Drug Misuse and Dependence UK Guidelines on Clinical Management Drug Misuse and Dependence UK Guidelines on Clinical Management

Total Page:16

File Type:pdf, Size:1020Kb

Drug Misuse and Dependence UK Guidelines on Clinical Management Drug Misuse and Dependence UK Guidelines on Clinical Management Drug misuse and dependence UK guidelines on clinical management Drug misuse and dependence UK guidelines on clinical management Prepared by Clinical Guidelines on Drug Misuse and Dependence Update 2017 Independent Expert Working Group Title: Drug misuse and dependence: UK guidelines on clinical management Recommended citation: Clinical Guidelines on Drug Misuse and Dependence Update 2017 Independent Expert Working Group (2017) Drug misuse and dependence: UK guidelines on clinical management. London: Department of Health Author: Clinical Guidelines on Drug Misuse and Dependence Update 2017 Independent Expert Working Group Publisher: Global and Public Health / Population Health / Healthy Behaviours / 25460 Document purpose: Guidance Publication date: July 2017 (minor revisions November 2017) Target audience: Healthcare professionals Providers and commissioners of treatment for people who misuse or are dependent on drugs Professional and regulatory bodies Service users and carers Contact details: Alcohol, Drugs & Tobacco Division Public Health England [email protected] You may re-use the text of this document (not including logos) free of charge in any format or medium, under the terms of the Open Government Licence. To view this licence, visit www.nationalarchives.gov.uk/ doc/open-government-licence/ © Crown copyright Published to gov.uk www.gov.uk/dh Contents 1 Contents Preface 5 Professor Sir John Strang 5 Chapter 1: Introduction 9 Chapter 2: Essential elements of treatment provision 15 2.1 Key points 15 2.2 Assessment, planning care and treatment 15 2.3 Delivery of treatment 27 2.4 Drug testing 28 2.5 General health assessment at presentation and in treatment 31 2.6 Effective communication with primary and secondary care services 35 2.7 Organisational factors for effective drug treatment 35 2.8 Intimate partner violence and domestic abuse 43 2.9 Planning and contracting or commissioning services 44 Chapter 3: Psychosocial components of treatment 47 3.1 Key points 47 3.2 Introduction 47 3.3 Core elements underpinning effective delivery 51 3.4 Making psychosocial interventions effective 52 3.5 Interventions focused on social network and family, friends and carers 56 3.6 Medication and psychosocial interventions 57 3.7 Delivering psychosocial interventions 58 3.8 Resources and further reading 81 3.9 References 81 Chapter 4: Pharmacological interventions 83 4.1 Key points 83 4.2 Prescribing 84 4.3 Choosing an appropriate opioid substitute 88 4.4 Induction onto methadone and buprenorphine substitution treatment 90 4.5 Supervised consumption 101 4.6 Assessing and responding to progress and failure to benefit 104 4.7 Opioid maintenance prescribing 110 4.8 Opioid detoxification 115 4.9 Naltrexone for relapse prevention 118 4.10 Pharmacological management of dependence on other drugs 119 4.11 Resources and further reading 124 4.12 References 125 2 Drug misuse and dependence: UK guidelines on clinical management Chapter 5: Criminal justice system 127 5.1 Key points 127 5.2 Introduction 128 5.3 Criminal justice systems in the community 130 5.4 Prisons and other secure environments 133 5.5 References 160 Chapter 6: Health considerations 163 6.1 Key points 163 6.2 Blood-borne viruses and other infections 163 6.3 Preventing drug-related deaths 174 6.4 Naloxone 178 6.5 Alcohol in drug treatment 183 6.6 Smoking and respiratory function 187 6.7 Oral health 190 6.8 References 194 Chapter 7: Specific treatment situations and populations 197 7.1 General key points 197 7.2 Pain management 197 7.3 Dependence on prescribed and over-the-counter opioids 205 7.4 Misuse of or dependence on gabapentinoids 208 7.5 Hospitalisation 209 7.6 Pregnancy and neonatal care 220 7.7 New psychoactive substances and club drugs 225 7.8 Image and performance enhancing drugs 229 7.9 Coexisting problems with mental health and substance use 231 7.10 Young people 240 7.11 Older people 247 7.12 References 252 Annexes 255 A1: Working group members and other contributors 257 A1.1 Members of the working group 257 A1.2 User and carer representatives 