Anesthesia/Anti-Convulsants: Carbamazepine Ethosuximide Halothane Lidocaine Phenytoin Valproic Acid Antibiotics: Aminoglycosides

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DRUGS Anesthesia/Anti-Convulsants: Carbamazepine Ethosuximide Halothane Lidocaine Phenytoin Valproic Acid Antibiotics: Aminoglycosides (Generic Examples: Gentamycin; Tobramycin; Amikacin) Amoxicillin Amphotericin B Ampicillin Azithromycin (A Special Macrolide) Ceftriaxone (Prototype 3rd Generation Cephalosporin) Chloramphenicol Chloroquine, Quinine and Mefloquine Ciprofloxacin (Prototype Fluoroquinolone) Clindamycin Demeclocycline (Another Tetracycline) Doxycycline (Prototype Tetracycline) Erythromycin (Prototype Macrolide) Indinavir Isoniazid Ketoconazole Metronidazole Nafcillin (Beta-Lactamase Resistant Penicillin) Praziquantel Rifampin Trimethoprim + Sulfamethoxazole Vancomycin Zidovudine Autonomic Drugs : Atropine Bethanechol Clonidine Cocaine Dobutamine Edrophonium Epinephrine Isoproteronol Labetalol (also Carvedilol) Methylphenidate Metoprolol Phenoxybenzamine Phentolamine Phenylepherine Physostigmine Pilocarpine Pindolol (also Acebutolol) Prazosin Propranolol Reserpine Ritodrine Blood D/O Drugs: Heparin Streptokinase TPA (Tissue Plasminogen Activator) Warfarin Cancer Drugs: 5-Fluoruracil + Folic Acid Bleomycin Busulfan Cisplatin Colchicine Cyclophoshamide Cyclosporine Dacarbazine Doxorubicin = Adriamycin Melphalan Methotrexate Vinchristine Cardiovascular Drugs: Amiodarone Captopril and Enalapril Digoxin Diltiazem Hydralazine Lidocaine Losartan Nifedipine Nitroglycerin and Isosorbide Dinitrate Nitroprusside Procainamide Quinidine Verapamil CNS Drugs: Alprazolam (Another Benzodiazepine) Desipramine (Secondary TCA) Diazepam (Prototype Benzoadiazepine) Flumazenil Fluoxetine Imipramine (Tertiary TCA) Lithium Phenelzine (MAO-I) Trancyclopromine (Another MAO-I) Triazolam (Another Benzodiazepine) Diuretics: Ethacrynic Acid Furosemide Hydrochlorothiazide GI Drugs: Cholestyramine Cimetidine Ipecac Lovastatin Niacin (Vitamin B3) Omeprazole Insulin/Hypoglycemics : Chlorpropamide (Prototye sulfonylurea : Tolbutamide, Glyburide, Glipizide) Regular Insulin NSAIDS/Analgesia : Acetomenophin ASA : Apirin (Acetylsalic Acid) Ibuprofen Indomethacin Meperidine Morphine (Prototype Opiate) Naloxone Oxycodone Zafirlukast Parkinsons/Antipsychotics : Bromocriptine Chlorpromazine Clozapine Haloperidol L-Dopa Selgiline Respiratory : Aminophylline/Theophylline Beclomethasone (Inhaled Steroid) Cromolyn Sodium Ipratrapium Prednisone Respiratory/Steriods: Ethinyl Estradiol (Synthetic Estrogen) Finasteride Leuprolide (GnRH Analog) Levothyroxine Medroxy Progesterone (Synthetic Progesterone) Octreotide Prednisone Prophylthiouracil Spironolactone Tamoxifen Misc. Drugs: Allopurinol Aurithroglucose Colchicine Diphenhydramine Ergotamine Tartrate Isoretinoin Penicillamine Sildenafil Sumatriptan .

