DOCSLIB.ORG

Update on Serotonin.Pdf

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Update on Serotonin.Pdf AUGUST 2006 IMPROVING PATIENT CARE THROUGH ESOTERIC LABORATORY TESTING VOLUME 31, NO. 8 Update on Serotonin Serotonin pathways regulate many systems in neuromuscular activity, cognitive function, the body, and disturbances in the serotonergic and mood control. Serotonin is released from (activated by or capable of liberating serotonin) presynaptic neurons and binds to postsynaptic system result in a wide range of problems. Drugs serotonin receptors, thereby exciting the that affect the serotonergic system are commonly postsynaptic neurons. The serotonin transporter used to treat psychiatric disorders, and inherited then carries serotonin back into the presynaptic differences in serotonin metabolism may alter neuron for subsequent reuse. Conversely, the patients’ responses to these drugs. In this review, enzyme monoamine oxidase (MAO) reduces we discuss serotonin metabolism, serotonin presynaptic serotonin levels by deamination syndrome, and new serotonin-related genetic (Figure 1). tests (pharmacogenetics). Serotonin in Enterochromaffin Cells Serotonin Metabolism Serotonin released from enterochromaffin cells Serotonin (5-hydroxytryptamine; 5-HT) is exerts a strong influence on the GI tract by synthesized from the amino acid tryptophan. increasing GI blood flow, motility, and fluid The body has 3 main serotonin pools: the central secretion. On its first pass through the liver, 30% nervous system (CNS), gastrointestinal (GI) to 80% of serotonin is metabolized, predominately enterochromaffin cells, and platelets. to 5-hydroxyindoleacetic acid (5-HIAA), which is excreted by the kidneys. Most of the remaining Serotonin and the Central Nervous System serotonin (90%) is metabolized in the lungs, also to 5-HIAA. Approximately 10% is taken up by Serotonin, a neurotransmitter, is an important platelets, where it remains until it is released regulator of the autonomic nervous system during the coagulation process. (including temperature regulation and GI motility), INSIDE THIS ISSUE Feature Psychiatric Genomic Tests New Test Announcements Update on Serotonin Quick Reference Guide • #88672 API2/MALT1, mRNA Detection by Reverse 2006 Education Calendar Ask Us Transcription-PCR • #80678 Chorionic Gonadotropin for Pregnancy, Serum AUGUST 2006 • WWW.MAYOREFERENCESERVICES.ORG/COMMUNIQUE/ • PAGE 1 Figure 1. Diagram of neurosynaptic serotonin (5-HT). Serotonin in Platelets Serotonin and Psychiatric Disorders Serotonin is stored in the platelets’ dense granules Anxiety and depression are often treated with drugs and released during platelet activation. It stimulates that increase CNS serotonin levels, either by: platelet aggregation and causes other local and • Reducing serotonin deamination (eg, monoamine systemic effects including vasodilation and oxidase inhibitors [MAOI]) constriction, blood pressure changes, and • Increasing serotonin precursors (eg, lithium) bronchoconstriction. • Acting as serotonin agonists (eg, trazodone) PAGE 2 • WWW.MAYOREFERENCESERVICES.ORG/COMMUNIQUE/ • AUGUST 2006 • Increasing serotonin levels in the nerve synapses drug. Other individuals demonstrate accelerated (eg, tricyclic antidepressants [TCAs], such as metabolism and may not experience the desired amitriptyline [Elavil], imipramine [Tofranil], therapeutic effects because the drug is rapidly and desipramine [Norpramin], and the selective inactivated and/or eliminated. Individuals with serotonin reuptake inhibitors [SSRIs], such as extra copies (duplication) of the functional CYP2D6 citalopram [Celexa], fluoxetine [Prozac], gene demonstrate accelerated metabolism (ultrarapid paroxetine [Paxil], sertraline [Zoloft], and metabolizers). escitalopram [Lexapro]). A number of polymorphisms have been identified Use of these drugs has become increasingly in the CYP2D6 gene that result in enzymatic widespread. However, some patients are deficiencies (Table 2). The frequency of these nonresponsive or respond slowly to these polymorphisms varies within major ethnic groups. medications, while other patients may develop CYP2D6 polymorphisms that result in poor serious side