Inoue Arita Yoshie, Akutsu Koichi, Yamamoto Takeshi, Kawanaka Hidekazu, Kitamura Mitsunobu, Murata Hiroshige, Miyachi Hideki, Hosokawa Yusuke, Tanaka Keiji, Shimizu Wataru
Division of Cardiovascular Intensive Care, Nippon Medical School Hospital, Japan.
Intern Med. 2016;55(14):1845-52. doi: 10.2169/internalmedicine.55.5924. Epub 2016 Jul 15.
Objective A fever is observed in approximately one-third of cases of acute aortic dissection (AAD); however, the causes remain unclear. We investigated the mechanism of a fever in AAD by measuring the serum concentrations of inflammatory markers, mediators of coagulation and fibrinolysis, and procalcitonin, a marker of bacterial infection. Methods We retrospectively studied 43 patients with medically treated AAD without apparent infection. Patients were divided into those with (Group A; n=19) and without (Group B; n=24) a maximum body temperature >38°C. We established which patients fulfilled the criteria for systemic inflammatory response syndrome (SIRS), and its relationship with a fever was examined. Mediators of inflammation, coagulation and fibrinolysis were compared by a univariate analysis. Factors independently associated with a fever were established by a multivariate analysis. Results The criteria for SIRS were fulfilled in a greater proportion of patients in Group A (79%) than in Group B (42%, p=0.001). There was no difference in the procalcitonin concentration between Groups A and B (0.15±0.17 ng/mL vs. 0.11±0.12 ng/mL, respectively; p=0.572). Serum procalcitonin concentrations lay within the normal range in all patients in whom it was measured, which showed that the fever was caused by endogenous mediators. On the multivariate analysis, there was a borderline significant relationship between a fever and the prothrombin time-International Normalized Ratio (p=0.065), likely reflecting the extrinsic pathway activity initiated by tissue factor. Conclusion Our findings suggest that a fever in AAD could be caused by SIRS, provoked by endogenous mediators that influence the extrinsic coagulation pathway without elevating the serum procalcitonin concentration.
在大约三分之一的急性主动脉夹层（AAD）病例中观察到发热；然而，其病因仍不清楚。我们通过测量炎症标志物、凝血和纤溶介质以及降钙素原（一种细菌感染标志物）的血清浓度，研究了AAD发热的机制。方法：我们回顾性研究了43例接受药物治疗且无明显感染的AAD患者。患者被分为最高体温>38°C的患者（A组；n = 19）和最高体温未超过38°C的患者（B组；n = 24）。我们确定了哪些患者符合全身炎症反应综合征（SIRS）的标准，并检查了其与发热的关系。通过单因素分析比较炎症、凝血和纤溶介质。通过多因素分析确定与发热独立相关的因素。结果：A组符合SIRS标准的患者比例（79%）高于B组（42%，p = 0.001）。A组和B组之间的降钙素原浓度无差异（分别为0.15±0.17 ng/mL和0.11±0.12 ng/mL；p = 0.572）。所有测量降钙素原的患者血清降钙素原浓度均在正常范围内，这表明发热是由内源性介质引起的。多因素分析显示，发热与凝血酶原时间-国际标准化比值之间存在临界显著关系（p = 0.065），这可能反映了由组织因子启动的外源性途径活性。结论：我们的数据表明，AAD发热可能由SIRS引起，SIRS由影响外源性凝血途径的内源性介质引发，而血清降钙素原浓度未升高。
