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Adverse Reactions to Hallucinogenic Drugs. 1Rnstttutton National Test
DOCUMENT RESUME ED 034 696 SE 007 743 AUTROP Meyer, Roger E. , Fd. TITLE Adverse Reactions to Hallucinogenic Drugs. 1rNSTTTUTTON National Test. of Mental Health (DHEW), Bethesda, Md. PUB DATP Sep 67 NOTE 118p.; Conference held at the National Institute of Mental Health, Chevy Chase, Maryland, September 29, 1967 AVATLABLE FROM Superintendent of Documents, Government Printing Office, Washington, D. C. 20402 ($1.25). FDPS PRICE FDPS Price MFc0.50 HC Not Available from EDRS. DESCPTPTOPS Conference Reports, *Drug Abuse, Health Education, *Lysergic Acid Diethylamide, *Medical Research, *Mental Health IDENTIFIEPS Hallucinogenic Drugs ABSTPACT This reports a conference of psychologists, psychiatrists, geneticists and others concerned with the biological and psychological effects of lysergic acid diethylamide and other hallucinogenic drugs. Clinical data are presented on adverse drug reactions. The difficulty of determining the causes of adverse reactions is discussed, as are different methods of therapy. Data are also presented on the psychological and physiolcgical effects of L.S.D. given as a treatment under controlled medical conditions. Possible genetic effects of L.S.D. and other drugs are discussed on the basis of data from laboratory animals and humans. Also discussed are needs for futher research. The necessity to aviod scare techniques in disseminating information about drugs is emphasized. An aprentlix includes seven background papers reprinted from professional journals, and a bibliography of current articles on the possible genetic effects of drugs. (EB) National Clearinghouse for Mental Health Information VA-w. Alb alb !bAm I.S. MOMS Of NAM MON tMAN IONE Of NMI 105 NUNN NU IN WINES UAWAS RCM NIN 01 NUN N ONMININI 01011110 0. -
The Effects of Antipsychotic Treatment on Metabolic Function: a Systematic Review and Network Meta-Analysis
The effects of antipsychotic treatment on metabolic function: a systematic review and network meta-analysis Toby Pillinger, Robert McCutcheon, Luke Vano, Katherine Beck, Guy Hindley, Atheeshaan Arumuham, Yuya Mizuno, Sridhar Natesan, Orestis Efthimiou, Andrea Cipriani, Oliver Howes ****PROTOCOL**** Review questions 1. What is the magnitude of metabolic dysregulation (defined as alterations in fasting glucose, total cholesterol, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, and triglyceride levels) and alterations in body weight and body mass index associated with short-term (‘acute’) antipsychotic treatment in individuals with schizophrenia? 2. Does baseline physiology (e.g. body weight) and demographics (e.g. age) of patients predict magnitude of antipsychotic-associated metabolic dysregulation? 3. Are alterations in metabolic parameters over time associated with alterations in degree of psychopathology? 1 Searches We plan to search EMBASE, PsycINFO, and MEDLINE from inception using the following terms: 1 (Acepromazine or Acetophenazine or Amisulpride or Aripiprazole or Asenapine or Benperidol or Blonanserin or Bromperidol or Butaperazine or Carpipramine or Chlorproethazine or Chlorpromazine or Chlorprothixene or Clocapramine or Clopenthixol or Clopentixol or Clothiapine or Clotiapine or Clozapine or Cyamemazine or Cyamepromazine or Dixyrazine or Droperidol or Fluanisone or Flupehenazine or Flupenthixol or Flupentixol or Fluphenazine or Fluspirilen or Fluspirilene or Haloperidol or Iloperidone -
A Nested Case–Control Study
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Golestan University of Medical Sciences Repository Schizophrenia Research 150 (2013) 416–420 Contents lists available at ScienceDirect Schizophrenia Research journal homepage: www.elsevier.com/locate/schres Medication and suicide risk in schizophrenia: A nested case–control study Johan Reutfors a,⁎, Shahram Bahmanyar a,b, Erik G. Jönsson c, Lena Brandt a, Robert Bodén a,d, Anders Ekbom a, Urban Ösby e,f a Centre for Pharmacoepidemiology (CPE), Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden b Faculty of Medicine, Golestan University of Medical Sciences, Gorgan, Iran c Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden d Department of Neuroscience, Psychiatry, Uppsala University, Uppsala, Sweden e