effects (eg, serotonin syndrome, metabolism are found in 7% to 10% of Caucasians, cardiac dysrhthmias, hypotension, convulsions, 2% of Africans and African Americans, and 1% of CNS depression, or worsening of depression). Asians. Individuals who are homozygous (2 copies Antidepressant drug selection may be more of 1 abnormality) or compound heterozygous effectively guided by pharmacogenetic testing. (1 copy of 2 different abnormalities) for the Molecular tests are currently available for genes polymorphisms associated with reduced enzyme encoding the hepatic enzymes responsible for activity are poor metabolizers. Individuals who are drug metabolism (cytochrome P450 enzymes), heterozygous, with 1 normal gene and 1 polymorphic for the serotonin receptor, and for the serotonin gene, will have a metabolism that is intermediate, transporter.1 between the extensive and poor metabolizers. Cytochrome P450-mediated Metabolism Identification of a patient’s CYP2D6 genotype of Serotonergic Drugs may allow appropriate dosing adjustments (#83180 Cytochrome P450 2D6 Genotyping). Patients who Metabolism of many drugs is accomplished by are poor metabolizers may need lower than usual cytochrome P450 (CYP) enzymes, a group of enzymes doses to achieve optimal response while avoiding located predominantly in the liver (Table 1). Of the toxicity. Patients who are ultrarapid metabolizers CYP enzymes, CYP2D6 is primarily responsible for may benefit from increased doses or conversion to the metabolism of a large number of commonly other drugs that are not primarily metabolized by prescribed drugs, including the SSRIs and TCAs. CYP2D6. A complicating factor in correlating CYP2D6 genotype with phenotype is that many CYP2D6–mediated drug metabolism is highly drugs (or their metabolites) may reduce CYP2D6 variable, and inherited differences have been catalytic activity (Table 1). For example, an described. Individuals without inactivating individual with an inherited pattern consistent polymorphisms, deletions, or duplications are with intermediate metabolizer status for the considered normal (referred to as extensive antidepressant amitriptyline (metabolized by metabolizers), designated as CYP2D6*1/*1. CYP2D6) may act as a poor metabolizer if he Some individuals have altered CYP2D6 gene or she also is taking a drug that decreases CYP2D6 sequences (polymorphisms) that result in synthesis activity such as celecoxib or quinidine. Consequently, of enzyme with decreased or absent catalytic activity. it is important to interpret the results of CYP testing These individuals metabolize SSRIs and TCAs poorly in the context of other coadministered drugs, as and may experience significant medication side effects individuals may require dosing changes greater or due to prolonged exposure to the active form of the less than predicted based upon genotype alone. AUGUST 2006 • WWW.MAYOREFERENCESERVICES.ORG/COMMUNIQUE/ • PAGE 3 Drugs That Undergo Metabolism By CYP2D6: Alpha-blocker: alprenolol, timolol Analgesic: codeine, oxycodone, tramadol Anticonvulsant: felbamate, mephobarbital Antidepressant: amitryptyline, clomipramine, desipramine, duloxetine, fluoxetine, fluvoxamine, imipramine, mirtazapine, nortriptyline, paroxetine, sertraline, venlafaxine Antidiabetic: phenformin Antiestrogen: tamoxifen Antihypertensive: diltiazem Antipsychotic: aripiprazole, chlorpromazine, haloperidol, perphenazine, risperidone, thioridazine Antitussive: dextromethorphan Beta-blocker: labetalol, metoprolol, propranolol Cardioactive: disopyramide, encainide, flecainide, lidocaine, mexiletine, propafenone Norepinephrine reuptake inhibitors: atomoxetine Stimulant: amphetamine Coadministration may decrease the rate of elimination of other drugs metabolized by CYP2D6 Drugs Known To Increase CYP2D6 Activity: Dexamethasone Coadministration of this drug increases the rate of excretion of CYP2D6-metabolized drugs, reducing the other drugs’ effectiveness. Drugs Known To Decrease CYP2D6 Activity: Analgesic: celecoxib, methadone Antidepressant: bupropion, clomipramine, citalopram, duloxatine, fluoxetine, paroxetine, and sertraline Antiemetic: metoclopramide Antineoplastic: doxorubicin Antipsychotic: chlorpromazine, haloperidol