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Sökning: L773:1398 5647 OR L773:1399 5618

  • Resultat 11-20 av 81
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  • Bosi, A., et al. (författare)
  • Quality of laboratory biomarker monitoring during treatment with lithium in patients with bipolar disorder
  • 2023
  • Ingår i: Bipolar Disorders. - : Wiley. - 1398-5647 .- 1399-5618. ; 25:6, s. 499-506
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundClinical guidelines recommend monitoring of creatinine and lithium throughout treatment with lithium. We here assessed the extent to which this occurs in healthcare in Sweden. MethodsThis is an observational study of all adults with bipolar disorder starting lithium therapy in Stockholm, Sweden, during 2007-2018. The main outcome was monitoring of blood lithium and creatinine at therapy initiation and/or once annually. The secondary outcome was monitoring of calcium and thyroid-stimulating hormone (TSH). Patients were followed up until therapy cessation, death, out-migration, or to the end of 2018. ResultsWe identified 4428 adults with bipolar disorder who started lithium therapy and were followed up for up to 11 years. Their median age was 39 years, and 63% were women. The median duration on lithium therapy was 4.3 (IQR: 1.9-7.45) years, and the majority who discontinued therapy started another mood stabilizer soon after. Overall, 21% started lithium therapy without assessing the serum/plasma concentration of creatinine. The proportion of people who did not have both lithium and creatinine measured increased from 21% in the first year to 33% in the eleventh year. The proportion with annual testing for TSH or calcium was slightly lower. As few as 16% of patients had both lithium and creatinine tested once annually during their complete time on lithium. ConclusionsIn a Swedish community sample, lithium and creatinine monitoring was inconsistent with guideline recommendations that call for measurement of annual biomarker levels.
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  • Di Simplicio, Martina, et al. (författare)
  • An investigation of mental imagery in bipolar disorder : Exploring "the mind's eye"
  • 2016
  • Ingår i: Bipolar Disorders. - : WILEY-BLACKWELL. - 1398-5647 .- 1399-5618. ; 18:8, s. 669-683
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: Mental imagery abnormalities occur across psychopathologies and are hypothesized to drive emotional difficulties in bipolar disorder (BD). A comprehensive assessment of mental imagery in BD is lacking. We aimed to test whether (i) mental imagery abnormalities (abnormalities in cognitive stages and subjective domains) occur in BD relative to non-clinical controls; and (ii) to determine the specificity of any abnormalities in BD relative to depression and anxiety disorders. Methods: Participants included 54 subjects in the BD group (depressed/euthymic; n=27 in each subgroup), subjects with unipolar depression (n=26), subjects with anxiety disorders (n=25), and non-clinical controls (n=27) matched for age, gender, ethnicity, education, and premorbid IQ. Experimental tasks assessed cognitive (non-emotional) measures of mental imagery (cognitive stages). Questionnaires, experimental tasks, and a phenomenological interview assessed subjective domains including spontaneous imagery use, interpretation bias, and emotional mental imagery. Results: (i) Compared to non-clinical controls, the BD combined group reported a greater impact of intrusive prospective imagery in daily life, more vivid and "real" negative images (prospective imagery task), and higher self-involvement (picture-word task). The BD combined group showed no clear abnormalities in cognitive stages of mental imagery. (ii) When depressed individuals with BD were compared to the depressed or anxious clinical control groups, no significant differences remained-across all groups, imagery differences were associated with affective lability and anxiety. Conclusions: Compared to non-clinical controls, BD is characterized by abnormalities in aspects of emotional mental imagery within the context of otherwise normal cognitive aspects. When matched for depression and anxiety, these abnormalities are not specific to BD-rather, imagery may reflect a transdiagnostic marker of emotional psychopathology.
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19.
  • Jansåker, Filip, et al. (författare)
  • Association between neighborhood deprivation and mortality in patients with schizophrenia and bipolar disorder—A nationwide follow-up study
  • 2023
  • Ingår i: Bipolar Disorders. - : Wiley. - 1398-5647 .- 1399-5618. ; 25:6, s. 489-498
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: The aim was to explore the association between neighborhood deprivation and all-cause mortality and cause-specific mortalities in patients with schizophrenia and bipolar disorder. A better understanding of this potential relationship may help to identify patients with schizophrenia and bipolar disorder with an increased mortality risk. Methods: This nationwide study included practically all adults (≥30 years) diagnosed with schizophrenia (n = 34,544) and bipolar disorder (n = 64,035) in Sweden (1997–2017). The association between neighborhood deprivation and mortality was explored using Cox regression. All models were conducted in both men and women and adjusted for individual-level sociodemographic factors and comorbidities. Results: There was an association between level of neighborhood deprivation and all-cause mortality in both groups. The adjusted hazard ratios for all-cause mortality associated with high compared to low neighborhood deprivation were 1.18 (95% confidence interval 1.11–1.25) in patients with schizophrenia and 1.33 (1.26–1.41) in patients with bipolar disorder. The two most common mortality causes in both groups were coronary heart disease and cancer. The mortality due to coronary heart disease increased when neighborhood deprivation increased and reached 1.37 (1.18–1.60) in patients with schizophrenia and 1.70 (1.44–2.01) in patients with bipolar disorder living in the most deprived neighborhoods. Conclusions: This study shows that neighborhood deprivation is an important risk factor for all-cause mortality and most cause-specific mortalities among patients with schizophrenia and bipolar disorder. These findings could serve as aid to policymakers when allocating healthcare resources and to clinicians who encounter patients with these conditions in deprived neighborhoods.
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  • Kalman, Janos L, et al. (författare)
  • Investigating polygenic burden in age at disease onset in bipolar disorder: Findings from an international multicentric study.
  • 2019
  • Ingår i: Bipolar disorders. - : Wiley. - 1399-5618 .- 1398-5647. ; 21:1, s. 68-75
  • Tidskriftsartikel (refereegranskat)abstract
    • Bipolar disorder (BD) with early disease onset is associated with an unfavorable clinical outcome and constitutes a clinically and biologically homogenous subgroup within the heterogeneous BD spectrum. Previous studies have found an accumulation of early age at onset (AAO) in BD families and have therefore hypothesized that there is a larger genetic contribution to the early-onset cases than to late onset BD. To investigate the genetic background of this subphenotype, we evaluated whether an increased polygenic burden of BD- and schizophrenia (SCZ)-associated risk variants is associated with an earlier AAO in BD patients.A total of 1995 BD type 1 patients from the Consortium of Lithium Genetics (ConLiGen), PsyCourse and Bonn-Mannheim samples were genotyped and their BD and SCZ polygenic risk scores (PRSs) were calculated using the summary statistics of the Psychiatric Genomics Consortium as a training data set. AAO was either separated into onset groups of clinical interest (childhood and adolescence [≤18years] vs adulthood [>18years]) or considered as a continuous measure. The associations between BD- and SCZ-PRSs and AAO were evaluated with regression models.BD- and SCZ-PRSs were not significantly associated with age at disease onset. Results remained the same when analyses were stratified by site of recruitment.The current study is the largest conducted so far to investigate the association between the cumulative BD and SCZ polygenic risk and AAO in BD patients. The reported negative results suggest that such a polygenic influence, if there is any, is not large, and highlight the importance of conducting further, larger scale studies to obtain more information on the genetic architecture of this clinically relevant phenotype.
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