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  • 1
    Online Resource
    Online Resource
    S. Karger AG ; 2005
    In:  Neuropsychobiology Vol. 52, No. 1 ( 2005), p. 11-16
    In: Neuropsychobiology, S. Karger AG, Vol. 52, No. 1 ( 2005), p. 11-16
    Abstract: The mechanisms underlying weight gain induced by psychopharmacological agents are poorly understood. Because the recently discovered enteric hormone, ghrelin, stimulates food intake, we hypothesized that increases in circulating ghrelin levels might mediate the weight gain caused by certain antidepressants and atypical antipsychotic drugs. Fifty-two patients receiving psychopharmacological treatments were included in the study: 16 patients received antidepressants that are not known to induce weight gain, and 13 patients received mirtazapine or trimipramine, which are antidepressants known to lead to weight gain; 6 patients received clozapine and olanzapine, which have the highest liability among the antipsychotics to cause weight gain, and 17 patients received other antipsychotics. Fasting venous blood samples for the measurement of ghrelin were drawn in the morning between 06:00 and 08:00 a.m. in the second week of treatment. Although psychopharmacological treatment induced significant weight changes in the expected directions (most prominent in the clozapine or olanzapine treatment group), ghrelin levels did not differ significantly between groups. Psychotropic drugs with different propensities to induce body weight gain are associated with similar concentrations of plasma ghrelin in psychiatric patients after a short period of treatment.
    Type of Medium: Online Resource
    ISSN: 0302-282X , 1423-0224
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2005
    detail.hit.zdb_id: 1483094-2
    SSG: 5,2
    SSG: 15,3
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  • 2
    In: Neuropsychobiology, S. Karger AG, Vol. 62, No. 1 ( 2010), p. 36-42
    Abstract: 〈 i 〉 Background: 〈 /i 〉 The late onset of therapeutic response and a relatively large proportion of nonresponders to antidepressants remain major concerns in clinical practice. Therefore, there is a critical need for effective medication strategies that augment treatment with antidepressants. 〈 i 〉 Methods: 〈 /i 〉 To review the available evidence on the use of lithium as an augmentation strategy to treat depressive episodes. 〈 i 〉 Results: 〈 /i 〉 More than 30 open-label studies and 10 placebo-controlled double-blind trials have demonstrated substantial efficacy of lithium augmentation in the acute treatment of depressive episodes. Most of these studies were performed in unipolar depression and included all major classes of antidepressants, however mostly tricyclics. A meta-analysis including 10 randomized placebo-controlled trials has provided evidence that lithium augmentation has a statistically significant effect on the response rate compared to placebo with an odds ratio of 3.11, which corresponds to a number-needed-to-treat of 5. The meta-analysis revealed a mean response rate of 41.2% in the lithium group and 14.4% in the placebo group. One placebo-controlled trial in the continuation treatment phase showed that responders to acute-phase lithium augmentation should be maintained on the lithium-antidepressant combination for at least 12 months to prevent early relapses. Preliminary studies to assess genetic influences on response probability to lithium augmentation have suggested a predictive role of the –50T/C single nucleotide polymorphism of the GSK3β gene. 〈 i 〉 Conclusion: 〈 /i 〉 Augmentation of antidepressants with lithium is currently the best-evidenced augmentation therapy in the treatment of depressed patients who do not respond to antidepressants.
    Type of Medium: Online Resource
    ISSN: 0302-282X , 1423-0224
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2010
    detail.hit.zdb_id: 1483094-2
    SSG: 5,2
    SSG: 15,3
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    In: Neuropsychobiology, S. Karger AG, Vol. 62, No. 1 ( 2010), p. 72-78
    Abstract: For more than half a decade, lithium has been successfully used to treat bipolar disorder. Worldwide, it is considered the first-line mood stabilizer. Apart from its proven antimanic and prophylactic effects, considerable evidence also suggests an antisuicidal effect in affective disorders. Lithium is also effectively used to augment antidepressant drugs in the treatment of refractory major depressive episodes and prevent relapses in recurrent unipolar depression. In contrast to many psychiatric drugs, lithium has outlasted various pharmacotherapeutic ‘fashions’, and remains an indispensable element in contemporary psychopharmacology. Nevertheless, data from pharmacogenetic studies of lithium are comparatively sparse, and these studies are generally characterized by small sample sizes and varying definitions of response. Here, we present an international effort to elucidate the genetic underpinnings of lithium response in bipolar disorder. Following an initiative by the International Group for the Study of Lithium-Treated Patients (www.IGSLI.org) and the Unit on the Genetic Basis of Mood and Anxiety Disorders at the National Institute of Mental Health,lithium researchers from around the world have formed the Consortium on Lithium Genetics (www.ConLiGen.org) to establish the largest sample to date for genome-wide studies of lithium response in bipolar disorder, currently comprising more than 1,200 patients characterized for response to lithium treatment. A stringent phenotype definition of response is one of the hallmarks of this collaboration. ConLiGen invites all lithium researchers to join its efforts.
