DOCSLIB.ORG

Dementia – Diagnostic and Therapeutic Interventions

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Dementia – Diagnostic and Therapeutic Interventions A Systematic Review Volume 2 June 2008 The Swedish Council on Technology Assessment in Health Care SBU • Statens beredning för medicinsk utvärdering SBU Evaluates Healthcare Technology SBU (the Swedish Council on Technology Assessment in Health Care) is a government agency that assesses the methods employed by medical professionals and institutions. In addition to analyzing the costs and benefits of various health care measures, the agency weighs Swedish clinical practice against the findings of medical research. The objective of SBU’s activities is to provide everyone who is involved in decisions about the conduct of health care with more complete and accurate information. We welcome you to visit our homepage on the Internet at www.sbu.se. SBU issues three series of reports. The first series, which appears in a yellow binding, presents assessments that have been carried out by the agency’s project groups. A lengthy summary, as well as a synopsis of measures proposed by the SBU Board of Directors and Scientific Advisory Committee, accompanies every assessment. Each report in the second, white-cover series focuses on current research in a parti- cular healthcare area for which assessments may be needed. The Alert Reports, the third series, focus on initial assessments of new healthcare measures. To order this report (No 172E/2) please contact: SBU Mailing Address: Box 5650, SE-114 86 Stockholm, Sweden Street Address: Tyrgatan 7 Tel: +46 8 412 32 00 Fax: +46 8 411 32 60 Internet: www.sbu.se E-mail: [email protected] Graphic Design: pmochco, www.pm.se Printing: Elanders Infologistics Väst AB, Mölnlycke 2008 ISBN 978-91-85413-24-9 • ISSN 1400-1403 Dementia – Diagnostic and Therapeutic Interventions A Systematic Review Project Group Olof Edhag Laura Fratiglioni Anders Norlund (Chair) Lars Gustafson (Project Director) Hedda Aguero-Eklund Ingrid Håkanson Liisa Palo-Bengtsson Ove Almkvist (Project Assistant) Magnus Sjögren Kenneth Asplund Aki Johanson Eva von Strauss Kaj Blennow Ingvar Karlsson Lars-Olof Wahlund Sirkka-Liisa Ekman Mona Kihlgren Gunhild Waldemar Knut Engedal Lena Kilander Anders Wallin Elisabet Englund Elisabet Londos Anders Wimo Sture Eriksson Jan Marcusson Dag Årsland Johan Fastbom Astrid Norberg Scientific Reviewers Per Edebalk Rurik Löfmark Anneli Sarvimäki Serge Gauthier Hans Melander Hilkka Soininen Lars Lannfelt Ingalill Rahm Matti Viitanen Kim Lützén Hallberg Reference Group Ann Hedberg Balkå P-O Sandman Bengt Winblad (Swedish Association (Umeå University) (Karolinska Institute) of Local Authorities Members from the and Regions) Alzheimer Associ- ation of Sweden and from the Dementia Association The Swedish Council on Technology Assessment in Health Care SBU • Statens beredning för medicinsk utvärdering Content 9. Diagnosing Dementia Disorders 17 Background 17 Diagnostic evaluation of dementia 17 The concept of mild cognitive impairment (MCI) 17 Guidelines for the diagnostic evaluation of dementia 19 European federation of neurological societies (EFNS) 19 guidelines [3] American Academy of Neurology guidelines [5] 20 Aims 21 Methods 21 Selection of papers 21 Classification of evidence 27 Summary of evidence 28 Laboratory screening tests that might detect 28 reversible cognitive impairment Tests that can be used to detect a dementia disorder 28 Single cognitive tests 28 Tests that identify specific dementia disorders 29 ApoE 29 Methods of diagnosing dementia disorders 29 Structural imaging (MRI/CT) 29 Functional imaging (PET, SPECT) 29 Neurophysiological methods (EEG, EEG) 29 CSF analyses 29 Methodological considerations 30 Lack of gold standard 31 Selection bias 31 Setting 31 Circularity bias 32 Recommendations for future research 32 References 34 Checklists regarding assessment of study quality for different chapters of this report are included in the electronic version of the SBU report on Dementia diseases at www.sbu.se 10. Identifying Secondary Dementia or Potential Reversible 35 Cognitive Impairment Thyroid disease and dementia 35 Background 35 Literature search for evidence 35 Search strategy 36 Results 36 Comments 37 References 46 11. Neurosyphilis and Dementia 49 Background 49 Literature search for evidence 50 Search strategy 50 Result 51 Comments 51 References 56 12. Vitamin B12, Folic Acid and Homocysteine, 57 Cognitive Impairment and Alzheimer’s Disease Conclusions 57 Background 57 Literature search strategy 58 Comments 60 Vitamin B12 60 Folic acid 60 Homocysteine 60 Treatment with vitamin B12 or folate 60 References 76 13. Evidence for Tests that can be used to Diagnose Dementia 79 Informant interview in the diagnostic 79 evaluation of patients with dementia Background 79 Literature search 80 Search strategy 80 Results 80 