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Current Awareness in Clinical Toxicology Editors: Damian Ballam Msc and Allister Vale MD
Current Awareness in Clinical Toxicology Editors: Damian Ballam MSc and Allister Vale MD February 2016 CONTENTS General Toxicology 9 Metals 38 Management 21 Pesticides 41 Drugs 23 Chemical Warfare 42 Chemical Incidents & 32 Plants 43 Pollution Chemicals 33 Animals 43 CURRENT AWARENESS PAPERS OF THE MONTH How toxic is ibogaine? Litjens RPW, Brunt TM. Clin Toxicol 2016; online early: doi: 10.3109/15563650.2016.1138226: Context Ibogaine is a psychoactive indole alkaloid found in the African rainforest shrub Tabernanthe Iboga. It is unlicensed but used in the treatment of drug and alcohol addiction. However, reports of ibogaine's toxicity are cause for concern. Objectives To review ibogaine's pharmacokinetics and pharmacodynamics, mechanisms of action and reported toxicity. Methods A search of the literature available on PubMed was done, using the keywords "ibogaine" and "noribogaine". The search criteria were "mechanism of action", "pharmacokinetics", "pharmacodynamics", "neurotransmitters", "toxicology", "toxicity", "cardiac", "neurotoxic", "human data", "animal data", "addiction", "anti-addictive", "withdrawal", "death" and "fatalities". The searches identified 382 unique references, of which 156 involved human data. Further research revealed 14 detailed toxicological case reports. Current Awareness in Clinical Toxicology is produced monthly for the American Academy of Clinical Toxicology by the Birmingham Unit of the UK National Poisons Information Service, with contributions from the Cardiff, Edinburgh, and Newcastle Units. The NPIS is commissioned by Public Health England Current Awareness in Clinical Toxicology Editors: Damian Ballam MSc and Allister Vale MD February 2016 Current Awareness in Clinical Toxicology is produced monthly for the American Academy of Clinical Toxicology by the Birmingham Unit of the UK National Poisons Information Service, with contributions from the Cardiff, Edinburgh, and Newcastle Units. -
Dezocine Exhibits Antihypersensitivity Activities in Neuropathy Through
www.nature.com/scientificreports OPEN Dezocine exhibits antihypersensitivity activities in neuropathy through spinal Received: 09 November 2016 Accepted: 19 January 2017 μ-opioid receptor activation and Published: 23 February 2017 norepinephrine reuptake inhibition Yong-Xiang Wang1, Xiao-Fang Mao1, Teng-Fei Li1, Nian Gong1 & Ma-Zhong Zhang2 Dezocine is the number one opioid painkiller prescribed and sold in China, occupying 44% of the nation’s opioid analgesics market today and far ahead of the gold-standard morphine. We discovered the mechanisms underlying dezocine antihypersensitivity activity and assessed their implications to antihypersensitivity tolerance. Dezocine, given subcutaneously in spinal nerve-ligated neuropathic rats, time- and dose-dependently produced mechanical antiallodynia and thermal antihyperalgesia, significantly increased ipsilateral spinal norepinephrine and serotonin levels, and induced less antiallodynic tolerance than morphine. Its mechanical antiallodynia was partially (40% or 60%) and completely (100%) attenuated by spinal μ-opioid receptor (MOR) antagonism or norepinephrine depletion/α2-adrenoceptor antagonism and combined antagonism of MORs and α2-adenoceptors, respectively. In contrast, antagonism of spinal κ-opioid receptors (KORs) and δ-opioid receptors (DORs) or depletion of spinal serotonin did not significantly alter dezocine antiallodynia. In addition, dezocine- delayed antiallodynic tolerance was accelerated by spinal norepinephrine depletion/α2-adenoceptor antagonism. Thus dezocine produces antihypersensitivity activity through spinal MOR activation and norepinephrine reuptake inhibition (NRI), but apparently not through spinal KOR and DOR activation, serotonin reuptake inhibition or other mechanisms. Our findings reclassify dezocine as the first analgesic of the recently proposed MOR-NRI, and reveal its potential as an alternative to as well as concurrent use with morphine in treating pain. -
Opioid Antagonists As Potential Therapeutics for Ischemic Stroke
