Publications by authors named "Thomas C Baghai"

80 Publications

Mental Health-Related Risk Factors and Interventions in Patients with Heart Failure. A Position Paper endorsed by the European Association of Preventive Cardiology (EAPC).

Eur J Prev Cardiol 2022 Feb 1. Epub 2022 Feb 1.

Department of Medical and Clinical Psychology, Center of Research on Psychology in Somatic diseases (CoRPS), Tilburg University, Tilburg, the Netherlands.

The prevalence and public health burden of chronic heart failure (CHF) in Europe is steadily increasing mainly caused by the ageing population and prolonged survival of CHF patients. Frequent hospitalizations, high morbidity and mortality rates, and enormous healthcare costs contribute to the health related burden. However, multidisciplinary frameworks that emphasize effective long-term management and the psychological needs of the patients are sparse. The present position paper endorsed by the European Association of Preventive Cardiology (EAPC) provides a comprehensive overview on the scientific evidence of psychosocial aspects of heart failure (HF). In order to synthesize newly available information and reinforce best medical practice, information was gathered via literature reviews and consultations of experts. It covers the evidence for aetiological and prospective psychosocial risk factors and major underlying psycho-biological mechanisms. The paper elucidates the need to include psycho social aspects in self-care concepts and critically resumes the current shortcomings of psychotherapeutic and psycho-pharmacological interventions. It also highlights the need for involvement of psychological support in device therapy for HF patients and finally calls for more, earlier and better palliative interventions in the final stage of HF progression.
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http://dx.doi.org/10.1093/eurjpc/zwac006DOI Listing
February 2022

SARS-CoV-2 Risk Management in Clinical Psychiatry: A Few Considerations on How to Deal With an Unrivaled Threat.

Front Psychiatry 2020 11;11:550. Epub 2020 Jun 11.

Department of Psychiatry and Psychotherapy, Bezirksklinikum, University of Regensburg, Regensburg, Germany.

The pandemic spread of the corona virus SARS-CoV-2 has even-handedly shattered national and international health systems and economies almost in an instant. As numbers of infections and COVID-19-related deaths rise from day to day, fears and uncertainties on how to deal with this unknown threat are extremely present both for individuals and societies as a whole. In this manuscript, we aim to exemplarily describe the bullet points concerning (a) the internal risk management, (b) the organizational and structural changes, and (c) the communicational strategies applied in a Psychiatric University Hospital in the Southern part of Germany. The authors are well aware about the fact that almost none of these considerations may be considered as evidence-based at the moment. However, the authors trust that these reflections and experiences may be useful as an orientation for similar risk constellations in other afflicted countries due to the temporal delay of the pandemic course.
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http://dx.doi.org/10.3389/fpsyt.2020.00550DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7300317PMC
June 2020

Major Depressive Disorder is Associated with Impaired Mitochondrial Function in Skin Fibroblasts.

Cells 2020 04 4;9(4). Epub 2020 Apr 4.

Department of Psychiatry and Psychotherapy, University of Regensburg, 93053 Regensburg, Germany.

Mitochondrial malfunction is supposed to be involved in the etiology and pathology of major depressive disorder (MDD). Here, we aimed to identify and characterize the molecular pathomechanisms related to mitochondrial dysfunction in adult human skin fibroblasts, which were derived from MDD patients or non-depressive control subjects. We found that MDD fibroblasts showed significantly impaired mitochondrial functioning: basal and maximal respiration, spare respiratory capacity, non-mitochondrial respiration and adenosine triphosphate (ATP)-related oxygen consumption was lower. Moreover, MDD fibroblasts harbor lower ATP levels and showed hyperpolarized mitochondrial membrane potential. To investigate cellular resilience, we challenged both groups of fibroblasts with hormonal (dexamethasone) or metabolic (galactose) stress for one week, and found that both stressors increased oxygen consumption but lowered ATP content in MDD as well as in non-depressive control fibroblasts. Interestingly, the bioenergetic differences between fibroblasts from MDD or non-depressed subjects, which were observed under non-treated conditions, could not be detected after stress. Our findings support the hypothesis that altered mitochondrial function causes a bioenergetic imbalance, which is associated with the molecular pathophysiology of MDD. The observed alterations in the oxidative phosphorylation system (OXPHOS) and other mitochondria-related properties represent a basis for further investigations of pathophysiological mechanisms and might open new ways to gain insight into antidepressant signaling pathways.
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http://dx.doi.org/10.3390/cells9040884DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7226727PMC
April 2020

The cytokine IL-17A as a marker of treatment resistance in major depressive disorder?

Eur J Neurosci 2021 01 19;53(1):172-182. Epub 2019 Dec 19.

Department of Psychiatry and Psychotherapy, University of Regensburg, Regensburg, Germany.

Major depression is a complex disease and-among others, inflammation appears to play an important role in its pathophysiology. In this study, we investigated a broad range of cytokines in depressed patients. Plasma levels of interleukin (IL)-12/ IL-23p40, IL-15, IL-16, IL-17A, IL-1α, IL-7, tumor necrosis factorβ and vascular endothelial growth factor were compared in 48 patients suffering from major depression before, after one and after six weeks of antidepressive treatment in relation to therapy response. Interestingly, the level of IL-17A turned out to rise significantly in the non-responder group compared to responder during antidepressive treatment. IL-17A is a pro-inflammatory cytokine that initiates the production of other cytokines, thereby inducing and mediating immune response. It is also involved in allergic and autoimmune-related diseases. The database investigating the role of IL-17A in major depressive disorder has grown within the last few years comparing levels of this cytokine in depressed patients versus healthy subjects. However, little is known about the expression of IL-17A during the course of antidepressive treatment. In summary, our study provides valuable evidence that this cytokine might serve as a marker of therapy resistance to antidepressants.
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http://dx.doi.org/10.1111/ejn.14636DOI Listing
January 2021

Minocycline alters behavior, microglia and the gut microbiome in a trait-anxiety-dependent manner.

Transl Psychiatry 2019 09 13;9(1):223. Epub 2019 Sep 13.

University of Regensburg, Department of Behavioural and Molecular Neurobiology, Regensburg Center of Neuroscience, Regensburg, Germany.

