免疫正常人和过敏性猝死者类胰蛋白酶含量测定

目的观察免疫正常人和过敏性猝死者血清类胰蛋白酶、IgE含量及类胰蛋白酶在咽喉、肺和小肠组织的表达,探讨过敏性猝死的诊断方法。方法采用荧光酶联免疫法（FEIA）测定115例正常人和6例过敏性猝死者血清类胰蛋白酶;采用酶联免疫吸附试验（ELISA）测定7例过敏性猝死者血清IgE含量;采用免疫组织化学方法观察15例过敏性猝死者咽喉、肺、小肠组织中类胰蛋白酶的表达,并采用BL-2000病理图像分析系统进行定量分析。结果①115例免疫正常人血清中类胰蛋白酶含量在0.80μg/L～8.86μg/L之间,性别之间无明显差异（P〉0.05）。20岁以下、21～40岁和41～60岁组之间血清中类胰蛋白酶含量无明显差别（P〉0.05）,而60岁以上组含量高于其他年龄组（P〈0.05）;②6例过敏性猝死者血清类胰蛋白酶含量均高于免疫正常人;③7例过敏性猝死者中有6例血清IgE水平高于正常值（〉333U/mL）;④过敏性猝死者咽喉、肺和小肠组织中类胰蛋白酶表达升高,与对照组之间有显著性差异（P〈0.01）。结论过敏性猝死者血清IgE、类胰蛋白酶含量及咽喉、肺和小肠组织类胰蛋白酶表达升高,可对敏性猝死的诊断有一定参考价值。     

过敏性休克死亡者肺组织类胰蛋白酶及类糜蛋白酶的表达

目的观察类胰蛋白酶与类糜蛋白酶在过敏性休克死亡人体肺组织中的表达,并探讨其在过敏性休克死亡法医学鉴定中的意义。方法应用荧光免疫组化法对类胰蛋白酶与类糜蛋白酶进行检测,同时以10例CO中毒死者为对照：采用图像分析仪及Image—pro plus 5．0．2软件进行图像分析,计算阳性肥大细胞数及类胰蛋白酶、类糜蛋白酶荧光表达强度。结果与对照组相比,实验组肺组织中类胰蛋白酶和类糜蛋白酶表达差异有统计学意义（P〈0．05）。结论过敏性休克死亡人体肺组织中类胰蛋白酶与类糜蛋白酶的表达增强．可作为过敏性休克死亡的形态学诊断依据。     

肥大细胞类胰蛋白酶的免疫组化染色观察

目的　观察过敏性休克死亡者咽喉、肺、小肠组织肥大细胞类胰蛋白酶 (MCT) ,探讨过敏性休克死亡法医鉴定的形态学依据。方法　交通事故致严重颅脑损伤死亡者 10例 (对照组 )、明确诊断为过敏性休克死亡者 15例(实验A组 )和羊水栓塞死亡者 8例 (实验B组 )的尸体 ,分别取其咽喉部、肺及小肠组织 ,石蜡切片 ,HE染色及用免疫组化超敏SP法进行MCT染色。结果　实验A组的咽喉部组织充血、水肿 ,咽喉部粘膜下层MCT增多 (MCT颗粒计数为 48 2 3 ) ;实验B组的咽喉部粘膜下层MCT增多 (MCT颗粒计数为 42 72 )。肺间质尤其是小支气管壁及小血管壁上MCT增多 (MCT颗粒计数分别为 46 98和 43 5 0 ) ,小肠粘膜层MCT增多 (MCT颗粒计数分别为 48 2 3和 42 72 )。对照组的咽喉部、肺和小肠MCT颗粒计数较少 ,分别为 7 79、 12 94和 2 0 2 5。实验A组与对照组相比 ,两组具有显著性差异 (P <0 0 1) ;实验A、B组相比 ,两组无显著性差异 (P >0 0 1)。结论　过敏性休克及羊水栓塞死亡的尸体 ,其咽喉部组织、肺组织及胃肠道组织MCT增多。     

类胰蛋白酶和IgE测定在过敏性猝死诊断中的应用研究

目的探讨过敏性猝死法医学鉴定的诊断方法和指标。方法采取10例正常人、9例过敏性猝死和19例其他死因（排除过敏反应、冠心病）尸体的静脉血，采用荧光酶联免疫法（Pharmacia UniCAP100过敏原定量分析仪）和酶联免疫吸附试验ELISA法分别测定血清肥大细胞类胰蛋白酶和]gE含量，采用免疫组化方法观察过敏性猝死和其他死因的肺组织中的肥大细胞类胰蛋白酶免疫组化染色。结果过敏性猝死者的血清类胰蛋白酶和IgE含量升高，与其他死因之间的差异具有显著性意义（P〈0．01），其他死因和正常人之间的差异无统计学意义（P〉0．05）；与其它死因相比，过敏性猝死肺组织中的肥大细胞类胰蛋白酶免疫组化阳性染色增强（P〈0．01）。结论过敏性猝死者血清IgE和肥大细胞类胰蛋白酶含量显著升高；过敏性猝死者肺组织中肥大细胞类胰蛋白酶染色增强。     