259 A1.3 Observers 259 A1.4 Secretariat 260 A1.5 Reviews and synopses 260 A1.6 Other contributors 261 Contents 3 A2: Governance 263 A2.1 Quality governance 263 A2.2 Confidentiality and safeguarding 266 A2.3 Non-medical prescribing 269 A3: Marketing authorisations 271 A3.1 ‘Off-label’ or ‘unlicensed’ prescribing 271 A3.2 Young people 272 A3.3 References 272 A4: Writing prescriptions 277 A4.1 General considerations 277 A4.2 Patient safety 277 A4.3 Legal and good practice requirements 278 A4.4 Minor amendments 281 A4.5 Additional country-specific rules 281 A4.6 Other considerations 283 A4.7 Examples of what to write on a prescription 284 A4.8 Private prescriptions 291 A4.9 Resources and further reading 292 A5: Interactions 293 A5.1 Medicinal interactions 293 A5.2 Interactions with illicit drugs 294 A5.3 Resources and further reading 295 A6: Travelling abroad with controlled drugs 303 A6.1 General 303 A6.2 Travelling for less than three months 303 A6.3 Travelling for three months or more 303 A7: Drugs and driving 305 A7.1 Key points 305 A7.2 Offences related to drug use and driving in the UK 305 A7.3 Driving licence requirements 306 A7.4 Risk assessment for driving 308 A7.5 Responsibilities of the prescribing clinician 308 A7.6 Information for patients 308 A7.7 References 310 A8: Glossary 311 4 Drug misuse and dependence: UK guidelines on clinical management List of figures Box 1: Full or comprehensive assessment of drug-using parents 19 Box 2: Principles for trauma-informed care 42 Table 1: A model of phased and layered interventions 50 Table 2: Signs of opiate withdrawal 86 Table 3: Responses to drug and alcohol misuse on top of an opioid prescription 109 Table 4: Approximate dosages equivalent to 5mg diazepam 122 Box 3: Naloxone and hostel scenario example 180 Box 4: Advice for achieving and maintaining good oral hygiene 193 Table 5: Special health needs of older people with substance use problems 249 Table 6: Marketing authorisations for medicines used in in adults 273 Table 7: Marketing authorisations for medicines used in in young people 275 Table 8: Examples of prescription writing 285 Table 9: Important interactions with methadone and buprenorphine 296 Table 10: Other clinically important interactions in substance misuse 300 Table 11: Some important interactions with HIV and hepatitis treatments 302 Preface 5 Preface Professor Sir John Strang It has been my great honour and pleasure to chair the independent expert working group updating the 2007 Clinical Guidelines. I am immensely grateful to the many colleagues who have served on the working group, or who have prepared documents and given evidence to us, and to the officials who have so actively supported us in our work. I am satisfied that this 2017 edition of the ‘Orange Book’ will help providers and commissioners to optimise the reach and effectiveness of the interventions they have the responsibility to deliver. The right treatment at the right time can be life-saving. It can also make a huge difference to the wellbeing and recovery of people with problems related to their drug use. Well-delivered treatment is greatly more effective than less competently delivered treatment. The Clinical Guidelines are designed to support you in meeting your responsibility to ensure evidence- based treatments are available and competently delivered. Guidelines guide – they are not intended to dictate the precise treatment for each patient. Rather, they are designed to guide the clinician and the commissioner in the provision of the right balance of interventions, which have the greatest likelihood to produce individual benefit and public good. The Clinical Guidelines also enable the clinician to assess whether a proposed treatment plan departs, and to what extent it departs, from evidence-based guidance on the specific treatment. As a general principle, the greater the extent to which a treatment plan departs from evidence-based guidelines, the greater the need to ensure that this departure from orthodox clinical practice is appropriate. Since my first involvement with the Clinical Guidelines more than a quarter of a century ago, the world of drug treatment has matured greatly, and so too has the manner in which we examine the available evidence. This is evident in the substantial and evidence-informed nature of the new 2017 Clinical Guidelines. Some of the problems individuals experience are new and require their own consideration, although many of the underlying principles of the provision of best care remain valid from previous iterations of the Clinical Guidelines. This is as we would expect it to be, since our knowledge grows incrementally with regard to the problems people experience and the ways in which we can help them to address these problems. Thus, some sections of the 2017 Clinical Guidelines contain new material, others echo earlier editions and others present updated revisions of earlier guidance. 