DOCSLIB.ORG

Module 1. Signalering – Concept Voor Commentaarronde

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Module 1. Signalering – Concept Voor Commentaarronde KIMO Klinische praktijkrichtlijn Xerostomie en hyposialie gerelateerd aan medicatie en polyfarmacie Module 1. Signalering – Concept voor commentaarronde 1 Xerostomie en hyposialie gerelateerd 2 aan medicatie en polyfarmacie 3 Module 1. Signalering 4 Uitgangsvraag 1. Bij gebruik van welke medicatie (soorten en/of aantal) moeten 5 mondzorgverleners alert zijn op problemen rond xerostomie en/of hyposialie? 6 1a. Gebruik bepaalde soorten medicatie 7 Uitwerking in PDO (PDO model i.p.v. PICO; PDO = patiënten/populatie, determinanten, outcome 8 (uitkomstmaat)): 9 P: Alle patiënten in de mondzorgpraktijk 10 D: Gebruik van bepaalde medicatie, namelijk 11 • ACE-remmers 12 • Alfablokkers 13 • Anesthetica (intraveneuze) 14 • Angiotensinereceptorblokkers (ARBs) 15 • Antidepressiva (overige) 16 • Antidepressiva (tricyclische) 17 • Anti-epileptica 18 • Antihistaminica 19 • Antihypertensiva (centraal aangrijpend) 20 • Antipsychotica 21 • Benzodiazepine-agonisten 22 • Bètablokkers 23 • Bisfosfonaten 24 • Calciumantagonisten 25 • CCR5-antagonisten 26 • Dihydropyridinen 27 • Diuretica 28 • Dopamine-agonisten 29 • H2-antagonisten 30 • Hiv-integraseremmers 31 • Hiv-non-nucleoside reverse-transcriptaseremmers 32 • Hiv-nucleoside reverse-transcriptaseremmers 33 • Hiv-proteaseremmers 34 • Lisdiuretica 35 • Lithiumzouten 36 • MAO-A-remmers 37 • MAO-B-remmers 38 • Medicamenten bij alcoholverslaving 39 • Medicamenten bij nicotineverslaving 40 • Monoklonale antilichamen bij maligniteiten 41 • Oncolytica 42 • Opioïden 43 • Parasympathicolytica (bronchodilatators) 1 KIMO Klinische praktijkrichtlijn Xerostomie en hyposialie gerelateerd aan medicatie en polyfarmacie Module 1. Signalering – Concept voor commentaarronde 44 • Platinaverbindingen (oncolytica) 45 • Protonpompremmers 46 • Psychostimulantia 47 • Serotonineheropnameremmers 48 • Spasmolytica (urologische) 49 • Spierrelaxantia 50 • Sympathicomimetica (bronchodilatators) 51 • Vasopressine-antagonisten 52 • Vermageringsmiddelen 53 • Xanthinederivaten (bronchodilatator theophylline) 54 55 O: Klachten/symptomen/bevindingen rond de speekselsecretie, namelijk 56 - Xerostomie 57 - Hyposialie 58 Aanbeveling 59 Mondzorgverleners dienen alert te zijn op het optreden van xerostomie en/of hyposialie. Indien 60 een patiënt meldt dat hij of zij hinder ondervindt van een droge mond of wanneer bij mondon- 61 derzoek tekenen worden gezien van monddroogheid, dient de mondzorgverlener na te gaan of de 62 patiënt medicamenten gebruikt waarvan bekend is dat deze xerostomie en/of hyposialie kunnen 63 veroorzaken. Dan dient ook de speekselsecretiesnelheid in rust en na stimulatie te worden beoor- 64 deeld. 65 Overwegingen 66 Medicatie kan een effect hebben op het centrale en perifere zenuwstelsel en/of op de musca- 67 rinerge, α- en β-adrenerge receptoren en/of op bepaalde peptidereceptoren op de speekselklie- 68 ren zelf. Hiertoe behoren in het bijzonder medicamenten die inwerken op het zenuwstelsel, op 69 het cardiovasculaire, urogenitale, musculoskelettale of pulmonaire systeem, en/of op het maag- 70 darmstelsel. Van veel medicamenten is wel bekend dat gebruik hiervan xerostomie en/of hypo- 71 sialie kan veroorzaken of bestaat hieromtrent een sterk vermoeden, maar helaas is vaak niet be- 72 kend of gebruik van die medicamenten resulteert in hyposialie. In dat kader zou het een aanbeve- 73 ling zijn om van iedere patiënt te weten wat zijn of haar speekselsecretiesnelheid in rust en na 74 stimulatie is onder gezonde omstandigheden, zodat kan worden vastgesteld of gebruik van medi- 75 catie bij die patiënt inderdaad heeft geresulteerd in hyposialie. Een algemene richtlijn is dat ie- 76 mand een drogemondgevoel (xerostomie) ervaart als de speekselsecretiesnelheid maximaal 50% 77 van diens normale speekselsecretiesnelheid bedraagt. Ook