Antiretroviral: indinavir, ritonavir Antistroke: ticlopidine Cardioactive: amiodarone, quinidine H-1 blocker: cimetidine, ranitidine Stimulant: cocaine Sympathomimetic: chlorpheniramine Coadministration will decrease the rate of metabolism of CYP2D6-metabolized drugs, increasing the possibility of toxicity. Table 1. Some of the known CYP2D6 metabolism and drug relationships. PAGE 4 • WWW.MAYOREFERENCESERVICES.ORG/COMMUNIQUE/ • AUGUST 2006 Serotonin Receptor Genotype response to SSRIs, putting the patient at increased risk for adverse drug reactions.3 The effects of serotonin occur after it binds Variations in the HTR2A and HTR2C genes to serotonin receptors, a large and diverse have been associated with increased risk of family of G protein-coupled receptors.2 At least tardive dyskinesia, a common and troubling 7 groups of serotonin receptors, each with medication side effect, in schizophrenic multiple polymorphisms, have been described.2 patients.4,5 Conversely, the presence of the Receptor proteins encoded by these gene HTR2A allele and HTR2C allele have been variants may demonstrate differing serotonin reported to predict favorable response to therapy binding affinity, differing signal transduction with clozapine, an antipsychotic agent.6 A capabilities,
Load more

Recommended publications
  • Pharmacology in MS Advanced Practice Management
    Pharmacology in MS Advanced Practice Management Heidi Maloni APRN, BC [email protected] Objectives • Discuss basic principles of pharmacology, pharmacokinetics and pharmacodynamics. • Describe the pharmacotherapeutics of drugs used in MS • Identify the role of advanced practice nurse in MS pharmacological management. Advanced Practice Pharmacology Background • Pharmacology: study of a drug’s effects within a living system • Each drug is identified by 3 names: chemical, generic, trade or marketing name N-4-(hydroxyphenyl) acetamide; acetaminophen; Tylenol sodium hypochlorite; bleach; Clorox 4-(diethylamino)-2-butynl ester hydrochloride; oxybutynin chloride; Ditropan • Drugs are derived from: plants, humans, animals, minerals, and chemical substances • Drugs are classified by clinical indication or body system APN Role Safe drug administration Nurses are professionally, legally, morally, and personally responsible for every dose of medication they prescribe or administer Know the usual dose Know usual route of administration Know significant side effects Know major drug interactions Know major contraindication Use the nursing process Pregnancy Safety • Teratogenicity: ability to produce an abnormality in the fetus (thalidomide) • Mutogenicity: ability to produce a genetic mutation (diethylstilbestrol, methotrexate) Pregnancy Safety Categories • A: studies indicate no risk to the fetus (levothyroxan; low dose vitamins, insulin) • B: studies indicate no risk to animal fetus; information in humans is not available (naproxen;acetaminophen; glatiramer
    [Show full text]
  • 2D6 Substrates 2D6 Inhibitors 2D6 Inducers
    Physician Guidelines: Drugs Metabolized by Cytochrome P450’s 1 2D6 Substrates Acetaminophen Captopril Dextroamphetamine Fluphenazine Methoxyphenamine Paroxetine Tacrine Ajmaline Carteolol Dextromethorphan Fluvoxamine Metoclopramide Perhexiline Tamoxifen Alprenolol Carvedilol Diazinon Galantamine Metoprolol Perphenazine Tamsulosin Amiflamine Cevimeline Dihydrocodeine Guanoxan Mexiletine Phenacetin Thioridazine Amitriptyline Chloropromazine Diltiazem Haloperidol Mianserin Phenformin Timolol Amphetamine Chlorpheniramine Diprafenone Hydrocodone Minaprine Procainamide Tolterodine Amprenavir Chlorpyrifos Dolasetron Ibogaine Mirtazapine Promethazine Tradodone Aprindine Cinnarizine Donepezil Iloperidone Nefazodone Propafenone Tramadol Aripiprazole Citalopram Doxepin Imipramine Nifedipine Propranolol Trimipramine Atomoxetine Clomipramine Encainide Indoramin Nisoldipine Quanoxan Tropisetron Benztropine Clozapine Ethylmorphine Lidocaine Norcodeine Quetiapine Venlafaxine Bisoprolol Codeine Ezlopitant Loratidine Nortriptyline Ranitidine Verapamil Brofaramine Debrisoquine Flecainide Maprotline olanzapine Remoxipride Zotepine Bufuralol Delavirdine Flunarizine Mequitazine Ondansetron Risperidone Zuclopenthixol Bunitrolol Desipramine Fluoxetine Methadone Oxycodone Sertraline Butylamphetamine Dexfenfluramine Fluperlapine Methamphetamine Parathion Sparteine 2D6 Inhibitors Ajmaline Chlorpromazine Diphenhydramine Indinavir Mibefradil Pimozide Terfenadine Amiodarone Cimetidine Doxorubicin Lasoprazole Moclobemide Quinidine Thioridazine Amitriptyline Cisapride