Progress in Neurobiology 182 (2019) 101679 Contents lists available at ScienceDirect Progress in Neurobiology journal homepage: www.elsevier.com/locate/pneurobio Perspective article Opioid antagonists as potential therapeutics for ischemic stroke T ⁎ ⁎ Nadia Peyraviana,b, Emre Dikicia,b, Sapna Deoa,b, Michal Toboreka,b, , Sylvia Daunerta,b,c, a Department of Biochemistry and Molecular Biology, Miller School of Medicine, University of Miami, USA b Dr. JT Macdonald Foundation Biomedical Nanotechnology Institute of the University of Miami, USA c University of Miami Clinical and Translational Science Institute, USA ARTICLE INFO ABSTRACT Keywords: Chronic use of prescription opioids exacerbates risk and severity of ischemic stroke. Annually, 6 million people Ischemic stroke die from stroke worldwide and there are no neuroprotective or neurorestorative agents to improve stroke out- Opioid antagonist comes and promote recovery. Prescribed opioids such as morphine have been shown to alter tight junction Blood brain barrier protein expression, resulting in the disruption of the blood brain barrier (BBB), ultimately leading to stroke Neuroprotection pathogenesis. Consequently, protection of the BBB has been proposed as a therapeutic strategy for ischemic Naloxone stroke. This perspective addresses the deficiency in stroke pharmacological options and examines a novel ap- Naltrexone plication and repurposing of FDA-approved opioid antagonists as a prospective neuroprotective therapeutic strategy to minimize BBB damage, reduce stroke severity, and promote neural recovery. Future directions discuss potential drug design and delivery methods to enhance these novel therapeutic targets. 1. Introduction modulate resulting microglia and macrophage activation in the is- chemic region to reduce neuroinflammation and prevent secondary As of 2017, the US government declared the opioid epidemic as a neurodegeneration resulting from phagocytosis of viable neurons. -
Supplemental Information
REVIEW ARTICLE Supplemental Information SEARCH STRATEGIES 7. exp Congenital Abnormalities/ or remifentanil or sufentanil or 8. (defect or cleft or heart defect tapentadol or tramadol or heroin Database: Ovid MEDLINE(R) In- or nalmefene or naloxone or Process and Other Nonindexed or gastroschisis or cryptorchidism or atresia or congenital or clubfoot naltrexone).mp. Citations and Ovid MEDLINE(R), or renal or craniosynostosis or 4. 1 or 2 or 3 1946 to Present hypospadias or malformation or 5. exp pregnancy/or exp pregnancy spina bifida or neural tube defect). outcome/ mp. 1. exp Analgesics, Opioid/ 6. exp teratogenic agent/ 9. 5 or 6 or 7 or 8 2. (opioid* or opiate*).mp. 7. exp congenital disorder/ 10. 4 and 9 3. (alfentanil or alphaprodine or 11. Limit 10 to (English language and 8. (defect or cleft or heart defect buprenorphine or butorphanol humans) or gastroschisis or cryptorchidism or codeine or dezocine or or atresia or congenital or clubfoot dihydrocodeine or fentanyl or Database: Ovid Embase, 1988– or renal or craniosynostosis or hydrocodone or hydromorphone 2016, Week 7 hypospadias or malformation or or levomethadyl or levorphanol spina bifida or neural tube defect). or meperidine or methadone or mp. 1. exp opiate/ morphine or nalbuphine or opium 9. 5 or 6 or 7 or 8 or oxycodone or oxymorphone 2. (opioid* or opiate*).mp. or pentazocine or propoxyphene 10. 4 and 9 3. (alfentanil or alphaprodine or or remifentanil or sufentanil or buprenorphine or butorphanol 11. Limit 10 to (human and English tapentadol or tramadol or heroin or codeine or dezocine or language and (article or book or or nalmefene or naloxone or book series or conference paper dihydrocodeine or fentanyl or “ ” naltrexone).mp. -
VHA/Dod CLINICAL PRACTICE GUIDELINE for the MANAGEMENT of POSTOPERATIVE PAIN
VHA/DoD CLINICAL PRACTICE GUIDELINE FOR THE MANAGEMENT OF POSTOPERATIVE PAIN Veterans Health Administration Department of Defense Prepared by: THE MANAGEMENT OF POSTOPERATIVE PAIN Working Group with support from: The Office of Performance and Quality, VHA, Washington, DC & Quality Management Directorate, United States Army MEDCOM VERSION 1.2 JULY 2001/ UPDATE MAY 2002 VHA/DOD CLINICAL PRACTICE GUIDELINE FOR THE MANAGEMENT OF POSTOPERATIVE PAIN TABLE OF CONTENTS Version 1.2 Version 1.2 VHA/DoD Clinical Practice Guideline for the Management of Postoperative Pain TABLE OF CONTENTS INTRODUCTION A. ALGORITHM & ANNOTATIONS • Preoperative Pain Management.....................................................................................................1 • Postoperative Pain Management ...................................................................................................2 B. PAIN ASSESSMENT C. SITE-SPECIFIC PAIN MANAGEMENT • Summary Table: Site-Specific Pain Management Interventions ................................................1 • Head and Neck Surgery..................................................................................................................3 - Ophthalmic Surgery - Craniotomies Surgery - Radical Neck Surgery - Oral-maxillofacial • Thorax (Non-cardiac) Surgery.......................................................................................................9 - Thoracotomy - Mastectomy - Thoracoscopy • Thorax (Cardiac) Surgery............................................................................................................16 -
