Risk of dementia and AD with prior exposure to NSAIDs in an elderly community-based cohort
Risk of dementia and AD with prior exposure to NSAIDs in an elderly community-based cohort
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DOI：
10.1212/wnl.0b013e3181a18691
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发表时间：
2009-06-02
期刊：
影响因子：
9.9
通讯作者：
Larson, E. B.
中科院分区：
文献类型：
--
作者：
Breitner, J. C. S.;Haneuse, S. J. P. A.;Larson, E. B.
背景：非甾体类抗炎药 (NSAID) 可以预防阿尔茨海默氏痴呆 (AD)。 方法：我们在入组时年龄≥ 65 岁（中位数 74.8）的成人思想变化队列中分析了既往 NSAID 暴露与痴呆和 AD 事件的关联。参与者是 Group Health 的成员，该组织提供 1977 年以来的计算机化药房配药记录。我们对 2,736 名无痴呆症的参与者进行了研究，并收集了大量先前的药房数据，每两年对他们进行一次长达 12 年的跟踪，以识别痴呆症和 AD。 Cox 比例风险回归评估了痴呆或 AD 与 NSAID 使用之间的关联，按 2 年分配的标准每日剂量 (SDD) 分级（例如，大量使用 = 500 + SDD），一些分析还添加了 NSAID 使用的连续两年期自我报告。 结果：药房记录确定 351 名参与者 (12.8%) 在入组时有大量 NSAID 使用史。另有 107 人在随访过程中成为重度用户。大约 476 人罹患痴呆症，其中 356 人患有 AD（中位发病年龄为 83.5 岁和 83.8 岁）。与 NSAID 可以预防 AD 的假设相反，药房定义的大量 NSAID 使用者表现出痴呆和 AD 的发病率增加，调整后的风险比为 1.66（95% 置信区间，1.24-2.24）和 1.57（95% 置信区间，1.10-2.23）。添加自我报告的暴露数据并没有改变这些结果。结论：这些发现与其他针对年轻队列的研究的结果不同。其他地方观察到的结果可能反映了非类固醇抗炎药（NSAID）使用者阿尔茨海默氏痴呆（AD）的延迟发作。可以想象，这种延迟可能会导致晚年 AD 发病率增加。 NSAID 使用与 AD 发病机制的关系需要进一步研究。神经病学（R）2009； 72：1899-1905
Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) may prevent Alzheimer dementia (AD).Methods: We analyzed the association of prior NSAID exposure with incident dementia and AD in the Adult Changes in Thought population-based cohort aged >= 65 years (median 74.8) at enrollment. Participants were members of Group Health, which provided computerized pharmacy dispensing records from 1977 onward. We studied 2,736 dementia-free enrollees with extensive prior pharmacy data, following them biennially for up to 12 years to identify dementia and AD. Cox proportional hazards regression assessed association of dementia or AD with NSAID use graded in standard daily doses (SDD) dispensed over 2 years (e.g., heavy use = 500 + SDD), with some analyses also adding consecutive biennial self-reports of NSAID use.Results: Pharmacy records identified 351 participants (12.8%) with history of heavy NSAID use at enrollment. Another 107 became heavy users during follow-up. Some 476 individuals developed incident dementia, 356 with AD (median onset ages 83.5 and 83.8 years). Contrary to the hypothesis that NSAIDs protect against AD, pharmacy-defined heavy NSAID users showed increased incidence of dementia and AD, with adjusted hazard ratios of 1.66 (95% confidence interval, 1.24-2.24) and 1.57 (95% confidence interval, 1.10-2.23). Addition of self-reported exposure data did not alter these results.Conclusions: These findings differ from those of other studies with younger cohorts. The results observed elsewhere may reflect delayed onset of Alzheimer dementia (AD) in nonsteroidal anti-inflammatory drug (NSAID) users. Conceivably, such delay could result in increased AD incidence in late old age. The relation of NSAID use and AD pathogenesis needs further investigation. Neurology (R) 2009; 72: 1899-1905