DOCSLIB.ORG

(12) Patent Application Publication (10) Pub. No.: US 2006/0058336A1 Nakanishi Et Al

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
(12) Patent Application Publication (10) Pub. No.: US 2006/0058336A1 Nakanishi Et Al US 20060058336A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2006/0058336A1 Nakanishi et al. (43) Pub. Date: Mar. 16, 2006 (54) PHARMACEUTICAL COMPOSITION FOR Publication Classification TREATMENT OF DRUG DEPENDENCE (51) Int. Cl. (76) Inventors: Shigetada Nakanishi, Kyoto-shi (JP); A6IK 31/4745 (2006.01) Takatoshi Hikida, Baltimore, MD A6IK 31/473 (2006.01) (US); Ira Pastan, Potomac, MD (US) A6IK 31/47 (2006.01) C d Add A6IK 31/4178 (2006.01) orrespondence Address: A6IK 31/407 (2006.01) BRCH STEWART KOLASCH & BRCH (52) U.S. Cl. ......................... 514/297; 514/310; 514/397; PO BOX 747 514/411 FALLS CHURCH, VA 22040-0747 (US) (21)21) AppAppl. No.: 10/493,4889 (57) ABSTRACT (22) PCT Filed: Feb. 26, 2004 (86) PCT No.: PCT/P04/02301 The present invention relates to the use of a medicinal Substance capable of enhancing or disinhibiting the actions Related U.S. Application Data of acetylcholine, and provides a pharmaceutical composition for treating drug dependence comprising Said Substance as (60) Provisional application No. 60/449,868, filed on Feb. an active ingredient, and a method of treating drug depen 27, 2003. dence using the Same. Patent Application Publication Mar. 16, 2006 Sheet 1 of 7 US 2006/0058336A1 Fig 1 ÁeM??edö?6Jau?uedopo?quu??osºuu9ul y--No.````*auquedoqbº O\/]LIA}} C?ksne10nN suequunooe eu||0?.0|Á?90W Patent Application Publication Mar. 16, 2006 Sheet 2 of 7 US 2006/0058336A1 Fig 2 Before After conditioningBefore conditioningAfter conditioning conditioning 8 O 500 6 O O 4. O -50 O 2 O O -1000 O -15 a T-tg F. : (mg/kg) T-wt Patent Application Publication Mar. 16, 2006 Sheet 3 of 7 US 2006/0058336A1 Fig 3 IT-tg O T-Wt Saline NaloxOne Patent Application Publication Mar. 16, 2006 Sheet 4 of 7 US 2006/0058336A1 Fig. 4 b Before After 3. Before . After conditioning conditioning g conditioning conditioning with morphine : 6OO with morphine 7 5o 2400 5O O s: ele g C 250 E 2O 3s O D il - Saline Donepezil E. g -Wt (1 mg/kg) T-tg Patent Application Publication Mar. 16, 2006 Sheet 5 of 7 US 2006/0058336A1 Fig 5 Before After b a Salie conditioning conditioning A Donepez J-BOO with cocaine N14 se 12 SOO 510 440 s 8 E 200 s 4. 2 w o 1 3 Day 0 1 2 3 4 S Dr.2 Saline Cocaine Saline d s 2Donepezil f-w e125 Galanthamine 25 s e100 s 7s s SO s 25 O - A-ard - Saline Saline Donee Sale Cocaire Cocaine (10 mg/kg) Day O S O Saline 175 Donepezil 150 5 125 to 7S 50 al 25 2 C O hu Day O 12 Saline cocaine Cocaine (10 mg/kg) Patent Application Publication Mar. 16, 2006 Sheet 6 of 7 US 2006/0058336A1 Fig 6 1S IT-tg 93 a 3 750. Before Afterwith conditioning Cocaine 500 S.g 3 2 250 2 O saline pilocarpine . Patent Application Publication Mar. 16, 2006 Sheet 7 of 7 US 2006/00583.36A1 Fig 7 Before After conditioning conditioning with alcohol SOO 4OO 300 200 1 OO Saline Donepezil - OO -200 US 2006/0058336A1 Mar. 16, 2006 PHARMACEUTICAL COMPOSITION FOR 0006 Throughout the present specification and claims, TREATMENT OF DRUG DEPENDENCE the term “drug dependence” means conditions including “Substance-related disorders' based on the criterion of TECHNICAL FIELD DSM-IV (Diagnostic and Statistical Manual of Mental Dis 0001. The present invention relates to the treatment of orders, Fourth Edition) of American Psychiatric Association, drug dependence, more specifically, to a pharmaceutical namely, Substance use disorders and Substance-induced dis composition for the treatment of drug dependence, which orders. comprises a medicinal Substance capable of enhancing or 0007. At present, there are few effective cures for drug disinhibiting the action of acetylcholine, a neurotransmitter, dependence. Cocaine- or amphetamine-dependence is cur in the central nervous system (CNS) and a method of rently treated by