6 Drug misuse and dependence: UK guidelines on clinical management Psychosocial and pharmacological approaches are considered within the Clinical Guidelines, as is the social context in which people experience their problems and are helped with their treatment and recovery. Pharmacological approaches remain extremely important and of clearly demonstrated efficacy and effectiveness for those with problems related to use of heroin or other opiates. But this approach is of limited relevance to treatment for those with problems related to use of other types of drug. For many who make contact with treatment services, it is also important to look broadly at the opportunity to address their psychological problems and the impact of past traumas, and to provide support to gain meaningful employment, stable housing, alongside family and other social support.
Recommended publications
  • Table 2. 2012 AGS Beers Criteria for Potentially
    Table 2. 2012 AGS Beers Criteria for Potentially Inappropriate Medication Use in Older Adults Strength of Organ System/ Recommendat Quality of Recomm Therapeutic Category/Drug(s) Rationale ion Evidence endation References Anticholinergics (excludes TCAs) First-generation antihistamines Highly anticholinergic; Avoid Hydroxyzin Strong Agostini 2001 (as single agent or as part of clearance reduced with e and Boustani 2007 combination products) advanced age, and promethazi Guaiana 2010 Brompheniramine tolerance develops ne: high; Han 2001 Carbinoxamine when used as hypnotic; All others: Rudolph 2008 Chlorpheniramine increased risk of moderate Clemastine confusion, dry mouth, Cyproheptadine constipation, and other Dexbrompheniramine anticholinergic Dexchlorpheniramine effects/toxicity. Diphenhydramine (oral) Doxylamine Use of diphenhydramine in Hydroxyzine special situations such Promethazine as acute treatment of Triprolidine severe allergic reaction may be appropriate. Antiparkinson agents Not recommended for Avoid Moderate Strong Rudolph 2008 Benztropine (oral) prevention of Trihexyphenidyl extrapyramidal symptoms with antipsychotics; more effective agents available for treatment of Parkinson disease. Antispasmodics Highly anticholinergic, Avoid Moderate Strong Lechevallier- Belladonna alkaloids uncertain except in Michel 2005 Clidinium-chlordiazepoxide effectiveness. short-term Rudolph 2008 Dicyclomine palliative Hyoscyamine care to Propantheline decrease Scopolamine oral secretions. Antithrombotics Dipyridamole, oral short-acting* May
    [Show full text]
  • Dofetilide (Tikosyn): a New Drug to Control Atrial Fibrillation
    CURRENT DRUG THERAPY WALID I. SALIBA, MD Section of Cardiac Electrophysiology and Pacing, CREDIT Department of Cardiology, Cleveland Clinic Dofetilide (Tikosyn): A new drug to control atrial fibrillation ABSTRACT OFETILIDE (Tikosyn), a new antiarrhyth- mic drug, can convert atrial fibrillation Dofetilide, a new class III antiarrhythmic agent, selectively and atrial flutter to sinus rhythm in approxi- blocks a specific cardiac potassium channel, lKr, increasing mately 30% of cases and maintain sinus the effective refractory period of the myocyte and thereby rhythm after electrical or pharmacologic con- terminating reentrant arrhythmias. Given orally, it appears version for up to 1 year in 60% to 70% of to effectively convert atrial fibrillation and atrial flutter to cases, without increasing the risk of sudden sinus rhythm and maintain sinus rhythm after conversion in death in patients at high risk. appropriately selected patients. This paper reviews the Such new drugs are needed, as many of the pharmacology of dofetilide, the evidence of its antiarrhythmic drugs in use up to now have effectiveness, and the appropriate precautions in using it. actually produced higher mortality rates in