Comments 81 References 88 14. Neuropsychological Tests as a Diagnostic Marker 91 of Dementia Conclusion 91 Introduction 91 Aim 91 Search strategy 92 Description of studies included and excluded 92 Results 93 Discussion 94 References 102 15. Evidence-based Evaluation of Single Cognitive Tests 103 as a Diagnostic Marker of Dementia Conclusions 103 Introduction 103 Search strategy 104 Results 105 Discussion 106 References 116 16. Genetic Markers 119 Conclusion 119 Causative genes for dementia disorders 119 Apolipoprotein E ε4 as a diagnostic marker of AD 120 Background 120 Literature search strategy 122 Results 122 ApoE ε4 allele as a marker of AD 123 in comparison with controls ApoE ε4 allele as marker of AD compared 124 to other dementia disorders ApoE ε4 allele as marker of AD compared to MCI 125 ApoE ε4 allele as marker of FTLD compared 125 to normal controls References 162 17. Structural and Functional Imaging of the Brain 171 in Dementia Workup Conclusions 171 Introduction 172 Search strategy 172 Structural imaging 173 Results 173 References 188 18. Functional Imaging’s Diagnostic Tool in Dementia 193 Workup Search Strategies Conclusions 193 Introduction 193 Search strategy 194 Results 195 References 208 19. Evidence Based Evaluation of EEG (Quantitative EEG 211 and Visual Rated EEG) Conclusions 211 Introduction 211 Search strategy 211 References 218 20. Cerebrospinal Fluid Biomarkers in AD 219 Conclusion 219 Background 219 Search strategy 220 Selection criteria 220 Analytical principles for CSF T-tau, P-tau and Aß42 221 CSF total tau (T-tau) 221 CSF ß-amyloid (Aß42) 222 CSF phosphorylated tau (P-tau) 222 Diagnostic performance of CSF markers for AD 223 CSF T-tau 223 Aß42 224 CSF P-tau 224 Combination of CSF markers 224 CFS markers in early Alzheimer’s disease and MCI 225 CFS markers in other cognitive, psychiatric 226 and neurological disorders References 276 21. Interventions in Dementia Disorders 285 Background 285 Questions of interest 286 Study quality and levels of evidence 287 Methodological aspects of pharmacological studies 288 Selection and setting 288 Which patients were included in the efficacy analyses: 289 ITT, ITT-LOCF or OC? Long-term effects 290 Concepts of care 291 Quality of life 292 References 293 22. Pharmacological Treatment of Dementia – 295 Established Drugs Conclusions 295 Adverse events 296 Other conclusions 296 Background 297 Acetylcholinesterase inhibitors (AChEIs) 297 Memantine 298 Aim 298 Methods 298 Strategy for searching the literature 298 Included trials: Acetylcholinesterase inhibitors in AD 299 Donepezil 299 Rivastigmine 300 Galantamine 300 Included trials: Memantine 300 Measurements of efficacy 301 Global function 301 Cognitive function 302 ADL 303 Behavioral disturbances and psychological symptoms 303 Measurements of acceptability and safety 303 Acetylcholinesterase inhibitors in AD 304 Presentation of results 304 Effects on global function, primary outcomes: 304 CIBIC+ and GBS Effects on global function, secondary outcomes 305 Effects on cognitive function, primary outcomes: 305 ADAS-cog Effects on cognitive function: secondary outcomes 306 Effects on ADL 307 Effects on BPSD 308 Moderate to severe dementia 308 Acceptability and tolerability 309 Results after short-term treatment, effects 311 of washout and placebo effects Prediction of response 311 Neuroimaging findings in RCTs 312 Comparisons among different acetylcholinesterase 313 inhibitors Memantine in AD and VaD 313 Global function 313 Cognitive function 314 ADL function and BPSD 314 Acceptability and tolerability 314 Combined memantine and donepezil treatment 315 Acetylcholinesterase inhibitors in VaD 315 Results for donepezil 315 Results for galantamine 317 Other neurodegenerative dementia disorders 317 Cholinesterase inhibitors in dementia with Lewy bodies 317 (DLB) Cholinesterase inhibitors in Parkinson’s disease (PD) 318 and dementia Frontotemporal dementia (FTD) 318 Cholinesterase inhibitors in Down syndrome 319 Need for research 319 References 354 23. Hypertension and Dementia 361 Conclusions 361 Background 361 Search of literature 361 Results 362 Need for research 363 References 364 24. Treatment of Depression in Dementia 365 Conclusions 365 Background 365 Search strategy 366 Search results 366 Effects of antidepressants on depression in dementia 367 Effects of antidepressants on non-depressive symptoms 368 References 378 25. Treatment of Psychotic and Behavioral Symptoms 381 in Dementia Conclusions 381 Background 382 Effects of antipsychotic treatment of psychotic 383 symptoms and BPSD Search 383 Results 383 Study on withdrawal of antipsychotic 386 treatment in dementia Treatment of BPSD with antidepressants 386 Rate of decline of cognitive symptoms 387 during antipsychotic treatment Effects of antipsychotics on cerebral 387
Recommended publications
  • United States Patent (19) (11) 4,232,002 Nogrady 45) Nov

