Havemann-Reinecke, Ursula

[["dc.bibliographiccitation.firstpage","133"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","138"],["dc.bibliographiccitation.volume","261"],["dc.contributor.author","Wedekind, Dirk"],["dc.contributor.author","Neumann, Karolin"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Engel, Kirsten Rita"],["dc.contributor.author","Jamrozinski, Katja"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.date.accessioned","2018-11-07T08:58:43Z"],["dc.date.available","2018-11-07T08:58:43Z"],["dc.date.issued","2011"],["dc.description.abstract","Elevations of serum homocysteine levels are a consistent finding in alcohol addiction. Serum S100B levels are altered in different neuropsychiatric disorders but not well investigated in alcohol withdrawal syndromes. Because of the close connection of S100B to ACTH and glutamate secretion that both are involved in neurodegeneration and symptoms of alcoholism the relationship of S100B and homocysteine to acute withdrawal variables has been examined. A total of 22 male and 9 female inpatients (mean age 46.9 +/- A 9.7 years) with an ICD-10 diagnosis of alcohol addiction without relevant affective comorbidity were examined on admission and after 24, 48, and 120 h during withdrawal. S100B and homocysteine levels in serum were collected, and severity of withdrawal symptoms (AWS-scale), applied withdrawal medication, initial serum ethanol levels and duration of addiction were recorded. Serum S100B and homocysteine levels declined significantly (P < .05) over time. Both levels declined with withdrawal syndrome severity. Females showed a trend to a more intense decline in serum S100B levels compared to males at day 5 (P = .06). Homocysteine levels displayed a negative relationship to applied amount of clomethiazole (P < .05) and correlated with age of onset of addiction. No withdrawal seizures were recorded during the trial. As it is known for homocysteine, S100B revealed to decline rapidly over withdrawal treatment in alcoholism. This effect is more pronounced in female patients. S100B could be of relevance in the neurobiology of alcohol withdrawal syndromes. It may be indirectly related to the level of stress level or glutamatergic activity during alcohol withdrawal."],["dc.identifier.doi","10.1007/s00406-010-0121-2"],["dc.identifier.isi","000287859300007"],["dc.identifier.pmid","20593192"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6616"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23711"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0940-1334"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","S100B and homocysteine in the acute alcohol withdrawal syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","German Journal of Psychiatry"],["dc.bibliographiccitation.lastpage","7"],["dc.contributor.author","Wedekind, Dirk"],["dc.contributor.author","Jacobs, Stefan"],["dc.contributor.author","Poser, Wolfgang"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Schneider, Udo"],["dc.contributor.author","Cimander, Konrad"],["dc.contributor.author","Engel, Kirsten"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.date.accessioned","2019-07-10T08:13:27Z"],["dc.date.available","2019-07-10T08:13:27Z"],["dc.date.issued","2009"],["dc.description.abstract","Objective: Previous reports on heroin and cocaine addicts showed drug-related and gender differences in psychiatric comorbidity, which has relevant consequences for treatment. However, studies vary substantially with respect to methods and timeframes. Studies on German patient groups are scarce. Methods: Data on psychiatric and somatic comorbidity, substance addiction history, present intake patterns and sociodemography were obtained from 43 female (n=11) and male (n=32) heroin and cocaine addicts in acute inpatient detoxification treatment or specified long-term treatment. A European Addiction-Severity-Index (EuropASI) based centre questionnaire and the Mini-DIPS were applied. Results: Treatment groups did not differ in psychiatric comorbidity. Female subjects, however, had a significantly higher prevalence of psychiatric comorbid diagnoses (p<.05), mostly anxiety and affective disorders which significantly correlated with low occupational status (p<.05).Patients in long-term treatment abused more other substances and had an earlier onset of regular substance abuse (in particular alcohol and cannabis) (p<.05). Conclusion: Heroin and cocaine addicted females are more likely than males to have affective and anxiety disorders. Long-term treatment attenders appear to be more severely addicted (earlier onset and additional abuse) than acute treatment patients but do not differ in comorbidity. However, no axis-II diagnoses were recorded and the sample-size was small. Results should be regarded as preliminary (German J Psychiatry 2009; 12: 1-7)."],["dc.identifier.fs","541930"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5950"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61249"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1455-1033"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Psychiatric Comorbidity and Gender Effects in Heroin and Cocaine-Addicted Patients in Specified Long-Term Treatment and Acute Inpatient Detoxification Treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1778"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Addiction