Department of Neurobiology, Care Sciences, and Society, Centre of Family Medicine (CeFAM), Karolinska Institutet, Stockholm, Sweden f Department of Psychiatry, Tiohundra AB, Norrtälje, Sweden article info abstract Article history: Introduction: Patients with schizophrenia are at increased risk of suicide, but data from controlled studies of Received 16 June 2013 pharmacotherapy in relation to suicide risk is limited. Received in revised form 28 August 2013 Aim: To explore suicide risk in schizophrenia in relation to medication with antipsychotics, antidepressants, Accepted 9 September 2013 and lithium. Available online 2 October 2013 Methods: Of all patients with a first clinical discharge diagnosis of schizophrenia or schizoaffective disorder in Stockholm County between 1984 and 2000 (n = 4000), patients who died by suicide within five years Keywords: from diagnosis were defined as cases (n = 84; 54% male). Individually matched controls were identified Schizophrenia Suicide from the same population. -
Pharmaceutical Appendix to the Tariff Schedule 2
Harmonized Tariff Schedule of the United States (2007) (Rev. 2) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2007) (Rev. 2) Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 2 Table 1. This table enumerates products described by International Non-proprietary Names (INN) which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service (CAS) registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known. ABACAVIR 136470-78-5 ACIDUM LIDADRONICUM 63132-38-7 ABAFUNGIN 129639-79-8 ACIDUM SALCAPROZICUM 183990-46-7 ABAMECTIN 65195-55-3 ACIDUM SALCLOBUZICUM 387825-03-8 ABANOQUIL 90402-40-7 ACIFRAN 72420-38-3 ABAPERIDONUM 183849-43-6 ACIPIMOX 51037-30-0 ABARELIX 183552-38-7 ACITAZANOLAST 114607-46-4 ABATACEPTUM 332348-12-6 ACITEMATE 101197-99-3 ABCIXIMAB 143653-53-6 ACITRETIN 55079-83-9 ABECARNIL 111841-85-1 ACIVICIN 42228-92-2 ABETIMUSUM 167362-48-3 ACLANTATE 39633-62-0 ABIRATERONE 154229-19-3 ACLARUBICIN 57576-44-0 ABITESARTAN 137882-98-5 ACLATONIUM NAPADISILATE 55077-30-0 ABLUKAST 96566-25-5 ACODAZOLE 79152-85-5 ABRINEURINUM 178535-93-8 ACOLBIFENUM 182167-02-8 ABUNIDAZOLE 91017-58-2 ACONIAZIDE 13410-86-1 ACADESINE 2627-69-2 ACOTIAMIDUM 185106-16-5 ACAMPROSATE 77337-76-9 -
Studies with Lysergic Acid Diethylamide in Regressed Schizophrenics
CHAPTER 15 _ Studies with Lysergic Acid Diethylamide in Regressed Schizophrenics By FREDERICK B. CHARAT AN, M.D. OF THE MANY studies carried out with lysergic acid diethylamide in the last 15 years, relatively few have dealt with regressed schizophrenics. Most workers have used comparatively small doses of LSD. Some gave up to 600 gamma orally. Others reported the effects of up to 500 gamma intra- muscularly, 180 gamma intravenously and 60 gamma intrathecally in small series of cases. Several investigators agreed that in chronic schizophrenics higher doses of LSD than those administered to undeteriorated schizo- phrenics and nonpsychotics have been required to produce psychic effects. Apart from the slight response of chronic schizophrenics to doses of LSD which lead to marked and characteristic effects in other subjects, tolerance to the drug seems to develop in as brief a period as three days. These differences in response to LSD pose some interesting problems. Is the lack of response in chronic schizophrenics merely an apparent one caused by their inability to communicate their inner experiences? Is it due to the development of some immune state connected with biochemical alter- ations produced during the psychosis? Is it the reflection of a metabolic difference between schizophrenics and non-schizophrenics? May it be a general manifestation of schizophrenic underresponsiveness to virtually any stress, once the chronic stagnant phase of the psychosis has been reached? Clear answers to all these questions cannot yet be given. The present investi- gation was undertaken to examine further the responses of chronic schizo- phrenics to large doses of LSD and also to observe the effect of other drugs upon this response. -
Perphenazine-151548-PI.Pdf
