Wang Tzu-Yun, Lee Sheng-Yu, Chen Shiou-Lan, Chung Yi-Lun, Li Chia-Ling, Chang Yun-Hsuan, Wang Liang-Jen, Chen Po See, Chen Shih-Heng, Chu Chun-Hsien, Huang San-Yuan, Tzeng Nian-Sheng, Hsieh Tsai-Hsin, Chiu Yen-Chu, Lee I Hui, Chen Kao-Chin, Yang Yen Kuang, Hong Jau-Shyong, Lu Ru-Band
Department of Psychiatry, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan (Drs T.-Y.W., S.-Y.L., S.-L.C., Ms Y.-L.C. Drs C.-L.L.,Y.-H.C., and P.S.C. , Ms T.-H.H., Drs I.H.L., K.-C.C., Y.K.Y., and R.-B.L.); Institute of Behavioral Medicine (Drs Y.K.Y. and R.-B.L.), and Institute of Allied Health Sciences (Dr Y.-H.C. and R.-B.L.), College of Medicine, and Addiction Research Center (Drs P.S.C., I.H.L, K.C.C., Y.K.Y., and R.-B.L.), National Cheng Kung University, Tainan, Taiwan; Department of Psychiatry, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan (Dr S.-Y.L.); Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University(KMU), Lipid Science and Aging Research Center, KMU, Kaohsiung, Taiwan (Dr S.-L.C.); Department of Psychiatry, Tri-Service General Hospital, School of Medicine, and Student Counseling Center (Dr N.-S.T.), National Defense Medical Center, Taipei, Taiwan (Dr S.-Y.H.); Department of Child and Adolescent Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan (Dr L.-J.W.); Department of Psychiatry, National Cheng Kung University Hospital, Dou-Liou Branch, Yunlin, Taiwan (Dr Y.K.Y.); Center for Neuropsychiatric Research, National Health Research Institutes, Miaoli, Taiwan (Dr R.-B.L.); Neurobiology Laboratory, NIH/NIEHS, Research Triangle Park, NC (Drs S.-H.C. and J.-S.H.); Deprtment of Psychology, Asia University, Taichung, Taiwan (Dr Y.-H.C.); Institute of Molecular Medicine (Dr C.-H.C.) , and Institute of Basic Medical Sciences (Ms Y.-L.C.), College of Medicine, National Cheng Kung University, Tainan, Taiwan ; Department of Biomedical Science and Environmental Biology, School of Life Science, Kaohsiung Medical University, Kaohsiung, Taiwan (Ms Y.-C.C.).
Int J Neuropsychopharmacol. 2016 Aug 12;19(8). doi: 10.1093/ijnp/pyw012. Print 2016 Aug.
Emerging evidence suggests that inflammation and neurodegeneration underlies bipolar disorder. To investigate biological markers of cytokines and brain-derived neurotrophic factor between bipolar I, bipolar II, and other specified bipolar disorder with short duration hypomania may support the association with inflammatory dysregulation and bipolar disorder and, more specifically, provide evidence for other specified bipolar disorder with short duration hypomania patients were similar to bipolar II disorder patients from a biological marker perspective.
We enrolled patients with bipolar I disorder (n=234), bipolar II disorder (n=260), other specified bipolar disorder with short duration hypomania (n=243), and healthy controls (n=140). Their clinical symptoms were rated using the Hamilton Depression Rating Scale and Young Mania Rating Scale. Inflammatory cytokine (tumor necrosis factor-α, C-reactive protein, transforming growth factor-β1, and interleukin-8) and brain-derived neurotrophic factor levels were measured in each group. Multivariate analysis of covariance and linear regression controlled for possible confounders were used to compare cytokine and brain-derived neurotrophic factor levels among the groups.
Multivariate analysis of covariance adjusted for age and sex and a main effect of diagnosis was significant (P<.001). Three of the 5 measured biomarkers (tumor necrosis factor-α, transforming growth factor-β1, and interleukin-8) were significantly (P=.006, .01, and <.001) higher in all bipolar disorder patients than in controls. Moreover, covarying for multiple associated confounders showed that bipolar I disorder patients had significantly higher IL-8 levels than did bipolar II disorder and other specified bipolar disorder with short duration hypomania patients in multivariate analysis of covariance (P=.03) and linear regression (P=.02) analyses. Biomarkers differences between bipolar II disorder and other specified bipolar disorder with short duration hypomania patients were nonsignificant.
The immunological disturbance along the bipolar spectrum was most severe in bipolar I disorder patients. Other specified bipolar disorder with short duration hypomania patients and bipolar II disorder patients did not differ in these biological markers.
新出现的证据表明炎症和神经退行性变是双相情感障碍的基础。研究双相I型障碍、双相II型障碍和其他特定的双相情感障碍伴短期轻躁狂发作患者之间细胞因子和脑源性神经营养因子的生物学标志物，可能支持炎症调节异常与双相情感障碍之间的关联，更具体地说，从生物学标志物角度为其他特定的双相情感障碍伴短期轻躁狂发作患者与双相II型障碍患者相似提供证据。
我们纳入了双相I型障碍患者（n = 234）、双相II型障碍患者（n = 260）、其他特定的双相情感障碍伴短期轻躁狂发作患者（n = 243）和健康对照者（n = 140）。使用汉密尔顿抑郁量表和杨氏躁狂量表对他们的临床症状进行评分。测量每组中炎症细胞因子（肿瘤坏死因子-α、C反应蛋白、转化生长因子-β1和白细胞介素-8）和脑源性神经营养因子水平。使用协方差多元分析和控制可能混杂因素的线性回归来比较各组之间的细胞因子和脑源性神经营养因子水平。
经年龄和性别调整的协方差多元分析以及诊断的主效应具有显著性（P <.001）。在所有双相情感障碍患者中，5种测量的生物标志物中的3种（肿瘤坏死因子-α、转化生长因子-β1和白细胞介素-8）显著高于对照组（P = 0.006、0.01和<.001）。此外，对多个相关混杂因素进行协变量调整后显示，在协方差多元分析（P = 0.03）和线性回归（P = 0.02）分析中，双相I型障碍患者的白细胞介素-8水平显著高于双相II型障碍和其他特定的双相情感障碍伴短期轻躁狂发作患者。双相II型障碍患者与其他特定的双相情感障碍伴短期轻躁狂发作患者之间的生物标志物差异不显著。
双相谱系中的免疫紊乱在双相I型障碍患者中最为严重。其他特定的双相情感障碍伴短期轻躁狂发作患者和双相II型障碍患者在这些生物学标志物方面没有差异。
Zotero 插件