics in an attempt to provide a new strategy for expanding the clinical research and medication of SHL preparations.

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Ahmane, Amel, Hocine Gacem, Karim Boulesbiaat, and Meriem Boullelli. "Pharmacokinetic interactions: from mechanisms to clinical relevance." Batna Journal of Medical Sciences (BJMS) 1, no. 2 (December 31, 2014): 85–95. http://dx.doi.org/10.48087/bjmstf.2014.1209.

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Among the various types of known drug interactions, those involving pharmacokinetic processes are more complex and dangerous. From digestive pH changes to plasma protein binding and induction or inhibition phenomena; current data used to define, with precision, the sites of interaction. The enzymes involved in metabolism, the transporters involved in tissue distribution and excretion of drugs, and nuclear receptors that regulate the expression of these enzymes and transporters are keys determinants that should be defined for each drug. The clinical relevance of a pharmacokinetic interaction is related to the magnitude of changes in drug concentrations and pharmacological properties of these. Good knowledge of the pharmacokinetic properties of drugs and the mechanisms involved in the genesis of these interactions is, then, needed to prevent and avoid theme.

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Zerjav, Sylvia, Gordon Tse, and Michael J. W. Scott. "Review of Duloxetine and Venlafaxine in Depression." Canadian Pharmacists Journal / Revue des Pharmaciens du Canada 142, no. 3 (May 2009): 144–52. http://dx.doi.org/10.3821/1913-701x-142.3.144.

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Objectives: To compare the efficacy and pharmacologic, pharmacokinetic, drug interaction and adverse effect profiles of duloxetine and venlafaxine. Methods: A systematic review of the literature pertaining to duloxetine and venlafaxine was conducted using a computer-aided search of MEDLINE and EMBASE for the period January 1988 to May 2008 with the following search terms: venlafaxine and duloxetine and depression, clinical studies, pharmacology, drug interactions, pharmacokinetics, adverse effects, safety, case reports and review articles. Results: Duloxetine and venlafaxine have comparable efficacy and share similar pharmacologic profiles but differ somewhat in their pharmacokinetic profiles, drug interactions and adverse effects. Both agents block the reuptake of serotonin and norepinephrine and both are substrates for the cytochrome P450 2D6 isoenzyme; however, duloxetine inhibits these enzymes to a moderate extent, whereas venlafaxine is only a weak inhibitor. Furthermore, duloxetine is more extensively bound to protein than venlafaxine. Venlafaxine is more likely to elevate blood pressure in a dose-related manner. Both duloxetine and venlafaxine have the potential to cause hepatic injury. Conclusions: Although venlafaxine and duloxetine have similar efficacy in the treatment of depression, differences in their adverse effects and pharmacokinetic profiles suggest that one agent may be preferred over the other in certain patient groups.

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Dukaew, Nahathai, Patcharawadee Thongkumkoon, Nutnicha Sirikaew, Sivamoke Dissook, Wannachai Sakuludomkan, Siripong Tongjai, Parameth Thiennimitr, et al. "Gut Microbiota-Mediated Pharmacokinetic Drug–Drug Interactions between Mycophenolic Acid and Trimethoprim-Sulfamethoxazole in Humans." Pharmaceutics 15, no. 6 (June 14, 2023): 1734. http://dx.doi.org/10.3390/pharmaceutics15061734.