PRESCRIBING INFORMATION PERPHENAZINE Perphenazine Tablets USP 2 mg , 4 mg, 8mg, and 16 mg Antipsychotic/Antiemetic AA Pharma Inc. DATE OF REVISION: April 12, 2012 1165 Creditsone Road, Unit #1 Vaughan, Ontario L4K 4N7 Control Number: 151548 PRESCRIBING INFORMATION PERPHENAZINE Perphenazine Tablets USP 2 mg, 4 mg, 8 mg and 16 mg THERAPEUTIC CLASSIFICATION Antipsychotic/Antiemetic ACTIONS AND CLINICAL PHARMACOLOGY Perphenazine is a piperazine phenothiazine derivative with antipsychotic, antiemetic and weak sedative activity. Perphenazine has actions similar to those of other phenothiazine derivatives but appears to be less sedating and to have a weak propensity for causing hypotension or potentiating the effects of CNS depressants and anesthetics. However, it produces a high incidence of extrapyramidal reactions. Perphenazine is well absorbed from the gastrointestinal tract. Onset of action following oral administration is 30 to 40 minutes. Duration of action is 3 to 4 hours. Perphenazine distributes to most body tissues with high concentrations being distributed into liver and spleen. Perphenazine enters the enterohepatic circulation and is excreted chiefly in the feces. INDICATIONS AND CLINICAL USE Perphenazine is indicated in the management of manifestations of psychotic disorders. It is also effective in controlling nausea and vomiting due to stimulation of the chemoreceptor trigger zone. 1 Perphenazine has not been shown effective for the management of behavioral complications in patients with mental retardation. CONTRAINDICATIONS Should not be administered in the presence of circulatory collapse, altered states of consciousness or comatose states, particularly when these are due to intoxication with central depressant drugs (alcohol, hypnotics, narcotics). It is contraindicated in severely depressed patients, in the presence of blood dyscrasias, liver disease, renal insufficiency, pheochromocytoma, or in patients with severe cardiovascular disorders or a history of hypersensitivity to phenothiazine derivatives. -
CENTRAL NERVOUS SYSTEM DEPRESSANTS Opioid Pain Relievers Anxiolytics (Also Belong to Psychiatric Medication Category) • Codeine (In 222® Tablets, Tylenol® No
CENTRAL NERVOUS SYSTEM DEPRESSANTS Opioid Pain Relievers Anxiolytics (also belong to psychiatric medication category) • codeine (in 222® Tablets, Tylenol® No. 1/2/3/4, Fiorinal® C, Benzodiazepines Codeine Contin, etc.) • heroin • alprazolam (Xanax®) • hydrocodone (Hycodan®, etc.) • chlordiazepoxide (Librium®) • hydromorphone (Dilaudid®) • clonazepam (Rivotril®) • methadone • diazepam (Valium®) • morphine (MS Contin®, M-Eslon®, Kadian®, Statex®, etc.) • flurazepam (Dalmane®) • oxycodone (in Oxycocet®, Percocet®, Percodan®, OxyContin®, etc.) • lorazepam (Ativan®) • pentazocine (Talwin®) • nitrazepam (Mogadon®) • oxazepam ( Serax®) Alcohol • temazepam (Restoril®) Inhalants Barbiturates • gases (e.g. nitrous oxide, “laughing gas”, chloroform, halothane, • butalbital (in Fiorinal®) ether) • secobarbital (Seconal®) • volatile solvents (benzene, toluene, xylene, acetone, naptha and hexane) Buspirone (Buspar®) • nitrites (amyl nitrite, butyl nitrite and cyclohexyl nitrite – also known as “poppers”) Non-Benzodiazepine Hypnotics (also belong to psychiatric medication category) • chloral hydrate • zopiclone (Imovane®) Other • GHB (gamma-hydroxybutyrate) • Rohypnol (flunitrazepam) CENTRAL NERVOUS SYSTEM STIMULANTS Amphetamines Caffeine • dextroamphetamine (Dexadrine®) Methelynedioxyamphetamine (MDA) • methamphetamine (“Crystal meth”) (also has hallucinogenic actions) • methylphenidate (Biphentin®, Concerta®, Ritalin®) • mixed amphetamine salts (Adderall XR®) 3,4-Methelynedioxymethamphetamine (MDMA, Ecstasy) (also has hallucinogenic actions) Cocaine/Crack -
Preparation of Metabolites by Chemical Reaction: Conversion of Antipsychotic Phenothiazines to Their Sulfoxides and Tertiary