Major depressive disorder is the main cause of disability worldwide with imperfect treatment options. However, novel therapeutic approaches are currently discussed, from augmentation strategies to novel treatments targeting the immune system or the microbiome-gut-brain axis. Therefore, we examined the potential beneficial effects of minocycline, a tetracycline antibiotic with pleiotropic, immunomodulatory action, alone or as augmentation of escitalopram on behavior, prefrontal microglial density, and the gut microbiome in rats selectively bred for high anxiety-like behavior (HAB). We show that concomitant with their high innate anxiety and depression, HABs have lower microglial numbers in the infralimbic and prelimbic prefrontal cortex and an altered gut microbiota composition compared with controls. Three weeks of minocycline treatment alleviated the depressive-like phenotype, further reduced microglial density, exclusively in male HAB rats, and reduced plasma concentrations of pro-inflammatory cytokines. However, coadministration of escitalopram, which had no effect alone, prevented these minocycline-induced effects. Moreover, minocycline led to a robust shift in cecal microbial composition in both HABs and rats non-selected for anxiety-like behavior. Minocycline markedly increased relative abundance of Lachnospiraceae and Clostridiales Family XIII, families known for their butyrate production, with a corresponding increase and positive correlation in plasma 3-OH-butyrate levels in a trait-dependent manner. Thus, our data suggest that the antidepressant effect of minocycline is sex- and trait-dependent, associated with a reduced microglial number in the prefrontal cortex, and with changes in microbial composition and their metabolites. These results further support the microbiome-gut-brain axis as potential target in the treatment of depression.
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http://dx.doi.org/10.1038/s41398-019-0556-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6744405PMC
September 2019

Classical Risk Factors and Inflammatory Biomarkers: One of the Missing Biological Links between Cardiovascular Disease and Major Depressive Disorder.

Int J Mol Sci 2018 06 12;19(6). Epub 2018 Jun 12.

Department of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Nußbaumstraße 7, D-80336 Munich, Germany.

Background: Cardiovascular disorders (CVD) and major depressive disorder (MDD) are the most frequent diseases worldwide responsible for premature death and disability. Behavioral and immunological variables influence the pathophysiology of both disorders. We therefore determined frequency and severity of MDD in CVD and studied whether MDD without CVD or other somatic diseases influences classical and inflammatory biomarkers of cardiovascular risk. In addition, we investigated the influence of proinflammatory cytokines on antidepressant treatment outcome.

Methods: In a case-control design, 310 adults (MDD patients without CVD, CVD patients, and cardiologically and psychiatrically healthy matched controls) were investigated. MDD patients were recruited after admission in a psychiatric university hospital. Primary outcome criteria were clinical depression ratings (HAM-D scale), vital signs, classical cardiovascular risk factors and inflammatory biomarkers which were compared between MDD patients and healthy controls.

Results: We detected an enhanced cardiovascular risk in MDD. Untreated prehypertension and signs directing to a metabolic syndrome were detected in MDD. Significantly higher inflammatory biomarkers such as the high sensitivity C-reaktive protein (hsCRP) and proinflammatory acute phase cytokines interleukine-1β (IL-1β) and interleukine-6 (IL-6) underlined the higher cardiovascular risk in physically healthy MDD patients. Surprisingly, high inflammation markers before treatment were associated with better clinical outcome and faster remission. The rate of MDD in CVD patients was high.

Conclusions: Patients suffering from MDD are at specific risk for CVD. Precise detection of cardiovascular risks in MDD beyond classical risk factors is warranted to allow effective prophylaxis and treatment of both conditions. Future studies of prophylactic interventions may help to provide a basis for prophylactic treatment of both MDD and CVD. In addition, the high risk for MDD in CVD patients was confirmed and underlines the requirement for clinical attention.
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http://dx.doi.org/10.3390/ijms19061740DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6032328PMC
June 2018

A standardized stepwise drug treatment algorithm for depression reduces direct treatment costs in depressed inpatients - Results from the German Algorithm Project (GAP3).

J Affect Disord 2018 03 13;228:173-177. Epub 2017 Nov 13.

Charité - Universitätsmedizin Berlin, Department of Psychiatry and Psychotherapy, Campus Charité Mitte, Berlin, Germany; Fliedner Klinik Berlin, Center for Psychiatry, Psychotherapy and Psychosomatic Medicine, Berlin, Germany.

Background: In a previous single center study we found that a standardized drug treatment algorithm (ALGO) was more cost effective than treatment as usual (TAU) for inpatients with major depression. This report aimed to determine whether this promising initial finding could be replicated in a multicenter study.

Methods: Treatment costs were calculated for two time periods: the study period (from enrolment to exit from study) and time in hospital (from enrolment to hospital discharge) based on daily hospital charges. Cost per remitted patient during the study period was considered as primary outcome.

Results: 266 patients received ALGO and 84 received TAU. For the study period, ALGO costs were significantly lower than TAU (ALGO: 7 848 ± 6 065 €; TAU: 10 033 ± 7 696 €; p = 0.04). For time in hospital, costs were not different (ALGO: 14 734 ± 8 329 €; TAU: 14 244 ± 8 419 €; p = 0.617). Remission rates did not differ for the study period (ALGO: 57.9%, TAU: 50.0%; p=0.201). Remission rates were greater in ALGO (83.3%) than TAU (66.2%) for time in hospital (p = 0.002). Cost per remission was lower in ALGO (13 554 ± 10 476 €) than TAU (20 066 ± 15 391 €) for the study period (p < 0.001) and for time in hospital (ALGO: 17 582 ± 9 939 €; TAU: 21 516 ± 12 718 €; p = 0.036).

Limitations: Indirect costs were not assessed. Different dropout rates in TAU and ALGO complicated interpretation.

Conclusions: Treatment algorithms enhance the cost effectiveness of the care of depressed inpatients, which replicates our prior results in an independent sample.
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http://dx.doi.org/10.1016/j.jad.2017.11.051DOI Listing
March 2018

Macrophage-Derived Chemokine: A Putative Marker of Pharmacological Therapy Response in Major Depression?

Neuroimmunomodulation 2017 13;24(2):106-112. Epub 2017 Sep 13.

Department of Psychiatry and Psychotherapy, University of Regensburg, Regensburg, Germany.

Introduction: Inflammatory processes play an important and complex role in the pathophysiology of major depressive disorder (MDD), but, so far, no specific investigation of chemokines exists.

Methods: In this study, we investigated the changes of plasma chemokine levels (eotaxin-1, eotaxin-3, IP-10, MCP-1, MCP-4, MDC, MIP-1α, MIP-1β, and TARC) in 47 MDD patients before (PRE) and after 1 and 6 weeks of pharmacological treatment (POST1 and POST6) in relation to the response to antidepressive therapy. We hypothesized that the direction of alterations in levels of chemokines would significantly differ between the 2 groups, responders and nonresponders.