psychotherapy, however, its effects are treating drug dependence with Such a Substance. poor, and there is no effective medical therapy available. Treatment with dopamine antagonists or agonists is consid BACKGROUND ART ered, however, there is little therapeutic effect. Psychotic disorders induced by cocaine or amphetamine are treated by 0002 Drug- or substance-dependence is a disorder Symptomatic treatment with antipsychotic drugs. Opium or caused by various types of addictive (dependence-produc nicotine dependence is treated by alternative Substances ing) Substances. The number of patients/drug abusers Suf Such as methadone or nicotine patch. Although Such therapy fering from drug dependence is estimated to exceed 30 may be effective on withdrawal Symptom, the dependence millions worldwide. The cost to society is high when social itself remains. Regarding benzodiazepine, it shows certain problems caused by drug-dependence-related organic men effects on withdrawal Symptoms of alcohol dependence, but tal disorder and Socially dysfunctional characteristics of it is ineffective on alcohol dependence per se. An alcohol drug dependent individuals are considered. Thus there is a deterrent disulfiram is useful in the rehabilitation period of Worldwide demand for an effective cure for drug depen alcohol dependence treatment but may cause noxious reac dence. tion when taken simultaneously with alcohol. Therefore, the 0003) There are two types of drug (substance) dependen administration of disulfiram must be combined with psy cies, psychological and physical. Psychological dependence chological or behavioral therapy, and hence causes practical refers to a condition wherein an organism possesses a inconvenience. An opioid receptor antagonist, naltrexone, heightened desire and compulsion for taking a certain drug. has been approved in the U.S.A. as a therapeutic medica Physical dependence refers to a condition wherein both ment, however, the effects of this drug is yet to be estab psychologically and physically morbid Symptoms (with lished. drawal Symptoms) occurs to an organism when the drug is 0008. The regions of the brain that are closely associated depleted from the body and the pharmacological effect with the reward System, the System closely related to drug thereof weakens or vanishes after having habituated to the dependence, include; ventral tegmental area (hereinafter, condition under the influence of an addictive drug. “VTA”), nucleus accumbens (NAc), locus ceruleus and 0004) To the onset of drug dependence, the involvement medial forebrain bundle. In particular, the dopaminergic of the CNS reward system has been elucidated. The reward system projecting from VTA to NAc plays the central role in System has been identified as the Site responsible for intrac the activation of the reward system (FIG. 1). FIG. 1 ranial Self Stimulation-related behaviors in animals and playS illustrates the dopaminergic pathway of the meSolimbic a role in eliciting Senses of pleasure, motivation, and eupho system. As seen from FIG. 1, the reward system functions ria. The treatment of drug dependence is made very difficult when dopamine derived from VTA acts on nerve cells of Since many addictive Substances have an activity of Stimu NAc. Cocaine increases the NAc dopamine level through lating this System, thereby eliciting Senses of pleasure in inhibition of dopamine transporters of nerve cells in the users, and the influence of Such activity remains even after NAc. It is also known that opium, amphetamine and alco the drug, as a causative agent, is depleted from the body. In hols elevate the NAc dopamine level. Therefore, increase of accordance with the Symptoms, addictive drugS/Substances dopamine level in NAc is implicated in inductive mecha are classified into the following types: morphine type, alco nism of drug dependence. hol type, barbiturate type, amphetamine type, cocaine type, 0009 From this viewpoint, the researches of this