Childhood interleukin-6, C-reactive protein and atopic disorders as risk factors for hypomanic symptoms in young adulthood: a longitudinal birth cohort study.
Childhood interleukin-6, C-reactive protein and atopic disorders as risk factors for hypomanic symptoms in young adulthood: a longitudinal birth cohort study.
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DOI：
10.1017/s0033291716001574
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发表时间：
2017-01
影响因子：
6.9
通讯作者：
Osborn, D. P. J.
中科院分区：
文献类型：
--
作者：
Hayes, J. F.;Khandaker, G. M.;Anderson, J.;Mackay, D.;Zammit, S.;Lewis, G.;Smith, D. J.;Osborn, D. P. J.
目前还没有关于儿童期炎症标志物和特应性疾病以及成年期轻躁狂症状风险的纵向研究。本研究检测了儿童期：（1）血清白细胞介素-6（IL-6）和C-反应蛋白（CRP）;（2）哮喘和/或湿疹是否与青年期轻躁狂特征相关。雅芳父母和儿童纵向研究（一项前瞻性普通人群英国出生队列研究）的参与者在9岁时（n = 4645）进行了IL-6和CRP测量的非空腹血液样本，父母在10岁之前回答了关于医生诊断的特应性疾病的问题（n = 7809）。这些参与者在22岁时完成了轻躁狂检查表（n = 3361）。在调整了年龄、性别、种族、社会经济状况、过去的心理和行为问题、体重指数和母亲产后抑郁症后，9岁时IL-6值最高的三分之一的参与者与最低的三分之一相比，到22岁时轻躁狂症状的风险增加[调整后的比值比1.77，95%置信区间（CI）1.10-2.85，p < 0.001]。儿童期较高的IL-6水平与成人轻躁狂特征呈剂量反应关系。在18岁时进一步调整抑郁症后，这种关联仍然存在（调整后的比值比1.70，95%CI 1.03-2.81，p = 0.038）。没有证据表明轻躁狂症状与儿童期CRP水平、哮喘或湿疹相关。儿童期较高水平的全身炎症标志物IL-6与青年期轻躁狂症状相关，表明炎症可能在躁狂症的病理生理学中发挥作用。炎症通路可能是双相情感障碍预防和干预的合适靶点。
There are no existing longitudinal studies of inflammatory markers and atopic disorders in childhood and risk of hypomanic symptoms in adulthood. This study examined if childhood: (1) serum interleukin-6 (IL-6) and C-reactive protein (CRP); and (2) asthma and/or eczema are associated with features of hypomania in young adulthood. Participants in the Avon Longitudinal Study of Parents and Children, a prospective general population UK birth cohort, had non-fasting blood samples for IL-6 and CRP measurement at the age of 9 years (n = 4645), and parents answered a question about doctor-diagnosed atopic illness before the age of 10 years (n = 7809). These participants completed the Hypomania Checklist at age 22 years (n = 3361). After adjusting for age, sex, ethnicity, socio-economic status, past psychological and behavioural problems, body mass index and maternal postnatal depression, participants in the top third of IL-6 values at 9 years, compared with the bottom third, had an increased risk of hypomanic symptoms by age 22 years [adjusted odds ratio 1.77, 95% confidence interval (CI) 1.10–2.85, p < 0.001]. Higher IL-6 levels in childhood were associated with adult hypomania features in a dose–response fashion. After further adjustment for depression at the age of 18 years this association remained (adjusted odds ratio 1.70, 95% CI 1.03–2.81, p = 0.038). There was no evidence of an association of hypomanic symptoms with CRP levels, asthma or eczema in childhood. Higher levels of systemic inflammatory marker IL-6 in childhood were associated with hypomanic symptoms in young adulthood, suggesting that inflammation may play a role in the pathophysiology of mania. Inflammatory pathways may be suitable targets for the prevention and intervention for bipolar disorder.