39 research outputs found

    Clinical correlates of high burden of general medical comorbidities in patients with bipolar disorder

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    Background: Bipolar disorder is associated with an increased burden of general medical conditions that might be related to a more severe illness course. Methods: This is a cross-sectional study that evaluated clinical correlates of general medical comorbidities in outpatients with bipolar disorder (BD) involving 203 adult patients with a DSM-IV diagnosis of BD, consecutively recruited from the Bipolar Research Program (PROTAHBI) in Porto Alegre, Brazil. Clinical, demographic and anthropometrical variables were systematically assessed, and general medical comorbidity was measured using the Cumulative Illness Rating Scale (CIRS). Results: The prevalence of one or more medical comorbidities was 90.1%. The most common were those from endocrine/metabolic/breast, neurologic and vascular categories. A high burden of general medical comorbidities (defined as CIRS total score ≥ 4) was related to increasing age and body mass index and longer duration of illness after controlling for confounding factors. Limitations: The cross-sectional design limits our ability to make causal conclusions. Also, our sample consisted of patients with longer illness duration from a tertiary clinic and may not generalize to the whole spectrum of bipolar disorder. Conclusions: BD was associated with a high burden of general medical conditions related to age, obesity and longer duration of illness. Medical comorbidities must be incorporated as a core feature in the development of effective treatment strategies for bipolar disorder

    Challenges and developments in research of the early stages of bipolar disorder

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    Recently, attention in the field of bipolar disorder (BD) has focused on prevention, including early detection and intervention, as these strategies have the potential to delay, lessen the severity, or even prevent full-blown episodes of BD. Although knowledge of the neurobiology of BD has advanced substantially in the last two decades, most research was conducted with chronic patients. The objective of this paper is to comprehensively review the literature regarding the early stages of BD, to explore recent discoveries on the neurobiology of these stages, and to discuss implications for research and clinical care. The following databases were searched: PubMed, PsycINFO, Cochrane Library, and SciELO. Articles published in English from inception to December 2015 were retrieved. Several research approaches were used, including examination of offspring studies, retrospective studies, prospective studies of clinical high-risk populations, and exploration of the progression after the first manic episode. Investigations with neuroimaging, cognition assessments, and biomarkers provide promising (although not definitive) evidence of alterations in the neural substrate during the at-risk stage. Research on BD should be expanded to encompass at-risk states and aligned with recent methodological progress in neuroscience

    Attenuated inflammatory response of monocyte-derived macrophage from patients with BD : a preliminary report

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    Background: Innate immune system dysfunction has been recognized as an important element in the pathophysiology of bipolar disorder (BD). We aimed to investigate whether there are differences in the response of macrophages derived from patients in the early stages and late stages of BD and healthy subjects. Methods: Human monocytes purified from peripheral blood mononuclear cells (PBMCs) of patients with BD type I (n = 18)—further classified into early- and late stage BD patients according to their functioning- and from healthy individuals (n = 10) were differentiated into macrophages in vitro. Monocyte-derived macrophages (M) were exposed to IFNγ plus LPS-M(IFNγ + LPS)- or IL-4-M(IL-4)—to induce their polarization into the classical (also called M1) or alternative (also called M2) activation phenotypes, respectively; or either Mψ were not exposed to any stimuli characterizing the resting state (denominated M0). In vitro secretion of cytokines, such as IL-1β, IL-6, IL-10, and TNF-α, was used as an index of macrophage activity. Results: M(IFNγ + LPS) from late-stage BD patients produced less amount of IL-1β, IL-6, and IL-10 when compared to early-stage BD patients and healthy controls. Following alternative activation, M(IL-4) derived from late-stage patients secreted less IL-6 compared to the other groups. TNFα was less secreted by all macrophage phenotypes derived from late-stage patients when compared to healthy controls only (p < 0.005). Mψ from late-stage patients exhibited lower production of IL-1β and IL-10 compared to macrophages from healthy subjects and early-stage patients respectively. Interestingly, cytokines secretion from M(IFNγ + LPS), M(IL-4) and Mψ were similar between early-stage patients and healthy controls. Conclusion: Our results suggest a progressive dysfunction in the response of peripheral innate immune cells of BD patients in the late stages of the illness. This failure in the regulation of the immune system function may be implicated in the multisystemic progression of BD

    Baixa ingesta de cálcio em portadoras de pré-eclâmpsia

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    Mediadores inflamatórios no transtorno bipolar

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    Objetivos: Comparar os níveis séricos de citocinas entre voluntários saudáveis e em pacientes bipolares tipo 1 em mania, depressão e eutimia. Comparar os níveis séricos de quimiocinas entre voluntários saudáveis e pacientes bipolares tipo 1 em eutimia. Metodologia: Sessenta e um pacientes bipolares foram recrutados para a avaliação dos níveis séricos de citocinas. Desses, 24 estavam eutímicos, e 23 e 24 estavam em mania e depressão, respectivamente. Este grupo foi comparado a outro, composto por 25 voluntários saudáveis. As seguintes citocinas foram exainadas através de citometria de fluxo: TNF-alfa, IL-2, IL-4, IL-6, IL-10, IFN-gama e comparadas entre os grupos. Além dessa análise, 30 pacientes bipolares tipo 1 foram comparados a igual número de voluntários saudáveis para estudar os níveis séricos das seguintes quimiocinas: CCL2, CCL3, CCL8, CCL 9, CCL10, CCL11 e CCL24, dosadas através de ELISA sandwich. Resultados: Duarnte a mania, as citocinas pró-inflamatórias IL-2, IL-4 e IL-6 estavam elevadas nos pacientes com TB em comparação com o grupo de voluntários saudáveis. Já os pacientes em episódio depressivo, apresentavam somente elevação da IL-6. Não houve modificação dos níveis de citocinas nos pacientes eutímicos, exceto pelo aumento da IL-4. Quanto as quimiocinas, enquanto os níveis séricos de CXCL10 estavam elevados nos pacientes bipolares, os níveis de CCL24 estavam diminuídos.Objectives: Compare serum levels of cytokines between healthy volunteers and patients with bipolar disorder type 1 in mania, depression and euthymia. Compare serum levels of chemokines between healthy volunteers and bipolar patients in euthymia. Methods: Sixty-one bipolar patients were recruited for assessment of serum cytokine levels. Of these, 14 were in euthymic state, 23 and 24 were in manic and depressive episodes, respectively. A healthy comparison group included 25 healthy volunteers. Cytokines involved in Th1/Th2 balance, such as TNF- , IL-2, IL-4, IL-6, IL-10, IFN- , were examined by flow cytometry. In addition, serum chemokine levels of 30 euthymic patients with BD type I and 30 healthy volunteers were investigated and compared. The chemokines assessed were CCL2, CCL3, CCL8, CCL 9, CCL10, CCL11, and CCL24. Results: During mania, proinflammatory cytokines, IL-2, IL-4 and IL-6, were increased in comparison with healthy subjects. Patients in depressive episode showed only increased IL-6 levels. There were no significant differences in cytokine levels between patients in remission and healthy subjects, except for IL-4. Regarding chemokines, patients with BD showed significant differences in chemokine levels when compared with healthy subjects. While serum levels of CXCL10 were increased, CCL24 levels were lower in bipolar patients when compared with controls. There was no statistical difference in the serum levels of CCL2, CCL3, CCL24, CXCL9, and CXCL11 between patients and controls
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