field cannabinoid type, organic Solvent type, khat type, and were focused on drugs that target dopamine itself or other hallucinogen type. Examples of Substances generally known neurotransmitters indirectly related to the dopaminergic to cause drug dependence include cocaine, opium (heroin, nervous System Such as Serotonin, GABA or glutamic acid, morphine, etc), alcohols, amphetamine (or amphetamine receptors thereof and intracellular signaling cascades asso like Substances), caffeine, cannabinoids, hallucinogen, ciated with dopamine receptors. However, no investigation inhalants, nicotine, phencyclidine (or phencyclidine-like of Such kind has resulted in the development of any Sub Substances), Sedatives, hypnotic agents and anxiolytic stance effective for the treatment of drug dependence So far. agents. Patients are often found to be dependent on more 0010 NAc contains cholinergic cells that produce ace than one type of these Substances. tylcholine (ACh), which is another neurotransmitter differ 0005 Most addictive drugs can cause dependence after a ent from dopamine. The present inventors have established Single administration and once the user is affected, the a method to Selectively eliminate cholinergic cells in the Symptoms Sometimes persist over a long term even after the NAc, and demonstrated that ACh has an antagonistic activ use is terminated. For these reasons, drug dependence is ity against dopamine activities and that the reduction of NAc considered as a chronical neurological disorder. Further ACh level by cholinergic cell elimination enhances the more, overdose of Such drugs may have a deteriorating effect sensitivity to cocaine in mice (Hikida et al., Proc. Natl. on living body and may even cause death. Acad. Sci. USA 98, 13351-13354 (2001)). US 2006/0058336A1 Mar. 16, 2006 DISCLOSURE OF INVENTION Substance, wherein Said Substance has an activity of 0.011 The present inventors, with consideration to the enhancing or disinhibiting the action of ACh. Situation above, have conducted an investigation with a 0024 (12) Use of a medicinal substance having an activ purpose of developing medicaments effective for the treat ity of enhancing or disinhibiting the action of ACh in the ment of drug dependence.
Load more

Recommended publications
  • (12) Patent Application Publication (10) Pub. No.: US 2006/0110428A1 De Juan Et Al
    US 200601 10428A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2006/0110428A1 de Juan et al. (43) Pub. Date: May 25, 2006 (54) METHODS AND DEVICES FOR THE Publication Classification TREATMENT OF OCULAR CONDITIONS (51) Int. Cl. (76) Inventors: Eugene de Juan, LaCanada, CA (US); A6F 2/00 (2006.01) Signe E. Varner, Los Angeles, CA (52) U.S. Cl. .............................................................. 424/427 (US); Laurie R. Lawin, New Brighton, MN (US) (57) ABSTRACT Correspondence Address: Featured is a method for instilling one or more bioactive SCOTT PRIBNOW agents into ocular tissue within an eye of a patient for the Kagan Binder, PLLC treatment of an ocular condition, the method comprising Suite 200 concurrently using at least two of the following bioactive 221 Main Street North agent delivery methods (A)-(C): Stillwater, MN 55082 (US) (A) implanting a Sustained release delivery device com (21) Appl. No.: 11/175,850 prising one or more bioactive agents in a posterior region of the eye so that it delivers the one or more (22) Filed: Jul. 5, 2005 bioactive agents into the vitreous humor of the eye; (B) instilling (e.g., injecting or implanting) one or more Related U.S. Application Data bioactive agents Subretinally; and (60) Provisional application No. 60/585,236, filed on Jul. (C) instilling (e.g., injecting or delivering by ocular ion 2, 2004. Provisional application No. 60/669,701, filed tophoresis) one or more bioactive agents into the Vit on Apr. 8, 2005. reous humor of the eye. Patent Application Publication May 25, 2006 Sheet 1 of 22 US 2006/0110428A1 R 2 2 C.6 Fig.