kan door de secretoire potentie van de 78 speekselklieren te weten, worden beoordeeld of stimulatie van de speekselsecretie succesvol kan 79 zijn als het het niet mogelijk is het medicatiegebruik aan te passen. Bij een patiënt die ten ge- 80 volge van medicatiegebruik xerostomie heeft, is gewoonlijk de speekselsecretiesnelheid in rust 81 verminderd. Na stimulatie kan vaak nog een (sub)normale speekselsecretiesnelheid worden be- 82 werkstelligd. Bij xerostomie ten gevolge van andere oorzaken is vaak de speekselsecretiesnelheid 83 zowel in rust als na stimulatie (sterk) verminderd. Dit is een belangrijk differentieeldiagnostisch 84 kenmerk. Voor praktische adviezen over meting van de speekselsecretiesnelheid wordt verwezen 85 naar het Advies Droge Mond van het Ivoren Kruis (1). Voor het meten en evalueren van de ernst 86 van xerostomie kan (de verkorte versie van) de Xerostomia Inventory worden gebruikt (2). 87 Onderbouwing 88 Voor het beantwoorden van uitgangsvraag 1 is gebruikgemaakt van een combinatie van methoden: 89 - Systematisch literatuuronderzoek (zie bijlage 1); 90 - Informatie van de Stichting Health Base (zie bijlage 2); 91 - Informatie zoals opgenomen in het boek MKA-chirurgie (Stegenga et al., Assen: van Gorcum, 92 2013, (zie bijlage 3); 2 KIMO Klinische praktijkrichtlijn Xerostomie en hyposialie gerelateerd aan medicatie en polyfarmacie Module 1. Signalering – Concept voor commentaarronde 93 - Systematisch verzamelde data over de bijwerking van medicamenten door de afdeling Orale 94 Geneeskunde van het Academisch Centrum Tandheelkunde Amsterdam (ACTA), in het kader 95 van het promotieonderzoek van W.M.H. Rademacher (zie bijlage 4). 96 Het geaggregeerde resultaat hiervan is weergegeven in de volgende conclusie: 97 Conclusie Er bestaat een associatie tussen het optreden van xerostomie en/of hyposialie en het gebruik van medicamenten uit de volgende medicamentgroepen (voor een volledige lijst van de medi- camentgroepen en de individuele medicamenten wordt verwezen naar bijlage 5): - Alfablokkers, in het bijzonder de selectieve alfa-1-blokkers (medicamenten bij prostaatklachten) - Allergeenextracten - Antiaritmica - Antibiotica: aminoglycosiden, antibacteriële medicamenten (overige), carba- penems, cefalosporinen, fluorochinolonen, macroliden, oxazolidinonen, penicilli- nen, tetracyclinen - Antidepressiva: selectieve serotonineheropnameremmers (SSRI), tricyclische an- tidepressiva (TCA), MAO-A-remmers, MAO-B-remmers - Antidiabetica: DPP4-remmers, GLP-1-agonisten, SGLT2-remmers - Anti-emetica - Anti-epileptica - Antiglaucoommedicamenten: NSAIDs (oculair), prostaglandine f-analoga, koolzuur- anhydrase(II)-remmers, bètablokkers (oculair), parasympathicolytica (oculair), sym- pathicomimetica (oculair) - Antihistaminica - Antihypertensiva: diuretica, bètablokkers, calciumantagonisten (overige), ACE-rem- mers, angiotensinereceptorblokkers, alfablokkers, antihypertensiva (centraal aan- grijpend), lisdiuretica, renineremmers - Antimycotica: antimycotica (overige), echinocandinen, imidazolen, triazolen - Anti-Parkinsonmedicatie: amantadine (groep), COMT-remmers, dopamine-agonis- ten, levodopa met decarboxylaseremmers, MAO-B-remmers, tertiaire aminen - Antipsychotica: antipsychotica (atypische), antipsychotica (klassieke), dopamine- antagonisten, lithiumzouten - Antitrombotica: anticoagulantia (direct werkende), glycoproteïne IIb/IIIa-recepto- rantagonisten, prostacycline-analoga, salicylaten - Antivirale medicamenten: antivirale medicamenten bij hepatitis (overige), fosfon- zuurderivaten, HCV-polymeraseremmers, HIV-integraseremmers, HIV-non-nucleo- side reverse-transcriptaseremmers, HIV-nucleoside reverse-transcriptaseremmers, HIV-proteaseremmers, nucleoside- en nucleotide-analoga, NS5A-remmers - Anxiolytica: benzodiazepine-agonisten, psychofarmaca (overige) - Bèta2-sympathicomimetica - Bisfosfonaten - Coxibs - Fosfodiësterase-5-remmers - H2-receptorantagonisten - Immunosuppressiva: calciumneurineremmers, immunosuppressiva (overige), MS- medicamenten, TNF-alfa-blokkers - Medicamenten bij alcohol-, nicotine- en opioïdverslaving - Prostaglandinesynthetaseremmers (NSAIDs) - Oncolytica: alkylerende medicamenten, anti-androgenen, antracyclinederivaten, aromataseremmers, gonadoreline-agonisten, interferonen, monoclonale antilicha- men bij maligniteiten, oncolytica (overige), progestagenen (exclusief 3 KIMO Klinische praktijkrichtlijn Xerostomie en hyposialie gerelateerd aan medicatie en polyfarmacie Module 1. Signalering – Concept voor commentaarronde anticonceptiva), proteïnekinaseremmers, pyrimidine-antagonisten, retinoïden (sys- temische), taxanen - Opioïden - Parasympathicolytica (inhalatie) - Protonpompremmers - Psychostimulantia: amfetaminen, psychostimulantia (overige) - Spierrelaxantia - Thyreomimetica - Triptanen - Urologische spasmolytica 98 4 KIMO Klinische praktijkrichtlijn Xerostomie en hyposialie gerelateerd aan medicatie en polyfarmacie Module 1. Signalering – Concept voor commentaarronde 99 1b. Polyfarmacie 100 Uitwerking in PDO (PDO model i.p.v. PICO; PDO = patiënten/populatie, determinanten, outcome 101 (uitkomstmaat)): 102 P: Alle patiënten in de mondzorgpraktijk 103 D: Polyfarmacie 104 O: Klachten/symptomen/bevindingen rond de speekselsecretie, namelijk 105 - Xerostomie 106 - Hyposialie 107 Aanbeveling 108 Mondzorgverleners dienen alert te zijn op het optreden van xerostomie en/of hyposialie bij men- 109 sen met polyfarmacie. Zie verder aanbeveling 1a. 110 Overwegingen 111 Hoewel de studies waarop de aanbeveling is gebaseerd voornamelijk een observationeel karakter 112 hebben, wijzen de uitkomsten van deze studies alle in dezelfde richting: hoe groter het aantal 113 medicamenten dat een patiënt gebruikt, des te groter is de kans op het ontwikkelen van xerosto- 114 mie en/of
Load more

Recommended publications
  • Experimental Dopamine Reuptake Inhibitors in Parkinson’S Disease: a Review of the Evidence
    Journal of Experimental Pharmacology Dovepress open access to scientific and medical research Open Access Full Text Article REVIEW Experimental Dopamine Reuptake Inhibitors in Parkinson’s Disease: A Review of the Evidence This article was published in the following Dove Press journal: Journal of Experimental Pharmacology Thomas Müller Abstract: Parkinson’s disease (PD) is the second most chronic neurodegenerative disorder worldwide. Deficit of monoamines, particularly dopamine, causes an individually varying Department of Neurology, St. Joseph Hospital Berlin-Weissensee, Berlin, compilation of motor and non-motor features. Constraint of presynaptic uptake extends 13088, Germany monoamine stay in the synaptic cleft. This review discusses possible benefits of dopamine reuptake inhibition for the treatment of PD. Translation of this pharmacologic principle into positive clinical study results failed to date. Past clinical trial designs did not consider a mandatory, concomitant stable inhibition of glial monoamine turnover, i.e. with mono­ amine oxidase B inhibitors. These studies focused on improvement of motor behavior and levodopa associated motor complications, which are fluctuations of motor and non-motor behavior. Future clinical investigations in early, levodopa- and dopamine agonist naïve patients shall also aim on alleviation of non-motor symptoms, like fatigue, apathy or cognitive slowing. Oral levodopa/dopa decarboxylase inhibitor application is inevitably necessary with advance of PD. Monoamine reuptake (MRT) inhibition improves the efficacy of levodopa, the blood brain barrier crossing metabolic precursor of dopamine. The pulsatile brain delivery pattern of orally administered levodopa containing formulations results in synaptic dopamine variability. Ups and downs of dopamine counteract the physiologic principle of continuous neurotransmission, particularly in nigrostriatal, respectively meso­ corticolimbic pathways, both of which regulate motor respectively non-motor behavior.