    [Show full text]
  • Advantages and Disadvantages of Beta- Adrenergic Blocking Drugs in Hypertension
    Reprinted from ANCIOLOCY Vol. 29, No. -I April 1978 Copyright 0 1978 Prinred in U.S.A. All Rights Rewrced Advantages and Disadvantages of Beta- Adrenergic Blocking Drugs in Hypertension Eoin T. O'Brien DUBLIN, IRELAND General Measures Elevation of blood pressure should be regarded as one of a number of potential risk factors for cardiovascular disease-albeit a major risk factor- rather than a disease per se.' It is important to identify additional risk factors in the hypertensive patient, not only because collectively these factors may greatly magnify the cardiovascular risk, but also because modification of them may, of itself, lower the blood pressure and thus alleviate the risk and save the patient the inconvenience, expense, and potential harm that may result from even the simplest of drug regimes. Careful consideration should be given to the patient's diet (particularly in relation to the calorie intake in the case of obesity, the cholesterol and saturated fat content in the case of hyperlipidemia and patients at high risk, and the salt content) and to smoking habits, physical activity. stress. personality, and drug therapy, especially anovulant preparations. Other diseases, such as diabetes mellitus, which are associated with a high incidence of hypertension and pri- mary causes of hypertension must be excluded. Although there is still no statistical evidence to show that modification of these risk factors-with the exception of tobacco and anovulant preparations-will actually reduce mortal- ity, it does seem prudent on the basis of the evidence available to encourage the hypertensive patient to adjust his or her life-style not only to reduce the cardiovascular risk,2 but also because in many instances the mildly hypertensive patient will respond to this approach alone.
    [Show full text]
  • The In¯Uence of Medication on Erectile Function
    International Journal of Impotence Research (1997) 9, 17±26 ß 1997 Stockton Press All rights reserved 0955-9930/97 $12.00 The in¯uence of medication on erectile function W Meinhardt1, RF Kropman2, P Vermeij3, AAB Lycklama aÁ Nijeholt4 and J Zwartendijk4 1Department of Urology, Netherlands Cancer Institute/Antoni van Leeuwenhoek Hospital, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands; 2Department of Urology, Leyenburg Hospital, Leyweg 275, 2545 CH The Hague, The Netherlands; 3Pharmacy; and 4Department of Urology, Leiden University Hospital, P.O. Box 9600, 2300 RC Leiden, The Netherlands Keywords: impotence; side-effect; antipsychotic; antihypertensive; physiology; erectile function Introduction stopped their antihypertensive treatment over a ®ve year period, because of side-effects on sexual function.5 In the drug registration procedures sexual Several physiological mechanisms are involved in function is not a major issue. This means that erectile function. A negative in¯uence of prescrip- knowledge of the problem is mainly dependent on tion-drugs on these mechanisms will not always case reports and the lists from side effect registries.6±8 come to the attention of the clinician, whereas a Another way of looking at the problem is drug causing priapism will rarely escape the atten- combining available data on mechanisms of action tion. of drugs with the knowledge of the physiological When erectile function is in¯uenced in a negative mechanisms involved in erectile function. The way compensation may occur. For example, age- advantage of this approach is that remedies may related penile sensory disorders may be compen- evolve from it. sated for by extra stimulation.1 Diminished in¯ux of In this paper we will discuss the subject in the blood will lead to a slower onset of the erection, but following order: may be accepted.