Biology"],["dc.bibliographiccitation.lastpage","1789"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Tomas-Roig, J"],["dc.contributor.author","Benito, E"],["dc.contributor.author","Agis-Balboa, RC"],["dc.contributor.author","Piscitelli, F"],["dc.contributor.author","Hoyer-Fender, S"],["dc.contributor.author","Di Marzo, V"],["dc.contributor.author","Havemann-Reinecke, U"],["dc.date.accessioned","2020-12-10T18:26:44Z"],["dc.date.available","2020-12-10T18:26:44Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1111/adb.12446"],["dc.identifier.issn","1355-6215"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16889"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76165"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Chronic exposure to cannabinoids during adolescence causes long-lasting behavioral deficits in adult mice"],["dc.title.alternative","Long-lasting WIN55212.2 effect"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","91"],["dc.bibliographiccitation.journal","BMC Psychiatry"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Gerchen, Martin Fungisai"],["dc.contributor.author","Ackermann, Verena"],["dc.contributor.author","Tarami, Asieh"],["dc.contributor.author","Treitz, Annika"],["dc.contributor.author","Flögel, Marlene"],["dc.contributor.author","Adler, Lothar"],["dc.contributor.author","Aldenhoff, Josef B."],["dc.contributor.author","Becker-Emner, Marianne"],["dc.contributor.author","Becker, Thomas"],["dc.contributor.author","Czernik, Adelheid"],["dc.contributor.author","Dose, Matthias"],["dc.contributor.author","Folkerts, Here"],["dc.contributor.author","Freese, Roland"],["dc.contributor.author","Guenther, Rolf"],["dc.contributor.author","Herpertz, Sabine"],["dc.contributor.author","Hesse, Dirk"],["dc.contributor.author","Kruse, Gunther"],["dc.contributor.author","Kunze, Heinrich"],["dc.contributor.author","Franz, Michael"],["dc.contributor.author","Lohrer, Frank"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Mielke, Andreas"],["dc.contributor.author","Müller-Isberner, Rüdiger"],["dc.contributor.author","Oestereich, Cornelia"],["dc.contributor.author","Pajonk, Frank-Gerald"],["dc.contributor.author","Pollmächer, Thomas"],["dc.contributor.author","Schneider, Udo"],["dc.contributor.author","Schwarz, Hans-Joachim"],["dc.contributor.author","Kröner-Herwig, Birgit"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:37Z"],["dc.date.available","2017-09-07T11:46:37Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Schizophrenia is the collective term for an exclusively clinically diagnosed, heterogeneous group of mental disorders with still obscure biological roots. Based on the assumption that valuable information about relevant genetic and environmental disease mechanisms can be obtained by association studies on patient cohorts of ≥ 1000 patients, if performed on detailed clinical datasets and quantifiable biological readouts, we generated a new schizophrenia data base, the GRAS (Göttingen Research Association for Schizophrenia) data collection. GRAS is the necessary ground to study genetic causes of the schizophrenic phenotype in a 'phenotype-based genetic association study' (PGAS). This approach is different from and complementary to the genome-wide association studies (GWAS) on schizophrenia. Methods: For this purpose, 1085 patients were recruited between 2005 and 2010 by an invariable team of traveling investigators in a cross-sectional field study that comprised 23 German psychiatric hospitals. Additionally, chart records and discharge letters of all patients were collected. Results: The corresponding dataset extracted and presented in form of an overview here, comprises biographic information, disease history, medication including side effects, and results of comprehensive cross-sectional psychopathological, neuropsychological, and neurological examinations. With >3000 data points per schizophrenic subject, this data base of living patients, who are also accessible for follow-up studies, provides a wide-ranging and standardized phenotype characterization of as yet unprecedented detail. Conclusions: The GRAS data base will serve as prerequisite for PGAS, a novel approach to better understanding 'the schizophrenias' through exploring the contribution of genetic variation to the schizophrenic phenotypes."],["dc.format.extent","20"],["dc.identifier.doi","10.1186/1471-244X-10-91"],["dc.identifier.gro","3150558"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5803"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7333"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The cross-sectional GRAS sample: a comprehensive phenotypical data collection of schizophrenic patients"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","387"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","CNS Neuroscience & Therapeutics"],["dc.bibliographiccitation.lastpage","395"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Tomas-Roig, Jordi"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Salinas-Riester, Gabriela"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.date.accessioned","2018-11-07T10:15:14Z"],["dc.date.available","2018-11-07T10:15:14Z"],["dc.date.issued","2016"],["dc.description.abstract","Aim and methodsDifferent types of insults to the CNS lead to axon demyelination. Remyelination occurs when the CNS attempts to recover from myelin loss and requires the activation of oligodendrocyte precursor cells. With the rationale that CB1 receptor is expressed in oligodendrocytes and marijuana consumption alters CNS myelination, we study the effects of the cannabinoid agonist WIN55212.2 in (1) an invitro model of oligodendrocyte differentiation and (2) the cuprizone model for demyelination. ResultsThe synthetic cannabinoid agonist WIN55212.2 at 1M increased the myelin basic protein mRNA and protein expression invitro. During cuprizone-induced acute demyelination, the administration of 0.5mg/kg WIN55212.2 confers more myelinated axons, increased the expression of retinoid X receptor alpha, and declined nogo receptor expression. Controversially, 1mg/kg of the drug increased the number of demyelinated axons and reduced the expression of nerve growth factor inducible, calreticulin and myelin-related genes coupling specifically with a decrease in 2,3-cyclic nucleotide 3 phosphodiesterase expression. ConclusionThe cannabinoid agonist WIN55212.2 promotes oligodendrocyte differentiation invitro. Moreover, 0.5mg/kg of the drug confers neuroprotection during cuprizone-induced demyelination, while 1mg/kg aggravates the demyelination process."],["dc.description.sponsorship","DFG CNMPB [CNMPB C1-6]; Northern German Addiction Research Federation"],["dc.identifier.doi","10.1111/cns.12506"],["dc.identifier.isi","000374377600007"],["dc.identifier.pmid","26842941"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13413"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40770"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley"],["dc.relation.issn","1755-5949"],["dc.relation.issn","1755-5930"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","The Cannabinoid CB1/CB2 Agonist WIN55212.2 Promotes Oligodendrocyte Differentiation In Vitro and Neuroprotection During the Cuprizone-Induced Central Nervous System Demyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1"],["dc.bibliographiccitation.journal","Substance Abuse Treatment Prevention and Policy"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Wedekind, Dirk"],["dc.contributor.author","Bandelow, Borwin"],["dc.contributor.author","Heitmann, Soren"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.contributor.author","Engel, Kirsten-Rita"],["dc.contributor.author","Huether, Gerald"],["dc.date.accessioned","2018-11-07T09:29:13Z"],["dc.date.available","2018-11-07T09:29:13Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Insecure early attachment experiences have been reported to play an important role in the manifestation in alcoholism. The purpose of this study was to investigate the relationship of attachment styles with anxiety, anxiety coping and dysfunctional personality styles, as well as with the prevalence of personality disorders, and adverse life-events in adolescence. Methods: 59 inpatient alcohol addicted male (n=43) and female (n=16) patients were characterized by an attachment style scale (Relationships-style-questionnaire-RSQ) and completed a questionnaire battery comprising the State-Trait-Anxiety-Inventory (STAI), the Anxiety-Coping-Inventory (ABI), Temperament-and-character-inventory (TCI), Personality-system-interaction-inventory (PSI), and gave information on sociodemography, alcohol history, and adolescent adverse events. A structured interview (SKID-II) was performed to diagnose personality disorders. Results: Only 33% of subjects had a secure attachment style. Insecure attachment was associated with significantly higher trait-anxiety, higher cognitive avoidance to control anxiety, and higher values on most personality style dimensions directed to the pathological pole. Conclusions: Despite the limitation due to a small sample size, the results of this study show that the consideration of attachment styles is of significance in the diagnosis and therapy of alcohol addiction. Attachment may characterize different styles to control emotional aspects, anxiety cues and interpersonal relationships in individuals suffering from alcohol addiction."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2013"],["dc.identifier.doi","10.1186/1747-597X-8-1"],["dc.identifier.isi","000317649000001"],["dc.identifier.pmid","23302491"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8903"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30968"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1747-597X"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Attachment style, anxiety coping, and personality-styles in withdrawn alcohol addicted inpatients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Tomas-Roig, J."],["dc.contributor.author","Agbemenyah, H. Y."],["dc.contributor.author","Celarain, N."],["dc.contributor.author","Quintana, E."],["dc.contributor.author","Ramió-Torrentà, Ll."],["dc.contributor.author","Havemann-Reinecke, U."],["dc.date.accessioned","2021-04-14T08:27:36Z"],["dc.date.available","2021-04-14T08:27:36Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41598-019-57290-1"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17128"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82344"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Dose-dependent effect of cannabinoid WIN-55,212-2 on myelin repair following a demyelinating insult"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","972141"],["dc.bibliographiccitation.