DOCSLIB.ORG

Drug Adherence Assessment Report

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Drug Adherence Assessment Report APPROVAL REQUIRED Patient: COMP, Sample report Acc #: 80139 Patient #: 1-49505 Birth: 4/5/1963 Doctor: Doctor, Test Age: 55 years Collection Date: 4/17/2018 1:27 PM Gender: Male Received in Lab: 4/17/2018 1:27 PM CT Drug Adherence Assessment Report Prescribed Medications: CYMBALTA, FIORICET, HYDROCODONE/APAP, NEURONTIN, NORTRIPTYLINE, SOMA, TRAMADOL, VENLAFAXINE, XANAX, CODEINE, PROMETHAZINE, STADOL, ACETAMINOPHEN, ABILIFY, CHLORPROMAZINE, TIAGABINE, TOPAMAX, BRINTELLIX, TRILEPTAL, GLUMETZA (Metformin), PALIPERIDONE, DARVON, CARBAMAZEPINE, TEGRETOL, GEODON, PLAVIX (CLOPIDOGREL), PREVACID (LANSOPRAZOLE), PANTOPRAZOLE, WARFARIN, SIMVASTATIN, OMEPRAZOLE, SUDAFED (Pseudoephedrine), INVEGA SUSTENNA, ZYLOPRIM (Allopurinol) CONSISTENT RESULTS - REPORTED MEDICATION DETECTED (PARENT DRUG AND/OR METABOLITE) REPORTED ANTICIPATED TEST DETECTION WINDOW PRESCRIPTION POSITIVE(S) OUTCOME ABILIFY Aripiprazole POSITIVE Plasma Half-Life: 75-94 hours ACETAMINOPHEN Acetaminophen POSITIVE Plasma Half-Life: 2-3 hours BRINTELLIX Vortioxetine POSITIVE Plasma Half-Life: 66 hours CHLORPROMAZINE Chlorpromazine POSITIVE Plasma Half-Life: 30 hours CODEINE Codeine POSITIVE Plasma Half-Life: 2-4 hours CODEINE Morphine POSITIVE Plasma Half-Life: 1.3-7 hours CODEINE Dihydrocodeine POSITIVE Plasma Half-Life: 4 hours CODEINE NorCodeine POSITIVE Plasma Half-Life: 2-4 hours CYMBALTA Duloxetine POSITIVE Plasma Half-Life: 8-17 hours FIORICET Acetaminophen POSITIVE Plasma Half-Life: 2-3 hours FIORICET Caffeine POSITIVE Plasma Half-Life: 5-6 hours GLUMETZA (Metformin) Metformin POSITIVE Plasma Half-Life: 6-7 hours HYDROCODONE/APAP Hydrocodone POSITIVE Plasma Half-Life: 3.5-9 hours HYDROCODONE/APAP Norhydrocodone POSITIVE Plasma Half-Life: 3.5-9 hours HYDROCODONE/APAP Hydromorphone POSITIVE Plasma Half-Life: 1.5-4 hours NEURONTIN Gabapentin POSITIVE Plasma Half-Life: 5-7 hours NORTRIPTYLINE Nortriptyline POSITIVE Plasma Half-Life: 26 hours PALIPERIDONE 9-Hydroxyrisperidone POSITIVE Plasma Half-Life: 5-6 days PROMETHAZINE Promethazine POSITIVE Plasma Half-Life: 16-19 hours SOMA Carisoprodol POSITIVE Plasma Half-Life: 2 hours SOMA Meprobamate POSITIVE Plasma Half-Life: 10 hours STADOL Butorphanol POSITIVE Plasma Half-Life: 18 hours TIAGABINE Tiagabine POSITIVE Plasma Half-Life: 2-5 hours TOPAMAX Topiramate POSITIVE Plasma Half-Life: 19-25 hours TRAMADOL Tramadol POSITIVE Plasma Half-Life: 4-8 hours TRAMADOL N-Desmethyl-Tramadol POSITIVE Plasma Half-Life: 4-10 hours TRAMADOL O-Desmethyl-Tramadol POSITIVE Plasma Half-Life: 4-10 hours TRILEPTAL Carbamazepine POSITIVE Plasma Half-Life: 18-65 hours TRILEPTAL Oxcarbazepine POSITIVE Plasma Half-Life: 1-5 hours Originally Reported On: 4/24/2018 1:03 PM Accession: 80139 Patient ID: 1-49505 Printed: 4/24/2018 7:20 PM Lab Results For: Sample report COMP Page 1 of 17 STAT[S] Corrected [C] Added [A] APPROVAL REQUIRED Patient: COMP, Sample report Acc #: 80139 Patient #: 1-49505 Birth: 4/5/1963 Doctor: Doctor, Test Age: 55 years Collection Date: 4/17/2018 1:27 PM Gender: Male Received in Lab: 4/17/2018 1:27 PM CT TRILEPTAL 10-11-Dihydro-10-Hydroxycarbamazepine POSITIVE Plasma Half-Life: 8-10 hours VENLAFAXINE Venlafaxine POSITIVE Plasma