    United States Patent (19) (11) 4,232,002 Nogrady 45) Nov

    United States Patent (19) (11) 4,232,002 Nogrady 45) Nov. 4, 1980 (54) PROCEDURES AND PHARMACEUTICAL (56) References Cited PRODUCTS FOR USE IN THE PUBLICATIONS ADMINISTRATION OF ANTHISTAMINES American Hospital Formulary Service, 1966, 4:00 Anti (75. Inventor: Stephen G. Nogrady, Sully, near histamine Drugs, Penarth, Great Britain Primary Examiner-Stanley J. Friedman Attorney, Agent, or Firm-Young & Thompson 73) Assignee: The Welsh National School of Medicine, Penarth, Great Britain 57 ABSTRACT An antihistamine of the benzhydrylether, alkylamine, or (21) Appl. No.: 965,171 benzocyloheptatiophene class is suitable for use in the therapeutic treatment or prophylaxis of reversible air (22 Filed: Nov.30, 1978 ways obstruction by inhalation. The antihistamine may be clemastine, chlorpheniramine or ketotifen and may (30) Foreign Application Priority Data be in the form of a composition in admixture with a diluent. The antihistamine can be administered from a Dec. 1, 1977 GB) United Kingdom ..................... 5.0020 pharmaceutical inhalation device which is designed to 51 Int. Cl. ......................... A61L 9/04; A61 K9/04; administer a dosage unit of the antihistamine. The inha A61K 31/44 lation device can be in the form of a pressurized aerosol 52 U.S. C. ........................................ 424/45; 424/46; inhaler or a dry powder insufflator. 424/263 58) Field of Search ............................ 424/263, 46, 45 5 Claims, No Drawings 4,232,002 1. 2 inhalation provides the equivalent of 0.1 to 5 mg. of PROCEDURES AND PHARMACEUTICAL clemastine, or 0.05 to 2.5 mg. of chlorpheniramine. The PRODUCTS FOR USE IN THE ADMINISTRATION drug may be inhaled in the form of a mist or nebulized OF ANTHISTAMINES spray, or as a cloud of fine solid particles, and may be inhaled from a variety of inhaler devices.
  • Anticoagulant Effects of Statins and Their Clinical Implications