clinical trials than did placebo, or cause unac- ceptable side effects. KEY POINTS This article reviews the mechanism of action, safety, effectiveness, and clinical use of Dofetilide is generally well tolerated but like other class III dofetilide. drugs can cause torsades de pointes. The risk is dose- dependent and can be minimized by adjusting the dosage • PROBLEMS WITH PREVIOUS DRUGS according to creatinine clearance and QT interval, by excluding patients with known risk factors for long QT A variety of drugs have been used to terminate syndrome and torsades de pointes, and by starting or prevent atrial and ventricular arrhythmias, treatment in an inpatient monitored setting for the first 3 but their safety, efficacy, and tolerability in days.
    [Show full text]
  • Medical Review Officer Manual
    Department of Health and Human Services Substance Abuse and Mental Health Services Administration Center for Substance Abuse Prevention Medical Review Officer Manual for Federal Agency Workplace Drug Testing Programs EFFECTIVE OCTOBER 1, 2010 Note: This manual applies to Federal agency drug testing programs that come under Executive Order 12564 dated September 15, 1986, section 503 of Public Law 100-71, 5 U.S.C. section 7301 note dated July 11, 1987, and the Department of Health and Human Services Mandatory Guidelines for Federal Workplace Drug Testing Programs (73 FR 71858) dated November 25, 2008 (effective October 1, 2010). This manual does not apply to specimens submitted for testing under U.S. Department of Transportation (DOT) Procedures for Transportation Workplace Drug and Alcohol Testing Programs (49 CFR Part 40). The current version of this manual and other information including MRO Case Studies are available on the Drug Testing page under Medical Review Officer (MRO) Resources on the SAMHSA website: http://www.workplace.samhsa.gov Previous Versions of this Manual are Obsolete 3 Table of Contents Chapter 1. The Medical Review Officer (MRO)........................................................................... 6 Chapter 2. The Federal Drug Testing Custody and Control Form ................................................ 7 Chapter 3. Urine Drug Testing ...................................................................................................... 9 A. Federal Workplace Drug Testing Overview..................................................................
    [Show full text]
  • What Are the Acute Treatments for Migraine and How Are They Used?
    2. Acute Treatment CQ II-2-1 What are the acute treatments for migraine and how are they used? Recommendation The mainstay of acute treatment for migraine is pharmacotherapy. The drugs used include (1) acetaminophen, (2) non-steroidal anti-inflammatory drugs (NSAIDs), (3) ergotamines, (4) triptans and (5) antiemetics. Stratified treatment according to the severity of migraine is recommended: use NSAIDs such as aspirin and naproxen for mild to moderate headache, and use triptans for moderate to severe headache, or even mild to moderate headache when NSAIDs were ineffective in the past. It is necessary to give guidance and cautions to patients having acute attacks, and explain the methods of using medications (timing, dose, frequency of use) and medication use during pregnancy and breast-feeding. Grade A Background and Objective The objective of acute treatment is to resolve the migraine attack completely and rapidly and restore the patient’s normal functions. An ideal treatment should have the following characteristics: (1) resolves pain and associated symptoms rapidly; (2) is consistently effective; (3) no recurrence; (4) no need for additional use of medication; (5) no adverse effects; (6) can be administered by the patients themselves; and (7) low cost. Literature was searched to identify acute treatments that satisfy the above conditions. Comments and Evidence The acute treatment drugs for migraine generally include (1) acetaminophens, (2) non-steroidal anti-inflammatory drugs (NSAIDs), (3) ergotamines, (4) triptans, and (5) antiemetics. For severe migraines including status migrainosus and migraine attacks refractory to treatment, (6) anesthetics, and (7) corticosteroids (dexamethasone) are used (Tables 1 and 2).1)-9) There are two approaches to the selection and sequencing of these medications: “step care” and “stratified care”.