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Mycophenolic acid (MPA) and trimethoprim-sulfamethoxazole (TMP-SMX) are commonly prescribed together in certain groups of patients, including solid organ transplant recipients. However, little is known about the pharmacokinetic drug–drug interactions (DDIs) between these two medications. Therefore, the present study aimed to determine the effects of TMP-SMX on MPA pharmacokinetics in humans and to find out the relationship between MPA pharmacokinetics and gut microbiota alteration. This study enrolled 16 healthy volunteers to take a single oral dose of 1000 mg mycophenolate mofetil (MMF), a prodrug of MPA, administered without and with concurrent use of TMP-SMX (320/1600 mg/day) for five days. The pharmacokinetic parameters of MPA and its glucuronide (MPAG) were measured using high-performance liquid chromatography. The composition of gut microbiota in stool samples was profiled using a 16S rRNA metagenomic sequencing technique during pre- and post-TMP-SMX treatment. Relative abundance, bacterial co-occurrence networks, and correlations between bacterial abundance and pharmacokinetic parameters were investigated. The results showed a significant decrease in systemic MPA exposure when TMP-SMX was coadministered with MMF. Analysis of the gut microbiome revealed altered relative abundance of two enriched genera, namely the genus Bacteroides and Faecalibacterium, following TMP-SMX treatment. The relative abundance of the genera Bacteroides, [Eubacterium] coprostanoligenes group, [Eubacterium] eligens group, and Ruminococcus appeared to be significantly correlated with systemic MPA exposure. Coadministration of TMP-SMX with MMF resulted in a reduction in systemic MPA exposure. The pharmacokinetic DDIs between these two drugs were attributed to the effect of TMP-SMX, a broad-spectrum antibiotic, on gut microbiota-mediated MPA metabolism.

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Hofmeister, Craig C., Xiaoxia Yang, Flavia Pichiorri, Ping Chen, Darlene M. Rozewski, Amy J. Johnson, Seungsoo Lee, et al. "Phase I Trial of Lenalidomide and CCI-779 in Patients With Relapsed Multiple Myeloma: Evidence for Lenalidomide–CCI-779 Interaction via P-Glycoprotein." Journal of Clinical Oncology 29, no. 25 (September 1, 2011): 3427–34. http://dx.doi.org/10.1200/jco.2010.32.4962.

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Abstract (sommario):

Purpose Multiple myeloma (MM) is an incurable plasma-cell neoplasm for which most treatments involve a therapeutic agent combined with dexamethasone. The preclinical combination of lenalidomide with the mTOR inhibitor CCI-779 has displayed synergy in vitro and represents a novel combination in MM. Patients and Methods A phase I clinical trial was initiated for patients with relapsed myeloma with administration of oral lenalidomide on days 1 to 21 and CCI-779 intravenously once per week during a 28-day cycle. Pharmacokinetic data for both agents were obtained, and in vitro transport and uptake studies were conducted to evaluate potential drug-drug interactions. Results Twenty-one patients were treated with 15 to 25 mg lenalidomide and 15 to 20 mg CCI-779. The maximum-tolerated dose (MTD) was determined to be 25 mg lenalidomide with 15 mg CCI-779. Pharmacokinetic analysis indicated increased doses of CCI-779 resulted in statistically significant changes in clearance, maximum concentrations, and areas under the concentration-time curves, with constant doses of lenalidomide. Similar and significant changes for CCI-779 pharmacokinetics were also observed with increased lenalidomide doses. Detailed mechanistic interrogation of this pharmacokinetic interaction demonstrated that lenalidomide was an ABCB1 (P-glycoprotein [P-gp]) substrate. Conclusion The MTD of this combination regimen was 25 mg lenalidomide with 15 mg CCI-779, with toxicities of fatigue, neutropenia, and electrolyte wasting. Pharmacokinetic and clinical interactions between lenalidomide and CCI-779 seemed to occur, with in vitro data indicating lenalidomide was an ABCB1 (P-gp) substrate. To our knowledge, this is the first report of a clinically significant P-gp–based drug-drug interaction with lenalidomide.

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Botts, Sheila R., and Cara Alfaro. "Antidepressant Drug Interactions." Journal of Pharmacy Practice 14, no. 6 (December 2001): 467–77. http://dx.doi.org/10.1177/089719001129040964.

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Abstract (sommario):

Second-generation antidepressants are more selective in their pharmacological mechanisms and offer fewer side effects and a safer toxicological profile than cyclic antidepressants and monoamine oxidase inhibitors. While the risk for pharmacodynamic interactions is more limited than with older agents with broader receptor effects, the risks for pharmacokinetic interactions is greater. The capacity of selective serotonin reuptake inhibitors to inhibit the metabolic activity of cytochrome P450 isozyme system has spurred over a decade of intense psychopharmacological and pharmacogenetics research to better the understanding of the significance of these interactions. Clinicians have had to increase their knowledge and understanding of drug interaction potential to better manage patients receiving these newer antidepressants. The following is a review of both pharmacodynamic and pharmacokinetic drug-drug interactions with antidepressants.