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With LAMOTRIGINE IN
were independent of seizure type. Cardiac abnormalities occurring in epilepsy with GTCS may potentially facilitate sudden cardiac death (SUDEP). ETHOSUXIMIDE, VALPROIC ACID, AND LAMOTRIGINE IN CHILDHOOD ABSENCE EPILEPSY Efficacy, tolerability, and neuropsychological effects of ethosuximide, valproic acid, and lamotrigine in children with newly diagnosed childhood absence epilepsy were compared in a double-blind, randomized, controlled clinical trial performed at six centers in the US and organized as a Study Group. Drug doses were incrementally increased until freedom from seizures or highest tolerable dose was reached, Primary outcome was freedom from treatment failure after 16 weeks therapy, and secondary outcome was attentional dysfunction. In a total of 453 children, the freedom-from-failure rates after 16 weeks were similar for ethosuximide (53%) and valproic acid (58%), and higher than the rate for lamotrigine (29%) (P<0.001). Attentional dysfunction was more common with valproic acid (49%) than with ethosuximide (33%) (P=0.03). (Glauser TA, Cnaan A, Shinnar S, et al. Ethosuximide, valproic acid, and lamotrigine in childhood absence epilepsy. N Engl J Med March 4 2010;362:790-799). (Reprints: Dr Tracy A Glauser, Cincinnati Children's Hospital, 3333 Burnett Ave, MLC 2015, Cincinnati, OH 45229. E- mail: [email protected]). COMMENT. "Older is better," is the conclusion of Vining EPG, in an editorial (N Engl J Med 2010;362:843-845). As generally accepted in US practice and confirmed by the above controlled trial, ethosuximide from the 1950s is the optimal initial therapy for childhood absence epilepsy without GTCS. Ethosuximide is equal to valproic acid in seizure control and superior in effects on attention.
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Fasted and Fed State Human Duodenal Fluids: Characterization, Drug Solubility, and Comparison to Simulated Fluids and with Human Bioavailability
European Journal of Pharmaceutics and Biopharmaceutics 163 (2021) 240–251 Contents lists available at ScienceDirect European Journal of Pharmaceutics and Biopharmaceutics journal homepage: www.elsevier.com/locate/ejpb Fasted and fed state human duodenal fluids: Characterization, drug solubility, and comparison to simulated fluids and with human bioavailability D. Dahlgren a, M. Venczel b,c, J.-P. Ridoux b,c, C. Skjold¨ a, A. Müllertz d, R. Holm e, P. Augustijns f, P.M. Hellstrom¨ g, H. Lennernas¨ a,* a Department of Pharmaceutical Biosciences, Biopharmaceutics, Uppsala University, Sweden b Global CMC Development Sanofi, Frankfurt, Germany c Global CMC Development Sanofi, Vitry, France d Physiological Pharmaceutics, University of Copenhagen, Copenhagen, Denmark e Drug Product Development, Janssen R&D, Johnson & Johnson, Beerse, Belgium f Drug Delivery and Disposition, KU Leuven, Leuven, Belgium g Department of Medical Sciences, Gastroenterology/Hepatology, Uppsala University, Sweden ARTICLE INFO ABSTRACT Keywords: Accurate in vivo predictions of intestinal absorption of low solubility drugs require knowing their solubility in Bioavailability physiologically relevant dissolution media. Aspirated human intestinal fluids (HIF) are the gold standard, fol Food effects lowed by simulated intestinal HIF in the fasted and fed state (FaSSIF/FeSSIF). However, current HIF charac Drug solubility terization data vary, and there is also some controversy regarding the accuracy of FaSSIF and FeSSIF for Human intestinal fluids predicting drug solubility in HIF. This study aimed at characterizing fasted and fed state duodenal HIF from 16 Drug absorption Drug dissolution human volunteers with respect to pH, buffer capacity, osmolarity, surface tension, as well as protein, phos Drug delivery pholipid, and bile salt content.