Half-Life: 3-7 hours VENLAFAXINE O-Desmethyl-Venlafaxine POSITIVE Plasma Half-Life: 9-13 hours XANAX Alprazolam POSITIVE Plasma Half-Life: 6-27 hours XANAX Alpha-hydroxyalprazolam POSITIVE Plasma Half-Life: 13-20 hours DARVON Propoxyphene POSITIVE Plasma Half-Life: 8-24 hours DARVON Norpropoxyphene POSITIVE Plasma Half-Life: 16-30 hours CARBAMAZEPINE Carbamazepine POSITIVE Plasma Half-Life: 18-65 hours CARBAMAZEPINE 10-11-Dihydro-10-Hydroxycarbamazepine POSITIVE Plasma Half-Life: 8-10 hours GEODON Ziprasidone POSITIVE Plasma Half-Life: 7-10 hours INVEGA SUSTENNA 9-Hydroxyrisperidone POSITIVE Plasma Half-Life: 5-6 days OMEPRAZOLE Omeprazole POSITIVE Plasma Half-Life: less than 1 hour PANTOPRAZOLE Pantoprazole POSITIVE Plasma Half-Life: 1 hour PLAVIX (CLOPIDOGREL) Clopidogrel POSITIVE Plasma Half-Life: 7-8 hours SIMVASTATIN Simvastatin POSITIVE Plasma Half-Life: SUDAFED (Pseudoephedrine) Pseudoephedrine POSITIVE Plasma Half-Life: 4-8 hours TEGRETOL Carbamazepine POSITIVE Plasma Half-Life: 18-65 hours TEGRETOL 10-11-Dihydro-10-Hydroxycarbamazepine POSITIVE Plasma Half-Life: 8-10 hours WARFARIN Warfarin POSITIVE Plasma Half-Life: 20-60 hours ZYLOPRIM (Allopurinol) Oxipurinol POSITIVE Plasma Half-Life: 1-2 hours INCONSISTENT RESULTS - REPORTED MEDICATION NOT DETECTED (NEITHER PARENT DRUG NOR METABOLITE) REPORTED ANTICIPATED TEST DETECTION WINDOW PRESCRIPTION POSITIVE(S) OUTCOME N/A N/A N/A N/A Originally Reported On: 4/24/2018 1:03 PM Accession: 80139 Patient ID: 1-49505 Printed: 4/24/2018 7:20 PM Lab Results For: Sample report COMP Page 2 of 17 STAT[S] Corrected [C] Added [A] APPROVAL REQUIRED Patient: COMP, Sample report Acc #: 80139 Patient #: 1-49505 Birth: 4/5/1963 Doctor: Doctor, Test Age: 55 years Collection Date: 4/17/2018 1:27 PM Gender: Male Received in Lab: 4/17/2018 1:27 PM CT INCONSISTENT RESULTS - ANALYTE DETECTED BUT NO CORRESPONDING PRESCRIPTION REPORTED DETECTED ILLICIT MEASURED CUTOFF TEST DETECTION WINDOW ANALYTE RESULT OUTCOME Buprenorphine No 200 <10 POSITIVE Plasma Half-Life: 26-42 hours Norbuprenorphine No 200 <10 POSITIVE Plasma Half-Life: 15-150 hours Fentanyl No 200 <5 POSITIVE Plasma Half-Life: 3-12 hours Norfentanyl No 200 <5 POSITIVE Plasma Half-Life: 9-10 hours Levorphanol No 200 <5 POSITIVE Plasma Half-Life: 11-30 hours Meperidine No 200 <5 POSITIVE Plasma Half-Life: 3-4 hours Methadone No 200 <5 POSITIVE Plasma Half-Life: 15-55 hours EDDP No 200 <5 POSITIVE Plasma Half-Life: 15-55 hours Oxycodone No 200 <5 POSITIVE Plasma Half-Life: 3-6 hours Noroxycodone No 200 <10 POSITIVE Plasma Half-Life: 3-6 hours Oxymorphone No 200 <10 POSITIVE Plasma Half-Life: 7.5-9.5 hours Tapentadol No 200 <10 POSITIVE Plasma Half-Life: 4 hours Clonazepam No 200 <5 POSITIVE Plasma Half-Life:19-60 hours 7-Aminoclonazepam No 200 <5 POSITIVE Plasma Half-Life: 30-92 hours Diazepam No 200 <5 POSITIVE Plasma Half-Life: 21-37 hours Nordiazepam No 200 <5 POSITIVE Plasma Half-Life: 36-200 hours Temazepam No 200 <5 POSITIVE Plasma Half-Life: 3-13 hours Oxazepam No 200 <5 POSITIVE Plasma Half-Life: 4-11 hours Lorazepam No 200 <125 POSITIVE Plasma Half-Life: 9-16 hours Alpha-Hydroxytriazolam No 200 <5 POSITIVE Plasma Half-Life: 3-4 hrs 6-Hydroxybuspirone No 200 <10 POSITIVE Plasma Half-Life: 3-4 hours Buspirone No 200 <10 POSITIVE Plasma Half-Life: 2-3 hours Triazolam