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Rapp, Robert P. "Pharmacokinetics and Pharmacodynamics of Intravenous and Oral Azithromycin: Enhanced Tissue Activity and Minimal Drug Interactions." Annals of Pharmacotherapy 32, no. 7-8 (July 1998): 785–93. http://dx.doi.org/10.1345/aph.17299.

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Abstract (sommario):

OBJECTIVE: To review the pharmacokinetics and pharmacodynamics of oral and intravenous azithromycin compared with other macrolide antibiotics, and to evaluate these differences and their relation to clinical effectiveness. DATA SOURCE: A MEDLINE search (1966–May 1998) was performed to identify applicable English-language clinical, animal, and microbiologic studies pertaining to pharmacokinetic and pharmacodynamic parameters. STUDY SELECTION: Relevant studies concerning microbiology, pharmacokinetics, tissue concentrations, pharmacodynamics, and the clinical effects of these parameters were selected. DATA SYNTHESIS: The structural modification that distinguishes the azalide antibiotics from the macrolide antibiotics is responsible for the pharmacokinetic and pharmacodynamic behavior of azithromycin, resulting in the high and sustained tissue and intracellular concentrations seen with this agent. Drug delivery to the site of infection by phagocytes and fibroblasts is the hallmark of azithromycin's tissue-directed pharmacodynamics, allowing for convenient once-daily, 5-day regimens for most infections that respond to oral therapy and 7–10 days for more serious infections requiring initial intravenous therapy. Metabolism is via hepatic pathways other than cytochrome P450, thus minimizing the risk of drug interactions. CONCLUSIONS: Compared with other macrolide antibiotics, the unique pharmacokinetic and pharmacodynamic features of azithromycin offer the potential for improved efficacy and safety from drug interactions. These attributes, combined with its once-daily dosing schedule, make azithromycin suitable for the treatment of many types of bacterial infection.

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Czyrski, Andrzej, Matylda Resztak, Paweł Świderski, Jan Brylak, and Franciszek K. Główka. "The Overview on the Pharmacokinetic and Pharmacodynamic Interactions of Triazoles." Pharmaceutics 13, no. 11 (November 19, 2021): 1961. http://dx.doi.org/10.3390/pharmaceutics13111961.

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Abstract (sommario):

Second generation triazoles are widely used as first-line drugs for the treatment of invasive fungal infections, including aspergillosis and candidiasis. This class, along with itraconazole, voriconazole, posaconazole, and isavuconazole, is characterized by a broad range of activity, however, individual drugs vary considerably in safety, tolerability, pharmacokinetics profiles, and interactions with concomitant medications. The interaction may be encountered on the absorption, distribution, metabolism, and elimination (ADME) step. All triazoles as inhibitors or substrates of CYP isoenzymes can often interact with many drugs, which may result in the change of the activity of the drug and cause serious side effects. Drugs of this class should be used with caution with other agents, and an understanding of their pharmacokinetic profile, safety, and drug-drug interaction profiles is important to provide effective antifungal therapy. The manuscript reviews significant drug interactions of azoles with other medications, as well as with food. The PubMed and Google Scholar bases were searched to collect the literature data. The interactions with anticonvulsants, antibiotics, statins, kinase inhibitors, proton pump inhibitors, non-nucleoside reverse transcriptase inhibitors, opioid analgesics, benzodiazepines, cardiac glycosides, nonsteroidal anti-inflammatory drugs, immunosuppressants, antipsychotics, corticosteroids, biguanides, and anticoagulants are presented. We also paid attention to possible interactions with drugs during experimental therapies for the treatment of COVID-19.

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Crismon, M. Lynn. "Pharmacokinetics and Drug Interactions of Cholinesterase Inhibitors Administered in Alzheimer's Disease." Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 18, no. 2P2 (March 4, 1998): 47–54. http://dx.doi.org/10.1002/j.1875-9114.1998.tb03878.x.