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Therapeutic Class Overview Anticonvulsants
Therapeutic Class Overview Anticonvulsants INTRODUCTION Epilepsy is a disease of the brain defined by any of the following (Fisher et al 2014): ○ At least 2 unprovoked (or reflex) seizures occurring > 24 hours apart; ○ 1 unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after 2 unprovoked seizures, occurring over the next 10 years; ○ Diagnosis of an epilepsy syndrome. Types of seizures include generalized seizures, focal (partial) seizures, and status epilepticus (Centers for Disease Control and Prevention [CDC] 2018, Epilepsy Foundation 2016). ○ Generalized seizures affect both sides of the brain and include: . Tonic-clonic (grand mal): begin with stiffening of the limbs, followed by jerking of the limbs and face . Myoclonic: characterized by rapid, brief contractions of body muscles, usually on both sides of the body at the same time . Atonic: characterized by abrupt loss of muscle tone; they are also called drop attacks or akinetic seizures and can result in injury due to falls . Absence (petit mal): characterized by brief lapses of awareness, sometimes with staring, that begin and end abruptly; they are more common in children than adults and may be accompanied by brief myoclonic jerking of the eyelids or facial muscles, a loss of muscle tone, or automatisms. ○ Focal seizures are located in just 1 area of the brain and include: . Simple: affect a small part of the brain; can affect movement, sensations, and emotion, without a loss of consciousness . Complex: affect a larger area of the brain than simple focal seizures and the patient loses awareness; episodes typically begin with a blank stare, followed by chewing movements, picking at or fumbling with clothing, mumbling, and performing repeated unorganized movements or wandering; they may also be called “temporal lobe epilepsy” or “psychomotor epilepsy” .
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Pharmacokinetic Drug–Drug Interactions Among Antiepileptic Drugs, Including CBD, Drugs Used to Treat COVID-19 and Nutrients
International Journal of Molecular Sciences Review Pharmacokinetic Drug–Drug Interactions among Antiepileptic Drugs, Including CBD, Drugs Used to Treat COVID-19 and Nutrients Marta Kara´zniewicz-Łada 1 , Anna K. Główka 2 , Aniceta A. Mikulska 1 and Franciszek K. Główka 1,* 1 Department of Physical Pharmacy and Pharmacokinetics, Poznan University of Medical Sciences, 60-781 Poznań,Poland; [email protected] (M.K.-Ł.); [email protected] (A.A.M.) 2 Department of Bromatology, Poznan University of Medical Sciences, 60-354 Poznań,Poland; [email protected] * Correspondence: [email protected]; Tel.: +48-(0)61-854-64-37 Abstract: Anti-epileptic drugs (AEDs) are an important group of drugs of several generations, rang- ing from the oldest phenobarbital (1912) to the most recent cenobamate (2019). Cannabidiol (CBD) is increasingly used to treat epilepsy. The outbreak of the SARS-CoV-2 pandemic in 2019 created new challenges in the effective treatment of epilepsy in COVID-19 patients. The purpose of this review is to present data from the last few years on drug–drug interactions among of AEDs, as well as AEDs with other drugs, nutrients and food. Literature data was collected mainly in PubMed, as well as google base. The most important pharmacokinetic parameters of the chosen 29 AEDs, mechanism of action and clinical application, as well as their biotransformation, are presented. We pay a special attention to the new potential interactions of the applied first-generation AEDs (carba- Citation: Kara´zniewicz-Łada,M.; mazepine, oxcarbazepine, phenytoin, phenobarbital and primidone), on decreased concentration Główka, A.K.; Mikulska, A.A.; of some medications (atazanavir and remdesivir), or their compositions (darunavir/cobicistat and Główka, F.K.
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Pharmacokinetic Interactions of Pioglitazone
Department of Clinical Pharmacology University of Helsinki Finland PHARMACOKINETIC INTERACTIONS OF PIOGLITAZONE Tiina Jaakkola ACADEMIC DISSERTATION To be presented, with the permission of the Medical Faculty of the University of Helsinki, for public examination in Auditorium 2 of Biomedicum, on August 24th, 2007, at 12 noon. Helsinki 2007 JJaakkola_Tiina_vaitos.inddaakkola_Tiina_vaitos.indd 1 117.7.20077.7.2007 221:11:231:11:23 Supervisors: Professor Pertti Neuvonen, MD Department of Clinical Pharmacology University of Helsinki Helsinki, Finland Docent Janne Backman, MD Department of Clinical Pharmacology University of Helsinki Helsinki, Finland Reviewers: Docent Kimmo Malminiemi, MD, MSc Department of Pharmacology, Clinical Pharmacology and Toxicology University of Tampere Tampere, Finland Professor emeritus Pertti Pentikäinen, MD Department of Medicine University of Helsinki Helsinki, Finland Opponent: Professor Kari Kivistö, MD Department of Pharmacology, Clinical Pharmacology and Toxicology University of Tampere Tampere, Finland ISBN 978-952-92-2224-7 (paperback) ISBN 978-952-10-4020-7 (PDF, http://ethesis.helsinki.fi ) Helsinki 2007 Yliopistopaino JJaakkola_Tiina_vaitos.inddaakkola_Tiina_vaitos.indd 2 117.7.20077.7.2007 221:11:551:11:55 JJaakkola_Tiina_vaitos.inddaakkola_Tiina_vaitos.indd 3 117.7.20077.7.2007 221:11:551:11:55 CONTENTS CONTENTS ABBREVIATIONS.......................................................................................................................................... 6 LIST OF ORIGINAL PUBLICATIONS.......................................................................................................