No 200 <5 POSITIVE Plasma Half-Life: 1-6 hours Prazepam No 200 <10 POSITIVE Plasma Half-Life: 29-224 hours Norchlordiazepoxide No 200 <10 POSITIVE Plasma Half-Life: 6-28 hours N-Desmethyl-Flunitrazepam No 200 <5 POSITIVE Plasma Half-Life: 16-35 hours Flunitrazepam No 200 <5 POSITIVE Plasma Half-Life: 16-35 hours Estazolam No 200 <5 POSITIVE Plasma Half-Life: 1-6 hours Clobazam No 200 <5 POSITIVE Plasma Half-Life:18 hours Chlordiazepoxide No 200 <5 POSITIVE Plasma Half-Life: 6-28 hours Clozapine No 200 <5 POSITIVE Plasma Half-Life: 14 hours Clozapine_N_oxide No 200 <10 POSITIVE Plasma Half-Life: 14 hours Fluphenazine No 200 <5 POSITIVE Plasma Half-Life: 14-15 hours Quetiapine No 200 <5 POSITIVE Plasma Half-Life: 6-7 hours Thioridazine No 200 <10 POSITIVE Plasma Half-Life: 5-26 hours Thiothixene No 200 <10 POSITIVE Plasma Half-Life: 4-24 hours Risperidone No 200 <5 POSITIVE Plasma Half-Life: 3 hours Olanzapine No 200 <10 POSITIVE Plasma Half-Life: 21-54 hours Asenapine No 200 <50 POSITIVE Plasma Half-Life: 24 hours Norquetiapine No 200 <50 POSITIVE Plasma Half-Life: 7-12 hours Originally Reported On: 4/24/2018 1:03 PM Accession: 80139 Patient ID: 1-49505 Printed: 4/24/2018 7:20 PM Lab Results For: Sample report COMP Page 3 of 17 STAT[S] Corrected [C] Added [A] APPROVAL REQUIRED Patient: COMP, Sample report Acc #: 80139 Patient #: 1-49505 Birth: 4/5/1963 Doctor: Doctor, Test Age: 55 years Collection Date: 4/17/2018 1:27 PM Gender: Male Received in Lab: 4/17/2018 1:27 PM CT Lurasidone No 200 <10 POSITIVE Plasma Half-Life:14-18 hours Iloperidone No 200 <10 POSITIVE Plasma Half-Life: 18-33 hours Dehydro Aripiprazole No 200 <125 POSITIVE Plasma Half-Life: 75-94 hours Haloperidol No 200 <5 POSITIVE Plasma Half-Life: 14-37 hours Amitriptyline No 200 <5 POSITIVE Plasma Half-Life: 10-28 hours Bupropion No 200 <5 POSITIVE Plasma Half-Life: 12-30 hours Citalopram No 200 <10 POSITIVE Plasma Half-Life: 35 hours Doxepin No 200 <5 POSITIVE Plasma-Half-Life: 8-25 hours Fluoxetine No 200 <5 POSITIVE Plasma Half-Life: 4 days Mirtazapine No 200 <5 POSITIVE Plasma Half-Life: 20-40 hours Paroxetine No 200 <10 POSITIVE Plasma Half-Life: 21 hours Sertraline No 200 <5 POSITIVE Plasma Half-Life: 23-26 hours Trazodone No 200 <5 POSITIVE Plasma Half-Life: 10-12 hours Clomipramine No 200 <5 POSITIVE Plasma Half-Life: 19-37 hours Vilazodone No 200 <125 POSITIVE Plasma Half-Life: 25 hours Yangonin No 200 <10 POSITIVE Plasma Half-Life: 9 hours Amoxapine No 200 <10 POSITIVE Plasma Half-Life: 8 hours Normirtazapine No 200 <1 POSITIVE Plasma Half-Life: 20-40 hours Norfluoxetine No 200 <10 POSITIVE Plasma Half-Life: 4-16 days Nordoxepin No 200 <5 POSITIVE Plasma Half-Life: 31 hours Milnacipran No 200 <1 POSITIVE Plasma Half-Life: 8 hours Hydroxybupropion No 200 <10 POSITIVE Plasma Half-Life: 12-30 hours D-L-Kavain No 200 <10 POSITIVE Plasma Half-Life: 9 hours Desmethoxyyangonin No 200 <50 POSITIVE Plasma Half-Life: 9 hours Dihydromethysticin No 200 <5 POSITIVE Plasma Half-Life: 9 hours Dihydrokavain No 200 <50 POSITIVE Plasma Half-Life: 9 hours Methysticin No 200 <5 POSITIVE
Load more

Recommended publications
  • Inhibitory Effect of Eslicarbazepine Acetate and S-Licarbazepine on 2 Nav1.5 Channels