    [Show full text]
  • Drug Class Review Antianginal Agents
    Drug Class Review Antianginal Agents 24:12.08 Nitrates and Nitrites 24:04.92 Cardiac Drugs, Miscellaneous Amyl Nitrite Isosorbide Dinitrate (IsoDitrate ER®, others) Isosorbide Mononitrate (Imdur®) Nitroglycerin (Minitran®, Nitrostat®, others) Ranolazine (Ranexa®) Final Report May 2015 Review prepared by: Melissa Archer, PharmD, Clinical Pharmacist Carin Steinvoort, PharmD, Clinical Pharmacist Gary Oderda, PharmD, MPH, Professor University of Utah College of Pharmacy Copyright © 2015 by University of Utah College of Pharmacy Salt Lake City, Utah. All rights reserved. Table of Contents Executive Summary ......................................................................................................................... 3 Introduction .................................................................................................................................... 4 Table 1. Antianginal Therapies .............................................................................................. 4 Table 2. Summary of Agents .................................................................................................. 5 Disease Overview ........................................................................................................................ 8 Table 3. Summary of Current Clinical Practice Guidelines .................................................... 9 Pharmacology ............................................................................................................................... 10 Table 4. Pharmacokinetic Properties
    [Show full text]
  • Properties and Units in Clinical Pharmacology and Toxicology
    Pure Appl. Chem., Vol. 72, No. 3, pp. 479–552, 2000. © 2000 IUPAC INTERNATIONAL FEDERATION OF CLINICAL CHEMISTRY AND LABORATORY MEDICINE SCIENTIFIC DIVISION COMMITTEE ON NOMENCLATURE, PROPERTIES, AND UNITS (C-NPU)# and INTERNATIONAL UNION OF PURE AND APPLIED CHEMISTRY CHEMISTRY AND HUMAN HEALTH DIVISION CLINICAL CHEMISTRY SECTION COMMISSION ON NOMENCLATURE, PROPERTIES, AND UNITS (C-NPU)§ PROPERTIES AND UNITS IN THE CLINICAL LABORATORY SCIENCES PART XII. PROPERTIES AND UNITS IN CLINICAL PHARMACOLOGY AND TOXICOLOGY (Technical Report) (IFCC–IUPAC 1999) Prepared for publication by HENRIK OLESEN1, DAVID COWAN2, RAFAEL DE LA TORRE3 , IVAN BRUUNSHUUS1, MORTEN ROHDE1, and DESMOND KENNY4 1Office of Laboratory Informatics, Copenhagen University Hospital (Rigshospitalet), Copenhagen, Denmark; 2Drug Control Centre, London University, King’s College, London, UK; 3IMIM, Dr. Aiguader 80, Barcelona, Spain; 4Dept. of Clinical Biochemistry, Our Lady’s Hospital for Sick Children, Crumlin, Dublin 12, Ireland #§The combined Memberships of the Committee and the Commission (C-NPU) during the preparation of this report (1994–1996) were as follows: Chairman: H. Olesen (Denmark, 1989–1995); D. Kenny (Ireland, 1996); Members: X. Fuentes-Arderiu (Spain, 1991–1997); J. G. Hill (Canada, 1987–1997); D. Kenny (Ireland, 1994–1997); H. Olesen (Denmark, 1985–1995); P. L. Storring (UK, 1989–1995); P. Soares de Araujo (Brazil, 1994–1997); R. Dybkær (Denmark, 1996–1997); C. McDonald (USA, 1996–1997). Please forward comments to: H. Olesen, Office of Laboratory Informatics 76-6-1, Copenhagen University Hospital (Rigshospitalet), 9 Blegdamsvej, DK-2100 Copenhagen, Denmark. E-mail: [email protected] Republication or reproduction of this report or its storage and/or dissemination by electronic means is permitted without the need for formal IUPAC permission on condition that an acknowledgment, with full reference to the source, along with use of the copyright symbol ©, the name IUPAC, and the year of publication, are prominently visible.