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Pharmacokinetic Interactions of Drugs with St John's Wort
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Mechanisms of Action of Antiepileptic Drugs
Review Mechanisms of action of antiepileptic drugs Epilepsy affects up to 1% of the general population and causes substantial disability. The management of seizures in patients with epilepsy relies heavily on antiepileptic drugs (AEDs). Phenobarbital, phenytoin, carbamazepine and valproic acid have been the primary medications used to treat epilepsy for several decades. Since 1993 several AEDs have been approved by the US FDA for use in epilepsy. The choice of the AED is based primarily on the seizure type, spectrum of clinical activity, side effect profile and patient characteristics such as age, comorbidities and concurrent medical treatments. Those AEDs with broad- spectrum activity are often found to exert an action at more than one molecular target. This article will review the proposed mechanisms of action of marketed AEDs in the US and discuss the future of AEDs in development. 1 KEYWORDS: AEDs anticonvulsant drugs antiepileptic drugs epilepsy Aaron M Cook mechanism of action seizures & Meriem K Bensalem-Owen† The therapeutic armamentarium for the treat- patients with refractory seizures. The aim of this 1UK HealthCare, 800 Rose St. H-109, ment of seizures has broadened significantly article is to discuss the past, present and future of Lexington, KY 40536-0293, USA †Author for correspondence: over the past decade [1]. Many of the newer AED pharmacology and mechanisms of action. College of Medicine, Department of anti epileptic drugs (AEDs) have clinical advan- Neurology, University of Kentucky, 800 Rose Street, Room L-455, tages over older, so-called ‘first-generation’ First-generation AEDs Lexington, KY 40536, USA AEDs in that they are more predictable in their Broadly, the mechanisms of action of AEDs can Tel.: +1 859 323 0229 Fax: +1 859 323 5943 dose–response profile and typically are associ- be categorized by their effects on the neuronal [email protected] ated with less drug–drug interactions.
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ACCOLATE® (Zafirlukast) TABLETS DESCRIPTION
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Chapter 25 Mechanisms of Action of Antiepileptic Drugs
Chapter 25 Mechanisms of action of antiepileptic drugs GRAEME J. SILLS Department of Molecular and Clinical Pharmacology, University of Liverpool _________________________________________________________________________ Introduction The serendipitous discovery of the anticonvulsant properties of phenobarbital in 1912 marked the foundation of the modern pharmacotherapy of epilepsy. The subsequent 70 years saw the introduction of phenytoin, ethosuximide, carbamazepine, sodium valproate and a range of benzodiazepines. Collectively, these compounds have come to be regarded as the ‘established’ antiepileptic drugs (AEDs). A concerted period of development of drugs for epilepsy throughout the 1980s and 1990s has resulted (to date) in 16 new agents being licensed as add-on treatment for difficult-to-control adult and/or paediatric epilepsy, with some becoming available as monotherapy for newly diagnosed patients. Together, these have become known as the ‘modern’ AEDs. Throughout this period of unprecedented drug development, there have also been considerable advances in our understanding of how antiepileptic agents exert their effects at the cellular level. AEDs are neither preventive nor curative and are employed solely as a means of controlling symptoms (i.e. suppression of seizures). Recurrent seizure activity is the manifestation of an intermittent and excessive hyperexcitability of the nervous system and, while the pharmacological minutiae of currently marketed AEDs remain to be completely unravelled, these agents essentially redress the balance between neuronal excitation and inhibition. Three major classes of mechanism are recognised: modulation of voltage-gated ion channels; enhancement of gamma-aminobutyric acid (GABA)-mediated inhibitory neurotransmission; and attenuation of glutamate-mediated excitatory neurotransmission. The principal pharmacological targets of currently available AEDs are highlighted in Table 1 and discussed further below.