    [Show full text]
  • Enhancement of Acetylcholinesterase Inhibitory Activity for the Soft Coral Associated Fungus Aspergillus Unguis SPMD-EGY by Media Composition
    Int. J. Pharm. Sci. Rev. Res., 41(2), November - December 2016; Article No. 64, Pages: 349-357 ISSN 0976 – 044X Research Article Enhancement of Acetylcholinesterase Inhibitory Activity for the Soft Coral Associated Fungus Aspergillus unguis SPMD-EGY by Media Composition Faten K. Abd El-Hady1*, Mohamed S. Abdel-Aziz2, Ahmed M.A. Souleman3, Zeinab A. El-Shahid1, Kamel H. Shaker4 1Chemistry of Natural Products Department, National Research Center, Egypt. 2Department of Microbial Chemistry, National Research Center, Egypt. 3Department of Phytochemistry and Plant Systematic, National Research Center, Egypt. 4Chemistry of Natural Compounds Department, National Research Center, Egypt. *Corresponding author’s E-mail: [email protected] Accepted on: 24-09-2016; Finalized on: 30-11-2016. ABSTRACT The soft coral fungus, Aspergillus unguis SPMD-EGY, was grown on different media to select the potential medium producing significant high acetyl-cholinesterase (AChE) inhibitory activity. Extract from Rice solid medium exhibited the highest inhibitory activity of AChE followed by PYMG medium in static conditions (culture filtrate and mycelia). Potato dextrose broth (PD) showed no AChE inhibitory activity but moderate activity was found with DOX broth medium under static conditions (culture filtrate and mycelia). Comparative study has been done for PYMG medium and our previous work. The chemical composition of the potent extracts was evaluated using GC/MS analysis. Rice solid medium extract (RS, 89% AChE inhibitory activity) solely contains nitrogenous compounds, fatty acids and their esters. PYMG medium(PY, 85% activity) showed the presence of two major compounds: 1,3-bis[2-hydroxyphenyl]-2-propen-1-one (33.6%) and D-friedoolean-14-en-3-one (39.8%), mild presence for the compounds 1,6,7-trimethyl-3-phenyl-9H-xanthen-9-one (3%) and 2,4,4’-trihydroxy-chalcone (3.2%).
    [Show full text]
  • The Effects of Donepezil, an Acetylcholinesterase Inhibitor, on Impaired Learning and Memory in Rodents
    Original Article Biomol Ther 26(3), 274-281 (2018) The Effects of Donepezil, an Acetylcholinesterase Inhibitor, on Impaired Learning and Memory in Rodents Chang Yell Shin1,2, Hae­Sun Kim1, Kwang­Ho Cha1, Dong Han Won1, Ji­Yun Lee2, Sun Woo Jang1,* and Uy Dong Sohn2,* 1Research Institute of Dong-A ST Co., Ltd., Yongin 17073, 2College of Pharmacy, Chung-Ang University, Seoul 06974, Republic of Korea Abstract A previous study in humans demonstrated the sustained inhibitory effects of donepezil on acetylcholinesterase (AChE) activity; however, the effective concentration of donepezil in humans and animals is unclear. This study aimed to characterize the effective concentration of donepezil on AChE inhibition and impaired learning and memory in rodents. A pharmacokinetic study of done- pezil showed a mean peak plasma concentration of donepezil after oral treatment (3 and 10 mg/kg) of approximately 1.2 ± 0.4 h and 1.4 ± 0.5 h, respectively; absolute bioavailability was calculated as 3.6%. Further, AChE activity was inhibited by increasing plasma concentrations of donepezil, and a maximum inhibition of 31.5 ± 5.7% was observed after donepezil treatment in hairless rats. Plasma AChE activity was negatively correlated with plasma donepezil concentration. The pharmacological effects of done- pezil are dependent upon its concentration and AChE activity; therefore, we assessed the effects of donepezil on learning and memory using a Y-maze in mice. Donepezil treatment (3 mg/kg) significantly prevented the progression of scopolamine-induced memory impairment in mice. As the concentration of donepezil in the brain increased, the recovery of spontaneous alternations also improved; maximal improvement was observed at 46.5 ± 3.5 ng/g in the brain.