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Abstract (sommario):

Cholinesterase inhibitors are the first agents to be successfully developed specifically for the treatment of cognitive decline associated with Alzheimer's disease. Basic knowledge of their pharmacokinetics is important to their appropriate administration. Their pharmacokinetics help determine the magnitude and duration of their pharmacologic effects, and also the manner in which they affect the degree of cholinesterase inhibition and recovery. The clinical utility of measuring these values in daily practice awaits further research. Drug interactions with cholinesterase inhibitors may occur by pharmacokinetic or pharmacodynamic mechanisms. For the most part, interactions that are mediated by the hepatic cytochrome P‐450 system have been inadequately evaluated.

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K, K., K. K, K. K, and K. K. "Oral Pharmacokinetic Drug-drug Interactions between Amifampridine and Acetaminophen in Rats." Yakhak Hoeji 68, no. 2 (March 30, 2024): 98–104. http://dx.doi.org/10.17480/psk.2024.68.2.98.

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Abstract (sommario):

Amifampridine, the first-line medication for Lambert-Eaton myasthenic syndrome (LEMS), is extensively metabolized by N-acetyltransferase 2 (NAT2). Drug-drug interactions (DDIs) can occur when co-administered with a NAT2 inhibitor and amifampridine. Acetaminophen is a widely used analgesic for mild to moderate pain, which is also known as a NAT2 inhibitor. In this work, we studied the effects of acetaminophen on the amifampridine pharmacokinetics in rats. Both acetaminophen (300 mg/kg) and amifampridine (2 mg/kg) were administered orally. In acetaminophen-treated rats, the systemic exposure to amifampridine significantly increased, and the ratio of the area under the plasma concentration-time curve for 3-N-acetylamifampridine to amifampridine (AUCm/AUCp) decreased markedly, which is likely due to the inhibition of NAT2 by acetaminophen. Also, the urinary amount excreted was increased in the acetaminophen-treated group, but the renal clearance remained unchanged. This oral pharmacokinetic drug-drug interaction study showed that orally administered acetaminophen significantly inhibits the NAT2-based metabolism of amifampridine and may cause meaningful DDIs.

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Lesko, L. J. "Pharmacokinetic Drug Interactions with Amiodarone." Clinical Pharmacokinetics 17, no. 2 (August 1989): 130–40. http://dx.doi.org/10.2165/00003088-198917020-00005.

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Venkatesan, K. "Pharmacokinetic Drug Interactions with Rifampicin." Clinical Pharmacokinetics 22, no. 1 (January 1992): 47–65. http://dx.doi.org/10.2165/00003088-199222010-00005.

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Periti, Piero, Teresita Mazzei, Enrico Mini, and Andrea Novelli. "Pharmacokinetic Drug Interactions of Macrolides." Clinical Pharmacokinetics 23, no. 2 (August 1992): 106–31. http://dx.doi.org/10.2165/00003088-199223020-00004.

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Riva, Roberto, Fiorenzo Albani, Manuela Contin, and Agostino Baruzzi. "Pharmacokinetic Interactions Between Antiepileptic Drugs." Clinical Pharmacokinetics 31, no. 6 (December 1996): 470–93. http://dx.doi.org/10.2165/00003088-199631060-00005.

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Giao, Phantrong, and Peter J. de Vries. "Pharmacokinetic Interactions of Antimalarial Agents." Clinical Pharmacokinetics 40, no. 5 (2001): 343–73. http://dx.doi.org/10.2165/00003088-200140050-00003.

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Unger, Matthias. "Pharmacokinetic drug interactions involvingGinkgo biloba." Drug Metabolism Reviews 45, no. 3 (July 19, 2013): 353–85. http://dx.doi.org/10.3109/03602532.2013.815200.

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Somogyi, Andrew, and Murray Muirhead. "Pharmacokinetic Interactions of Cimetidine 1987." Clinical Pharmacokinetics 12, no. 5 (May 1987): 321–66. http://dx.doi.org/10.2165/00003088-198712050-00002.

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Oesterheld, Jessica R., Scott C. Armstrong, and Kelly L. Cozza. "Ecstasy: Pharmacodynamic and Pharmacokinetic Interactions." Psychosomatics 45, no. 1 (March 2004): 84–87. http://dx.doi.org/10.1176/appi.psy.45.1.84.

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Pleuvry, Barbara J. "Pharmacodynamic and pharmacokinetic drug interactions." Anaesthesia & Intensive Care Medicine 6, no. 4 (April 2005): 129–33. http://dx.doi.org/10.1383/anes.6.4.129.63634.