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Therapeutic Drug Monitoring of Antiepileptic Drugs by Use of Saliva
REVIEW ARTICLE Therapeutic Drug Monitoring of Antiepileptic Drugs by Use of Saliva Philip N. Patsalos, FRCPath, PhD*† and Dave J. Berry, FRCPath, PhD† INTRODUCTION Abstract: Blood (serum/plasma) antiepileptic drug (AED) therapeu- Measuring antiepileptic drugs (AEDs) in serum or tic drug monitoring (TDM) has proven to be an invaluable surrogate plasma as an aid to personalizing drug therapy is now a well- marker for individualizing and optimizing the drug management of established practice in the treatment of epilepsy, and guidelines patients with epilepsy. Since 1989, there has been an exponential are published that indicate the particular features of epilepsy and increase in AEDs with 23 currently licensed for clinical use, and the properties of AEDs that make the practice so beneﬁcial.1 recently, there has been renewed and extensive interest in the use of The goal of AED therapeutic drug monitoring (TDM) is to saliva as an alternative matrix for AED TDM. The advantages of saliva ’ ﬂ optimize a patient s clinical outcome by supporting the man- include the fact that for many AEDs it re ects the free (pharmacolog- agement of their medication regimen with the assistance of ically active) concentration in serum; it is readily sampled, can be measured drug concentrations/levels. The reason why TDM sampled repetitively, and sampling is noninvasive; does not require the has emerged as an important adjunct to treatment with the expertise of a phlebotomist; and is preferred by many patients, AEDs arises from the fact that for an individual patient
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Farmacopea De 2021 (Lista De Medicamentos Cubiertos)
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Β-Hydroxybutyrate Detection with Proton MR Spectroscopy In
ORIGINAL RESEARCH PEDIATRICS ␤-Hydroxybutyrate Detection with Proton MR Spectroscopy in Children with Drug-Resistant Epilepsy on the Ketogenic Diet X J.N. Wright, X R.P. Saneto, and X S.D. Friedman ABSTRACT BACKGROUND AND PURPOSE: The ketogenic diet, including both classic and modified forms, is an alternative to antiepileptic medica- tions used in the treatment of drug-resistant epilepsy. We sought to evaluate the utility of proton MR spectroscopy for the detection of ␤-hydroxybutyrate in a cohort of children with epilepsy treated with the ketogenic diet and to correlate brain parenchymal metabolite ratios obtained from spectroscopy with ␤-hydroxybutyrate serum concentrations. MATERIALS AND METHODS: Twenty-three spectroscopic datasets acquired at a TE of 288 ms in children on the ketogenic diet were analyzed with LCModel using a modified basis set that included a simulated ␤-hydroxybutyrate resonance. Brain parenchymal metabolite ratios were calculated. Metabolite ratios were compared with serum ␤-hydroxybutyrate concentrations, and partial correlation coeffi- cients were calculated using patient age as a covariate. RESULTS: ␤-hydroxybutyrate blood levels were highly correlated to brain ␤-hydroxybutyrate levels, referenced as either choline, crea- tine, or N-acetylaspartate. They were inversely but more weakly associated with N-acetylaspartate, regardless of the ratio denominator. No strong concordance with lactate was demonstrated. CONCLUSIONS: Clinical MR spectroscopy in pediatric patients on the ketogenic diet demonstrated measurable ␤-hydroxybutyrate, with a strong correlation to ␤-hydroxybutyrate blood levels. These findings may serve as an effective tool for noninvasive monitoring of ketosis in this population. An inverse correlation between serum ␤-hydroxybutyrate levels and brain tissue N-acetylaspartate suggests that altered amino acid handling contributes to the antiepileptogenic effect of the ketogenic diet.
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