    bioRxiv preprint doi: https://doi.org/10.1101/2020.04.24.059188; this version posted August 14, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 Inhibitory effect of eslicarbazepine acetate and S-licarbazepine on 2 Nav1.5 channels 3 Theresa K. Leslie1, Lotte Brückner 1, Sangeeta Chawla1,2, William J. Brackenbury1,2* 4 1Department of Biology, University of York, Heslington, York, YO10 5DD, UK 5 2York Biomedical Research Institute, University of York, Heslington, York, YO10 5DD, UK 6 * Correspondence: Dr William J. Brackenbury, Department of Biology and York Biomedical 7 Research Institute, University of York, Wentworth Way, Heslington, York YO10 5DD, UK. Email: 8 [email protected]. Tel: +44 1904 328284. 9 Keywords: Anticonvulsant, cancer, epilepsy, eslicarbazepine acetate, Nav1.5, S-licarbazepine, 10 voltage-gated Na+ channel. 11 Abstract 12 Eslicarbazepine acetate (ESL) is a dibenzazepine anticonvulsant approved as adjunctive treatment for 13 partial-onset epileptic seizures. Following first pass hydrolysis of ESL, S-licarbazepine (S-Lic) 14 represents around 95 % of circulating active metabolites. S-Lic is the main enantiomer responsible 15 for anticonvulsant activity and this is proposed to be through the blockade of voltage-gated Na+ 16 channels (VGSCs). ESL and S-Lic both have a voltage-dependent inhibitory effect on the Na+ current 17 in N1E-115 neuroblastoma cells expressing neuronal VGSC subtypes including Nav1.1, Nav1.2, 18 Nav1.3, Nav1.6 and Nav1.7.
    [Show full text]
  • Eslicarbazepine Acetate Longer Procedure No
    European Medicines Agency London, 19 February 2009 Doc. Ref.: EMEA/135697/2009 CHMP ASSESSMENT REPORT FOR authorised Exalief International Nonproprietary Name: eslicarbazepine acetate longer Procedure No. EMEA/H/C/000987 no Assessment Report as adopted by the CHMP with all information of a commercially confidential nature deleted. product Medicinal 7 Westferry Circus, Canary Wharf, London, E14 4HB, UK Tel. (44-20) 74 18 84 00 Fax (44-20) 74 18 84 16 E-mail: [email protected] http://www.emea.europa.eu TABLE OF CONTENTS 1. BACKGROUND INFORMATION ON THE PROCEDURE........................................... 3 1.1. Submission of the dossier ...................................................................................................... 3 1.2. Steps taken for the assessment of the product..................................................................... 3 2. SCIENTIFIC DISCUSSION................................................................................................. 4 2.1. Introduction............................................................................................................................ 4 2.2. Quality aspects ....................................................................................................................... 5 2.3. Non-clinical aspects................................................................................................................ 8 2.4. Clinical aspects....................................................................................................................
    [Show full text]
  • 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 Pozna´n,Poland; [email protected] (M.K.-Ł.); [email protected] (A.A.M.) 2 Department of Bromatology, Poznan University of Medical Sciences, 60-354 Pozna´n,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.
