The Clinical Research, Investigation, and Systems Modeling of Acute Illness Laboratory, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
PLoS One. 2010 Nov 4;5(11):e13852. doi: 10.1371/journal.pone.0013852.
To determine whether inflammatory and hemostasis response in patients hospitalized for pneumonia varies by age and whether these differences explain higher mortality in the elderly.
In an observational cohort of subjects with community-acquired pneumonia (CAP) recruited from emergency departments (ED) in 28 hospitals, we divided subjects into 5 age groups (<50, 51-64, 65-74, 75-84, and ≥85). We measured circulating levels of inflammatory (TNF, IL-6, and IL-10), hemostasis (D-dimer, Factor IX, thrombin-antithrombin complex, antithrombin and plasminogen-activator inhibitor-1), and cell-surface markers (TLR-2, TLR-4, and HLA-DR) during the first week of hospitalization and at discharge and compared 90-day mortality. We used logistic regression to compare odds ratios (OR) for 90-day mortality between age groups, adjusting for differences in pre-infection factors alone and then additionally adjusting for immune markers.
Of 2,183 subjects, 495, 444, 403, 583, and 258 subjects were <50, 51-64, 65-74, 75-84, and ≥85 years of age, respectively. Large age-related differences were observed in 90-day mortality (0.82% vs. 3.2% vs. 6.4% vs. 12.8% vs. 13.6%, p<0.01). No age-related differences in inflammatory and cell surface markers occurred during the first week. Older subjects had higher pro-coagulant markers on ED presentation and over first week (p ≤ 0.03), but these differences were modest (1.0-1.7-fold differences). Odds of death for older adults changed minimally in models incorporating differences in hemostasis and inflammatory markers (for subjects ≥ 85 compared to those <50, OR = 4.36, when adjusted for pre-infection factors and OR = 3.49 when additionally adjusted for hemostasis markers). At discharge, despite clinical recovery as evidenced by normal vital signs in >85% subjects, older subjects had modestly increased hemostasis markers and IL-6 levels (p<0.01).
Modest age-related increases in coagulation response occur during hospitalization for CAP; however these differences do not explain the large differences in mortality. Despite clinical recovery, immune resolution may be delayed in older adults at discharge.
确定因肺炎住院的患者的炎症和止血反应是否因年龄而异，以及这些差异是否可以解释老年人的死亡率更高。
在从 28 家医院的急诊科招募的社区获得性肺炎（CAP）的观察性队列中，我们将受试者分为 5 个年龄组（<50 岁、51-64 岁、65-74 岁、75-84 岁和≥85 岁）。我们在住院的第一周和出院时测量了循环中的炎症（TNF、IL-6 和 IL-10）、止血（D-二聚体、IX 因子、凝血酶-抗凝血酶复合物、抗凝血酶和纤溶酶原激活物抑制剂-1）和细胞表面标志物（TLR-2、TLR-4 和 HLA-DR），并比较了 90 天的死亡率。我们使用逻辑回归比较了 90 天死亡率的优势比（OR），仅调整了感染前因素，然后还调整了免疫标志物。
在 2183 名受试者中，<50 岁、51-64 岁、65-74 岁、75-84 岁和≥85 岁的患者分别为 495、444、403、583 和 258 例。90 天死亡率有较大的年龄相关差异（0.82%比 3.2%比 6.4%比 12.8%比 13.6%，p<0.01）。炎症和细胞表面标志物在第一周内没有年龄相关性差异。老年患者在急诊科就诊时和整个第一周的促凝标志物均较高（p≤0.03），但差异较小（1.0-1.7 倍）。在纳入止血和炎症标志物差异的模型中，老年患者的死亡风险变化不大（与<50 岁相比，年龄≥85 岁的患者 OR=4.36，调整感染前因素后的 OR=3.49）。出院时，尽管超过 85%的患者生命体征正常，表明临床康复，但老年患者的止血标志物和 IL-6 水平略有升高（p<0.01）。
CAP 住院期间凝血反应适度增加与年龄相关；然而，这些差异并不能解释死亡率的巨大差异。尽管临床康复，但老年人在出院时的免疫恢复可能会延迟。