Results: Among the investigated chemokines, only the level of macrophage-derived chemokine (MDC) changed significantly in relation to therapy response. MDC levels were significantly elevated in the responder group at POST6.

Discussion: MDC is a constitutively expressed chemokine involved in the pathophysiology of infectious and neoplastic diseases. This is the first study providing valuable hints that MDC might serve as a marker of pharmacological therapy response in MDD.
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http://dx.doi.org/10.1159/000479739DOI Listing
June 2018

"I Am I and My Bacterial Circumstances": Linking Gut Microbiome, Neurodevelopment, and Depression.

Front Psychiatry 2017 22;8:153. Epub 2017 Aug 22.

Department of Psychiatry and Psychotherapy, University of Regensburg, Regensburg, Germany.

Recently, there has been renewed interest in the role played by microbiome in both human health and human disease. A correct equilibrium between the human host and their microorganisms is important for an appropriate physiological function. Extensive research has shown that microbes that inhabit the gastrointestinal tract-or gut microbiota-are involved not only in both nutritive and digestive activities but also in immunological processes. Moreover, the gut microbiome influences both central nervous system and energy homeostasis. An altered gut microbiome has been associated with the pathophysiology of different diseases, including neuropsychiatric disorders. Apparently, both environmental-diet, exposition to antibiotics, and infections-and host-genetic factors have a strong influence on gut microbiome, modulating the risk for neuropsychiatric illness. Also, early life disruption of the microbiome-gut-brain (MGB) axis has been associated with an increased risk of developing depression later in life, suggesting a link between gut microbiome, neurodevelopment, and depression. This review aims to contribute to this growing area of research by exploring the role played by the gut microbiome in neurodevelopment and in the etiology of the depressive syndrome, including nutritional, immunological, and energy homeostasis approaches.
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http://dx.doi.org/10.3389/fpsyt.2017.00153DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5572414PMC
August 2017

How Effective Is Algorithm-Guided Treatment for Depressed Inpatients? Results from the Randomized Controlled Multicenter German Algorithm Project 3 Trial.

Int J Neuropsychopharmacol 2017 09;20(9):721-730

Charité - Universitätsmedizin Berlin, Department of Psychiatry and Psychotherapy, Campus Charité Mitte, Berlin, Germany; Universität Regensburg, Department of Psychiatry and Psychotherapy, Regensburg, Germany; East London NHS Foundation Trust, City and Hackney Centre for Mental Health, Donald Winnicott Centre, London, United Kingdom; kbo-Lech-Mangfall-Klinik Garmisch-Partenkirchen, Department of Psychiatry and Psychotherapy, Garmisch-Partenkirchen, Germany; Ludwig-Maximilians-Universität, Department of Psychiatry and Psychotherapy, München, Germany; kbo-Isar-Amper-Klinikum, Department of Psychiatry and Psychotherapy, München, Germany; Heinrich-Heine-Universität Düsseldorf, Department of Psychiatry and Psychotherapy, Düsseldorf, Germany; Institut für Psychologische Medizin, Haag, Germany; St. Joseph-Krankenhaus, Department of Psychiatry and Psychotherapy, Berlin, Germany; LWL-Klinikum Gütersloh, Department of Psychiatry and Psychotherapy, Gütersloh, Germany; Universitätsklinikum Carl Gustav Carus, Department of Psychiatry and Psychotherapy, Technische Universität Dresden, Dresden, Germany; Jena University Hospital, Department of Medical Statistics, Informatics and Documentation, Friedrich-Schiller-Universität Jena, Jena, Germany; Fliedner Klinik Berlin, Center for Psychiatry, Psychotherapy and Psychosomatic Medicine.

Background: Treatment algorithms are considered as key to improve outcomes by enhancing the quality of care. This is the first randomized controlled study to evaluate the clinical effect of algorithm-guided treatment in inpatients with major depressive disorder.

Methods: Inpatients, aged 18 to 70 years with major depressive disorder from 10 German psychiatric departments were randomized to 5 different treatment arms (from 2000 to 2005), 3 of which were standardized stepwise drug treatment algorithms (ALGO). The fourth arm proposed medications and provided less specific recommendations based on a computerized documentation and expert system (CDES), the fifth arm received treatment as usual (TAU). ALGO included 3 different second-step strategies: lithium augmentation (ALGO LA), antidepressant dose-escalation (ALGO DE), and switch to a different antidepressant (ALGO SW). Time to remission (21-item Hamilton Depression Rating Scale ≤9) was the primary outcome.

Results: Time to remission was significantly shorter for ALGO DE (n=91) compared with both TAU (n=84) (HR=1.67; P=.014) and CDES (n=79) (HR=1.59; P=.031) and ALGO SW (n=89) compared with both TAU (HR=1.64; P=.018) and CDES (HR=1.56; P=.038). For both ALGO LA (n=86) and ALGO DE, fewer antidepressant medications were needed to achieve remission than for CDES or TAU (P<.001). Remission rates at discharge differed across groups; ALGO DE had the highest (89.2%) and TAU the lowest rates (66.2%).

Conclusions: A highly structured algorithm-guided treatment is associated with shorter times and fewer medication changes to achieve remission with depressed inpatients than treatment as usual or computerized medication choice guidance.
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http://dx.doi.org/10.1093/ijnp/pyx043DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5581493PMC
September 2017

Neurobiology of depression: A neurodevelopmental approach.

World J Biol Psychiatry 2018 08 3;19(5):349-359. Epub 2017 Mar 3.

a Department of Psychiatry and Psychotherapy , University of Regensburg, Regensburg, Germany.

Objectives: The main aims of this paper are to review and evaluate the neurobiology of the depressive syndrome from a neurodevelopmental perspective.

Methods: An English language literature search was performed using PubMed.

Results: Depression is a complex syndrome that involves anatomical and functional changes that have an early origin in brain development. In subjects with genetic risk for depression, early stress factors are able to mediate not only the genetic risk but also gene expression. There is evidence that endocrine and immune interactions have an important impact on monoamine function and that the altered monoamine signalling observed in the depressive syndrome has a neuro-endocrino-immunological origin early in the development.