    [Show full text]
  • Eslicarbazepine Acetate: a New Improvement on a Classic Drug Family for the Treatment of Partial-Onset Seizures
    Drugs R D DOI 10.1007/s40268-017-0197-5 REVIEW ARTICLE Eslicarbazepine Acetate: A New Improvement on a Classic Drug Family for the Treatment of Partial-Onset Seizures 1 1 1 Graciana L. Galiana • Angela C. Gauthier • Richard H. Mattson Ó The Author(s) 2017. This article is an open access publication Abstract Eslicarbazepine acetate is a new anti-epileptic drug belonging to the dibenzazepine carboxamide family Key Points that is currently approved as adjunctive therapy and monotherapy for partial-onset (focal) seizures. The drug Eslicarbazepine acetate is an effective and safe enhances slow inactivation of voltage-gated sodium chan- treatment option for partial-onset seizures as nels and subsequently reduces the activity of rapidly firing adjunctive therapy and monotherapy. neurons. Eslicarbazepine acetate has few, but some, drug– drug interactions. It is a weak enzyme inducer and it Eslicarbazepine acetate improves upon its inhibits cytochrome P450 2C19, but it affects a smaller predecessors, carbamazepine and oxcarbazepine, by assortment of enzymes than carbamazepine. Clinical being available in a once-daily regimen, interacting studies using eslicarbazepine acetate as adjunctive treat- with a smaller range of drugs, and causing less side ment or monotherapy have demonstrated its efficacy in effects. patients with refractory or newly diagnosed focal seizures. The drug is generally well tolerated, and the most common side effects include dizziness, headache, and diplopia. One of the greatest strengths of eslicarbazepine acetate is its ability to be administered only once per day. Eslicar- 1 Introduction bazepine acetate has many advantages over older anti- epileptic drugs, and it should be strongly considered when Epilepsy is a common neurological disorder affecting over treating patients with partial-onset epilepsy.
    [Show full text]
  • Epilepsy & Behavior
    Epilepsy & Behavior 80 (2018) 365–369 Contents lists available at ScienceDirect Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh Brief Communication Eslicarbazepine acetate as a replacement for levetiracetam in people with epilepsy developing behavioral adverse events Virupakshi Jalihal a, Rohit Shankar b,c,⁎, William Henley c, Mary Parrett d, Phil Tittensor e, Brendan N. McLean d, Ammad Ahmed f, Josemir W. Sander g,h,i a Ramaiah Medical College and Hospitals, Bengaluru, Karnataka 560054, India b Cornwall Partnership NHS Foundation Trust, Threemilestone Industrial Estate, Truro TR4 9LD, UK c Exeter Medical School, Knowledge Spa, Royal Cornwall Hospital, Truro, Cornwall TR1 3HD, UK d Royal Cornwall Hospital, Truro, Cornwall TR1 3LJ, UK e Royal Wolverhampton NHS Trust, UK f Bial Pharma Ltd., Admiral House, Windsor SL4 3BL, UK g NIHR University College London Hospitals Biomedical Research Centre, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK h Chalfont Centre for Epilepsy, Chalfont St Peter, Buckinghamshire SL9 0RJ, UK i Stichting Epilepsie Instellingen Nederland (SEIN), Achterweg 5, 2103 SW Heemstede, Netherlands article info abstract Article history: Background: Psychiatric and behavioral side effects (PBSEs) are a major cause of antiepileptic drug (AED) Received 13 November 2017 withdrawal. Levetiracetam (LEV) is a recognized first-line AED with good seizure outcomes but recognized Revised 16 January 2018 with PBSEs. Eslicarbazepine (ESL) is considered to function similarly to an active metabolite of the commonly Accepted 17 January 2018 used carbamazepine (CBZ). Carbamazepine is used as psychotropic medication to assist in various psychiatric Available online 5 February 2018 illnesses such as mood disorders, aggression, and anxiety.