    Anticoagulant Effects of Statins and Their Clinical Implications

    Review Article 1 Anticoagulant effects of statins and their clinical implications Anetta Undas1; Kathleen E. Brummel-Ziedins2; Kenneth G. Mann2 1Institute of Cardiology, Jagiellonian University School of Medicine, and John Paul II Hospital, Krakow, Poland; 2Department of Biochemistry, University of Vermont, Colchester, Vermont, USA Summary cleavage, factor V and factor XIII activation, as well as enhanced en- There is evidence indicating that statins (3-hydroxy-methylglutaryl dothelial thrombomodulin expression, resulting in increased protein C coenzyme A reductase inhibitors) may produce several cholesterol-inde- activation and factor Va inactivation. Observational studies and one ran- pendent antithrombotic effects. In this review, we provide an update on domized trial have shown reduced VTE risk in subjects receiving statins, the current understanding of the interactions between statins and blood although their findings still generate much controversy and suggest that coagulation and their potential relevance to the prevention of venous the most potent statin rosuvastatin exerts the largest effect. thromboembolism (VTE). Anticoagulant properties of statins reported in experimental and clinical studies involve decreased tissue factor ex- Keywords pression resulting in reduced thrombin generation and attenuation of Blood coagulation, statins, tissue factor, thrombin, venous throm- pro-coagulant reactions catalysed by thrombin, such as fibrinogen boembolism Correspondence to: Received: August 30, 2013 Anetta Undas, MD, PhD Accepted after major revision: October 15, 2013 Institute of Cardiology, Jagiellonian University School of Medicine Prepublished online: November 28, 2013 80 Pradnicka St., 31–202 Krakow, Poland doi:10.1160/TH13-08-0720 Tel.: +48 12 6143004, Fax: +48 12 4233900 Thromb Haemost 2014; 111: ■■■ E-mail: [email protected] Introduction Most of these additional statin-mediated actions reported are independent of blood cholesterol reduction.
  • Antihistamine Therapy in Allergic Rhinitis

    Antihistamine Therapy in Allergic Rhinitis

    CLINICAL REVIEW Antihistamine Therapy in Allergic Rhinitis Paul R. Tarnasky, MD, and Paul P. Van Arsdel, Jr, MD Seattle, Washington Allergic rhinitis is a common disorder that is associated with a high incidence of mor­ bidity and considerable costs. The symptoms of allergic rhinitis are primarily depen­ dent upon the tissue effects of histamine. Antihistamines are the mainstay of therapy for allergic rhinitis. Recently, a second generation of antihistamines has become available. These agents lack the adverse effect of sedation, which is commonly associated with older antihistamines. Current practice of antihistamine therapy in allergic rhinitis often involves random selection among the various agents. Based upon the available clinical trials, chlorpheniramine appears to be the most reasonable initial antihistaminic agent. A nonsedating antihis­ tamine should be used initially if a patient is involved in activities where drowsiness is dangerous. In this comprehensive review of allergic rhinitis and its treatment, the cur­ rent as well as future options in antihistamine pharmacotherapy are emphasized. J Fam Pract 1990; 30:71-80. llergic rhinitis is a common condition afflicting some­ defined by the period of exposure to those agents to which A where between 15 and 30 million people in the United a patient is sensitive. Allergens in seasonal allergic rhinitis States.1-3 The prevalence of disease among adolescents is consist of pollens from nonflowering plants such as trees, estimated to be 20% to 30%. Two thirds of the adult grasses, and weeds. These pollens generally create symp­ allergic rhinitis patients are under 30 years of age.4-6 Con­ toms in early spring, late spring through early summer, sequently, considerable costs are incurred in days lost and fall, respectively.
  • Antiplatelets, Anticoagulants and Bleeding Risk and Ppis