    [Show full text]
  • COPD Agents Review – October 2020 Page 2 | Proprietary Information
    COPD Agents Therapeutic Class Review (TCR) October 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]. October 2020
    [Show full text]
  • CORGARD® TABLETS Nadolol Tablets USP
    CORGARD® TABLETS Nadolol Tablets USP Rx Only DESCRIPTION CORGARD (nadolol) is a synthetic nonselective beta-adrenergic receptor blocking agent designated chemically as 1-(tert-butylamino)-3-[(5,6,7,8-tetrahydro-cis-6,7-dihydroxy-1- naphthyl)oxy]-2-propanol. Structural formula: C17H27NO4 MW 309.40 Nadolol is a white crystalline powder. It is freely soluble in ethanol, soluble in hydrochloric acid, slightly soluble in water and in chloroform, and very slightly soluble in sodium hydroxide. CORGARD (nadolol) is available for oral administration as 20 mg, 40 mg, and 80 mg tablets. Inactive ingredients: microcrystalline cellulose, colorant (FD&C Blue No. 2), corn starch, magnesium stearate, povidone (except 20 mg and 40 mg), and other ingredients. CLINICAL PHARMACOLOGY CORGARD (nadolol) is a nonselective beta-adrenergic receptor blocking agent. Clinical pharmacology studies have demonstrated beta-blocking activity by showing (1) reduction in heart rate and cardiac output at rest and on exercise, (2) reduction of systolic and diastolic blood pressure at rest and on exercise, (3) inhibition of isoproterenol-induced tachycardia, and (4) reduction of reflex orthostatic tachycardia. CORGARD (nadolol) specifically competes with beta-adrenergic receptor agonists for available beta receptor sites; it inhibits both the beta1 receptors located chiefly in cardiac muscle and the beta2 receptors located chiefly in the bronchial and vascular musculature, inhibiting the chronotropic, inotropic, and vasodilator responses to beta-adrenergic stimulation proportionately. CORGARD has no intrinsic sympathomimetic activity and, unlike some other beta-adrenergic blocking agents, nadolol has little direct myocardial depressant activity and does not have an anesthetic-like membrane- stabilizing action. Animal and human studies show that CORGARD slows the sinus rate and depresses AV conduction.
    [Show full text]
  • Comparison of Different Alpha-Blocker Combinations in Male Hypertensives with Refractory Lower Urinary Tract Symptoms
    대한남성과학회지：제 29 권 제 3 호 2011년 12월 Korean J Androl. Vol. 29, No. 3, December 2011 http://dx.doi.org/10.5534/kja.2011.29.3.242 Comparison of Different Alpha-blocker Combinations in Male Hypertensives with Refractory Lower Urinary Tract Symptoms Keon Cheol Lee1, Jong Gu Kim2, Sung Yong Cho1, Joon Sung Jeon1, In Rae Cho1 Department of Urology, 1Inje University Ilsanpaik Hospital, Goyang, 2Happy Urology Clinic, Ansan, Korea =Abstract= Purpose: We compared the efficacy and safety profiles of dose increase, traditional combination methods, and combining different alpha blockers in hypertensive males with lower urinary tract symptom (LUTS) refractory to an initial dose of 4 mg doxazosin. Materials and Methods: Between 2000 and 2005, 374 male patients with LUTS and hypertension unresponsive to 4 weeks of 4 mg doxazosin were enrolled. The subjects were randomly classified into 3 groups, 8 mg/day of doxazosin (D group), 4 mg of doxazosin plus 0.2 mg/day of tamsulosin (DT group), and 4 mg doxazosin plus 5 mg/day finasteride (DF group). Patients were evaluated based on their International Prostate Symptom Score (IPSS), quality of life (QOL), uroflowmetry and blood pressure (BP) and adverse events (AEs) at the baseline and 3 and 12 months after treatment. Results: The 269 patients (71.9%) were followed for at least 1 year (D group n=84, DT group n=115, and DF group n=70). The clinical parameters before and after initial 4 mg/day doxazosin were not different among the 3 groups. IPSS improvement after 3 months and maximal flow rate (Qmax) improvement after 3 and 12 months were significantly higher in the D and DT groups than the DF group (p＜0.05).
