Brunkhorst F M, Clark A L, Forycki Z F, Anker S D
Krankenhaus Zehlendorf, Department of Internal Medicine, Berlin, Germany.
Int J Cardiol. 1999 Dec 15;72(1):3-10. doi: 10.1016/s0167-5273(99)00118-7.
Exposure to bacterial endotoxin, perhaps due to bowel congestion or ischaemia and altered gut permeability, may result in immune activation that is characteristic for patients with severe heart failure. It is known that blood procalcitonin rises in response to bacterial endotoxin exposure.
We measured procalcitonin in a group of 29 patients with acute cardiogenic shock and no sign of infection (all without bacteraemia) and 26 with septic shock. Blood was analysed for procalcitonin, interleukin-6, tumour necrosis factor-alpha (TNF-alpha), c-reactive protein (CRP) and neopterin. Patients were managed conventionally in an intensive care unit with no further experimental procedures.
Three cardiogenic (10%) and seven septic shock patients (27%) survived. Most patients with acute heart failure surviving 12 h or more (18 of 20) developed a pyrexia (738.0 degrees C) of unknown origin in the absence of positive cultures, with a rise in procalcitonin (1.4+/-0.8 to 48.0+/-16.2 ng/ml, P<0.001), CRP (76.5+/-16.4 to 154.7+/-22.9 mg/l, P<0.001) and neopterin (20.7+/-3.5 to 41.2+/-6.7 nmol/l, P<0.001). Patients with septic shock had higher initial levels of cytokines, and higher peak levels. Those with heart failure surviving (n=3) and those dying in the first 12 h (n=9) had no rise in cytokine levels. The patients with high procalcitonin had a higher temperature (38.9+/-0.3 vs. 37.3+/-0.23 degrees C, P<0.05), TNF-alpha (43.95+/-9.64 vs. 16.43+/-4.33 pg/ml; P<0.005) and CRP (146.1+/-18.4 vs. 68.2+/-39.6 mg/ml, P<0.005). Peak procalcitonin levels correlated with peak temperature (r=0.74, P<0.001).
Cardiogenic shock causes a pyrexia of unknown origin in patients surviving for 12 h and that is associated with a rise in procalcitonin levels. This lends support to the hypothesis that patients with cardiogenic shock may be being exposed to bacterial endotoxin at a time when bowel wall congestion and or ischaemia is likely to be present.
接触细菌内毒素,可能是由于肠道充血或缺血以及肠道通透性改变,可能导致免疫激活,这是重症心力衰竭患者的特征。已知血液降钙素原会因接触细菌内毒素而升高。
我们测量了29例急性心源性休克且无感染迹象(均无菌血症)患者和26例感染性休克患者的降钙素原。对血液进行降钙素原、白细胞介素-6、肿瘤坏死因子-α(TNF-α)、C反应蛋白(CRP)和新蝶呤分析。患者在重症监护病房接受常规治疗,未进行进一步的实验操作。
3例心源性休克患者(10%)和7例感染性休克患者(27%)存活。大多数存活12小时或更长时间的急性心力衰竭患者(20例中的18例)在无阳性培养结果的情况下出现不明原因发热(体温≥38.0℃),降钙素原升高(1.4±0.8至48.0±16.2 ng/ml,P<0.001),CRP升高(76.5±16.4至154.7±22.9 mg/l,P<0.001),新蝶呤升高(20.7±3.5至41.2±6.7 nmol/l,P<0.001)。感染性休克患者的细胞因子初始水平和峰值水平更高。存活的心源性休克患者(n = 3)和在最初12小时内死亡的患者(n = 9)的细胞因子水平没有升高。降钙素原水平高的患者体温更高(38.9±0.3 vs. 37.3±0.23℃,P<0.05),TNF-α更高(43.95±9.64 vs. 16.43±4.33 pg/ml;P<0.005),CRP更高(146.1±18.4 vs. 68.2±39.6 mg/ml,P<0.005)。降钙素原峰值水平与峰值体温相关(r = 0.74,P<0.001)。
心源性休克会导致存活12小时的患者出现不明原因发热,且与降钙素原水平升高有关。这支持了这样一种假设,即心源性休克患者在可能存在肠壁充血和/或缺血时可能接触到细菌内毒素。