    Antiplatelets, Anticoagulants and Bleeding Risk and Ppis

    GP INFOSHEET – ANTITHROMBOTICS AND BLEEDING RISK Author(s): Dr. Stuart Rison; Dr. John Robson; Version: 1.6; Last updated 28/11/2019 ANTIPLATELETS, ANTICOAGULANTS AND BLEEDING RISK – WHICH AGENTS AND FOR HOW LONG?; WHY USE PPIs? KEY RECOMMENDATION Patients taking anticoagulants or antiplatelet medicines at high bleed risk should be considered for a Proton Pump Inhibitor (PPI). PPIs reduce bleeding risk by 70% or more. Patients age 65 years or more on anticoagulants or antiplatelet agents are at increased risk because of their age and bleeding risk continues to rise exponentially at older ages. PPIs are recommended in patients on anticoagulants or antiplatelet agents: o At any age with previous GI bleeding o Age 75 years or older o 65 years or older with additional risk factors (see box below) o Interacting medication Dual antiplatelet therapy (DAPT) for cardiac conditions - typically aspirin + clopidogrel - is rarely justified for more than 1 year. Review use for more than one 1 year and in conjunction with the cardiologist consider whether this can revert to a single agent. Dual-pathway therapy for atrial fibrillation - both an anticoagulant and one or more antiplatelet agents- is also rarely justified for longer than 1 year. Consider anticoagulant alone with appropriate specialist advice. ADDITIONAL GI-BLEED RISK FACTORS Anaemia Hb <11g/L Impaired renal function (eGFR<30) Upper GI inflammation (and of course previous GI bleeding) Liver disease Interacting medicines (NSAIDs, SSRI/SNRIs, bisphosphonates, lithium, spironolactone, phenytoin, carbamazepine) WHAT DO WE MEAN BY ANTITHROMBOTICS? Antithrombotics reduce blood clot formation1. There are two main categories: 1. Antiplatelet agent – inhibit platelet aggregation e.g.
  • Current Status of Antifibrinolytics in Cardiopulmonary Bypass and Elective Deep Hypothermic Circulatory Arrest Jeffrey A

    Current Status of Antifibrinolytics in Cardiopulmonary Bypass and Elective Deep Hypothermic Circulatory Arrest Jeffrey A

    Anesthesiology Clin N Am 21 (2003) 527–551 Current status of antifibrinolytics in cardiopulmonary bypass and elective deep hypothermic circulatory arrest Jeffrey A. Green, MD*, Bruce D. Spiess, MD Department of Anesthesiology, Virginia Commonwealth University, Medical College of Virginia Campus, 1200 East Broad Street, PO Box 980695, Richmond, VA 23209 USA Bleeding after cardiopulmonary bypass Cardiopulmonary bypass (CPB) alters the hemostatic balance and predisposes cardiac surgery patients to an increased risk of microvascular bleeding. Bleeding and the need for transfusion are among the most common complications of cardiac surgery. In fact, until recently, blood transfusions seemed to be required for about 50% of all cardiac surgery patients [1]. Currently, CPB accounts for 10% to 20% of the transfusions performed in the United States [2,3]. Transfusion, however, exposes patients to added risks such as infectious disease transmission [4], transfusion reactions [5], graft-versus-host disease [6], transfusion-induced lung injury [7], and decreased resistance to postoperative infection [8,9]. Transfusion increases the risk of infection by 35% to 300% and increases the risk of pneumonia in coronary artery bypass (CABG) patients by 5% per unit transfused [10]. The primary purported benefit of transfusion, increased oxygen carrying capacity, has not been definitively proven. Excessive postoperative bleeding may necessitate surgical reexploration, increasing morbidity, and mortality. Postoperatively, the risk of excessive bleeding is 11% [11], and 5% to 7% of patients lose more than 2 L of blood in the first 24 hours after CPB [12]. Reexploration for hemorrhage is required in 3.6% to 4.2% of patients [13], and mortality rates range from 10% to 22% [14].
  • Antithrombotic Therapy for VTE Disease, 10Th Ed, 2016