Conclusions: Neurodevelopment is a key aspect to understand the whole neurobiology of depression.
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http://dx.doi.org/10.1080/15622975.2017.1289240DOI Listing
August 2018

The sex-dependent role of the glucocorticoid receptor in depression: variations in the NR3C1 gene are associated with major depressive disorder in women but not in men.

Eur Arch Psychiatry Clin Neurosci 2017 Mar 22;267(2):123-133. Epub 2016 Aug 22.

Department of Psychiatry and Psychotherapy, Ludwig-Maximilians-University Munich, Nussbaumstrasse 7, 80336, Munich, Germany.

Genetic variations in the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR) have been associated with maladaptive stress responses and major depressive disorder (MDD). In a case-control study design, we examined whether single nucleotide polymorphisms (SNPs) and haploid genotype (haplotype) associations of MR gene NR3C2, GR gene NR3C1 and genes of GR chaperone molecules FK506 binding protein 5 (FKBP5) and corticotrophin-releasing hormone receptor 1 (CRHR1) differed between healthy subjects (n = 634) and inpatients with major depressive disorder (n = 412). All analyses were conducted for women and men separately. After conservative correction of Type-I-error to obtain reliable p values, one SNP in the NR3C1 gene, namely rs6195, showed a significant association with the presence of a major depression (p = 0.048) in females. In contrast, NR3C2, FKBP5 and CRHR1 polymorphisms were not significantly associated with MDD. No haplotype effects could be identified. Our results support the notion of an association between variants of GR-related genes in women and the pathophysiology of depression: females suffering from MDD showed a more than three times higher frequency of the T/C polymorphism compared to controls, which thus seems to increase the vulnerability to depression in females.
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http://dx.doi.org/10.1007/s00406-016-0722-5DOI Listing
March 2017

The sex-dependent role of the glucocorticoid receptor in depression: variations in the NR3C1 gene are associated with major depressive disorder in women but not in men.

Eur Arch Psychiatry Clin Neurosci 2017 Mar 22;267(2):123-133. Epub 2016 Aug 22.

Department of Psychiatry and Psychotherapy, Ludwig-Maximilians-University Munich, Nussbaumstrasse 7, 80336, Munich, Germany.

Genetic variations in the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR) have been associated with maladaptive stress responses and major depressive disorder (MDD). In a case-control study design, we examined whether single nucleotide polymorphisms (SNPs) and haploid genotype (haplotype) associations of MR gene NR3C2, GR gene NR3C1 and genes of GR chaperone molecules FK506 binding protein 5 (FKBP5) and corticotrophin-releasing hormone receptor 1 (CRHR1) differed between healthy subjects (n = 634) and inpatients with major depressive disorder (n = 412). All analyses were conducted for women and men separately. After conservative correction of Type-I-error to obtain reliable p values, one SNP in the NR3C1 gene, namely rs6195, showed a significant association with the presence of a major depression (p = 0.048) in females. In contrast, NR3C2, FKBP5 and CRHR1 polymorphisms were not significantly associated with MDD. No haplotype effects could be identified. Our results support the notion of an association between variants of GR-related genes in women and the pathophysiology of depression: females suffering from MDD showed a more than three times higher frequency of the T/C polymorphism compared to controls, which thus seems to increase the vulnerability to depression in females.
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http://dx.doi.org/10.1007/s00406-016-0722-5DOI Listing
March 2017

Characteristics and differences in treatment outcome of inpatients with chronic vs. episodic major depressive disorders.

J Affect Disord 2015 Mar 10;173:126-33. Epub 2014 Nov 10.

Charité - Universitätsmedizin Berlin, Department of Psychiatry and Psychotherapy, Campus Charité Mitte, Berlin, Germany; Fliedner Hospital Berlin, Germany.

Background: Approximately 20-30% of patients with Major depressive disorder (MDD) develop a chronic course of their disease. Chronic depression is associated with increased health care utilisation, hospitalisation and a higher disease burden. We identified clinical correlates and differences in treatment response of chronic MDD (cMDD) patients compared with non-chronic episodic depression in a huge sample of depressive inpatients.

Methods: Data were collected from 412 inpatients who had been diagnosed with a major depressive episode (MDE; according to ICD-10) and scored 15 or higher on the 21-item Hamilton Depression Rating Scale (HRSD-21). All subjects were participants in the German Algorithm Project, phase 3 (GAP3). Patients who were diagnosed with a MDE within the last two years or longer (herein referred to as CD) were compared with non-chronic depressive patients (herein referred to as non-CD). CD and non-CD patients were assessed for the following: psychosocial characteristics, symptom reduction from hospital admission to discharge, symptom severity at discharge, remission and response rates, and pharmacological treatment during inpatient treatment. The primary outcome measure was the HRSD-21.

Results: 13.6% (n=56) of patients met the criteria for chronic depression. Compared with non-CD patients, patients with CD showed increased axis I comorbidities (74% vs. 52%, χ(2) (1)=7.31, p=.02), a higher level of depressive symptoms at baseline and discharge, increased duration of inpatient treatment (64.8 vs. 53.3 days; t=2.86, p=.03) and lower response (HRSD: 60.0% vs. 72.0%; χ(2) (1)=3.61, p<.04; BDI: 40.5% vs. 54.2%; χ(2) (1)=3.56, p=.04) and remission rates (BDI 17.9.% vs. 29.7%; χ(2) (1)=3.42, p=.05. However, both groups achieved a comparable symptom reduction during inpatient treatment. The prescribed pharmacological strategy had no significant influence on treatment outcome in patients with CD.

Conclusion: Inpatients with CD show higher symptom severity, lower response and remission rates and a longer duration of inpatient treatment, although they achieve comparable symptom reduction during treatment. These findings support the need to recognise CD and its defining characteristics as a distinct subclass of depression.
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http://dx.doi.org/10.1016/j.jad.2014.10.059DOI Listing
March 2015

The influence of Hatha yoga as an add-on treatment in major depression on hypothalamic-pituitary-adrenal-axis activity: a randomized trial.

J Psychiatr Res 2014 Jun 11;53:76-83. Epub 2014 Mar 11.

Department of Psychiatry and Psychotherapy, University Regensburg, Germany.

Objectives: The impact of Hatha yoga as add-on treatment to quetiapine fumarate extended release (QXR) or escitalopram (ESC) in depressed patients on hypothalamic-pituitary-adrenal (HPA) axis activity was assessed.