    [Show full text]
  • Muscarinic Acetylcholine Receptor
    mAChR Muscarinic acetylcholine receptor mAChRs (muscarinic acetylcholine receptors) are acetylcholine receptors that form G protein-receptor complexes in the cell membranes of certainneurons and other cells. They play several roles, including acting as the main end-receptor stimulated by acetylcholine released from postganglionic fibersin the parasympathetic nervous system. mAChRs are named as such because they are more sensitive to muscarine than to nicotine. Their counterparts are nicotinic acetylcholine receptors (nAChRs), receptor ion channels that are also important in the autonomic nervous system. Many drugs and other substances (for example pilocarpineand scopolamine) manipulate these two distinct receptors by acting as selective agonists or antagonists. Acetylcholine (ACh) is a neurotransmitter found extensively in the brain and the autonomic ganglia. www.MedChemExpress.com 1 mAChR Inhibitors & Modulators (+)-Cevimeline hydrochloride hemihydrate (-)-Cevimeline hydrochloride hemihydrate Cat. No.: HY-76772A Cat. No.: HY-76772B Bioactivity: Cevimeline hydrochloride hemihydrate, a novel muscarinic Bioactivity: Cevimeline hydrochloride hemihydrate, a novel muscarinic receptor agonist, is a candidate therapeutic drug for receptor agonist, is a candidate therapeutic drug for xerostomia in Sjogren's syndrome. IC50 value: Target: mAChR xerostomia in Sjogren's syndrome. IC50 value: Target: mAChR The general pharmacol. properties of this drug on the The general pharmacol. properties of this drug on the gastrointestinal, urinary, and reproductive systems and other… gastrointestinal, urinary, and reproductive systems and other… Purity: >98% Purity: >98% Clinical Data: No Development Reported Clinical Data: No Development Reported Size: 10mM x 1mL in DMSO, Size: 10mM x 1mL in DMSO, 1 mg, 5 mg 1 mg, 5 mg AC260584 Aclidinium Bromide Cat. No.: HY-100336 (LAS 34273; LAS-W 330) Cat.