    [Show full text]
  • Effects of Acute Intravenous Administration of Pentamidine, a Typical Herg-Trafficking Inhibitor, on the Cardiac Repolarization Process of Halothane-Anesthetized Dogs
    J Pharmacol Sci 110, 476 – 482 (2009)4 Journal of Pharmacological Sciences ©2009 The Japanese Pharmacological Society Full Paper Effects of Acute Intravenous Administration of Pentamidine, a Typical hERG-Trafficking Inhibitor, on the Cardiac Repolarization Process of Halothane-Anesthetized Dogs Hirofumi Yokoyama1,2, Yuji Nakamura1, Hiroshi Iwasaki1, Yukitoshi Nagayama1,2,3, Kiyotaka Hoshiai1,2,3, Yoshitaka Mitsumori1, and Atsushi Sugiyama1,2,* 1Department of Pharmacology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi 409-3898, Japan 2Yamanashi Research Center of Clinical Pharmacology, Fuefuki, Yamanashi 406-0023, Japan 3Sugi Institute of Biological Science, Co., Ltd., Hokuto, Yamanashi 408-0044, Japan Received February 27, 2009; Accepted June 16, 2009 Abstract. Although acute treatment of pentamidine does not directly modify any ionic channel function in the heart at clinically relevant concentrations, its continuous exposure can prolong QT interval. Recent in vitro studies have indicated that hERG trafficking inhibition may play an important role in the onset of pentamidine-induced long QT syndrome. In this study, we examined acute in vivo electropharmacological effects of pentamidine using the halothane- anesthetized canine model (n = 5). The clinically relevant total dose of 4 mg/kg of pentamidine (namely, 1 mg/kg, i.v. over 10 min followed by 3 mg/kg, i.v. over 10 min with a pause of 20 min) decreased the mean blood pressure, ventricular contraction, preload to the left ventricle, and peripheral vascular resistance. Pentamidine also enhanced the atrioventricular conduction in parallel with its cardiohemodynamic actions, but it gradually prolonged both the ventricular repolarization period and effective refractory period, whereas no significant change was detected in the intraventricular conduction.
    [Show full text]
  • Intranasal Rhinitis Agents
    Intranasal Rhinitis Agents Therapeutic Class Review (TCR) February 1, 2020 No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, digital scanning, or via any information storage or retrieval system without the express written consent of Magellan Rx Management. All requests for permission should be mailed to: Magellan Rx Management Attention: Legal Department 6950 Columbia Gateway Drive Columbia, Maryland 21046 The materials contained herein represent the opinions of the collective authors and editors and should not be construed to be the official representation of any professional organization or group, any state Pharmacy and Therapeutics committee, any state Medicaid Agency, or any other clinical committee. This material is not intended to be relied upon as medical advice for specific medical cases and nothing contained herein should be relied upon by any patient, medical professional or layperson seeking information about a specific course of treatment for a specific medical condition. All readers of this material are responsible for independently obtaining medical advice and guidance from their own physician and/or other medical professional in regard to the best course of treatment for their specific medical condition. This publication, inclusive of all forms contained herein, is intended to be educational in nature and is intended to be used for informational purposes only. Send comments and suggestions to [email protected].