Methods: 60 inpatients suffering from major depressive disorder (MDD) according to DSM-IV were randomized for a 5 week treatment with Yoga or not (control group) and with either QXR (300 mg/day) or ESC (10 mg/day). Serial dexamethasone/corticotropin releasing hormone (DEX/CRH) tests were performed to assess HPA axis function. The Hamilton Depression Rating Scale (21-HAMD) was used weekly.

Results: A more pronounced down regulation of the HPA axis activity due to yoga could not be detected. The stepwise long term cortisol reduction was seen in both medication groups, irrespectively of yoga add-on treatment. In addition, cortisol improvers in week 1 of therapy (reduction in cortisol peak value within the DEX/CRH test) reached significant greater amelioration of depressive symptoms after 5 weeks.

Conclusions: Our results suggest that antidepressant agents down regulate HPA axis function to a greater extent than additional Hatha yoga treatment. Moreover, an early reduction of HPA system hyperactivity after one week of pharmacological treatment seems to raise the possibility of a favorable treatment response.
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http://dx.doi.org/10.1016/j.jpsychires.2014.02.022DOI Listing
June 2014

Effects of escitalopram/quetiapine combination therapy versus escitalopram monotherapy on hypothalamic-pituitary-adrenal-axis activity in relation to antidepressant effectiveness.

J Psychiatr Res 2014 May 31;52:15-20. Epub 2014 Jan 31.

Department of Psychiatry and Psychotherapy, Ludwig-Maximilians-University Munich, Nussbaumstrasse 7, 80336 Munich, Germany.

The hypothalamic-pituitary-adrenocortical (HPA) system is believed to play an important role in the pathophysiology of major depressive disorder. In this context, the atypical antipsychotic quetiapine (QUE) has been shown to inhibit HPA system activity in healthy subjects. In this study we investigated whether the putative inhibitory effects of QUE on HPA system activity may contribute to its antidepressant efficacy. We analyzed the effects of QUE as an augmentation to the selective serotonin reuptake inhibitor (SSRI) escitalopram (ESC) on HPA system activity in comparison to a monotherapy with ESC in relation to the antidepressant effectiveness. HPA axis activity (cortisol and ACTH) was measured by means of the dexamethasone/corticotropin-releasing hormone (DEX/CRH) test which was performed before (week 0) and during (week 1, week 5) antidepressant psychopharmacotherapy. The combination therapy, but not the ESC monotherapy showed significantly inhibiting effects on HPA system activity leading to stepwise down-regulation. ACTH concentrations were reduced in the ESC/QUE group during five weeks of treatment. The inhibitory effect of QUE maybe involved in its antidepressant effects as an augmentation strategy.
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http://dx.doi.org/10.1016/j.jpsychires.2014.01.013DOI Listing
May 2014

Impact on cortisol and antidepressant efficacy of quetiapine and escitalopram in depression.

Psychoneuroendocrinology 2014 Jan 23;39:141-151. Epub 2013 Oct 23.

Department of Psychiatry and Psychotherapy, Ludwig-Maximilian-University, Munich, Germany.

Background: In this study, the impact of quetiapine fumarate extended release (QXR) and escitalopram (ESC) on HPA axis activity was investigated in depressed patients in relationship to antidepressant efficacy.

Methods: In a randomized, open-label 5-week trial 60 inpatients suffering from major depression (DSM-IV criteria) were treated for 5 weeks with either QXR (300 mg/day) or ESC (10mg/day). The dexamethasone/CRH (DEX/CRH) test was performed before treatment, after 1, and after 5 weeks of treatment. Cortisol (COR) AUC values were used to assess HPA axis function. The Hamilton Depression Rating Scale was used weekly to estimate antidepressant efficacy.

Results: QXR and ESC showed comparable antidepressant effects but strongly differed in their impact on HPA axis activity. In the QXR group, a marked inhibition of COR AUC levels was observed which was most pronounced after one week of treatment but showed a partial re-increase after 5 weeks of treatment. In contrast, ESC transiently stimulated COR AUC values (week 1) whereas COR AUC levels at week 0 and week 5 were comparable. COR improvement at week 1 (defined as COR peak value reduction between DEX/CRH test 1 and 2) was significantly associated with better clinical outcome.

Conclusion: Apparently, different effects on HPA axis activity reflect distinct pharmacoendocrinological properties of psychotropic drugs.
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http://dx.doi.org/10.1016/j.psyneuen.2013.10.008DOI Listing
January 2014

Tryptophan metabolism and immunogenetics in major depression: a role for interferon-γ gene.

Brain Behav Immun 2013 Jul 15;31:128-33. Epub 2013 Apr 15.

Department of Psychiatry, Ludwig-Maximilian University Munich, Nussbaumstr. 7, D-80336 Munich, Germany.

The tryptophan metabolism and immune activation play a role in pathophysiology of major depressive disorders. The pro-inflammatory cytokine interferon-γ transcriptionally induces the indoleamine 2,3-dioxygenase enzyme that degrades the tryptophan and thus induces serotonin depletion. The polymorphism of certain cytokine genes was reported to be associated with major depression. We investigated the association between interferon-γ (IFNγ) gene CA repeat polymorphism, the profile of serotonin and tryptophan pathway metabolites and clinical parameters in 125 depressed patients and 93 healthy controls. Compared to controls, serum tryptophan and 5-hydroxyindoleacetic acid (5HIAA) concentrations in the patients were significantly lower and serum kynurenine concentrations were significantly higher at baseline (p<0.0001). The presence of IFNγ CA repeat allele 2 homozygous has significant association with higher kynurenine concentrations in controls (F=4.47, p=0.038) as well as in patients (F=3.79, p=0.045). The existence of interferon-γ CA repeat allele 2 (homo- or heterozygous) showed significant association with increase of tryptophan breakdown over time during the study period (F=6.0, p=0.019). The results indicated the association between IFNγ CA repeat allele 2, tryptophan metabolism and the effect of medication.
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http://dx.doi.org/10.1016/j.bbi.2013.04.003DOI Listing
July 2013

Translocator protein (18 kDa) (TSPO) as a therapeutic target for anxiety and neurologic disorders.

Eur Arch Psychiatry Clin Neurosci 2012 Nov 26;262 Suppl 2:S107-12. Epub 2012 Aug 26.

Department of Psychiatry and Psychotherapy, University Regensburg, Universitätsstraße 84, 93053 Regensburg, Germany.

