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      Depressive und Angststörungen bei somatischen Krankheiten

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          Zusammenfassung

          Depressiv-ängstliche Störungen sind bei den unterschiedlichen somatischen Erkrankungen häufig. Sie sind nicht nur als Reaktion auf die Situation der Erkrankung zu verstehen, sondern in ein komplexes Bedingungsgefüge eingebettet. Sie sind besonders häufig bei Erkrankungen, die das Zentralnervensystem oder endokrine Regulationssysteme direkt betreffen. Es besteht ein enger Zusammenhang zur Chronizität, Schwere und Prognose der Erkrankung. Eigenständige Effekte von diversen pharmakologischen Substanzgruppen sind wahrscheinlich.

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          The prevalence of comorbid depression in adults with diabetes: a meta-analysis.

          To estimate the odds and prevalence of clinically relevant depression in adults with type 1 or type 2 diabetes. Depression is associated with hyperglycemia and an increased risk for diabetic complications; relief of depression is associated with improved glycemic control. A more accurate estimate of depression prevalence than what is currently available is needed to gauge the potential impact of depression management in diabetes. MEDLINE and PsycINFO databases and published references were used to identify studies that reported the prevalence of depression in diabetes. Prevalence was calculated as an aggregate mean weighted by the combined number of subjects in the included studies. We used chi(2) statistics and odds ratios (ORs) to assess the rate and likelihood of depression as a function of type of diabetes, sex, subject source, depression assessment method, and study design. A total of 42 eligible studies were identified; 20 (48%) included a nondiabetic comparison group. In the controlled studies, the odds of depression in the diabetic group were twice that of the nondiabetic comparison group (OR = 2.0, 95% CI 1.8-2.2) and did not differ by sex, type of diabetes, subject source, or assessment method. The prevalence of comorbid depression was significantly higher in diabetic women (28%) than in diabetic men (18%), in uncontrolled (30%) than in controlled studies (21%), in clinical (32%) than in community (20%) samples, and when assessed by self-report questionnaires (31%) than by standardized diagnostic interviews (11%). The presence of diabetes doubles the odds of comorbid depression. Prevalence estimates are affected by several clinical and methodological variables that do not affect the stability of the ORs.
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            International experiences with the Hospital Anxiety and Depression Scale--a review of validation data and clinical results.

            More than 200 published studies from most medical settings worldwide have reported experiences with the Hospital Anxiety and Depression Scale (HADS) which was specifically developed by Zigmond and Snaith for use with physically ill patients. Although introduced in 1983, there is still no comprehensive documentation of its psychometric properties. The present review summarizes available data on reliability and validity and gives an overview of clinical studies conducted with this instrument and their most important findings. The HADS gives clinically meaningful results as a psychological screening tool, in clinical group comparisons and in correlational studies with several aspects of disease and quality of life. It is sensitive to changes both during the course of diseases and in response to psychotherapeutic and psychopharmacological intervention. Finally, HADS scores predict psychosocial and possibly also physical outcome.
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              Cytokines sing the blues: inflammation and the pathogenesis of depression.

              Increasing amounts of data suggest that inflammatory responses have an important role in the pathophysiology of depression. Depressed patients have been found to have higher levels of proinflammatory cytokines, acute phase proteins, chemokines and cellular adhesion molecules. In addition, therapeutic administration of the cytokine interferon-alpha leads to depression in up to 50% of patients. Moreover, proinflammatory cytokines have been found to interact with many of the pathophysiological domains that characterize depression, including neurotransmitter metabolism, neuroendocrine function, synaptic plasticity and behavior. Stress, which can precipitate depression, can also promote inflammatory responses through effects on sympathetic and parasympathetic nervous system pathways. Finally, depression might be a behavioral byproduct of early adaptive advantages conferred by genes that promote inflammation. These findings suggest that targeting proinflammatory cytokines and their signaling pathways might represent a novel strategy to treat depression.
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                Author and article information

                Journal
                978-3-540-33129-2
                10.1007/978-3-540-33129-2
                Psychiatrie und Psychotherapie
                Psychiatrie und Psychotherapie
                978-3-540-24583-4
                978-3-540-33129-2
                13 August 2009
                : 1501-1566
                Affiliations
                [1 ]GRID grid.411095.8, ISNI 0000000404772585, Klinik und Poliklinik für Psychiatrie und Psychotherapie, , Klinikum der Ludwig-Maximilians-Universität München, ; Nußbaumstr. 7, 80336 München,
                [2 ]GRID grid.5252.0, ISNI 000000041936973X, Inn-Salzach-Klinikum Wasserburg a. Inn · Rosenheim · Freilassing Fachkrankenhaus für Psychiatrie, Psychotherapie, Psychosomatische Medizin und Neurologie Akademisches Lehrkrankenhaus, , Ludwig-Maximilians-Universität München, ; Gabersee 7, 83512 Wasserburg am Inn,
                [3 ]GRID grid.11598.34, ISNI 0000000089882476, Klinik für Psychiatrie, , Medizinische Universität Graz, ; Auenbruggerplatz 31, 8036 Graz, Österreich
                GRID grid.11598.34, ISNI 0000000089882476, Klinik für Psychiatrie, , Medizinische Universität Graz, ; Auenbruggerplatz 31, 8036 Graz, Österreich
                Article
                57
                10.1007/978-3-540-33129-2_57
                7122024
                e457dd52-0998-4fec-9c36-51b50c9df5ec
                © Springer Medizin Verlag Heidelberg 2008

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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