    [Show full text]
  • Comparative Efficacy and Acceptability of Pharmacological Treatments in the Acute Phase Treatment of Bipolar Depression: a Multi
    COMPARATIVE EFFICACY AND ACCEPTABILITY OF PHARMACOLOGICAL TREATMENTS IN THE ACUTE PHASE TREATMENT OF BIPOLAR DEPRESSION: A MULTIPLE TREATMENT META-ANALYSIS [PROTOCOL] Tomofumi Miura, Toshi A. Furukawa, Hisashi Noma, Shiro Tanaka, Keisuke Motomura, Hiroshi Mitsuyasu, Satomi Katsuki, Andrea Cipriani, Sarah Stockton, John Geddes, Georgia Salanti, Shigenobu Kanba Background Description of the condition In late 19th century, Emil Kraepelin classified the major endogenous psychoses into two psychotic illnesses, manic-depressive illness and dementia praecox (Kraepelin’s dichotomy) (Trede et al. , 2005). His concept of manic-depressive illness had covered all of the major clinical forms of severe, moderate and mild melancholia. In 1957, Leonhard proposed to distinguish Kraepelin’s manic-depressive illness into bipolar illness, in which patients had histories of both depression and mania, and monopolar illness, in which patients only had histories of depression (Leonhard, 1979). This basic idea of the bipolar-unipolar distinction was supported by Angst and by Perris in 1966 (Angst, 1966, Perris, 1966), and it continues in the recent diagnostic classification system of mood disorders in DSM-IV(American Psychiatric Association, 1994) and ICD-10 (WHO, 1993). Bipolar disorder is a complex disorder, which is characterized by recurrent episodes of depression and mania (bipolar I disorder) or hypomania (bipolar II disorder)(American Psychiatric Association, 1994). The lifetime prevalence of any bipolar disorders, bipolar I and II disorders have been estimated at 1.1%, 0.7% and 0.5% respectively using the World Mental Health Survey version of the WHO Composite International Diagnostic Interview (Suppes et al. , 2001). The mean age at onset of bipolar disorder is reported to be in the early 20s, but its complex clinical features make its diagnosis difficult and there is a difference of about 8 years between age at onset and age at first treatment (Suppes, Leverich, 2001).
    [Show full text]
  • Test Summary Sheet For
    Test Summary Sheet for: 8054B Postmortem, Expanded with NPS, Blood (Forensic) The following test codes are contained in this document: 1. 8054B Postmortem, Expanded with NPS, Blood (Forensic) 2. 50000B Acetaminophen Confirmation, Blood (Forensic) 3. 52250B Alcohols and Acetone Confirmation, Blood (Forensic) 4. 52143B Alfentanil and Sufentanil Confirmation, Blood (Forensic) 5. 52168B Amitriptyline and Metabolite Confirmation, Blood (Forensic) 6. 52239B Amoxapine Confirmation, Blood (Forensic) 7. 52485B Amphetamines Confirmation, Blood (Forensic) 8. 52416B Aripiprazole Confirmation, Blood (Forensic) 9. 52007B Atomoxetine Confirmation, Blood (Forensic) 10. 50011B Barbiturates Confirmation, Blood (Forensic) 11. 52365B Bath Salts Confirmation, Blood (Forensic) 12. 52367B Bath Salts Confirmation, Blood (Forensic) 13. 50012B Benzodiazepines Confirmation, Blood (Forensic) 14. 52443B Benztropine Confirmation, Blood (Forensic) 15. 52245B Brompheniramine Confirmation, Blood (Forensic) 16. 52011B Bupivacaine Confirmation, Blood (Forensic) 17. 52012B Bupropion and Metabolite Confirmation, Blood (Forensic) 18. 52444B Buspirone Confirmation, Blood (Forensic) 19. 52198B Cannabinoids Confirmation, Blood (Forensic) 20. 52015B Carbamazepine and Metabolite Confirmation, Blood (Forensic) 21. 52017B Carisoprodol and Metabolite Confirmation, Blood (Forensic) 22. 52440B Chlorpheniramine Confirmation, Blood (Forensic) 23. 52272B Chlorpromazine Confirmation, Blood (Forensic) 24. 52482B Citalopram Confirmation, Blood (Forensic) 25. 52274B Clomipramine and Metabolite
    [Show full text]
  • Pharmacokinetic and Pharmacodynamic Interactions Between Antiepileptics and Antidepressants Domenico Italiano University of Messina, Italy
    University of Kentucky UKnowledge Psychiatry Faculty Publications Psychiatry 11-2014 Pharmacokinetic and Pharmacodynamic Interactions between Antiepileptics and Antidepressants Domenico Italiano University of Messina, Italy Edoardo Spina University of Messina, Italy Jose de Leon University of Kentucky, [email protected] Right click to open a feedback form in a new tab to let us know how this document benefits oy u. Follow this and additional works at: https://uknowledge.uky.edu/psychiatry_facpub Part of the Psychiatry and Psychology Commons Repository Citation Italiano, Domenico; Spina, Edoardo; and de Leon, Jose, "Pharmacokinetic and Pharmacodynamic Interactions between Antiepileptics and Antidepressants" (2014). Psychiatry Faculty Publications. 40. https://uknowledge.uky.edu/psychiatry_facpub/40 This Article is brought to you for free and open access by the Psychiatry at UKnowledge. It has been accepted for inclusion in Psychiatry Faculty Publications by an authorized administrator of UKnowledge. For more information, please contact [email protected]. Pharmacokinetic and Pharmacodynamic Interactions between Antiepileptics and Antidepressants Notes/Citation Information Published in Expert Opinion on Drug Metabolism & Toxicology, v. 10, Issue 11, p. 1457-1489. © 2014 Taylor & Francis Group This is an Accepted Manuscript of an article published by Taylor & Francis Group in Expert Opinion on Drug Metabolism & Toxicology in Nov. 2014, available online: http://www.tandfonline.com/10.1517/ 17425255.2014.956081 Digital Object Identifier (DOI) http://dx.doi.org/10.1517/17425255.2014.956081 This article is available at UKnowledge: https://uknowledge.uky.edu/psychiatry_facpub/40 1 This is an Accepted Manuscript of an article published by Taylor & Francis Group in Expert Opinion on Drug Metabolism & Toxicology in Nov.