The translocator protein (18 kD) (TSPO) plays a crucial role for the synthesis of neurosteroids by promoting the transport of cholesterol to the inner mitochondrial membrane, which is the rate-limiting step in neurosteroidogenesis. Neurosteroids are allosteric modulators of GABA(A) receptor function, which plays an important role in the pathophysiology of anxiety disorders. The TSPO ligand XBD173 enhances GABAergic neurotransmission by promoting neurosteroidogenesis without direct effects at the GABA(A) receptor. In humans, XBD173 shows potent antipanic efficacy without sedation and withdrawal after 7 days of treatment. XBD173 therefore appears to be a promising compound for rapid anxiolytic efficacy with a favorable side-effect profile. Furthermore, TSPO ligands show neuroprotective and antiinflammatory effects in experimental models of peripheral neuropathies and traumatic brain injury. These compounds might therefore also be valuable for the treatment of neurologic diseases with inflammation-related pathophysiology.
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http://dx.doi.org/10.1007/s00406-012-0352-5DOI Listing
November 2012

DNA methylation analysis of the angiotensin converting enzyme (ACE) gene in major depression.

PLoS One 2012 13;7(7):e40479. Epub 2012 Jul 13.

Department of Psychiatry and Psychotherapy, Ludwig-Maximilians-University Munich, Munich, Germany.

Background: The angiotensin converting enzyme (ACE) has been repeatedly discussed as susceptibility factor for major depression (MD) and the bi-directional relation between MD and cardiovascular disorders (CVD). In this context, functional polymorphisms of the ACE gene have been linked to depression, to antidepressant treatment response, to ACE serum concentrations, as well as to hypertension, myocardial infarction and CVD risk markers. The mostly investigated ACE Ins/Del polymorphism accounts for ~40%-50% of the ACE serum concentration variance, the remaining half is probably determined by other genetic, environmental or epigenetic factors, but these are poorly understood.

Materials And Methods: The main aim of the present study was the analysis of the DNA methylation pattern in the regulatory region of the ACE gene in peripheral leukocytes of 81 MD patients and 81 healthy controls.

Results: We detected intensive DNA methylation within a recently described, functional important region of the ACE gene promoter including hypermethylation in depressed patients (p = 0.008) and a significant inverse correlation between the ACE serum concentration and ACE promoter methylation frequency in the total sample (p = 0.02). Furthermore, a significant inverse correlation between the concentrations of the inflammatory CVD risk markers ICAM-1, E-selectin and P-selectin and the degree of ACE promoter methylation in MD patients could be demonstrated (p = 0.01 - 0.04).

Conclusion: The results of the present study suggest that aberrations in ACE promoter DNA methylation may be an underlying cause of MD and probably a common pathogenic factor for the bi-directional relationship between MD and cardiovascular disorders.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0040479PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3396656PMC
March 2013

[Ketamine-induced vesicopathy].

Psychiatr Prax 2012 Jan 10;39(1):43-5. Epub 2012 Jan 10.

Klinik und Poliklinik für Psychiatrie, Psychotherapie und Psychosomatik, Ludwig-Maximilians-Universität, München.

We report about a 25-year-old patient with transnasal ketamine abuse over years presenting with severe irritative urinary dysfunction (imperative urinary urgency, pollakisuria, dysuria) and severe alguria. Cystoscopia showed ketamine-induced vesicopathy with errosive cystitis; other etiologies could be excluded. Despite serious effort the patient was not motivated for abstinence from ketamine. After two ineffecient therapies with botulinum toxin A (200 and 400 I. E.) injected into the bladder, a prostate preserving cystectomia and ileum neobladder were mandatory.
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http://dx.doi.org/10.1055/s-0031-1292789DOI Listing
January 2012

Executive summary of the report by the WPA section on pharmacopsychiatry on general and comparative efficacy and effectiveness of antidepressants in the acute treatment of depressive disorders.

Eur Arch Psychiatry Clin Neurosci 2012 Feb 15;262(1):13-22. Epub 2011 Nov 15.

Department of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Nußbaumstraße 7, 80336, Munich, Germany.

Current gold standard in the treatment of depression includes pharmacotherapeutic and psychotherapeutic strategies together with social support. Due to the actually discussed controversies concerning the differential efficacy of antidepressants, a contribution to a comprehensive clarification seems to be necessary to avert further deterioration and uncertainty from patients, relatives, and their treating psychiatrists and general practitioners. Both efficacy and clinical effectiveness of antidepressants in the treatment of depressive disorders can be confirmed. Clinically meaningful antidepressant treatment effects were confirmed in different types of studies. Methodological issues of randomized controlled studies, meta-analyses, and effectiveness studies will be discussed. Furthermore, actual data about the differential efficacy and effectiveness of antidepressants with distinct pharmacodynamic properties and about outcome differences in studies using antidepressants and/or psychotherapy are discussed. This is followed by a clinically oriented depiction-the differential clinical effectiveness of different pharmacodynamic modes of action of antidepressants in different subtypes of depressive disorders. It can be summarized that the spectrum of different antidepressant treatments has broadened during the last decades. The efficacy and clinical effectiveness of antidepressants is statistically significant and clinically relevant and proven repeatedly. For further optimizing antidepressant treatment plans, clearly structured treatment algorithms and the implementation of psychotherapy seem to be useful. A modern individualized antidepressant treatment in most cases is a well-tolerated and efficacious tool to minimize the negative impact of the otherwise devastating and life-threatening outcome of depressive disorders.
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http://dx.doi.org/10.1007/s00406-011-0274-7DOI Listing
February 2012

General and comparative efficacy and effectiveness of antidepressants in the acute treatment of depressive disorders: a report by the WPA section of pharmacopsychiatry.

Eur Arch Psychiatry Clin Neurosci 2011 Nov;261 Suppl 3:207-45

Department of Psychiatry and Psychotherapy, Ludwig-Maximilian-University of Munich, Nussbaumstrasse 7, 80336, Munich, Germany.