    [Show full text]
  • Study Protocol
    Clinical Study Protocol A 24-WEEK PHASE 2, DOUBLE-BLIND, RANDOMIZED, PLACEBO- CONTROLLED, SINGLE-CENTER SAFETY AND EFFICACY STUDY TO EVALUATE OVERALL SAFETY AND TOLERABILITY OF CO- ADMINISTRATION OF TESOFENSINE AND METOPROLOL IN SUBJECTS WITH HYPOTHALAMIC INJURY-INDUCED OBESITY (HIO), AND WITH A 24-WEEK OPEN-LABEL EXTENSION, IN TOTAL 48 WEEKS Sponsor: Saniona, A/S Baltorpvej 154 DK2750 Ballerup Denmark Protocol number: TM005 Protocol version: 5.0 Date: 10 December 2019 EudraCT number: 2018-003672-12 The information contained in this document is provided in confidence. It is understood that this information will not be disclosed to others without prior agreement with Saniona A/S, according to the statement in the Clinical Study Protocol, and in accordance with the confidentiality agreement. Saniona A/S Clinical Study Protocol TM005 CONFIDENTIAL CLINICAL STUDY PROTOCOL SYNOPSIS A 24-week phase 2, double-blind (DB), randomized, placebo- controlled, single-center safety and efficacy study to evaluate overall safety and tolerability of co-administration of Study title tesofensine and metoprolol in subjects with hypothalamic injury-induced obesity (HIO), and with a 24-week open-label extension, in total 48 weeks. Saniona, A/S Baltorpvej 154 Study sponsor DK2750 Ballerup Denmark Phase 2a Number of sites 1 site; Rigshospitalet (RH), Copenhagen, Denmark Sample size Minimum of 12 and maximum of 25 adult subjects with HIO. DB, randomized, placebo-controlled, single-center study followed by an open-label extension period. The study will have two
    [Show full text]
  • (19) United States (12) Patent Application Publication (10) Pub
    US 20130289061A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2013/0289061 A1 Bhide et al. (43) Pub. Date: Oct. 31, 2013 (54) METHODS AND COMPOSITIONS TO Publication Classi?cation PREVENT ADDICTION (51) Int. Cl. (71) Applicant: The General Hospital Corporation, A61K 31/485 (2006-01) Boston’ MA (Us) A61K 31/4458 (2006.01) (52) U.S. Cl. (72) Inventors: Pradeep G. Bhide; Peabody, MA (US); CPC """"" " A61K31/485 (201301); ‘4161223011? Jmm‘“ Zhu’ Ansm’ MA. (Us); USPC ......... .. 514/282; 514/317; 514/654; 514/618; Thomas J. Spencer; Carhsle; MA (US); 514/279 Joseph Biederman; Brookline; MA (Us) (57) ABSTRACT Disclosed herein is a method of reducing or preventing the development of aversion to a CNS stimulant in a subject (21) App1_ NO_; 13/924,815 comprising; administering a therapeutic amount of the neu rological stimulant and administering an antagonist of the kappa opioid receptor; to thereby reduce or prevent the devel - . opment of aversion to the CNS stimulant in the subject. Also (22) Flled' Jun‘ 24’ 2013 disclosed is a method of reducing or preventing the develop ment of addiction to a CNS stimulant in a subj ect; comprising; _ _ administering the CNS stimulant and administering a mu Related U‘s‘ Apphcatlon Data opioid receptor antagonist to thereby reduce or prevent the (63) Continuation of application NO 13/389,959, ?led on development of addiction to the CNS stimulant in the subject. Apt 27’ 2012’ ?led as application NO_ PCT/US2010/ Also disclosed are pharmaceutical compositions comprising 045486 on Aug' 13 2010' a central nervous system stimulant and an opioid receptor ’ antagonist.
    [Show full text]
  • Classification Decisions Taken by the Harmonized System Committee from the 47Th to 60Th Sessions (2011
    CLASSIFICATION DECISIONS TAKEN BY THE HARMONIZED SYSTEM COMMITTEE FROM THE 47TH TO 60TH SESSIONS (2011 - 2018) WORLD CUSTOMS ORGANIZATION Rue du Marché 30 B-1210 Brussels Belgium November 2011 Copyright © 2011 World Customs Organization. All rights reserved. Requests and inquiries concerning translation, reproduction and adaptation rights should be addressed to [email protected]. D/2011/0448/25 The following list contains the classification decisions (other than those subject to a reservation) taken by the Harmonized System Committee ( 47th Session – March 2011) on specific products, together with their related Harmonized System code numbers and, in certain cases, the classification rationale. Advice Parties seeking to import or export merchandise covered by a decision are advised to verify the implementation of the decision by the importing or exporting country, as the case may be. HS codes Classification No Product description Classification considered rationale 1. Preparation, in the form of a powder, consisting of 92 % sugar, 6 % 2106.90 GRIs 1 and 6 black currant powder, anticaking agent, citric acid and black currant flavouring, put up for retail sale in 32-gram sachets, intended to be consumed as a beverage after mixing with hot water. 2. Vanutide cridificar (INN List 100). 3002.20 3. Certain INN products. Chapters 28, 29 (See “INN List 101” at the end of this publication.) and 30 4. Certain INN products. Chapters 13, 29 (See “INN List 102” at the end of this publication.) and 30 5. Certain INN products. Chapters 28, 29, (See “INN List 103” at the end of this publication.) 30, 35 and 39 6. Re-classification of INN products.