    [Show full text]
  • Drug-Facilitated Sexual Assault Panel, Blood
    DRUG-FACILITATED SEXUAL ASSAULT PANEL, BLOOD Blood Specimens (Order Code 70500) Alcohols Analgesics, cont. Anticonvulsants, cont. Antihistamines, cont. Ethanol Phenylbutazone Phenytoin Cyclizine Amphetamines Piroxicam Pregabalin Diphenhydramine Amphetamine Salicylic Acid* Primidone Doxylamine BDB Sulindac* Topiramate Fexofenadine Benzphetamine Tapentadol Zonisamide Guaifenesin Ephedrine Tizanidine Antidepressants Hydroxyzine MDA Tolmetin Amitriptyline Loratadine MDMA Tramadol Amoxapine Oxymetazoline* Mescaline* Anesthetics Bupropion Pyrilamine Methcathinone Benzocaine Citalopram Tetrahydrozoline Methamphetamine Bupivacaine Clomipramine Triprolidine Phentermine Etomidate Desipramine Antipsychotics PMA Ketamine Desmethylclomipramine 9-hydroxyrisperidone Phenylpropanolamine Lidocaine Dosulepin Aripiprazole Pseudoephedrine Mepivacaine Doxepin Buspirone Analgesics Methoxetamine Duloxetine Chlorpromazine Acetaminophen Midazolam Fluoxetine Clozapine Baclofen Norketamine Fluvoxamine Fluphenazine Buprenorphine Pramoxine* Imipramine Haloperidol Carisoprodol Procaine 1,3-chlorophenylpiperazine (mCPP) Mesoridazine Cyclobenzaprine Rocuronium Mianserin* Norclozapine Diclofenac Ropivacaine Mirtazapine Olanzapine Etodolac Antibiotics Nefazodone Perphenazine Fenoprofen Azithromycin* Nordoxepin Pimozide Hydroxychloroquine Chloramphenicol* Norfluoxetine Prochlorperazine Ibuprofen Ciprofloxacin* Norsertraline Quetiapine Ketoprofen Clindamycin* Nortriptyline Risperidone Ketorolac Erythromycin* Norvenlafaxine Thioridazine Meclofenamic Acid* Levofloxacin* Paroxetine
    [Show full text]
  • Hallucinogens: an Update
    National Institute on Drug Abuse RESEARCH MONOGRAPH SERIES Hallucinogens: An Update 146 U.S. Department of Health and Human Services • Public Health Service • National Institutes of Health Hallucinogens: An Update Editors: Geraline C. Lin, Ph.D. National Institute on Drug Abuse Richard A. Glennon, Ph.D. Virginia Commonwealth University NIDA Research Monograph 146 1994 U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service National Institutes of Health National Institute on Drug Abuse 5600 Fishers Lane Rockville, MD 20857 ACKNOWLEDGEMENT This monograph is based on the papers from a technical review on “Hallucinogens: An Update” held on July 13-14, 1992. The review meeting was sponsored by the National Institute on Drug Abuse. COPYRIGHT STATUS The National Institute on Drug Abuse has obtained permission from the copyright holders to reproduce certain previously published material as noted in the text. Further reproduction of this copyrighted material is permitted only as part of a reprinting of the entire publication or chapter. For any other use, the copyright holder’s permission is required. All other material in this volume except quoted passages from copyrighted sources is in the public domain and may be used or reproduced without permission from the Institute or the authors. Citation of the source is appreciated. Opinions expressed in this volume are those of the authors and do not necessarily reflect the opinions or official policy of the National Institute on Drug Abuse or any other part of the U.S. Department of Health and Human Services. The U.S. Government does not endorse or favor any specific commercial product or company.
    [Show full text]
  • Airway Receptors
    Postgraduate Medical Journal (1989) 65, 532- 542 Postgrad Med J: first published as 10.1136/pgmj.65.766.532 on 1 August 1989. Downloaded from Mechanisms of Disease Airway receptors Peter J. Barnes Department of Thoracic Medicine, National Heart and Lung Institute, Dovehouse Street, London SW3 6L Y, UK. Introduction Airway smooth muscle tone is influenced by many indirect action which, in part, is due to activation of a hormones, neurotransmitters, drugs and mediators, cholinergic reflex, since the bronchoconstriction may which produce their effects by binding to specific be reduced by a cholinergic antagonist. Other surface receptors on airway smooth muscle cells. mediators may have a bronchoconstrictor effect Bronchoconstriction and bronchodilatation may which, in the case of adenosine, is due to mast cell therefore be viewed in terms of receptor activation or mediator release,2 or in the case of platelet-activating blockade and the contractile state of airway smooth factor due to platelet products.3 muscle is probably the resultant effect of interacting excitatory and inhibitory receptors. Epithelial-derived relaxantfactor It is important to recognize that airway calibre is not only the result of airway smooth muscle tone, but in Recently there has been considerable interest in the asthma it is likely that airway narrowing may also be possibility of a relaxant factor released from airway explained by oedema of the bronchial wall (resulting epithelial cells, which may be analogous to relaxant factor.4 The presence of from microvascular leakage) and to luminal plugging endothelial-derived by copyright. by viscous mucus secretions and extravasated plasma airway epithelium in bovine airways in vitro reduces proteins, which may be produced by a 'soup' of the sensitivity to and maximum contractile effect of mediators released from inflammatory cells, including spasmogens, such as histamine, acetylcholine or mast cells, macrophages and eosinophils.
    [Show full text]