    [Show full text]
  • Download PDF (131K)
    doi: 10.2169/internalmedicine.6261-20 Intern Med 60: 2251-2254, 2021 http://internmed.jp 【 CASE REPORT 】 Cholinergic Crisis Owing to Distigmine Bromide Complicated by Hyperosmolar Hyperglycemic State Kazumasa Kotake 1, Atsuhito Tone 2, Satoko Watanabe 2, Mayumi Senoo 2, Mitsuhiro Kaneto 2, Yusuke Imai 2, Sanae Teshigawara 2, Yasuhiro Kawakami 1 and Tatsuaki Nakatou 2 Abstract: Distigmine bromide is widely used to treat neurogenic bladder and causes cholinergic crisis, a serious side effect. We herein report about a patient with distigmine bromide-induced cholinergic crisis complicated by a hyperosmolar hyperglycemic state (HHS). On admission, the patient was diagnosed with HHS based on the medical history and laboratory test results. However, she also had bradycardia, miosis, and low plasma cholinesterase activity. We later found that she had received distigmine bromide, which led to a diagnosis of cholinergic crisis. We suggest that the exacerbation of pathology, including HHS, can cause cholinergic crisis in patients receiving distigmine bromide. Key words: distigmine bromide, cholinergic crisis, hyperosmolar hyperglycemic state, bradycardia, miosis, low plasma cholinesterase activity (Intern Med 60: 2251-2254, 2021) (DOI: 10.2169/internalmedicine.6261-20) ness. Her activities of daily living required full assistance, Introduction and her food intake had been gradually decreasing for the preceding few days; however, her condition worsened after Distigmine bromide is classified as a cholinesterase in- lunch on the day of admission. She had a history of type 2 hibitor and is used for the treatment of underactive neuro- diabetes, hypertension, dementia, neurogenic bladder, cata- genic bladder. In older adults, detrusor contractility, urine ract, angina, Meniere’s disease, disc herniation, and colorec- flow, and bladder sensation are significantly reduced.
    [Show full text]
  • Biol. Pharm. Bull. 42(7): 1064-1068 (2019)
    1064 Biol. Pharm. Bull. 42, 1064–1068 (2019) Vol. 42, No. 7 Review Effects of Distigmine on the Mechanical Activity of Urinary Bladder Smooth Muscle Keisuke Obara* and Yoshio Tanaka Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toho University; 2–2–1 Miyama, Funabashi, Chiba 274–8510, Japan. Received February 28, 2019; accepted April 24, 2019 Distigmine bromide (distigmine) is a reversible carbamate cholinesterase (ChE) inhibitor. Its principle clinical application is in the treatment of myasthenia gravis. Distigmine is also used as a remedy for dysuria and glaucoma. Its effectiveness in the management of dysuria has been demonstrated in several clinical re- ports. Distigmine may improve (enhance) urinary bladder smooth muscle (UBSM) contraction during mic- turition by inhibiting acetylcholine (ACh) decomposition. However, the pharmacological effects of distigmine on UBSM have not been adequately studied so far. In this review article, we summarize the reported effects of distigmine on the contractile responses elicited by exogenous and endogenous ACh in isolated UBSM preparations. We also discuss the effects of distigmine on the UBSM basal tone and the contractile response of UBSM to ATP, which is co-released with ACh from parasympathetic nerve terminals. Key words distigmine bromide; urinary bladder smooth muscle; cholinesterase inhibitor; acetylcholine; adenosine triphosphate 1. INTRODUCTION 2. EFFECTS OF DISTIGMINE ON UBSM CONTRAC- TILE RESPONSES ELICITED BY EXOGENOUS CON- Distigmine bromide (distigmine)
    [Show full text]
  • 12.2% 122,000 135M Top 1% 154 4,800
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE We are IntechOpen, provided by IntechOpen the world’s leading publisher of Open Access books Built by scientists, for scientists 4,800 122,000 135M Open access books available International authors and editors Downloads Our authors are among the 154 TOP 1% 12.2% Countries delivered to most cited scientists Contributors from top 500 universities Selection of our books indexed in the Book Citation Index in Web of Science™ Core Collection (BKCI) Interested in publishing with us? Contact [email protected] Numbers displayed above are based on latest data collected. For more information visit www.intechopen.com Chapter Anticholinesterases Zeynep Özdemir and Mehmet Abdullah Alagöz Abstract Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) are known serine hydrolase enzymes responsible for the hydrolysis of acetylcholine (ACh). Although the role of AChE in cholinergic transmission is well known, the role of BChE has not been elucidated sufficiently. The hydrolysis of acetylcholine in the synaptic healthy brain cells is mainly carried out by AChE; it is accepted that the contribution to the hydrolysis of BChE is very low, but both AChE and BChE are known to play an active role in neuronal development and cholinergic transmission. Myasthenia gravis (MG) is a muscle disease characterized by weakness in skeletal muscles and rapid fatigue. Anticholinesterases, which are not only related to the immune origin of the disease but also have only symp- tomatic benefit, have an indispensable role in the treatment of MG. Pyridostigmine, distigmine, neostigmine, and ambenonium are the standard anticholinesterase drugs used in the symptomatic treatment of MG.