    Antithrombotic Therapy for VTE Disease, 10Th Ed, 2016

    [ Evidence-Based Medicine ] Antithrombotic Therapy for VTE Disease CHEST Guideline and Expert Panel Report Clive Kearon, MD, PhD; Elie A. Akl, MD, MPH, PhD; Joseph Ornelas, PhD; Allen Blaivas, DO, FCCP; David Jimenez, MD, PhD, FCCP; Henri Bounameaux, MD; Menno Huisman, MD, PhD; Christopher S. King, MD, FCCP; Timothy A. Morris, MD, FCCP; Namita Sood, MD, FCCP; Scott M. Stevens, MD; Janine R. E. Vintch, MD, FCCP; Philip Wells, MD; Scott C. Woller, MD; and COL Lisa Moores, MD, FCCP BACKGROUND: We update recommendations on 12 topics that were in the 9th edition of these guidelines, and address 3 new topics. METHODS: We generate strong (Grade 1) and weak (Grade 2) recommendations based on high- (Grade A), moderate- (Grade B), and low- (Grade C) quality evidence. RESULTS: For VTE and no cancer, as long-term anticoagulant therapy, we suggest dabigatran (Grade 2B), rivaroxaban (Grade 2B), apixaban (Grade 2B), or edoxaban (Grade 2B) over vitamin K antagonist (VKA) therapy, and suggest VKA therapy over low-molecular-weight heparin (LMWH; Grade 2C). For VTE and cancer, we suggest LMWH over VKA (Grade 2B), dabigatran (Grade 2C), rivaroxaban (Grade 2C), apixaban (Grade 2C), or edoxaban (Grade 2C). We have not changed recommendations for who should stop anticoagulation at 3 months or receive extended therapy. For VTE treated with anticoagulants, we recommend against an inferior vena cava filter (Grade 1B). For DVT, we suggest not using compression stockings routinely to prevent PTS (Grade 2B). For subsegmental pulmonary embolism and no proximal DVT, we suggest clinical surveillance over anticoagulation with a low risk of recurrent VTE (Grade 2C), and anticoagulation over clinical surveillance with a high risk (Grade 2C).
  • Medicines Classification Committee

    Medicines Classification Committee

    Medicines Classification Committee Meeting date 1 May 2017 58th Meeting Title Reclassification of Sedating Antihistamines Medsafe Pharmacovigilance Submitted by Paper type For decision Team Proposal for The Medicines Adverse Reactions Committee (MARC) recommended that the reclassification to committee consider reclassifying sedating antihistamines to prescription prescription medicines when used in children under 6 years of age for the treatment of medicine for some nausea and vomiting and travel sickness [exact wording to be determined by indications the committee]. Reason for The purpose of this document is to provide the committee with an overview submission of the information provided to the MARC about safety concerns associated with sedating antihistamines and reasons for recommendations. Associated March 2013 Children and Sedating Antihistamines Prescriber Update articles February 2010 Cough and cold medicines clarification – antihistamines Medsafe website Safety information: Use of cough and cold medicines in children – new advice Medicines for Alimemazine Diphenhydramine consideration Brompheniramine Doxylamine Chlorpheniramine Meclozine Cyclizine Promethazine Dexchlorpheniramine New Zealand Some oral sedating antihistamines available without exposure to a prescription (pharmacist-only and pharmacy only), sedating therefore usage data is not easily available. antihistamines Table of Contents 1.0 PURPOSE ......................................................................................................................................
  • AHFS Pharmacologic-Therapeutic Classification (2012).Pdf

