Gutjahr Ewgenija, Madea Burkhard
Institute of Forensic Medicine, University of Bonn, Stiftsplatz 12, 53111, Bonn, Germany.
Institute of Forensic Medicine, University of Bonn, Stiftsplatz 12, 53111, Bonn, Germany.
Forensic Sci Int. 2019 Apr;297:315-325. doi: 10.1016/j.forsciint.2019.02.026. Epub 2019 Feb 23.
Providing evidence of asphyxia death is a challenging issue in forensic pathology. Besides helpful macroscopical signs (e.g. strangulation mark, lung edema), recent data from literature indicate that the time of protracted asphyxia suffices to trigger an increase of giant cells and a migration of inflammatory cells from the bone marrow to the lung, thus offering a help in diagnosis of asphyxia death. In search of new valid asphyxia markers, the present study examined this hypothesis and investigated the leading role of pre-existing lung tissue cells and their functional state in reaction patterns to asphyxia. In specimens of suffocated human lungs following a short (n = 13) and a long asphyxia terminal episode (n = 15), and controls (sudden cardiovascular (n = 11) and traumatic deaths (n = 7)), the count of alveolar phagocytes, megakaryocytes, giant and mast cells, using H&E and toluidine blue staining, was performed. To show macrophage activation, immunohistochemical stainings for CD68, late (25F9) and early (MRP-8/-14) stage inflammatory markers were used. Measuring concentration of tryptase in femoral blood acted as a parameter for mast cell degranulation and consequently their activation. Results showed the lack of specificity of macroscopical parameters despite an association of suffocation with heavy lung edema. No significant differences in the numbers of inflammatory cells in the lungs of different case groups were detected. The doubling of MRP-8- and a five-fold elevation of MRP-14-positive cells compared to cardiovascular controls, proved an early activation state of pre-exiting monocytes in protracted asphyxia. These activated monocytes induced the degranulation of mast cells, resulting in slightly elevated tryptase levels in suffocation compared to cardiovascular controls. In summary, the duration of asphyxia (max. 20 min in cases investigated) only suffices to cause changes on molecular level, being not detectable in any specific macroscopical or histological form in the lung. Despite a potential utility of this molecular insight in individual cases, these results point to the classic doctrine of the evaluation of a rounded overall picture, accentuating on the proof of the ligature tool and the marks of suffocation process.
在法医病理学中，提供窒息死亡的证据是一个具有挑战性的问题。除了有用的宏观体征（如勒痕、肺水肿）外，文献中的最新数据表明，长时间窒息足以引发巨细胞数量增加以及炎症细胞从骨髓迁移至肺部，从而有助于窒息死亡的诊断。为了寻找新的有效窒息标志物，本研究检验了这一假设，并研究了肺组织中既有细胞及其功能状态在窒息反应模式中的主导作用。在经历短时间（n = 13）和长时间窒息终末期（n = 15）的窒息人肺标本，以及对照组（突发心血管疾病死亡（n = 11）和创伤性死亡（n = 7））中，使用苏木精-伊红染色和甲苯胺蓝染色对肺泡吞噬细胞、巨核细胞、巨细胞和肥大细胞进行计数。为显示巨噬细胞活化，使用了针对CD68、晚期（25F9）和早期（MRP-8/-14）阶段炎症标志物的免疫组织化学染色。测量股静脉血中类胰蛋白酶的浓度作为肥大细胞脱颗粒及活化的参数。结果显示，尽管窒息与重度肺水肿有关，但宏观参数缺乏特异性。不同病例组肺内炎症细胞数量未检测到显著差异。与心血管疾病对照组相比，MRP-8阳性细胞数量翻倍，MRP-14阳性细胞数量增加五倍，证明在长时间窒息中既有单核细胞处于早期活化状态。这些活化的单核细胞诱导肥大细胞脱颗粒，导致窒息组类胰蛋白酶水平相较于心血管疾病对照组略有升高。总之，窒息持续时间（本研究中最长20分钟）仅足以引起分子水平的变化，在肺中无法以任何特定的宏观或组织学形式检测到。尽管这种分子层面的见解在个别案例中可能有用，但这些结果指向了全面评估的经典原则，强调了勒颈工具的证据和窒息过程的痕迹。