    [Show full text]
  • Inhibitory Effect of Eslicarbazepine Acetate and S-Licarbazepine on 2 Nav1.5 Channels
    bioRxiv preprint doi: https://doi.org/10.1101/2020.04.24.059188; this version posted June 26, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 Inhibitory effect of eslicarbazepine acetate and S-licarbazepine on 2 Nav1.5 channels 3 Theresa K. Leslie1, Lotte Brückner 1, Sangeeta Chawla1,2, William J. Brackenbury1,2* 4 1Department of Biology, University of York, Heslington, York, YO10 5DD, UK 5 2York Biomedical Research Institute, University of York, Heslington, York, YO10 5DD, UK 6 * Correspondence: Dr William J. Brackenbury, Department of Biology and York Biomedical 7 Research Institute, University of York, Wentworth Way, Heslington, York YO10 5DD, UK. Email: 8 [email protected]. Tel: +44 1904 328284. 9 Keywords: Anticonvulsant, cancer, epilepsy, eslicarbazepine acetate, Nav1.5, S-licarbazepine, 10 voltage-gated Na+ channel. 11 Abstract 12 Eslicarbazepine acetate (ESL) is a dibenzazepine anticonvulsant approved as adjunctive treatment for 13 partial-onset epileptic seizures. Following first pass hydrolysis of ESL, S-licarbazepine (S-Lic) 14 represents around 95 % of circulating active metabolites. S-Lic is the main enantiomer responsible 15 for anticonvulsant activity and this is proposed to be through the blockade of voltage-gated Na+ 16 channels (VGSCs). ESL and S-Lic both have a voltage-dependent inhibitory effect on the Na+ current 17 in N1E-115 neuroblastoma cells expressing neuronal VGSC subtypes including Nav1.1, Nav1.2, 18 Nav1.3, Nav1.6 and Nav1.7.
    [Show full text]
  • A History of the Pharmacological Treatment of Bipolar Disorder
    International Journal of Molecular Sciences Review A History of the Pharmacological Treatment of Bipolar Disorder Francisco López-Muñoz 1,2,3,4,* ID , Winston W. Shen 5, Pilar D’Ocon 6, Alejandro Romero 7 ID and Cecilio Álamo 8 1 Faculty of Health Sciences, University Camilo José Cela, C/Castillo de Alarcón 49, 28692 Villanueva de la Cañada, Madrid, Spain 2 Neuropsychopharmacology Unit, Hospital 12 de Octubre Research Institute (i+12), Avda. Córdoba, s/n, 28041 Madrid, Spain 3 Portucalense Institute of Neuropsychology and Cognitive and Behavioural Neurosciences (INPP), Portucalense University, R. Dr. António Bernardino de Almeida 541, 4200-072 Porto, Portugal 4 Thematic Network for Cooperative Health Research (RETICS), Addictive Disorders Network, Health Institute Carlos III, MICINN and FEDER, 28029 Madrid, Spain 5 Departments of Psychiatry, Wan Fang Medical Center and School of Medicine, Taipei Medical University, 111 Hsin Long Road Section 3, Taipei 116, Taiwan; [email protected] 6 Department of Pharmacology, Faculty of Pharmacy, University of Valencia, Avda. Vicente Andrés, s/n, 46100 Burjassot, Valencia, Spain; [email protected] 7 Department of Pharmacology and Toxicology, Faculty of Veterinary Medicine, Complutense University, Avda. Puerta de Hierro, s/n, 28040 Madrid, Spain; [email protected] 8 Department of Biomedical Sciences (Pharmacology Area), Faculty of Medicine and Health Sciences, University of Alcalá, Crta. de Madrid-Barcelona, Km. 33,600, 28871 Alcalá de Henares, Madrid, Spain; [email protected] * Correspondence: fl[email protected] or [email protected] Received: 4 June 2018; Accepted: 13 July 2018; Published: 23 July 2018 Abstract: In this paper, the authors review the history of the pharmacological treatment of bipolar disorder, from the first nonspecific sedative agents introduced in the 19th and early 20th century, such as solanaceae alkaloids, bromides and barbiturates, to John Cade’s experiments with lithium and the beginning of the so-called “Psychopharmacological Revolution” in the 1950s.