Current gold standard approaches to the treatment of depression include pharmacotherapeutic and psychotherapeutic interventions with social support. Due to current controversies concerning the efficacy of antidepressants in randomized controlled trials, the generalizability of study findings to wider clinical practice and the increasing importance of socioeconomic considerations, it seems timely to address the uncertainty of concerned patients and relatives, and their treating psychiatrists and general practitioners. We therefore discuss both the efficacy and clinical effectiveness of antidepressants in the treatment of depressive disorders. We explain and clarify useful measures for assessing clinically meaningful antidepressant treatment effects and the types of studies that are useful for addressing uncertainties. This includes considerations of methodological issues in randomized controlled studies, meta-analyses, and effectiveness studies. Furthermore, we summarize the differential efficacy and effectiveness of antidepressants with distinct pharmacodynamic properties, and differences between studies using antidepressants and/or psychotherapy. We also address the differential effectiveness of antidepressant drugs with differing modes of action and in varying subtypes of depressive disorder. After highlighting the clinical usefulness of treatment algorithms and the divergent biological, psychological, and clinical efforts to predict the effectiveness of antidepressant treatments, we conclude that the spectrum of different antidepressant treatments has broadened over the last few decades. The efficacy and clinical effectiveness of antidepressants is statistically significant, clinically relevant, and proven repeatedly. Further optimization of treatment can be helped by clearly structured treatment algorithms and the implementation of psychotherapeutic interventions. Modern individualized antidepressant treatment is in most cases a well-tolerated and efficacious approach to minimize the negative impact of otherwise potentially devastating and life-threatening outcomes in depressive disorders.
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http://dx.doi.org/10.1007/s00406-011-0259-6DOI Listing
November 2011

[Antidepressants for mild depressive disorders].

Psychiatr Prax 2011 Aug 30;38(6):270-3. Epub 2011 Aug 30.

Klinik für Psychiatrie und Psychotherapie Ludwig-Maximilians-Universität Nussbaumstrasse 7 80336 München.

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http://dx.doi.org/10.1055/s-0031-1276865DOI Listing
August 2011

[Cannabinoid-induced hyperemesis].

Psychiatr Prax 2011 Apr 1;38(3):147-9. Epub 2011 Apr 1.

Klinik und Poliklinik für Psychiatrie, Psychotherapie und Psychosomatik, Ludwig-Maximilians-Universität, München, Germany.

In this case report, we describe a 29 year-old male patient with a history of chronic cannabis abuse presenting with recurrent vomiting, intense nausea and abdominal pain. Abstinence from cannabis resolved both vomiting and abdominal pain. We conclude that in case of chronic cannabis abuse, patients presenting with severe and chronic nausea, vomiting, accompanied by abdominal pain and compulsive behaviour (hot bathing), in the absence of other obvious causes, the diagnosis of cannabinoid-induced hyperemesis syndrome should be considered.
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http://dx.doi.org/10.1055/s-0030-1266067DOI Listing
April 2011

Major depressive disorder is associated with cardiovascular risk factors and low Omega-3 Index.

J Clin Psychiatry 2011 Sep 14;72(9):1242-7. Epub 2010 Dec 14.

Department of Psychiatry and Psychotherapy, Ludwig Maximilian University of Munich, Nussbaumstrasse 7, D-80336 Munich, Germany.

Objective: Cardiovascular disease (CVD) and major depressive disorder (MDD) are frequent worldwide and have a high comorbidity rate. Omega-3 fatty acids have been suggested as disease modulators for both CVD and MDD. Therefore, we studied whether polyunsaturated fatty acids and the Omega-3 Index may represent markers for assessment of the cardiovascular risk in somatically healthy patients suffering from MDD.

Method: We conducted a case-control study from July 2004 to December 2007 in 166 adults (86 inpatients with MDD but without CVD from the Department of Psychiatry and Psychotherapy and 80 age- and sex-matched healthy controls from an outpatient clinic of the Division of Preventive Cardiology, Ludwig Maximilian University of Munich, Germany). Information gathered at baseline included MDD diagnosis according to DSM-IV criteria, depression ratings, conventional cardiovascular risk factors, and fatty acid and interleukin-6 determinations. Fatty acid composition was analyzed according to the HS-Omega-3 Index methodology. During the study, patients received no supplementation with omega-3 fatty acids. The main inclusion criteria were the diagnosis of MDD according to DSM-IV and a 17-item Hamilton Depression Rating Scale (HDRS-17) score of at least 17. Treatment response and remission were defined using the HDRS-17.

Results: Several conventional risk factors such as high triglyceride (mean, 152 mg/dL vs 100 mg/dL; P < .001) and fasting glucose (mean, 96 mg/dL vs 87 mg/dL; P = .005) values as well as greater waist circumference (mean, 97 cm vs 87 cm; P = .019) and higher body mass index (calculated as kg/m(2); mean, 26 vs 24; P = .011) were more prevalent in MDD patients in comparison with controls. The Omega-3 Index (mean, 3.9% vs 5.1%; P < .001) and individual omega-3 fatty acids were significantly lower in MDD patients. An Omega-3 Index < 4% was associated with high concentrations of the proinflammatory cytokine interleukin-6 (χ(2) = 7.8, P = .02).

Conclusions: Conventional cardiovascular risk factors, the Omega-3 Index, and interleukin-6 levels indicated an elevated cardiovascular risk profile in MDD patients currently free of CVD. Our results support the employment of strategies to reduce the cardiovascular risk in still cardiovascularly healthy MDD patients by targeting conventional risk factors and the Omega-3 Index.
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http://dx.doi.org/10.4088/JCP.09m05895bluDOI Listing
September 2011

Translocator protein (18 kDa) (TSPO) as a therapeutic target for neurological and psychiatric disorders.

Nat Rev Drug Discov 2010 Dec;9(12):971-88

Department of Psychiatry and Psychotherapy, Ludwig-Maximilians University, Nussbaumstrasse 7, 80336 Munich, Germany.

The translocator protein (18 kDa) (TSPO) is localized primarily in the outer mitochondrial membrane of steroid-synthesizing cells, including those in the central and peripheral nervous system. One of its main functions is the transport of the substrate cholesterol into mitochondria, a prerequisite for steroid synthesis. TSPO expression may constitute a biomarker of brain inflammation and reactive gliosis that could be monitored by using TSPO ligands as neuroimaging agents. Moreover, initial clinical trials have indicated that TSPO ligands might be valuable in the treatment of neurological and psychiatric disorders. This Review focuses on the biology and pathophysiology of TSPO and the potential of currently available TSPO ligands for the diagnosis and treatment of neurological and psychiatric disorders.
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http://dx.doi.org/10.1038/nrd3295DOI Listing
December 2010

Agomelatine: The evidence for its place in the treatment of depression.

Core Evid 2010 Jun 15;4:171-9. Epub 2010 Jun 15.

Department of Psychiatry and Psychotherapy, Ludwig-Maximilians-University, Munich, Germany.