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Blei, Andres. "Pharmacokinetic-Hemodynamic Interactions in Cirrhosis." Seminars in Liver Disease 6, no. 04 (November 1986): 299–308. http://dx.doi.org/10.1055/s-2008-1040612.

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Back, David, Sara Gibbons, and Saye Khoo. "Pharmacokinetic Drug Interactions with Nevirapine." JAIDS Journal of Acquired Immune Deficiency Syndromes 34 (September 2003): S8—S14. http://dx.doi.org/10.1097/00126334-200309011-00003.

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Tarirai, Clemence, Alvaro M. Viljoen, and Josias H. Hamman. "Herb–drug pharmacokinetic interactions reviewed." Expert Opinion on Drug Metabolism & Toxicology 6, no. 12 (November 11, 2010): 1515–38. http://dx.doi.org/10.1517/17425255.2010.529129.

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Brüggemann, Roger J. M., Jan-Willem C. Alffenaar, Nicole M. A. Blijlevens, Eliane M. Billaud, Jos G. W. Kosterink, Paul E. Verweij, and David M. Burger. "Pharmacokinetic drug interactions of azoles." Current Fungal Infection Reports 2, no. 1 (March 2008): 20–27. http://dx.doi.org/10.1007/s12281-008-0004-4.

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Knežević, Sandra, Francesca Filippi-Arriaga, Andrej Belančić, Tamara Božina, Jasenka Mršić-Pelčić, and Dinko Vitezić. "Metabolic Syndrome Drug Therapy: The Potential Interplay of Pharmacogenetics and Pharmacokinetic Interactions in Clinical Practice: A Narrative Review." Diabetology 5, no. 4 (September 3, 2024): 406–29. http://dx.doi.org/10.3390/diabetology5040031.

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Abstract (sommario):

Metabolic syndrome (MetS) presents a significant global health challenge, characterized by a cluster of metabolic alterations including obesity, hypertension, insulin resistance/dysglycemia, and atherogenic dyslipidemia. Advances in understanding and pharmacotherapy have added complexity to MetS management, particularly concerning drug interactions and pharmacogenetic variations. Limited literature exists on drug–drug–gene interactions (DDGIs) and drug–drug–transporter gene interactions (DDTGIs), which can significantly impact pharmacokinetics and pharmacodynamics, affecting treatment outcomes. This narrative review aims to address the following three key objectives: firstly, shedding a light on the PK metabolism, transport, and the pharmacogenetics (PGx) of medicines most commonly used in the MetS setting (relevant lipid-lowering drugs, antihypertensives and antihyperglycemics agents); secondly, exemplifying potential clinically relevant pharmacokinetic drug interactions, including drug–drug interactions, DDGIs, and DDTGIs; and, thirdly, describing and discussing their potential roles in clinical practice. This narrative review includes relevant information found with the use of interaction checkers, pharmacogenetic databases, clinical pharmacogenetic practice guidelines, and literature sources, guided by evidence-based medicine principles.

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Choi, Min-Koo, and Im-Sook Song. "Pharmacokinetic Drug–Drug Interactions and Herb–Drug Interactions." Pharmaceutics 13, no. 5 (April 23, 2021): 610. http://dx.doi.org/10.3390/pharmaceutics13050610.

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Rodriguez-Vera, Leyanis, Xuefen Yin, Mohammed Almoslem, Karolin Romahn, Brian Cicali, Viera Lukacova, Rodrigo Cristofoletti, and Stephan Schmidt. "Comprehensive Physiologically Based Pharmacokinetic Model to Assess Drug–Drug Interactions of Phenytoin." Pharmaceutics 15, no. 10 (October 18, 2023): 2486. http://dx.doi.org/10.3390/pharmaceutics15102486.