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Eichentopf, Luzie; 1Department of Molecular Neuroimaging, Medical Faculty Mannheim, Central Institute of Mental Health, Heidelberg University, Mannheim, Germany"],["dc.contributor.affiliation","Hiemke, Christoph; 2Department of Psychiatry and Psychotherapy, Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center of Mainz, Mainz, Germany"],["dc.contributor.affiliation","Conca, Andreas; 3Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP)-Work Group “Therapeutic Drug Monitoring”, Nürnberg, Germany"],["dc.contributor.affiliation","Engelmann, Jan; 5Department of Psychiatry and Psychotherapy, Johannes Gutenberg University Medical Center Mainz, Mainz, Germany"],["dc.contributor.affiliation","Gerlach, Manfred; 3Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP)-Work Group “Therapeutic Drug Monitoring”, Nürnberg, Germany"],["dc.contributor.affiliation","Havemann-Reinecke, Ursula; 3Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP)-Work Group “Therapeutic Drug Monitoring”, Nürnberg, Germany"],["dc.contributor.affiliation","Hefner, Gudrun; 3Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP)-Work Group “Therapeutic Drug Monitoring”, Nürnberg, Germany"],["dc.contributor.affiliation","Florio, Vincenzo; 9Department of Psychiatry, Comprensorio Sanitario di Bolzano, Bolzano, Italy"],["dc.contributor.affiliation","Kuzin, Maxim; 3Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP)-Work Group “Therapeutic Drug Monitoring”, Nürnberg, Germany"],["dc.contributor.affiliation","Lieb, Klaus; 11Department of Psychiatry and Psychotherapy, University Medical Center Mainz, Mainz, Germany"],["dc.contributor.affiliation","Reis, Margareta; 12Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden"],["dc.contributor.affiliation","Riemer, Thomas G.; 14Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institute of Clinical Pharmacology and Toxicology, Berlin, Germany"],["dc.contributor.affiliation","Serretti, Alessandro; 15Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy"],["dc.contributor.affiliation","Schoretsanitis, Georgios; 3Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP)-Work Group “Therapeutic Drug Monitoring”, Nürnberg, Germany"],["dc.contributor.affiliation","Zernig, Gerald; 3Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP)-Work Group “Therapeutic Drug Monitoring”, Nürnberg, Germany"],["dc.contributor.affiliation","Gründer, Gerhard; 1Department of Molecular Neuroimaging, Medical Faculty Mannheim, Central Institute of Mental Health, Heidelberg University, Mannheim, Germany"],["dc.contributor.affiliation","Hart, Xenia M.; 1Department of Molecular Neuroimaging, Medical Faculty Mannheim, Central Institute of Mental Health, Heidelberg University, Mannheim, Germany"],["dc.contributor.author","Eichentopf, Luzie"],["dc.contributor.author","Hiemke, Christoph"],["dc.contributor.author","Conca, Andreas"],["dc.contributor.author","Engelmann, Jan"],["dc.contributor.author","Gerlach, Manfred"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.contributor.author","Hefner, Gudrun"],["dc.contributor.author","Florio, Vincenzo"],["dc.contributor.author","Kuzin, Maxim"],["dc.contributor.author","Lieb, Klaus"],["dc.contributor.author","Hart, Xenia M."],["dc.date.accessioned","2022-12-01T08:31:36Z"],["dc.date.available","2022-12-01T08:31:36Z"],["dc.date.issued","2022-10-17"],["dc.date.updated","2022-11-11T13:12:31Z"],["dc.description.abstract","Introduction\r\n A titration within a certain therapeutic reference range presupposes a relationship between the blood concentration and the therapeutic effect of a drug. However, this has not been systematically investigated for escitalopram. Furthermore, the recommended reference range disagrees with mean steady state concentrations (11–21 ng/ml) that are expected under the approved dose range (10–20 mg/day). This work systematically investigated the relationships between escitalopram dose, blood levels, clinical effects, and serotonin transporter occupancy.\r\n \r\n \r\n Methods\r\n Following our previously published methodology, relevant articles were systematically searched and reviewed for escitalopram.\r\n \r\n \r\n Results\r\n Of 1,032 articles screened, a total of 30 studies met the eligibility criteria. The included studies investigated escitalopram blood levels in relationship to clinical effects (9 studies) or moderating factors on escitalopram metabolism (12 studies) or serotonin transporter occupancy (9 studies). Overall, the evidence for an escitalopram concentration/effect relationship is low (level C).\r\n \r\n \r\n Conclusion\r\n Based on our findings, we propose a target range of 20–40 ng/ml for antidepressant efficacy of escitalopram. In maintenance treatment, therapeutic response is expected, when titrating patients above the lower limit. The lower concentration threshold is strongly supported by findings from neuroimaging studies. The upper limit for escitalopram’s reference range rather reflects a therapeutic maximum than a tolerability threshold, since the incidence of side effects in general is low. Concentrations above 40 ng/ml should not necessarily result in dose reductions in case of good clinical efficacy and tolerability. Dose-related escitalopram concentrations in different trials were more than twice the expected concentrations from guideline reports.\r\n \r\n \r\n Systematic review registration\r\n \r\n [\r\n https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=215873\r\n ], identifier [CRD42020215873]."],["dc.identifier.doi","10.3389/fpsyt.2022.972141"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118213"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1664-0640"],["dc.relation.isreplacedby","hdl:2/118213"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Systematic review and meta-analysis on the therapeutic reference range for escitalopram: Blood concentrations, clinical effects and serotonin transporter occupancy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]