    [Show full text]
  • Compositions and Methods for Selective Delivery of Oligonucleotide Molecules to Specific Neuron Types
    (19) TZZ ¥Z_T (11) EP 2 380 595 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 26.10.2011 Bulletin 2011/43 A61K 47/48 (2006.01) C12N 15/11 (2006.01) A61P 25/00 (2006.01) A61K 49/00 (2006.01) (2006.01) (21) Application number: 10382087.4 A61K 51/00 (22) Date of filing: 19.04.2010 (84) Designated Contracting States: • Alvarado Urbina, Gabriel AT BE BG CH CY CZ DE DK EE ES FI FR GB GR Nepean Ontario K2G 4Z1 (CA) HR HU IE IS IT LI LT LU LV MC MK MT NL NO PL • Bortolozzi Biassoni, Analia Alejandra PT RO SE SI SK SM TR E-08036, Barcelona (ES) Designated Extension States: • Artigas Perez, Francesc AL BA ME RS E-08036, Barcelona (ES) • Vila Bover, Miquel (71) Applicant: Nlife Therapeutics S.L. 15006 La Coruna (ES) E-08035, Barcelona (ES) (72) Inventors: (74) Representative: ABG Patentes, S.L. • Montefeltro, Andrés Pablo Avenida de Burgos 16D E-08014, Barcelon (ES) Edificio Euromor 28036 Madrid (ES) (54) Compositions and methods for selective delivery of oligonucleotide molecules to specific neuron types (57) The invention provides a conjugate comprising nucleuc acid toi cell of interests and thus, for the treat- (i) a nucleic acid which is complementary to a target nu- ment of diseases which require a down-regulation of the cleic acid sequence and which expression prevents or protein encoded by the target nucleic acid as well as for reduces expression of the target nucleic acid and (ii) a the delivery of contrast agents to the cells for diagnostic selectivity agent which is capable of binding with high purposes.
    [Show full text]
  • Monoamine Reuptake Inhibitors in Parkinson's Disease
    Hindawi Publishing Corporation Parkinson’s Disease Volume 2015, Article ID 609428, 71 pages http://dx.doi.org/10.1155/2015/609428 Review Article Monoamine Reuptake Inhibitors in Parkinson’s Disease Philippe Huot,1,2,3 Susan H. Fox,1,2 and Jonathan M. Brotchie1 1 Toronto Western Research Institute, Toronto Western Hospital, University Health Network, 399 Bathurst Street, Toronto, ON, Canada M5T 2S8 2Division of Neurology, Movement Disorder Clinic, Toronto Western Hospital, University Health Network, University of Toronto, 399BathurstStreet,Toronto,ON,CanadaM5T2S8 3Department of Pharmacology and Division of Neurology, Faculty of Medicine, UniversitedeMontr´ eal´ and Centre Hospitalier de l’UniversitedeMontr´ eal,´ Montreal,´ QC, Canada Correspondence should be addressed to Jonathan M. Brotchie; [email protected] Received 19 September 2014; Accepted 26 December 2014 Academic Editor: Maral M. Mouradian Copyright © 2015 Philippe Huot et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The motor manifestations of Parkinson’s disease (PD) are secondary to a dopamine deficiency in the striatum. However, the degenerative process in PD is not limited to the dopaminergic system and also affects serotonergic and noradrenergic neurons. Because they can increase monoamine levels throughout the brain, monoamine reuptake inhibitors (MAUIs) represent potential therapeutic agents in PD. However, they are seldom used in clinical practice other than as antidepressants and wake-promoting agents. This review article summarises all of the available literature on use of 50 MAUIs in PD. The compounds are divided according to their relative potency for each of the monoamine transporters.