    AHFS Pharmacologic-Therapeutic Classification (2012).Pdf

    AHFS Pharmacologic-Therapeutic Classification 4:00 Antihistamine Drugs 4:04 First Generation Antihistamines 4:04.04 Ethanolamine Derivatives 4:04.08 Ethylenediamine Derivatives 4:04.12 Phenothiazine Derivatives 4:04.16 Piperazine Derivatives 4:04.20 Propylamine Derivatives 4:04.92 Miscellaneous Derivatives 4:08 Second Generation Antihistamines 4:92 Other Antihistamines* 8:00 Anti-infective Agents 8:08 Anthelmintics 8:12 Antibacterials 8:12.02 Aminoglycosides 8:12.06 Cephalosporins 8:12.06.04 First Generation Cephalosporins 8:12.06.08 Second Generation Cephalosporins 8:12.06.12 Third Generation Cephalosporins 8:12.06.16 Fourth Generation Cephalosporins 8:12.07 Miscellaneous -Lactams 8:12.07.04 Carbacephems 8:12.07.08 Carbapenems 8:12.07.12 Cephamycins 8:12.07.16 Monobactams 8:12.08 Chloramphenicol 8:12.12 Macrolides 8:12.12.04 Erythromycins 8:12.12.12 Ketolides 8:12.12.92 Other Macrolides 8:12.16 Penicillins 8:12.16.04 Natural Penicillins 8:12.16.08 Aminopenicillins 8:12.16.12 Penicillinase-resistant Penicillins 8:12.16.16 Extended-spectrum Penicillins 8:12.18 Quinolones 8:12.20 Sulfonamides 8:12.24 Tetracyclines 8:12.24.12 Glycylcyclines 8:12.28 Antibacterials, Miscellaneous 8:12.28.04 Aminocyclitols 8:12.28.08 Bacitracins 8:12.28.12 Cyclic Lipopeptides 8:12.28.16 Glycopeptides 8:12.28.20 Lincomycins 8:12.28.24 Oxazolidinones 8:12.28.28 Polymyxins 8:12.28.30 Rifamycins 8:12.28.32 Streptogramins 8:12.28.92 Other Miscellaneous Antibacterials* 8:14 Antifungals 8:14.04 Allylamines 8:14.08 Azoles 8:14.16 Echinocandins 8:14.28 Polyenes 8:14.32
  • LITERATURE REVIEW Drug Review

    LITERATURE REVIEW Drug Review

    LITERATURE REVIEW Drug Review Document ID: N04-023 Author: Julie Qidwai Date: December 2004 National Advanced Driving Simulator 2401 Oakdale Blvd. Iowa City, IA 52242-5003 Fax (319) 335-4658 TABLE OF CONTENTS 1 Introduction ............................................................................................................................ 1 2 Alprazolam.............................................................................................................................. 1 3 Amitriptyline........................................................................................................................... 2 4 Biperiden................................................................................................................................. 2 5 Brompheniramine .................................................................................................................. 2 6 Butorphanol ............................................................................................................................ 2 7 Cetirizine................................................................................................................................. 3 8 Chloroquine ............................................................................................................................ 3 9 Chlorpheniramine .................................................................................................................. 4 10 Clemastine..............................................................................................................................
  • Identification of SARS-Cov-2 Entry Inhibitors Among Already Approved

    Identification of SARS-Cov-2 Entry Inhibitors Among Already Approved

    www.nature.com/aps ARTICLE Identification of SARS-CoV-2 entry inhibitors among already approved drugs Li Yang1, Rong-juan Pei2, Heng Li1,3, Xin-na Ma4, Yu Zhou1, Feng-hua Zhu1, Pei-lan He1, Wei Tang1, Ye-cheng Zhang2, Jin Xiong2, Shu-qi Xiao2, Xian-kun Tong1, Bo Zhang2 and Jian-ping Zuo1,3,4 To discover effective drugs for COVID-19 treatment amongst already clinically approved drugs, we developed a high throughput screening assay for SARS-CoV-2 virus entry inhibitors using SARS2-S pseudotyped virus. An approved drug library of 1800 small molecular drugs was screened for SARS2 entry inhibitors and 15 active drugs were identified as specific SARS2-S pseudovirus entry inhibitors. Antiviral tests using native SARS-CoV-2 virus in Vero E6 cells confirmed that 7 of these drugs (clemastine, amiodarone, trimeprazine, bosutinib, toremifene, flupenthixol, and azelastine) significantly inhibited SARS2 replication, reducing supernatant viral RNA load with a promising level of activity. Three of the drugs were classified as histamine receptor antagonists with clemastine showing the strongest anti-SARS2 activity (EC50 = 0.95 ± 0.83 µM). Our work suggests that these 7 drugs could enter into further in vivo studies and clinical investigations for COVID-19 treatment. Keywords: COVID-19; SARS-CoV-2; virus entry inhibitors; high throughput screening assay; approved drug library; histamine receptor antagonists; clemastine 1234567890();,: Acta Pharmacologica Sinica (2021) 42:1347–1353; https://doi.org/10.1038/s41401-020-00556-6 INTRODUCTION drugs with high activity and specificity that will be of critical Since the outbreak of COVID-19, there have been ~15 million benefit for our long-term control of this emerging disease.
  • Antithrombotic Therapy in Hypertension: a Cochrane Systematic Review

