Department of Medicine, Academic Medical Centre, University of Amsterdam, PO Box 22660, 1100 DD Amsterdam, The Netherlands.
J Psychiatr Res. 2012 Oct;46(10):1339-45. doi: 10.1016/j.jpsychires.2012.06.015. Epub 2012 Jul 28.
Delirium, a frequently occurring, devastating disease, is often underdiagnosed, especially in dementia. Serum anticholinergic activity (SAA) was proposed as a disease marker as it may reflect delirium's important pathogenetic mechanism, cholinergic deficiency. We assessed the association of serum anticholinergic activity with delirium and its risk factors in a longitudinal study on elderly hip fracture patients.
Consecutive elderly patients admitted for hip fracture surgery (n = 142) were assessed longitudinally for delirium, risk factors, and serum markers (IL-6, cortisol, and SAA). Using a sophisticated statistical design, we evaluated the association between SAA and delirium in general and with adjustments, but also the temporal course, including the events fracture, surgery, and potential delirium, individual confounders, and a propensity score.
Among elderly hip fracture patients 51% developed delirium, these showed more risk factors (p < 0.001), and complications (p < 0.05). Uncontrolled SAA levels (463 samples) were significantly higher in the delirium group (4.2 vs. 3.4 pmol/ml) and increased with delirium onset, but risk factors absorbed the effect. Using mixed-modeling we found a significant increase in SAA concentration (7.6% (95%CI 5.0-10.2, p < 0.001)) per day, which was modified by surgery and delirium, but this effect was confounded by cognitive impairment and IL-6 values. Confounder control by propensity scores resulted in a disappearance of delirium-induced SAA increase.
Delirium-predisposing factors are closely associated with changes in the temporal profile of serum anticholinergic activity and thus neutralize the previously documented association between higher SAA levels and delirium. An independent relationship of SAA to delirium presence is highly questionable.
谵妄是一种经常发生且具有破坏性的疾病,往往诊断不足,尤其是在痴呆患者中。血清抗胆碱能活性(SAA)被认为是一种疾病标志物,因为它可能反映了谵妄的重要发病机制,即胆碱能缺乏。我们在一项关于老年髋部骨折患者的纵向研究中,评估了血清抗胆碱能活性与谵妄及其危险因素的相关性。
连续入组因髋部骨折手术而入院的老年患者(n=142),进行纵向评估谵妄、危险因素和血清标志物(IL-6、皮质醇和 SAA)。我们采用复杂的统计设计,评估了 SAA 与谵妄的一般相关性和调整后的相关性,还评估了时间进程,包括骨折、手术和潜在的谵妄事件、个体混杂因素和倾向评分。
在老年髋部骨折患者中,51%发生了谵妄,这些患者有更多的危险因素(p<0.001)和并发症(p<0.05)。未控制的 SAA 水平(463 个样本)在谵妄组中显著升高(4.2 vs. 3.4 pmol/ml),并随着谵妄的发生而增加,但危险因素吸收了这种影响。使用混合模型,我们发现 SAA 浓度每天显著增加(7.6%(95%CI 5.0-10.2,p<0.001)),这种增加受到手术和谵妄的影响,但这种影响受到认知障碍和 IL-6 值的混杂。通过倾向评分控制混杂因素导致了谵妄引起的 SAA 增加的消失。
谵妄易感因素与血清抗胆碱能活性的时间谱变化密切相关,从而使先前记录的较高 SAA 水平与谵妄之间的关联失去作用。SAA 与谵妄存在的独立关系是非常值得怀疑的。