    [Show full text]
  • Pharmaceuticals and Medical Devices Safety Information No
    Pharmaceuticals and Medical Devices Safety Information No. 260 August 2009 Table of Contents 1. Tricyclic and tetracyclic antidepressants, associated with aggression ................................................................................................... 3 2. Important Safety Information .................................................................. 9 .1. Telmisartan ··························································································· 9 .2. Phenytoin, Phenytoin/Phenobarbital, Phenytoin/Phenobarbital/ Caffeine and Sodium Benzoate, Phenytoin Sodium ··························· 13 3. Revision of PRECAUTIONS (No. 208) Lamotrigine (and 9 others) ············································································ 17 4. List of products subject to Early Post-marketing Phase Vigilance ..................................................... 21 This Pharmaceuticals and Medical Devices Safety Information (PMDSI) is issued based on safety information collected by the Ministry of Health, Labour and Welfare. It is intended to facilitate safer use of pharmaceuticals and medical devices by healthcare providers. PMDSI is available on the Pharmaceuticals and Medical Devices Agency website (http://www.pmda.go.jp/english/index.html) and on the MHLW website (http://www.mhlw.go.jp/, Japanese only). Published by Translated by Pharmaceutical and Food Safety Bureau, Pharmaceuticals and Medical Devices Agency Ministry of Health, Labour and Welfare Pharmaceutical and Food Safety Bureau, Office of Safety I, Ministry of
    [Show full text]
  • Acetylcholinesterase Inhibitors of Natural Origin
    ® International Journal of Biomedical and Pharmaceutical Sciences ©2009 Global Science Books Acetylcholinesterase Inhibitors of Natural Origin Melanie-Jayne R. Howes1* • Peter J. Houghton2 1 Royal Botanic Gardens, Jodrell Laboratory, Kew, Richmond, Surrey, United Kingdom 2 Department of Pharmacy, King's College London, Franklin-Wilkins Building, London, United Kingdom Corresponding author : * [email protected] ABSTRACT The endogenous neurotransmitter acetylcholine (ACh), found in vertebrates, stimulates cholinergic (muscarinic and nicotinic) receptors to mediate cholinergic neuronal transmission. ACh has a short half-life, as it is rapidly hydrolysed in the neuronal synaptic cleft by the enzyme acetylcholinesterase (AChE). Modulation of cholinergic function has been recognised as a therapeutic target in some disease states and one approach to achieve this is to prolong the action of ACh through the use of AChE inhibitors. Consequently, AChE inhibitors have been investigated for a number of therapeutic applications including glaucoma, myasthenia gravis, anti-muscarinic poisoning and dementia. Many inhibitors of AChE have been derived from natural sources, with alkaloids generally being the most potent, although other compounds including some terpenoids have also been shown to inhibit AChE. It is particularly interesting that of the four drugs currently licensed in Europe to alleviate cognitive symptoms in Alzheimer’s disease, two (galantamine and rivastigmine) are derived from natural sources. Natural products continue to be investigated
    [Show full text]
  • Antimyasthenics