    [Show full text]
  • Drug Induced QT Prolongation and Torsades De Pointes (Tdp)
    Drug induced QT prolongation and Torsades de Pointes (TdP) Mark Friesen, PharmD March 13, 2013 Conflict of Interest None TdP: Learning objectives To review the pathophysiology of QT prolongation and TdP To become aware of the risk factors (including medication- related) for QT prolongation and TdP To understand and apply a systematic approach for dealing with drug interactions that may cause prolonged QT and TdP Clinical Scenario You receive an order for a patient: Levofloxacin 500 mg PO daily Fluconazole 400 mg PO daily Your drug interaction program flags this as a major interaction due to QT prolonging effect of both drugs increasing risk for TdP. What do you do? TdP: History Quinidine associated syncope since 1920’s Congenital syndromes with prolonged QT and syncope or sudden death described in 1950’s, and early 1960’s. 1966 Francois Dessertenne described a specific EKG form of polymorphic VT he termed “torsades de pointes” Over past decade single most common cause of drug withdrawal/restriction from market 9 structurally unrelated non-cardiac drugs: terfenadine, astemizole, grepafloxicin, terodiline, droperidol, terodiline, droperidol, lidoflazaine, sertindole, levomethadyl, cisapride TdP: Definition Polymorphic VT with a preexistant prolonged QT interval Ventricular Action Potential Ca++ Na+ IKr IKs IKr Channel: hERG controlled Delayed repolarization=prolonged QT interval Mechanism of Torsades de Pointes Early afterdepolarizations (extra beat) Transmural reentry (Unusual pathway) Mechanisms Of Drug - Induced QT Prolongation
    [Show full text]
  • Novel Formulations for Treatment of Migraine
    (19) TZZ _T (11) EP 2 756 756 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 23.07.2014 Bulletin 2014/30 A01N 43/42 (2006.01) A61K 31/44 (2006.01) (21) Application number: 14165112.5 (22) Date of filing: 24.04.2009 (84) Designated Contracting States: • Turanin, John AT BE BG CH CY CZ DE DK EE ES FI FR GB GR Emeryville, CA California 94608 (US) HR HU IE IS IT LI LT LU LV MC MK MT NL NO PL • Hawley, Roger PT RO SE SI SK TR Emeryville, CA California 94608 (US) • Schuster, Jeffrey, A. (30) Priority: 28.04.2008 US 48463 Bolinas, CA California 94924 (US) (62) Document number(s) of the earlier application(s) in (74) Representative: Duxbury, Stephen et al accordance with Art. 76 EPC: Arnold & Siedsma 09739139.5 / 2 273 880 Pettenkoferstrasse 37 80336 München (DE) (71) Applicant: Zogenix, Inc. Emeryville CA 94608 (US) Remarks: This application was filed on 17-04-2014 as a (72) Inventors: divisional application to the application mentioned • Farr, Stephen J. under INID code 62. Orinda, CA California 94563 (US) (54) Novel formulations for treatment of migraine (57) Systems and methods are described for treating Systems that are self contained, portable, prefilled, and un-met medical needs in migraine and related conditions simple to self administer at the onset of a migraine attack such as cluster headache. Included are treatments that are disclosed, and preferably include a needle-free in- are both rapid onset and long acting, which include sus- jector and a high viscosity formulation, to eliminate such tained release formulations, and combination products, issues as fear of self administration with needles, and Also included are treatments for multiple symptoms of needle stick and cross contamination.