Measures and CDS for Safer Opioid Prescribing: a Literature Review
Measures and CDS for Safer Opioid Prescribing: A Literature Review Measures and CDS for Safer Opioid Prescribing: A Literature Review Executive Summary The U.S. opioid epidemic continues to pose significant challenges for patients, families, clinicians, and public health policy. Opioids are responsible for an estimated 315,000 deaths (from 1999 to 2016) and have caused 115 deaths per day.1 In 2017, the U.S. Department of Health and Human Services declared the opioid epidemic a public health crisis.2 The total economic burden of opioid abuse in the United States has been estimated to be $78.5 billion per year.3 Although providing care for chronic opioid users is important, equally vital are efforts to prevent so-called opioid-naïve patients (patients with no history of opioid use) from developing regular opioid use, misuse, or abuse. However, much remains unclear regarding what role clinician prescribing habits play and what duration or dose of opioids may safely be prescribed without promoting long-term use.4,5 In 2013, ECRI Institute convened the Partnership for Health IT Patient Safety, and its component, single-topic-focused workgroups followed. For this subject, the Electronic Health Record Association (EHRA): Measures and Clinical Decision Support (CDS) for Safer Opioid Prescribing workgroup included members from the Healthcare Information and Management Systems Society (HIMSS) EHRA and the Partnership team. The project was oriented towards exploring methods to enable a synergistic cycle of performance measurement and identifying electronic health record (EHR)/health information technology (IT)–enabled approaches to support healthcare organizations’ ability to assess and measure opioid prescribing. -
Original Article Preoperative Intravenous Administration Of
Int J Clin Exp Med 2016;9(9):18451-18457 www.ijcem.com /ISSN:1940-5901/IJCEM0016462 Original Article Preoperative intravenous administration of dezocine for cesarean section under epidural anesthesia: effects on maternal well-being and neonatal outcome Keqiang He, Jianhui Pan, Liguo Hu, Ruiting Wang, Ling Hu Department of Anesthesia, Affiliated Provincial Hospital of Anhui Medical University, Hefei 230001, China Received September 19, 2015; Accepted January 21, 2016; Epub September 15, 2016; Published September 30, 2016 Abstract: We evaluated the efficacy and safety of preoperative intravenous administration of dezocine for comfort- able birth by cesarean section under epidural anesthesia. Sixty primigravida women with full-term singletons un- derwent elective cesarean section, and were randomly divided into three groups. Patients in groups A and B were intravenously injected with 5 and 10 mg of dezocine, 10 min before skin incision, whereas patients in group C were intravenously injected with saline. We recorded data on visceral traction responses and intraoperative adverse reactions, such as nausea and vomiting. While the neonate was being delivered, the umbilical arterial and venous blood gas values were determined. The Apgar scores at 1, 5, and 10 min after delivery, as well as the Neurologic Adaptive and Capacity Score (NACS) at 15 min, 2 h, and 24 h, were recorded. The “fineness rate” required to relieve the traction reaction in group B was higher than that in group C (P < 0.05). The intraoperative Modified Observer’s Assessment of Alertness/Sedation (MOAA/S) scores of groups A and B were lower than that of group C, and the time period that the intraoperative MOAA/S score was ≤ 4 points was longer in group B (P < 0.05). -
Evidence-Based Guidelines for the Pharmacological Management of Substance Abuse, Harmful Use, Addictio
444324 JOP0010.1177/0269881112444324Lingford-Hughes et al.Journal of Psychopharmacology 2012 BAP Guidelines BAP updated guidelines: evidence-based guidelines for the pharmacological management of substance abuse, Journal of Psychopharmacology 0(0) 1 –54 harmful use, addiction and comorbidity: © The Author(s) 2012 Reprints and permission: sagepub.co.uk/journalsPermissions.nav recommendations from BAP DOI: 10.1177/0269881112444324 jop.sagepub.com AR Lingford-Hughes1, S Welch2, L Peters3 and DJ Nutt 1 With expert reviewers (in alphabetical order): Ball D, Buntwal N, Chick J, Crome I, Daly C, Dar K, Day E, Duka T, Finch E, Law F, Marshall EJ, Munafo M, Myles J, Porter S, Raistrick D, Reed LJ, Reid A, Sell L, Sinclair J, Tyrer P, West R, Williams T, Winstock A Abstract The British Association for Psychopharmacology guidelines for the treatment of substance abuse, harmful use, addiction and comorbidity with psychiatric disorders primarily focus on their pharmacological management. They are based