396 Journal of Health Science, 50(4) 396–406 (2004) Preparation of Metabolites N-oxides from parent drug could be confirmed when the collisional energy was decreased to 10 eV. 1H- and by Chemical Reaction: 13C-NMR spectral data confirmed the structure of the Conversion of Antipsychotic prepared mianserin N-oxide to be 2-oxide. In conclu- sion, a simple and rapid preparation method for oxide Phenothiazines to their metabolites of phenothiazines and tertiary amino cy- Sulfoxides and Tertiary clic antidepressants available as analytical standards was established. Amino Cyclic Key words —–— metabolite, chemical preparation, ox- Antidepressants ide, phenothiazine, cyclic antidepressants, mass spectros- to their N-Oxide with copy Hydrogen Peroxide Using Titanosilicate INTRODUCTION Catalyst The identification and quantification of drugs Akira Ogamo* and Mariko Fukumoto ingested into human bodies require comprehensive information covering the target drugs themselves and School of Pharmaceutical Sciences, Kitasato University, their metabolites. To carry out a quantitative analy- Shirokane 5–9–1, Minato-ku, Tokyo 108–8641, Japan sis, the standard substances of metabolites are es- (Received March 5, 2004; Accepted April 11, 2004) sential. Some important metabolites can be obtained as commercial products, but many metabolites, es- The aim of this study was to establish a prepara- pecially those of new drugs, are difficult to obtain tion method needed to analyze the metabolites of an as standard samples. These problems have been analytical procedure for antipsychotic phenothiazines solved by using experimental animals or isolated and tertiary amino cyclic antidepressants by chemical enzyme systems originating from biological mate- reaction. These drugs were oxidized to their sulfoxide rials. -
Phenothiazine Poisoning a Review of 48 Cases
Refer to: Barry D, Meyskens FL Jr, Becker CE: Phenothiazine poison- ing-A review of 48 cases. Calif Med 118:1-5, Jan 1973 California Medicine THE WESTERN JOURNAL OF MEDICINE Phenothiazine Poisoning A Review of 48 Cases DANIEL BARRY, B.A., FRANK L. MEYSKENS, JR., M.D., AND CHARLES E. BECKER, M.D., San Francisco * Of 48 cases of phenothiazine poisoning that were analyzed, 34 were attributed to stuicide attempts, nine to accidental ingestion, and five to drug reactions. As outpatient treatment of schizophrenia increases, cases of over- dose with phenothiazine drugs may be expected to increase also. The prescribing of multiple phenothiazines and antidepressants is probably contributory to the occurrence of mixed drug ingestions. The symptoms and signs of phenothiazine poisoning are largely predictable if the atropine-like, alpha-blocking, quinidine-like, and extrapyramidal actions of phenothiazines are appreciated, Unexplain- able tachypnea and paradoxical miosis were noted in severe cases. In one case in the study phenothiazine intoxication was present in the newborn infant of a schizophrenic mother. PHENOTHIAZINES ARE BECOMING household drugs tionable advertising campaigns advocating phe- in Califomnia. The closing of state hospitals with nothiazines for the treatment of a wide variety the concomitant institution of mass outpatient of ailments have made these drugs generally treatment of chronic schizophrenics through com- available. The high incidence of schizophrenia munity mental health centers, and recent quesv in young adulthood and the increasing suicide From the Detoxification Unit, San Francisco General Hospital, and rate in this age group" suggest that phenothia- the Department of Clinical Pharmacology, University of California, San Francisco. -
Guidance on the Treatment of Antipsychotic Induced Hyperprolactinaemia in Adults
Guidance on the Treatment of Antipsychotic Induced Hyperprolactinaemia in Adults Version 1 GUIDELINE NO RATIFYING COMMITTEE DRUGS AND THERAPEUTICS GROUP DATE RATIFIED April 2014 DATE AVAILABLE ON INTRANET NEXT REVIEW DATE April 2016 POLICY AUTHORS Nana Tomova, Clinical Pharmacist Dr Richard Whale, Consultant Psychiatrist In association with: Dr Gordon Caldwell, Consultant Physician, WSHT . If you require this document in an alternative format, ie easy read, large text, audio, Braille or a community language, please contact the Pharmacy Team on 01243 623349 (Text Relay calls welcome). Contents Section Title Page Number 1. Introduction 2 2. Causes of Hyperprolactinaemia 2 3. Antipsychotics Associated with 3 Hyperprolactinaemia 4. Effects of Hyperprolactinaemia 4 5. Long-term Complications of Hyperprolactinaemia 4 5.1 Sexual Development in Adolescents 4 5.2 Osteoporosis 4 5.3 Breast Cancer 5 6. Monitoring & Baseline Prolactin Levels 5 7. Management of Hyperprolactinaemia 6 8. Pharmacological Treatment of 7 Hyperprolactinaemia 8.1 Aripiprazole 7 8.2 Dopamine Agonists 8 8.3 Oestrogen and Testosterone 9 8.4 Herbal Remedies 9 9. References 10 1 1.0 Introduction Prolactin is a hormone which is secreted from the lactotroph cells in the anterior pituitary gland under the influence of dopamine, which exerts an inhibitory effect on prolactin secretion1. A reduction in dopaminergic input to the lactotroph cells results in a rapid increase in prolactin secretion. Such a reduction in dopamine can occur through the administration of antipsychotics which act on dopamine receptors (specifically D2) in the tuberoinfundibular pathway of the brain2. The administration of antipsychotic medication is responsible for the high prevalence of hyperprolactinaemia in people with severe mental illness1. -