Introduction: Depressive disorders are among the main causes of disability due to disease. In spite of recent progress in the pharmacotherapy of depression, there is still a high nonresponse rate of approximately 30% to the first antidepressant treatment. Furthermore, the latency of several weeks until sufficient clinical improvement and the risk of side effects remain unresolved problems. Therefore, there is still further need for the development of new antidepressants. In the last years a variety of melatonin receptor agonists have been synthesized and evaluated for the treatment of sleep disorders. Animal studies suggested that agomelatine (S-20098), a synthetic melatonergic MT(1) and MT(2) receptor agonist with serotonin receptor antagonistic properties, may have additional activating properties and may represent a new approach in the treatment of depression.

Aims: Clinical trials that have demonstrated efficacy and safety of agomelatine for the treatment of depression are reviewed.

Evidence Review: In clinical trials, including phase III studies, superior efficacy compared to placebo and good efficacy compared to standard antidepressants was shown for agomelatine for the acute treatment of major depression. In all studies published so far agomelatine was safe and the overall tolerability profile was superior to selective serotonin reuptake inhibitors or selective serotonin and norepinephrine reuptake inhibitors.

Place In Therapy: Agomelatine may represent a novel perspective in the treatment of acute depression. The improvement of sleep disturbances, the tolerability in terms of sexual side effects, and the lack of withdrawal symptoms after abrupt discontinuation of treatment may represent important clinical benefits compared to established antidepressants.
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http://dx.doi.org/10.2147/ce.s6005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2899775PMC
June 2010

Prevalence and treatment outcome in anxious versus nonanxious depression: results from the German Algorithm Project.

J Clin Psychiatry 2010 Aug 13;71(8):1047-54. Epub 2010 Jul 13.

Charité-Universitätsmedizin Berlin, Department of Psychiatry and Psychotherapy, Campus Charité Mitte, Berlin, Germany.

Objective: The objective of this study was to explore the prevalence of anxious depression in an inpatient population, to describe its clinical and sociodemographic correlates, and to compare treatment outcomes between patients with anxious and nonanxious depression. Furthermore, the efficacy of algorithm-guided treatment versus treatment as usual in patients with anxious versus nonanxious depression was evaluated.

Method: Data were collected on 429 inpatients with the diagnosis of a depressive episode (according to ICD-10) and a score of ≥ or = 15 on the 21-item Hamilton Depression Rating Scale (HDRS-21). The German Algorithm Project, phase 3 (GAP3), was conducted between 2000 and 2005 in 10 psychiatric departments throughout Germany. A baseline HDRS-21 anxiety/somatization factor score of ≥ or = 7 was considered indicative of anxious depression. Remission was defined as an HDRS-21 score or ≤ = 9. To evaluate the efficacy of algorithm-guided treatment, patients were randomly assigned into 3 groups: 2 different treatment algorithms or treatment as usual.

Results: The prevalence of anxious depression was 49%. Patients with anxious depression were more likely than those with nonanxious depression to be older (mean ± SD = 45.3 ± 12.8 vs 42.9 ± 12.0 years, odds ratio [OR] = 1.02 [95% CI, 1.00-1.03], P = .046), retired (70% vs 30%, OR = 3.09 [95% CI, 1.70-5.62], P = .000), without school qualification (74% vs 26%, OR = 3.11 [95% CI, 1.09-8.83], P = .035), more severely depressed (mean ± SD HDRS-21 score = 20.1 ± 5.0 vs 18.5 ± 4.4, OR = 1.08 [95% CI, 1.03-1.12], P = .001), and more likely to have a longer duration of the current episode (mean ± SD = 20.9 ± 26.2 vs 13.7 ± 14.3 weeks, OR = 1.02 [95% CI, 1.01-1.03], P = .011). Patients with anxious depression were more likely to display a variety of melancholic features. In patients with anxious depression compared to those with nonanxious depression, remission was less likely to be achieved (48.6% vs 61.5%, OR = 0.63 [95% CI, 0.42-0.92], P = .018) and took longer to occur (mean ± SD = 44 ± 3.4 vs 30 ± 2.8 days, HR = 0.65 [95% CI, 0.50-0.85], P = .001). There was no significant interaction with the treatment mode with regard to remission (Wald = 0.20, P = .890).

Conclusions: Anxious depression is common in patients diagnosed with depression. The poorer treatment outcome in patients with anxious depression demonstrates the need to address the issue of specific treatment strategies for this subgroup. However, anxious depression has no moderating effect on the efficacy of algorithm-guided treatment.

Trial Registration: http://www.germanctr.de/ Identifier: DRKS00000161.
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http://dx.doi.org/10.4088/JCP.09m05650bluDOI Listing
August 2010

Glyoxalase-I mRNA expression and CCK-4 induced panic attacks.

J Psychiatr Res 2011 Jan 9;45(1):60-3. Epub 2010 Jun 9.

Department of Psychiatry and Psychotherapy, Ludwig-Maximilian-University, Nussbaumstrasse 7, 80336 Munich, Germany.

Rationale: There is evidence that the anti-glycation enzyme glyoxalase-1 (GLO1) may play a role in anxiety-related behaviour. However, discordant findings between GLO1 expression and anxiety-related behaviour have been observed in animal models. Because no data are available on the relation between GLO1 mRNA expression and human anxiety so far, we investigated the expression of GLO1 mRNA in peripheral blood cells in relation to cholecystokinin-tetrapeptide (CCK-4) induced panic anxiety in healthy subjects as an established model of human anxiety in healthy volunteers.

Methods: Twenty-three healthy subjects underwent challenge with CCK-4. GLO1 mRNA expression was assessed by quantitative real-time polymerase chain reaction prior to CCK-4 injection. Baseline anxiety was assessed with the State-Trait-Anxiety-Inventory (STAI) and panic response was measured with the Panic Symptom Scale (PSS).

Results: CCK-4 elicited a marked anxiety response accompanied by a significant increase in heart rate. GLO1 mRNA expression did not correlate with state or trait anxiety nor with severity of CCK-4 induced anxiety.

Conclusions: The lack of correlation between GLO1 mRNA expression and CCK-4 induced panic severity suggests that GLO1 is not involved into the acute panic response to CCK-4 in healthy volunteers. Therefore, further studies are needed to clarify the involvement of GLO1 in anxiety disorders at baseline and in anxiety challenge paradigms to resolve the apparent contradictions of preclinical studies concerning the relationship between GLO1 expression and anxiety.
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http://dx.doi.org/10.1016/j.jpsychires.2010.05.008DOI Listing
January 2011
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