    [Show full text]
  • Ehealth DSI [Ehdsi V2.2.2-OR] Ehealth DSI – Master Value Set
    MTC eHealth DSI [eHDSI v2.2.2-OR] eHealth DSI – Master Value Set Catalogue Responsible : eHDSI Solution Provider PublishDate : Wed Nov 08 16:16:10 CET 2017 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 1 of 490 MTC Table of Contents epSOSActiveIngredient 4 epSOSAdministrativeGender 148 epSOSAdverseEventType 149 epSOSAllergenNoDrugs 150 epSOSBloodGroup 155 epSOSBloodPressure 156 epSOSCodeNoMedication 157 epSOSCodeProb 158 epSOSConfidentiality 159 epSOSCountry 160 epSOSDisplayLabel 167 epSOSDocumentCode 170 epSOSDoseForm 171 epSOSHealthcareProfessionalRoles 184 epSOSIllnessesandDisorders 186 epSOSLanguage 448 epSOSMedicalDevices 458 epSOSNullFavor 461 epSOSPackage 462 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 2 of 490 MTC epSOSPersonalRelationship 464 epSOSPregnancyInformation 466 epSOSProcedures 467 epSOSReactionAllergy 470 epSOSResolutionOutcome 472 epSOSRoleClass 473 epSOSRouteofAdministration 474 epSOSSections 477 epSOSSeverity 478 epSOSSocialHistory 479 epSOSStatusCode 480 epSOSSubstitutionCode 481 epSOSTelecomAddress 482 epSOSTimingEvent 483 epSOSUnits 484 epSOSUnknownInformation 487 epSOSVaccine 488 © eHealth DSI eHDSI Solution Provider v2.2.2-OR Wed Nov 08 16:16:10 CET 2017 Page 3 of 490 MTC epSOSActiveIngredient epSOSActiveIngredient Value Set ID 1.3.6.1.4.1.12559.11.10.1.3.1.42.24 TRANSLATIONS Code System ID Code System Version Concept Code Description (FSN) 2.16.840.1.113883.6.73 2017-01 A ALIMENTARY TRACT AND METABOLISM 2.16.840.1.113883.6.73 2017-01
    [Show full text]
  • Pharmacotherapies for Obesity: Past, Current, and Future Therapies
    Hindawi Publishing Corporation Journal of Obesity Volume 2011, Article ID 179674, 18 pages doi:10.1155/2011/179674 Review Article Pharmacotherapies for Obesity: Past, Current, and Future Therapies Lisa L. Ioannides-Demos, Loretta Piccenna, and John J. McNeil Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Alfred Centre, Commercial Road, Melbourne, VIC 3004, Australia Correspondence should be addressed to Lisa L. Ioannides-Demos, [email protected] Received 4 August 2010; Accepted 24 September 2010 Academic Editor: A. Halpern Copyright © 2011 Lisa L. Ioannides-Demos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Past therapies for the treatment of obesity have typically involved pharmacological agents usually in combination with a calorie- controlled diet. This paper reviews the efficacy and safety of pharmacotherapies for obesity focusing on drugs approved for long- term therapy (orlistat), drugs approved for short-term use (amfepramone [diethylpropion], phentermine), recently withdrawn therapies (rimonabant, sibutamine) and drugs evaluated in Phase III studies (taranabant, pramlintide, lorcaserin and tesofensine and combination therapies of topiramate plus phentermine, bupropion plus naltrexone, and bupropion plus zonisamide). No current pharmacotherapy possesses the efficacy needed to produce substantial weight loss in morbidly obese patients. Meta- analyses support a significant though modest loss in bodyweight with a mean weight difference of 4.7 kg (95% CI 4.1 to 5.3 kg) for rimonabant, 4.2 kg (95% CI 3.6 to 4.8 kg) for sibutramine and 2.9 kg (95% CI 2.5 to 3.2 kg) for orlistat compared to placebo at ≥12 months.
    [Show full text]
  • BMJ Open Is Committed to Open Peer Review. As Part of This Commitment We Make the Peer Review History of Every Article We Publish Publicly Available
    BMJ Open: first published as 10.1136/bmjopen-2018-027935 on 5 May 2019. Downloaded from BMJ Open is committed to open peer review. As part of this commitment we make the peer review history of every article we publish publicly available. When an article is published we post the peer reviewers’ comments and the authors’ responses online. We also post the versions of the paper that were used during peer review. These are the versions that the peer review comments apply to. The versions of the paper that follow are the versions that were submitted during the peer review process. They are not the versions of record or the final published versions. They should not be cited or distributed as the published version of this manuscript. BMJ Open is an open access journal and the full, final, typeset and author-corrected version of record of the manuscript is available on our site with no access controls, subscription charges or pay-per-view fees (http://bmjopen.bmj.com). If you have any questions on BMJ Open’s open peer review process please email [email protected] http://bmjopen.bmj.com/ on September 26, 2021 by guest. Protected copyright. BMJ Open BMJ Open: first published as 10.1136/bmjopen-2018-027935 on 5 May 2019. Downloaded from Treatment of stable chronic obstructive pulmonary disease: a protocol for a systematic review and evidence map Journal: BMJ Open ManuscriptFor ID peerbmjopen-2018-027935 review only Article Type: Protocol Date Submitted by the 15-Nov-2018 Author: Complete List of Authors: Dobler, Claudia; Mayo Clinic, Evidence-Based Practice Center, Robert D.