explicitly on the available evidence and presented as recommendations to aid clinical decision making for practitioners alongside a detailed review of the evidence. A consensus meeting, involving experts in the treatment of these disorders, reviewed key areas and considered the strength of the evidence and clinical implications. The guidelines were drawn up after feedback from participants. The guidelines primarily cover the pharmacological management of withdrawal, short- and long-term substitution, maintenance of abstinence and prevention of complications, where appropriate, for substance abuse or harmful use or addiction as well management in pregnancy, comorbidity with psychiatric disorders and in younger and older people. Keywords Substance misuse, addiction, guidelines, pharmacotherapy, comorbidity Introduction guidelines (e.g. -
Quadazocine Decreases Responding Reinforced by Ethanol, Sucrose, and Phencyclidine Fluid Deliveries in Rhesus Monkeys: Comparison to Naltrexone’S Effects
Psychopharmacology (1999) 144:316–322 © Springer-Verlag 1999 ORIGINAL INVESTIGATION Keith L. Williams · Eric D. Pakarinen James H. Woods Quadazocine decreases responding reinforced by ethanol, sucrose, and phencyclidine fluid deliveries in rhesus monkeys: comparison to naltrexone’s effects Received: 24 June 1998 / Accepted: 18 February 1999 Abstract Rationale: The endogenous opioid system experiments, and thus we cannot rule out rate-dependent may mediate the reinforcing effects of ethanol as well as effects of the antagonists. sweet-tasting solutions. For example, opioid antagonists, such as naltrexone, reduce ethanol- and sucrose-rein- Key words Opioid antagonists · Alcohol reinforcement · forced responding in rhesus monkeys. If these effects are Self-administration · Primates due to blockade of the µ-receptor, then an opioid antago- nist such as quadazocine with a receptor selectivity pro- file similar to that of naltrexone should reduce respond- Introduction ing at doses correlated with its µ-selectivity. Objectives: To determine whether quadazocine would reduce re- The endogenous opioid system modulates alcohol drink- sponding for ethanol and sucrose at µ-selective doses, ing. In preclinical and clinical studies, opioid antagonists and whether quadazocine and naltrexone would reduce reduce alcohol drinking. For instance, we have previous- responding for a bitter-tasting drug solution such as ly shown that naltrexone (NTX) pretreatment in rhesus phencyclidine. Methods: Rhesus monkeys were given monkeys reduced oral ethanol self-administration access to ethanol, sucrose, or phencyclidine concurrently (Williams et al. 1998). In other studies using many dif- with water. Prior to the drinking sessions, quadazocine ferent animal species, NTX and other opioid antagonists (0.032–3.2 mg/kg) or saline was injected intramuscular- reduced oral ethanol self-administration (Levine and ly. -
Noribogaine Is a G-Protein Biased ᅢホᅡᄎ-Opioid Receptor Agonist
Neuropharmacology 99 (2015) 675e688 Contents lists available at ScienceDirect Neuropharmacology journal homepage: www.elsevier.com/locate/neuropharm Noribogaine is a G-protein biased k-opioid receptor agonist * Emeline L. Maillet a, , Nicolas Milon a, Mari D. Heghinian a, James Fishback a, Stephan C. Schürer b, c, Nandor Garamszegi a, Deborah C. Mash a, 1 a DemeRx, Inc., R&D Laboratory, Life Science & Technology Park, 1951 NW 7th Ave, Suite 300, Miami, FL 33136, USA b University of Miami, Center for Computational Science, 1320 S, Dixie Highway, Gables One Tower #600.H, Locator Code 2965, Coral Gables, FL 33146-2926, USA c Miller School of Medicine, Molecular and Cellular Pharmacology, 14th Street CRB 650 (M-857), Miami, FL 33136, USA article info abstract Article history: Noribogaine is the long-lived human metabolite of the anti-addictive substance ibogaine. Noribogaine Received 13 January 2015 efficaciously reaches the brain with concentrations up to 20 mM after acute therapeutic dose of 40 mg/kg Received in revised form ibogaine in animals. Noribogaine displays atypical opioid-like components in vivo, anti-addictive effects 18 August 2015 and potent modulatory properties of the tolerance to opiates for which the mode of action remained Accepted 19 August 2015 uncharacterized thus far. Our binding experiments and computational simulations indicate that nor- Available online 21 August 2015 ibogaine may bind to the orthosteric morphinan binding site of the opioid receptors. Functional activities of noribogaine at G-protein and non G-protein pathways of the mu and kappa opioid receptors were Chemical compounds studied in this article: Noribogaine hydrochloride (PubChem CID: characterized. -
Methylenedioxymethamphetamine Therapy Be Used to Treat Alcohol Use Disorder?