    Type of Medium: Online Resource
    ISSN: 0302-282X , 1423-0224
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2010
    detail.hit.zdb_id: 1483094-2
    SSG: 5,2
    SSG: 15,3
    Library Location Call Number Volume/Issue/Year Availability
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  • 4
    In: Pharmacopsychiatry, Georg Thieme Verlag KG, Vol. 56, No. 05 ( 2023-09), p. 182-187
    Abstract: Introduction Longitudinal study is an essential methodology for understanding disease trajectories, treatment effects, symptom changes, and long-term outcomes of affective disorders. Daily self-charting of mood and other illness-related variables is a commonly recommended intervention. With the widespread acceptance of home computers in the early 2000s, automated tools were developed for patient mood charting, such as ChronoRecord, a software validated by patients with bipolar disorder. The purpose of this study was to summarize the daily mood, sleep, and medication data collected with ChronoRecord, and highlight some of the key research findings. Lessons learned from implementing a computerized tool for patient self-reporting are also discussed. Methods After a brief training session, ChronoRecord software for daily mood charting was installed on a home computer and used by 609 patients with affective disorders. Results The mean age of the patients was 40.3±11.8 years, a mean age of onset was 22±11.2 years, and 71.4% were female. Patients were euthymic for 70.8% of days, 15.1% had mild depression, 6.6% had severe depression, 6.6% had hypomania, and 0.8% had mania. Among all mood groups, 22.4% took 1–2 medications, 37.2% took 3–4 medications, 25.7 took 5–6 medications, 11.6% took 7–8 medications, and 3.1% took 〉 8 medications. Conclusion The daily mood charting tool is a useful tool for increasing patient involvement in their care, providing detailed patient data to the physician, and increasing understanding of the course of illness. Longitudinal data from patient mood charting was helpful in both clinical and research settings.
    Type of Medium: Online Resource
    ISSN: 0176-3679 , 1439-0795
    RVK:
    Language: English
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2023
    detail.hit.zdb_id: 2041961-2
    SSG: 15,3
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  • 5
    In: Neuropsychopharmacology, Springer Science and Business Media LLC
    Abstract: Patients with bipolar disorder (BD) show alterations in both gray matter volume (GMV) and white matter (WM) integrity compared with healthy controls (HC). However, it remains unclear whether the phenotypically distinct BD subtypes (BD-I and BD-II) also exhibit brain structural differences. This study investigated GMV and WM differences between HC, BD-I, and BD-II, along with clinical and genetic associations. N = 73 BD-I, n = 63 BD-II patients and n = 136 matched HC were included. Using voxel-based morphometry and tract-based spatial statistics, main effects of group in GMV and fractional anisotropy (FA) were analyzed. Associations between clinical and genetic features and GMV or FA were calculated using regression models. For FA but not GMV, we found significant differences between groups. BD-I patients showed lower FA compared with BD-II patients ( p tfce-FWE = 0.006), primarily in the anterior corpus callosum. Compared with HC, BD-I patients exhibited lower FA in widespread clusters ( p tfce-FWE 〈 0.001), including almost all major projection, association, and commissural fiber tracts. BD-II patients also demonstrated lower FA compared with HC, although less pronounced ( p tfce-FWE = 0.049). The results remained unchanged after controlling for clinical and genetic features, for which no independent associations with FA or GMV emerged. Our findings suggest that, at a neurobiological level, BD subtypes may reflect distinct degrees of disease expression, with increasing WM microstructure disruption from BD-II to BD-I. This differential magnitude of microstructural alterations was not clearly linked to clinical and genetic variables. These findings should be considered when discussing the classification of BD subtypes within the spectrum of affective disorders.
    Type of Medium: Online Resource
    ISSN: 0893-133X , 1740-634X
    RVK:
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2024
    detail.hit.zdb_id: 2008300-2
    SSG: 15,3
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