1 Unit of Legal Medicine, S. Bortolo General Hospital, Vicenza, Italy.
2 Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
Int J Immunopathol Pharmacol. 2018 Jan-Dec;32:2058738418776526. doi: 10.1177/2058738418776526.
Current scientific consensus about the physiopathology in the progression from severe sepsis to septic shock and death focuses on myocardial contractile dysfunction. Nevertheless, objective parameters to establish a pathological correlate of a fatal outcome are lacking; then a cause of death due to sepsis can remain an unsolved problem. We first reviewed all death cases recorded at our institutions during the period from 2007 until 2015. Then, we conducted a retrospective study of a selected autopsy series of people who had received "sepsis" as cause of death. Two pathologists re-examined the heart sections while the most suitable myocardial sample for each case was stained for immunohistochemistry with antibodies targeted for specific inflammatory-related molecules. We used specific antibodies for the following markers: alpha-smooth muscle actin (alpha-SMA); fibronectin; matrix metallopeptidase 9 (MMP-9); intercellular adhesion molecule 1 (ICAM-1); caspase-3; lactoferrin (LF); cluster differentiation 15 (CD15). The statistical significance of differences was assessed using student's t-test for unpaired data or non-parametric Mann-Whitney or Wilcoxon tests for skewed variables or one-way analysis of variance and post hoc Scheffe's test for continuous variables and Pearson's χ-test for discrete variables. Linear regression analysis was used to determine the presence of a correlation between continuous variables. At our institutions, 2220 deaths have been recorded during the period study. Sepsis accounted as a cause of death for the 20% of total. We finally enrolled 56 cases; of these, only 20 were positive for microbiological analysis. At histological examination, clear inflammation was detectable in the 32% of cases; otherwise, immunohistochemical reaction showed a positive reaction for LF and CD15 in more than a half cases (56%). We still ignore all the underlying mechanisms of sepsis and all its pathophysiological connections with cardiac metabolism; in this sense, we aim to corroborate the diagnostic value of anti-LF and anti-CD15 staining for the post-mortem detection of myocardial inflammation.
目前,关于从严重脓毒症到感染性休克和死亡的病理生理学的科学共识集中在心肌收缩功能障碍上。然而,缺乏确定致命结果的病理相关的客观参数;因此,由于败血症导致的死亡仍然是一个悬而未决的问题。我们首先回顾了我们机构在 2007 年至 2015 年期间记录的所有死亡病例。然后,我们对一组死因诊断为“败血症”的尸检进行了回顾性研究。两位病理学家重新检查了心脏切片,同时为每个病例选择最合适的心肌样本进行针对特定炎症相关分子的免疫组织化学染色。我们使用了以下标记物的特异性抗体:α-平滑肌肌动蛋白(alpha-SMA);纤维连接蛋白;基质金属蛋白酶 9(MMP-9);细胞间黏附分子 1(ICAM-1);半胱天冬酶 3;乳铁蛋白(LF);簇分化 15(CD15)。使用学生 t 检验(用于非配对数据)或非参数 Mann-Whitney 或 Wilcoxon 检验(用于偏态变量)、方差分析和事后 Scheffe 检验(用于连续变量)和 Pearson χ 检验(用于离散变量)评估差异的统计学意义。使用线性回归分析确定连续变量之间存在相关性。在我们的机构中,在研究期间记录了 2220 例死亡。败血症占总死亡人数的 20%。我们最终纳入了 56 例病例;其中,只有 20 例的微生物分析结果为阳性。在组织学检查中,32%的病例可检测到明显的炎症;否则,免疫组化反应显示超过一半(56%)的病例 LF 和 CD15 呈阳性反应。我们仍然忽略了败血症的所有潜在机制及其与心脏代谢的所有病理生理联系;在这个意义上,我们旨在证实抗 LF 和抗 CD15 染色对死后心肌炎症检测的诊断价值。