Journal of Psychedelic Studies 1(1), pp. 1–9 (2017) DOI: 10.1556/2054.01.2016.003 First published online December 27, 2016 Can 3,4,-methylenedioxymethamphetamine therapy be used to treat alcohol use disorder? BEN SESSA* Imperial College London, London, England, UK (Received: September 2, 2016; revised manuscript received: November 28, 2016; accepted: December 3, 2016) Treating people with alcohol use disorder has been an important target area for psychedelic research – both in the first studies of the 1950s and during the Psychedelic Renaissance of the last 10 years. To date, most studies have looked at the classical psychedelic drugs as adjuncts to psychotherapy; with attention paid to the psychospiritual aspect of the experience as a central therapeutic process in effecting abstinence from drinking. Psychotherapy assisted with 3,4,-methylenedioxymethamphetamine (MDMA) has never been explored for treating alcohol use disorder. However, MDMA has some unique pharmacological characteristics – particularly its capacity for reducing the fear response and facilitating engagement in therapy around past psychological trauma – that could make it a useful candidate for tackling the core features of alcohol use disorder. This paper briefly describes the burden of alcohol use disorders and the history of psychedelic-assisted psychotherapy in the field of addictions. It gives the theoretical and experimental justification for MDMA-assisted psychotherapy for treating people with alcohol use disorder and introduces a forthcoming study from Bristol and London, UK, exploring the role for MDMA in treating a person with this challenging condition. Keywords: MDMA, alcohol use disorder, dependence, psychedelic, trauma, LSD INTRODUCTION primarily on post-traumatic stress disorder (PTSD). -
Panic Attack Following Addition of Nalmefene to Methylphenidate in A
International Journal of Medical and Pharmaceutical Case Reports 9(3): 1-5, 2017; Article no.IJMPCR.34856 ISSN: 2394-109X, NLM ID: 101648033 Panic Attack Following Addition of Nalmefene to Methylphenidate in a Patient with Comorbid Alcohol Use Disorder and Attention Deficit Hyperactivity Disorder: A Case Report Arda Karagöl 1* 1Department of Psychiatry, Ba şkent University School of Medicine, Bahçelievler, Ankara, Turkey. Author’s contribution The sole author designed, analyzed and interpreted and prepared the manuscript. Article Information DOI: 10.9734/IJMPCR/2017/34856 Editor(s): (1) Syed A. A. Rizvi, Department of Pharmaceutical Sciences, College of Pharmacy, Nova Southeastern University, USA. Reviewers: (1) Samuel T. Gontkovsky, Wisconsin School of Professional Psychology, United States. (2) Victor Chidi Onyencho, University of Maiduguri, Nigeria. Complete Peer review History: http://www.sciencedomain.org/review-history/19821 Received 15 th June 2017 th Case Study Accepted 29 June 2017 Published 3rd July 2017 ABSTRACT Aim: Our aim is to describe a previously unreported potential interaction of nalmefene with methylphenidate and discuss possible mechanisms and precautions. Presentation of Case: A 40-year-old man with ADHD taking long-acting methylphenidate developed alcohol use disorder. Nalmefene was prescribed. Following his first bedtime administration, he awoke with panic attack symptoms and concomitant suicidal and homicidal ideation. These symptoms resolved 45 minutes after he received diazepam. Discussion: Hypotheses for this reaction include a previously undescribed nalmefene– methylphenidate interaction causing elevated levels of either drug and leading to anxiety and panic symptoms, dysphoria, and suicidal/homicidal ideation. ADHD and alcohol abuse disorder are common comorbidities and treatment with both methylphenidate and nalmefene is a reasonable approach.