    Antimyasthenics This chapter includes those drugs used for their their reaction to an anticholinesterase. Intravenous edro- • Plasma exchange provides a dramatic but short-lived anticholinesterase action in the treatment of myasthe- phonium preceded by atropine (Tensilon test) is the most improvement and is useful as a short-term measure in nia gravis and related neuromuscular disorders. Other commonly used anticholinesterase test because of its rapid myasthenic crisis to improve ill patients while other groups of drugs playing an important role in the man- onset and short duration of action. Severe adverse effects therapies take effect, but there is no evidence that repeat- agement of myasthenia are the corticosteroids (p.1490) can occasionally occur so testing should only be undertak- ed plasma exchange combined with immunosuppres- en when facilities for endotracheal intubation and control- sion is superior to immunosuppression alone. A similar and some drugs with immunosuppressant actions dis- led ventilation are immediately available. A positive result short-term benefit has been seen from the use of high- cussed in the chapters on Antineoplastics (p.635) and is considered to be a rapid but temporary increase in mus- dose intravenous normal immunoglobulins; however, a Immunosuppressants (p.1810). cle strength. Repetitive nerve stimulation is also used as a systematic review considered further study to be war- diagnostic test but, like the anticholinesterase test, is not ranted. Eaton-Lambert myasthenic syndrome specific for myasthenia gravis. Computed tomography or • Thymectomy may be offered to all patients sufficiently Eaton-Lambert myasthenic syndrome is a rare auto-im- magnetic resonance imaging may be used to detect thymo- fit to undergo surgery unless they have minimal symp- mune disease of the neuromuscular junction.
    [Show full text]
  • Guidelines for Biological Treatment of Schizophrenia, Part 2
    The World Journal of Biological Psychiatry, 2013; 14: 2–44 GUIDELINES World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for Biological Treatment of Schizophrenia, Part 2: Update 2012 on the long-term treatment of schizophrenia and management of antipsychotic-induced side effects ALKOMIET HASAN 1 , PETER FALKAI1 , THOMAS WOBROCK 2 , JEFFREY LIEBERMAN 3 , BIRTE GLENTHOJ 4 , WAGNER F. GATTAZ 5 , FLORENCE THIBAUT6 & HANS-JÜ RGEN M Ö LLER 1 , WFSBP Task force on Treatment Guidelines for Schizophrenia * 1 Department of Psychiatry and Psychotherapy, Ludwig-Maximilians-University, Munich, Germany, 2 Centre of Mental Health, Darmstadt-Dieburg Clinics, Darmstadt, Germany, 3 Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York State Psychiatric Institute, Lieber Center for Schizophrenia Research, New York, USA, 4 Center for Neuropsychiatric Schizophrenia Research & Center for Clinical Intervention and Neuropsychiatric Schizophrenia Research, Copenhagen University Hospital, Psychiatric Center Glostrup, Denmark, 5 Department of Psychiatry, University of Sao Paulo, Brazil, and 6 University Hospital Ch. Nicolle, Faculty of Medicine, INSERM, Rouen, France Abstract These updated guidelines are based on a fi rst edition of the World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for biological treatment of schizophrenia published in 2006. For this 2012 revision, all available publications pertaining to the biological treatment of schizophrenia were reviewed systematically to allow for an evidence- based update. These guidelines provide evidence-based practice recommendations that are clinically and scientifi cally meaningful. They are intended to be used by all physicians diagnosing and treating people suffering from schizophrenia. Based on the fi rst version of these guidelines, a systematic review of the MEDLINE/PUBMED database and the Cochrane Library, in addition to data extraction from national treatment guidelines, has been performed for this update.