Neuroleptic Malignant Syndrome in a Patient
Psychiatria Danubina, 2018; Vol. 30, Suppl. 7, pp 415-417 Conference paper © Medicinska naklada - Zagreb, Croatia NEUROLEPTIC MALIGNANT SYNDROME IN A PATIENT TREATED WITH CLOTIAPINE Clémentine Lantin, Miriam Franco, François-Xavier Dekeuleneer, Didier Chamart & Juan Martin Tecco Mental Health Unit, Centre Hospitalier Universitaire et Psychiatrique de Mons-Borinage (CHUP-MB), Mons, Belgium SUMMARY Background: Neuroleptic malignant syndrome (NMS), which is linked to the use of antipsychotic medication, is a potentially lethal neurological emergency. The interest of our study is that NMS induced by the use of clotiapine has never previously been described. Subjects and methods: We present the case of a 61-year old man whose sleep disorders were treated with clotiapine 40 mg/day. After 7 days of taking 40 mg clotiapine, the patient presented with a deterioration of his general health which had gradually taken hold, with altered consciousness accompanied by generalised muscle rigidity and hypersalivation. Laboratory blood tests revealed elevated levels of Creatine Phosphokinase (CPK) at 812 U/l. The patient was diagnosed with NMS and treated accordingly. Results: The mechanism that underlies the appearance of NMS remains largely unknown. Clotiapine is a second-generation antipsychotic, first released onto the market in the 1970s, and is available in a few countries, including Belgium. NMS is treated as a medical emergency due to the possibility of morbidity and death. The first step in the treatment of NMS consists in withholding the agent suspected of provoking the symptoms. Conclusions: NMS is difficult to diagnose due to a great variability in clinical presentations and the absence of specific tests and laboratory results. -
Trilafon Tablets & Trilafon Injection Final Printed Labeling
PAGE 1 TRILAFON TABLETS & TRILAFON INJECTION FINAL PRINTED LABELING 1 TRILAFON Ò 2 brand of perphenazine, USP 3 Tablets, 4 Injection 5 6 DESCRIPTION TRILAFON products contain perphenazine, USP (4-[3-(2- 7 chlorophenothiazin-10-yl)propyl]-1-piper-azineethanol), a piperazinyl phenothiazine 8 having the chemical formula, C21H26CIN3OS. They are available as Tablets, 2, 4, 9 8, and 16 mg; and Injection, perphenazine 5 mg per 1 mL. 10 The inactive ingredients for TRILAFON Tablets, 2, 4, 8, and 16 mg, include: 11 acacia, black iron oxide, butylparaben, calcium phosphate, calcium sulfate, 12 carnauba wax, corn starch, lactose, magnesium stearate, sugar, titanium dioxide, 13 and white wax. The inactive ingredients for TRILAFON Injection include: citric 14 acid, sodium bisulfite, sodium hydroxide, and water. 15 ACTIONS Perphenazine has actions at all levels of the central nervous system, 16 particularly the hypothalamus. However, the site and mechanism of action of 17 therapeutic effect are not known. 18 CLINICAL PHARMACOLOGY Pharmacokinetics: Following oral administration 19 of TRILAFON® Tablets, mean peak plasma perphenazine concentrations were 20 observed between 1 to 3 hours. The plasma elimination half-life of perphenazine 21 was independent of dose and ranged between 9 and 12 hours. In a study in which 22 normal volunteers (n=12) received TRILAFON 4 mg q8h for 5 days, steady-state 23 concentrations of perphenazine were reached within 72 hours. Mean (%CV) Cmax 24 and Cmin values for perphenazine and 7-hydroxyperphenazine at steady-state are 25 listed below: 26 ParameterPerphenazine 7-Hydroxyperphenazine 27 Cmax (pg/mL) 984 (43) 509 (25) 28 Cmin (pg/mL) 442 (76) 350 (56) 1 PAGE 2 TRILAFON TABLETS & TRILAFON INJECTION FINAL PRINTED LABELING 29 Peak 7-hydroxyperphenazine concentrations were observed between 2 to 4 hours 30 with a terminal phase half-life ranging between 9.9 to 18.8 hours.