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Abstract (sommario):

Regulatory agencies worldwide expect that clinical pharmacokinetic drug–drug interactions (DDIs) between an investigational new drug and other drugs should be conducted during drug development as part of an adequate assessment of the drug’s safety and efficacy. However, it is neither time nor cost efficient to test all possible DDI scenarios clinically. Phenytoin is classified by the Food and Drug Administration as a strong clinical index inducer of CYP3A4, and a moderate sensitive substrate of CYP2C9. A physiologically based pharmacokinetic (PBPK) platform model was developed using GastroPlus® to assess DDIs with phenytoin acting as the victim (CYP2C9, CYP2C19) or perpetrator (CYP3A4). Pharmacokinetic data were obtained from 15 different studies in healthy subjects. The PBPK model of phenytoin explains the contribution of CYP2C9 and CYP2C19 to the formation of 5-(4′-hydroxyphenyl)-5-phenylhydantoin. Furthermore, it accurately recapitulated phenytoin exposure after single and multiple intravenous and oral doses/formulations ranging from 248 to 900 mg, the dose-dependent nonlinearity and the magnitude of the effect of food on phenytoin pharmacokinetics. Once developed and verified, the model was used to characterize and predict phenytoin DDIs with fluconazole, omeprazole and itraconazole, i.e., simulated/observed DDI AUC ratio ranging from 0.89 to 1.25. This study supports the utility of the PBPK approach in informing drug development.

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Albitar, Orwa, Sabariah Noor Harun, Hadzliana Zainal, Baharudin Ibrahim, and Siti Maisharah Sheikh Ghadzi. "Population Pharmacokinetics of Clozapine: A Systematic Review." BioMed Research International 2020 (January 8, 2020): 1–10. http://dx.doi.org/10.1155/2020/9872936.

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Abstract (sommario):

Background and Objective. Clozapine is a second-generation antipsychotic drug that is considered the most effective treatment for refractory schizophrenia. Several clozapine population pharmacokinetic models have been introduced in the last decades. Thus, a systematic review was performed (i) to compare published pharmacokinetics models and (ii) to summarize and explore identified covariates influencing the clozapine pharmacokinetics models. Methods. A search of publications for population pharmacokinetic analyses of clozapine either in healthy volunteers or patients from inception to April 2019 was conducted in PubMed and SCOPUS databases. Reviews, methodology articles, in vitro and animal studies, and noncompartmental analysis were excluded. Results. Twelve studies were included in this review. Clozapine pharmacokinetics was described as one-compartment with first-order absorption and elimination in most of the studies. Significant interindividual variations of clozapine pharmacokinetic parameters were found in most of the included studies. Age, sex, smoking status, and cytochrome P450 1A2 were found to be the most common identified covariates affecting these parameters. External validation was only performed in one study to determine the predictive performance of the models. Conclusions. Large pharmacokinetic variability remains despite the inclusion of several covariates. This can be improved by including other potential factors such as genetic polymorphisms, metabolic factors, and significant drug-drug interactions in a well-designed population pharmacokinetic model in the future, taking into account the incorporation of larger sample size and more stringent sampling strategy. External validation should also be performed to the previously published models to compare their predictive performances.

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Li, Ying, Yin Wu, Ya-Jing Li, Lu Meng, Cong-Yang Ding, and Zhan-Jun Dong. "Effects of Silymarin on the In Vivo Pharmacokinetics of Simvastatin and Its Active Metabolite in Rats." Molecules 24, no. 9 (April 28, 2019): 1666. http://dx.doi.org/10.3390/molecules24091666.

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Abstract (sommario):

Herein, the effect of silymarin pretreatment on the pharmacokinetics of simvastatin in rats was evaluated. To ensure the accuracy of the results, a rapid and sensitive UPLC–MS/MS method was established for simultaneous quantification of simvastatin (SV) and its active metabolite simvastatin acid (SVA). This method was applied for studying the pharmacokinetic interactions in rats after oral co-administration of silymarin (45 mg/kg) and different concentrations of SV. The major pharmacokinetic parameters, including Cmax, tmax, t1/2, mean residence time (MRT), elimination rate constant (λz) and area under the concentration-time curve (AUC0–12h), were calculated using the non-compartmental model. The results showed that the co-administration of silymarin and SV significantly increased the Cmax and AUC0–12h of SVA compared with SV alone, while there was no significant difference with regards to Tmax and t1/2. However, SV pharmacokinetic parameters were not significantly affected by silymarin pretreatment. Therefore, these changes indicated that drug-drug interactions may occur after co-administration of silymarin and SV.

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