    [Show full text]
  • Ep 3064490 A1
    (19) TZZ¥ZZ_T (11) EP 3 064 490 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 07.09.2016 Bulletin 2016/36 C07D 223/28 (2006.01) (21) Application number: 15195474.0 (22) Date of filing: 19.11.2015 (84) Designated Contracting States: (72) Inventors: AL AT BE BG CH CY CZ DE DK EE ES FI FR GB • Zaramella, Simone GR HR HU IE IS IT LI LT LU LV MC MK MT NL NO 35010 Vigodarzere (PD) (IT) PL PT RO RS SE SI SK SM TR • Rossi, Emiliano Designated Extension States: 35135 Padova (IT) BA ME • De Lucchi, Ottorino Designated Validation States: 35126 Padova (IT) MA MD • Serafini, Siro 36100 Vicenza (VI) (IT) (30) Priority: 06.03.2015 IT VI20150064 (74) Representative: Leganza, Alessandro (71) Applicant: F.I.S.- Fabbrica Italiana Sintetici S.p.A. F.I.S. - Fabbrica Italiana Sintetici S.p.A. 36075 Alte di Montecchio Maggiore (VI) (IT) Viale Milano, 26 36075 Montecchio Maggiore (VI) (IT) (54) IMPROVED PROCESS FOR THE PREPARATION OF ESLICARBAZEPINE AND ESLICARBAZEPINE ACETATE (57) Objectof the present invention isan improved process for thepreparation ofElsicarbazepine and Eslicarbazepine acetate by means of chiral Ruthenium catalysts. EP 3 064 490 A1 Printed by Jouve, 75001 PARIS (FR) EP 3 064 490 A1 Description Technical Field 5 [0001] The object of the present invention is an improved process for the synthesis of the pharmaceutically active substances known as Eslicarbazepine and Eslicarbazepine acetate. Background Art 10 [0002] Eslicarbazepine acetate is an anticonvulsant active pharmaceutical ingredient approved in Europe and in US for the treatment of epilepsy.
    [Show full text]
  • Brand Name: Aptiom Generic Name: Eslicarbazepine Manufacturer: Sunovion Pharmaceuticals Inc1 Product Availability: FDA Approved November 2013
    Brand Name: Aptiom Generic Name: eslicarbazepine Manufacturer: Sunovion Pharmaceuticals Inc1 Product Availability: FDA approved November 2013. Anticipated availability is late 2014.2 Drug Class: Anticonvulsant, central nervous system agent, voltage-gated sodium channel blocker 3,4 Uses: Labeled uses: Adjunctive treatment of partial seizures3,4 Unlabeled uses: None o Under investigation for use as monotherapy for treatment of focal epilepsy or partial-onset seizures5 o Under investigation as a possible treatment for bipolar disorder3,5,6 Mechanism of Action: Like many other anticonvulsants, the exact mechanism of action of eslicarbazepine is unknown. The antiepileptic action of the drug is theorized to be due to the blockage of voltage-gated sodium channels. Studies indicate that eslicarbazepine and its metabolites competitively interact with voltage-gated sodium channels to inhibit sustained repetitive neuronal firing, with enhanced inhibitory selectivity for rapidly firing neurons.1,3 Pharmacokinetics: Absorption: 1,3 Tmax 1-4 hours Vd 61 L t ½ 13-20 hours Clearance 20 mL/min GFR 80-120 mL/min Protein binding < 40% (% to albumin unknown) Bioavailability > 90% Metabolism: 1,3 Eslicarbazepine is rapidly metabolized to its major active metabolite eslicarbazepine (91%) by hydrolytic first-pass metabolism. Minor active metabolites are R-licarbazepine (5%) and oxcarbazepine (1%). In in vitro studies, eslicarbazepine acetate was found to be a moderate inhibitor of CYP2C19 and an inducer of CYP3A4. Studies with eslicarbazepine in fresh human hepatocytes showed only mild activation of UGT1A1- mediated glucuronidation. Eslicarbazepine showed no clinical inhibitory effects on CYP1A2, CYP2A6, CYP2B6, CYP2D6, CYP2E1, and CYP3A4 and did not undergo autoinduction. Elimination: 1,3 Eslicarbazepine metabolites are eliminated primarily by renal excretion in the unchanged and glucuronide conjugate forms.
    [Show full text]