    [Show full text]
  • Safety and Efficacy of Ibutilide in Cardioversion of Atrial Flutter And
    J Am Board Fam Med: first published as 10.3122/jabfm.2011.01.080096 on 5 January 2011. Downloaded from CLINICAL REVIEW Safety and Efficacy of Ibutilide in Cardioversion of Atrial Flutter and Fibrillation Madhuri Nair, MD, Lekha K. George, MD, and Santhosh K. G. Koshy, MD This article reviews the safety and efficacy of ibutilide for use in patients with atrial fibrillation and flut- ter. Ibutilide, a class III antiarrhythmic agent, is primarily used for conversion of atrial flutter and fi- brillation and is a good alternative to electrical cardioversion. Ibutilide has a conversion rate of up to 75% to 80% in recent-onset atrial fibrillation and flutter; the conversion rate is higher for atrial flutter than for atrial fibrillation. It is also safe in the conversion of chronic atrial fibrillation/flutter among patients receiving oral amiodarone therapy. Ibutilide pretreatment facilitates transthoracic defibrilla- tion and decreases the energy requirement of electrical cardioversion by both monophasic and biphasic shocks. Pretreatment with ibutilide before electrical defibrillation has a conversion rate of 100% com- pared with 72% with no pretreatment. Ibutilide is also safe and efficient in the treatment of atrial fibril- lation in patients who have had cardiac surgery, and in accessory pathway–mediated atrial fibrillation where the conversion rate of ibutilide is as high as 95%. There is up to a 4% risk of torsade de pointes and a 4.9% risk of monomorphic ventricular tachycardia. Hence, close monitoring in an intensive care unit setting is warranted during and at least for 4 hours after drug infusion. The anticoagulation strat- egy is the same as for any other mode of cardioversion.(J Am Board Fam Med 2011;24:86–92.) Keywords: Antiarrhythmics, Arrhythmia, Atrial Fibrillation, Cardiovascular Disorders, Cardioversion, Drug Ther- copyright.
    [Show full text]
  • Concentration Dependent Cardiotoxicity of Terodiline in Patients Treated for Urinary Incontinence
    Br HeartJ7 1995;74:53-56 53 Concentration dependent cardiotoxicity of terodiline in patients treated for urinary incontinence Simon H L Thomas, P Daniel Higham, Kenneth Hartigan-Go, Farhad Kamali, Peter Wood, Ronald W F Campbell, Gary A Ford Abstract Terodiline hydrochloride is an antimuscarinic Objective-Terodiline, an antimuscarinic drug with calcium antagonist properties' and calcium antagonist drug, was used to which was used for treating urinary inconti- treat detrusor instability but was with- nence caused by detrusor instability.2 The drawn in 1991 after provoking serious drug was withdrawn in 1991 after reports of ventricular arrhythmias associated with cardiac dysrhythmia including bradycardia, increases in the corrected QT interval heart block, ventricular fibrillation, and ven- (QTc). This research was performed to tricular tachycardia, usually of the torsade de relate drug induced electrocardiographic pointes-type34 and associated with QT pro- changes in asymptomatic recipients to longation. Plasma terodiline concentrations plasma concentrations of the R( +) and were very high in one affected patient. S(-) terodiline enantiomers. Predisposing factors for terodiline associated Setting-Urological and geriatric clinics torsade de pointes were old age, coexisting and wards. ischaemic heart disease, co-prescription of Subjects-Asymptomatic patients taking other cardioactive drugs, and hypokalaemia. terodiline in stable dose. Torsade de pointes is associated with Methods-Electrocardiograms (50 mm/s) abnormal prolongation of the ventricular were collected from patients while they refractory period which results in a long QT were taking terodiline and compared with interval on the electrocardiogram and is often ECGs obtained before or after terodiline. drug induced.5 Increased dispersion of ven- QT interval, heart rate corrected QT tricular recovery may be important in the interval (QTc), and QT dispersion (QTd) development of this arrhythmia and indirect were measured.