    Antithrombotic Therapy in Hypertension: a Cochrane Systematic Review

    Journal of Human Hypertension (2005) 19, 185–196 & 2005 Nature Publishing Group All rights reserved 0950-9240/05 $30.00 www.nature.com/jhh ORIGINAL ARTICLE Antithrombotic therapy in hypertension: a Cochrane Systematic review DC Felmeden and GYH Lip Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK Although elevated systemic blood pressure (BP) results on one large trial, ASA taken for 5 years reduced in high intravascular pressure, the main complications myocardial infarction (ARR, 0.5%, NNT 200 for 5 years), of hypertension are related to thrombosis rather than increased major haemorrhage (ARI, 0.7%, NNT 154), and haemorrhage. It therefore seemed plausible that use of did not reduce all cause mortality or cardiovascular antithrombotic therapy may be useful in preventing mortality. In two small trials, warfarin alone or in thrombosis-related complications of elevated BP. The combination with ASA did not reduce stroke or coronary objectives were to conduct a systematic review of the events. Glycoprotein IIb/IIIa inhibitors as well as ticlopi- role of antiplatelet therapy and anticoagulation in dine and clopidogrel have not been sufficiently eval- patients with BP, to address the following hypotheses: uated in patients with elevated BP. To conclude for (i) antiplatelet agents reduce total deaths and/or major primary prevention in patients with elevated BP, anti- thrombotic events when compared to placebo or other platelet therapy with ASA cannot be recommended active treatment; and (ii) oral anticoagulants reduce total since the magnitude of benefit, a reduction in myocar- deaths and/or major thromboembolic events when dial infarction, is negated by a harm of similar magni- compared to placebo or other active treatment.
  • Use of Antithrombotic Medications in the Presence of Neuraxial Anesthesia

    Use of Antithrombotic Medications in the Presence of Neuraxial Anesthesia

    Guideline: Use of Antithrombotic Medications In The Presence of Neuraxial Anesthesia Use of Antithrombotic Medications In The Presence of Neuraxial Anesthesia Purpose of Guidelines: To establish appropriate administration and timing of antithrombotic medications before, during, and after the use of neuraxial anesthesia to minimize the risk of bleeding. Definitions: Neuraxial Anesthesia = Delivery of anesthetic medication requiring placement of catheters or needles into the epidural or spinal space Antithrombotic Medications = Anticoagulant, antiplatelet, and thrombolytic medications Background1-3: Spinal (or epidural) hematomas are a rare but catastrophic complication of neuraxial anesthesia. The risk of hematoma development is increased in the presence of antithrombotic medication. Patients undergoing neuraxial anesthesia must have the risks of bleeding from neuraxial interventions balanced with the underlying and ongoing risk of thromboembolism necessitating anticoagulation. Recommendations for the management of specific antithrombotics in patients undergoing neuraxial anesthesia are provided in the following Tables: o Table 1. Management of Intravenous and Subcutaneous Anticoagulation Therapy in Patients Undergoing Neuraxial Anesthesia o Table 2. Management of ORAL Anticoagulation Therapy in Patients Undergoing Neuraxial Anesthesia o Table 3. Management of ORAL and Intravenous Antiplatelet and Thrombolytic Therapy in Patients Undergoing Neuraxial Anesthesia Workflow if a Contradicted Medication is Prescribed: Providers will have