    [Show full text]
  • Anti-Obesity Drugs: a Review About Their Effects and Their Safety
    Obesidade. Drogas - segurança - efeitos adversos Anti-obesity drugs: a review about their effects and their safety. Derosa G, Maffioli P. Expert Opin Drug Saf. 2012 May;11(3):459-71. Epub 2012 Mar 23. Source University of Pavia, Fondazione IRCCS Policlinico S. Matteo, Department of Internal Medicine and Therapeutics , P.le C. Golgi, 2 - 27100 Pavia , Italy +39 0382 526217 ; +39 0382 526259 ; [email protected]. Abstract Introduction: Amphetamines, rimonabant and sibutramine licenses as anti-obesity drugs have been withdrawn because of their adverse effects. In fact, orlistat is the only available long-term treatment for obesity. Areas covered: The efficacy and safety of long-term drug therapy is very important in the management obesity; for this reason, the authors decided to conduct a review on the efficacy and safety of current, past and future pharmacotherapies for weight loss. Expert opinion: Orlistat is a good choice for the treatment of obesity, because of its safety on cardiovascular events and its positive effects on diabetic control, even if it is not as effective as rimonabant or sibutramine in reducing body weight. Regarding emerging anti-obesity therapies in diabetic people, we currently have drugs that have already been marketed including the glucagon-like peptide-1 (GLP-1) receptor agonists exenatide and liraglutide; other than improving glycemic control, they also suppress appetite reducing body weight. Moreover, some other drugs are currently in study such as tesofensine, phentermine + topiramate, bupropion + naltrexone and bupropion + zonisamide. Furthermore, several additional gut hormone-based treatments for obesity are under investigation in Phase II and III clinical trials, with particular focus on ghrelin, peptide YY, pancreatic polypeptide, amylin and oxyntomodulin.
    [Show full text]
  • Pharmacotherapy of Obesity: Limits and Perspectives
    American Journal of Cardiovascular Drugs https://doi.org/10.1007/s40256-019-00328-6 REVIEW ARTICLE Pharmacotherapy of Obesity: Limits and Perspectives Pamela Rosa‑Gonçalves1 · David Majerowicz1 © Springer Nature Switzerland AG 2019 Abstract Obesity is a severe worldwide epidemic. Obesity comorbidities, such as type 2 diabetes mellitus, hypertension, and ath‑ erosclerosis, are costly for patients and governments. The treatment of obesity involves several facets, including lifestyle changes, bariatric surgery, and pharmacotherapy. As changes in lifestyle require considerable patient commitment that is sometimes unachievable, and surgery is expensive and invasive, pharmacotherapy is the primary option for most patients. This review describes the pharmacotherapy currently available in the USA, Europe, and Brazil, focusing on its limitations. We then analyze the results from clinical trials of new drug candidates. Most drugs cause weight loss of < 4 kg compared with controls, and severe adverse efects have caused a number of drugs to be withdrawn from the market in several coun‑ tries. Drugs under development have not shown more signifcant weight loss or reduced adverse efects. We conclude that a signifcant portion of obese patients have few treatment options because of the adverse efects and minimal weight loss associated with current pharmacotherapy. However, drugs currently under development appear unable to change this scenario in the near future. Thus, it is essential that new compounds are developed and new molecular targets studied so obesity can be efciently treated in all patients in the future. Key Points 1 Introduction The adverse efects, efcacy, and cost associated with Obesity is a chronic disease with a multifactorial etiology current pharmacotherapy for obesity restricts the range that results from genetic, physiological, behavioral, environ‑ of treated patients.
    [Show full text]