    [Show full text]
  • Anatomical Classification Guidelines V2020 EPHMRA ANATOMICAL
    EPHMRA ANATOMICAL CLASSIFICATION GUIDELINES 2020 Anatomical Classification Guidelines V2020 "The Anatomical Classification of Pharmaceutical Products has been developed and maintained by the European Pharmaceutical Marketing Research Association (EphMRA) and is therefore the intellectual property of this Association. EphMRA's Classification Committee prepares the guidelines for this classification system and takes care for new entries, changes and improvements in consultation with the product's manufacturer. The contents of the Anatomical Classification of Pharmaceutical Products remain the copyright to EphMRA. Permission for use need not be sought and no fee is required. We would appreciate, however, the acknowledgement of EphMRA Copyright in publications etc. Users of this classification system should keep in mind that Pharmaceutical markets can be segmented according to numerous criteria." © EphMRA 2020 Anatomical Classification Guidelines V2020 CONTENTS PAGE INTRODUCTION A ALIMENTARY TRACT AND METABOLISM 1 B BLOOD AND BLOOD FORMING ORGANS 28 C CARDIOVASCULAR SYSTEM 35 D DERMATOLOGICALS 50 G GENITO-URINARY SYSTEM AND SEX HORMONES 57 H SYSTEMIC HORMONAL PREPARATIONS (EXCLUDING SEX HORMONES) 65 J GENERAL ANTI-INFECTIVES SYSTEMIC 69 K HOSPITAL SOLUTIONS 84 L ANTINEOPLASTIC AND IMMUNOMODULATING AGENTS 92 M MUSCULO-SKELETAL SYSTEM 102 N NERVOUS SYSTEM 107 P PARASITOLOGY 118 R RESPIRATORY SYSTEM 120 S SENSORY ORGANS 132 T DIAGNOSTIC AGENTS 139 V VARIOUS 141 Anatomical Classification Guidelines V2020 INTRODUCTION The Anatomical Classification was initiated in 1971 by EphMRA. It has been developed jointly by Intellus/PBIRG and EphMRA. It is a subjective method of grouping certain pharmaceutical products and does not represent any particular market, as would be the case with any other classification system.
    [Show full text]
  • PH 1.14 Parasympathomimetics Cholinergic Drugs Cholinergic and Adrenergic System
    . At the end of this session, the student should be able to: • Describe cholinergic transmission • Enumerate types of cholinergic receptors, clinically relevant sites where present & response on stimulation PH 1.14 • Enumerate choline esters & alkaloids & mention clinical uses of each Parasympathomimetics with basis • Enumerate anticholinesterases, describe their important uses with Cholinergic drugs preferred agent & basis of use • Describe clinically relevant differences between Physostigmine & Neostigmine • Explain why Physostigmine is preferred for t/t of glaucoma & Belladona poisoning • Explain why Edrophonium is used for diagnostic purpose but not 1 preferred for therapeutic purpose 2 Parasympathetic Nervous System (Craniosacral Outflow) • Explain why anticholinesterases are not used for reversing the action SA & AV Node Bronchi/Bronchial of succinylcholine Circular Muscle of Iris Glands Ciliary Muscle • Explain t/t of early mushroom poisoning & acute organophosphate Stomach poisoning • Write a brief note on: Small Intestine Lacrimal Gland a) Edrophonium Bile Ducts b) Pralidoxime Gallbladder c) Cholinergic crisis Submaxillary & Kidney Sublingual d) Myasthenic crisis Glands Large Intestine Bladder Parotid Gland Genitalia 3 4 Sympathetic Nervous System (Thoracolumbar Outflow) Radial Muscle of Iris Ciliary Muscle Cholinergic and Adrenergic System Sublingual,Submaxillary & Parotid Gland • Accordingly: Pilomotor Muscles SA & AV Nodes Sweat Glands His-Purkinje System – Cholinergic Drugs, i.e. they act by releasing Myocardium acetylcholine Bronchi/Bronchial Glands • But also utilize nitric oxide (NO) or peptides for transmission Stomach Blood Vessels – Noradrenergic (commonly called "adrenergic") Drugs - Kidneys act by releasing norepinephrine (NA) Paravertebral Ganglia Intestines Bladder/ Genitalia Prevertebral Ganglia 5 6 1 . Sites of Cholinergic Transmission Schematic diagram comparing some anatomic 1. All preganglionic sites (Both Parasympathetic and sympathetic) and neurotransmitter features of autonomic and 2.
    [Show full text]