In patients with stable heart failure, soluble TNF-receptor 2 is associated with increased risk for depressive symptoms.

In patients with stable heart failure, soluble TNF-receptor 2 is associated with increased risk for depressive symptoms.
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DOI:
10.1177/1099800413496454
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发表时间:
2014-07
影响因子:
2.5
通讯作者:
Irwin M
Irwin M
中科院分区:
医学4区
文献类型:
--
作者:
Moughrabi S;Evangelista LS;Habib SI;Kassabian L;Breen EC;Nyamathi A;Irwin M

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研究人员提出生物(炎症)和心理(抑郁)因素可能是心力衰竭(HF)患者预后较差和再入院的潜在机制。然而,调查这些患者炎症和抑郁症状之间联系的研究很少。我们检测了HF门诊患者炎症标志物c反应蛋白(CRP)、白细胞介素(IL)-6和可溶性肿瘤坏死因子受体2 (sTNR2)水平与抑郁症状之间的关系。55例患有纽约心脏协会II、III或IV级心衰(分别为49%、47%和4%)和平均射血分数(EF) 29.9±7.1%的患者(74.5%男性,60%白人,平均年龄71.6±11.3岁)完成了患者健康问卷(PHQ)-9,作为抑郁症状的测量指标。我们还获得了身高、体重、CRP、IL-6和sTNFR2水平。我们使用多变量回归来评估PHQ-9评分对每个炎症标志物的预测价值。22名(40%)参与者报告抑郁症状(PHQ-9评分≥5)。在控制了年龄、性别、体重指数、HF病因、EF和他汀类药物使用后,我们发现sTNFR2 (β = 0.35, p = 0.01)和IL-6 (β = 0.30, p = 0.04)水平之间存在显著相关性,但CRP (β = -)无显著相关性。96, p = .52),抑郁评分。我们的发现为越来越多的证据提供了支持,即炎症加剧可以解释抑郁症对心衰的影响。卫生保健提供者应该筛查心衰患者的抑郁,因为他们可能有更高的炎症增强和不良预后的风险。
Researchers have proposed biological (inflammation) and psychological (depression) factors as potential mechanisms for poorer outcomes and readmissions in heart failure (HF) patients. However, studies investigating the link between inflammation and depressive symptoms in these patients are few. We examined the relationships between levels of the inflammatory markers C-reactive protein (CRP), interleukin (IL)-6, and soluble tumor necrosis factor receptor 2 (sTNR2) and depressive symptoms in HF outpatients. 55 patients (74.5% men; 60% Whites; mean age 71.6 ± 11.3 years) with New York Heart Association Class II, III, or IV HF (49%, 47%, and 4%, respectively) and mean ejection fraction (EF) 29.9 ± 7.1% completed the Patient Health Questionnaire (PHQ)-9 as a measure of depressive symptoms. We also obtained height, weight, and CRP, IL-6, and sTNFR2 levels. We used multivariate regressions to assess the predictive value of PHQ-9 scores on each inflammatory marker. 22 (40%) participants reported depressive symptoms (PHQ-9 score ≥ 5). After controlling for age, gender, body mass index, HF etiology, EF, and statin use, we found significant relationships between levels of both sTNFR2 (β = .35, p = .01) and IL-6 (β = .30, p = .04), but not CRP (β = −.96, p = .52), and depression scores. Our findings add to a growing body of evidence supporting the proposition that heightened inflammation explains the effect depression has on HF. Health care providers should screen for depression in HF patients, as they may be at higher risk of augmented inflammation and poor outcomes.
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