    [Show full text]
  • Supplementary Materials
    Supplementary Materials Table S1. The significant drug pairs in potential DDIs examined by the two databases. Micromedex Drugs.com List of drugs paired PK-PD Mechanism details 1. Amiodarone— PD Additive QT-interval prolongation Dronedarone 2. Amiodarone— PK CYP3A inhibition by Ketoconazole Ketoconazole 3. Ciprofloxacin— PD Additive QT-interval prolongation Dronedarone 4. Cyclosporine— PK CYP3A inhibition by Cyclosporine Dronedarone 5. Dronedarone— PK CYP3A inhibition by Erythromycin Erythromycin 6. Dronedarone— PD Additive QT-interval prolongation Flecainide 7. Dronedarone— PK CYP3A4 inhibition by Itraconazole Itraconazole 8. Dronedarone— PK Contraindication Major CYP3A inhibition by Ketoconazole Ketoconazole 9. Dronedarone— PD Additive QT-interval prolongation Procainamide PD 10. Dronedarone—Sotalol Additive QT-interval prolongation 11. Felodipine— PK CYP3A inhibition by Itraconazole Itraconazole 12. Felodipine— PK CYP3A inhibition by Ketoconazole Ketoconazole 13. Itraconazole— PK CYP3A inhibition by Itraconazole Nisoldipine 14. Ketoconazole— PK CYP3A inhibition by Ketoconazole Nisoldipine 15. Praziquantel— PK CYP induction by Rifampin Rifampin PD 1. Amikacin—Furosemide Additive or synergistic toxicity 2. Aminophylline— Decreased clearance of PK Ciprofloxacin Theophylline by Ciprofloxacin 3. Aminophylline— PK Decreased hepatic metabolism Mexiletine 4. Amiodarone— PD Additive effects on QT interval Ciprofloxacin 5. Amiodarone—Digoxin PK P-glycoprotein inhibition by Amiodarone 6. Amiodarone— PD, PK Major Major Additive effects on QT Erythromycin prolongation, CYP3A inhibition by Erythromycin 7. Amiodarone— PD, PK Flecainide Antiarrhythmic inhibition by Amiodarone, CYP2D inhibition by Amiodarone 8. Amiodarone— PK CYP3A inhibition by Itraconazole Itraconazole 9. Amiodarone— PD Antiarrhythmic inhibition by Procainamide Amiodarone 10. Amiodarone— PK CYP induction by Rifampin Rifampin PD Additive effects on refractory 11. Amiodarone—Sotalol potential 12. Amiodarone— PK CYP3A inhibition by Verapamil Verapamil 13.
    [Show full text]
  • Download Article (PDF)
    Use of astemizole in a large group practice TIMOTHY J. CRAIG, DO MARK GREENWALD, MD VANESSA KAUFFMANN JILL CRAIG, MS Astemizole was released in 1988. Shortly after the release of astemizole and terfe­ In late 1992, a new warning label was added nadine, it became evident that both were associat­ in response to reports of syncope and death ed with prolonged QT intervals and arrhythmias, from arrhythmia. Records of patients given new mainly torsades de pointes. Because of this associ­ prescriptions for astemizole were reviewed ation, the Food and Drug Administration (FDA) and to assess compliance with the warnings in a the manufacturers provided a warning letter to large multispecialty practice. The indication physicians in 1992.1 For astemizole, the warning was appropriate in 89% of cases. Excessive stated: (1) That arrhythmias have usually occurred doses were used in 4% of cases. Two percent when the dose of 10 mg/d (the recommended dose) of prescriptions were given to patients with was exceeded. Exceeding this dose and the use of contraindications. Only two complications loading doses should be avoided. (2) Serum levels were documented. Despite carrying a drug of astemizole may be elevated by ketoconazole, ery­ warning, astemizole continues to be used thromycin;, and itraconazole. These drugs should inappropriately and is a medicolegal concern. not be used together. (3) Presyncope and syncope Education and drug evaluations can be used may precede fatal arrhythmias and calls for dis­ to enhance compliance and decrease the risk continuing astemizole. (4) The drug should be avoid­ associated with the use of astemizole. ed in patients with significant liver disease.
    [Show full text]