类胰蛋白酶在过敏性休克死者心肺肠组织中的表达

目的观察过敏性休克死亡者心、肺及空肠组织中类胰蛋白酶免疫荧光表达的强度,为过敏性休克死亡提供法医学鉴定依据。方法运用免疫荧光染色法对过敏性休克死亡者心、肺及空肠组织进行类胰蛋白酶染色,荧光显微镜观察并采集图像,Image-pro plus6.2软件进行图像分析并计算阳性颗粒数,运用SPSS17.0软件进行统计学分析。结果过敏性休克死亡者心、肺及空肠组织中类胰蛋白酶的表达均明显高于对照组(P0.05),其差异具有统计学意义。结论当高度怀疑过敏性休克但无法获得满意的血液标本时,检测其心、肺及空肠组织中类胰蛋白酶的免疫表达可作为过敏性休克死亡法医学鉴定的辅助手段。     

性窒息诱发冠心病猝死1例

1 案例 葛某,男,64岁,退休工人.某日中午邻居告知其子女.葛某尾内白天持续亮着灯且近期一直未见其人.其子女打开反锁的大门,发现葛某死于家中,遂报警.据其子女反映,葛某平素性格孤僻,与子女来往甚少,其妻死后长期独居,平素有"露阴癖",偶与其他异性交往.     

冠心病合并冠状动脉血栓猝死的法医病理学特征

目的探讨冠心病合并冠状动脉血栓形成导致猝死的法医学特征。方法收集96例因冠心病而猝死的案例,并将其分为血栓形成组与无血栓形成组,对发病时间、诱因、病理特征等方面进行分析。结果两组都以男性为主,在季节和时间节律分布、诱因构成上差异无统计学意义,但血栓形成组中年龄〈40岁发病率更高;血栓形成组的心脏质量和冠脉狭窄程度低于无血栓形成组,而两组冠脉粥样硬化累及的支数（≥2）、累及长度及合并心梗等指标差异均无统计学意义,但血栓形成组有低于无血栓形成组的趋势。结论两组人群都以男性为主且发病诱因、冠脉病变部位及致死机制相似,但血栓形成组的发病年龄较轻,心脏的病变程度较低,法医学解剖中当认真鉴别。     

冠心病猝死者心肌中SOCS-1和Bax的表达

目的采用免疫组化方法,观察细胞因子信号转导抑制因子-1(SOCS-1)和Bax在冠心病猝死(SCD)者心肌中的表达情况,探讨其对SCD诊断的意义。方法 25例诊断为SCD者心脏样本为实验组,25例非心血管疾病猝死者心脏样本为对照组。应用免疫组织化学方法检测SOCS-1和Bax在心肌中的表达,应用SPSS 17.0软件进行统计处理,组间比较采用秩和检验。结果 SCD猝死者心肌SOCS-1与Bax的表达明显高于对照组,Uc值SOCS-1为5.830 6,Bax为5.573,两种指标组间比较,差异均有显著性意义(P<0.01);SCD组中SOCS-1表达阳性以上且Bax表达弱阳性以上有22例,而正常对照组仅有1例。结论 SOCS-1与Bax均可能参与了细胞凋亡的过程,检测两种指标在心肌中阳性表达,可以为SCD的诊断提供客观依据,且联合检测可提高SCD诊断的特异性。     

急性心功能障碍大鼠心肌中BNP的表达

目的研究大鼠急性心功能障碍时心肌组织中脑钠肽(brain natriuretic peptide,BNP)的表达变化,探讨BNP在急性心功能障碍的法医学诊断中的应用价值。方法建立大鼠急性心功能障碍模型,运用免疫组织化学、Western印迹法、实时RT-PCR等技术检测心功能障碍过程中心肌组织BNP蛋白和BNP mRNA的表达变化。结果随心功能障碍持续时间增加,免疫阳性着色不断增强。1～2h主要表现为弱阳性,4～6h心肌细胞主要表现为阳性,10～12h大鼠心肌细胞表现为强阳性。Western印迹法和实时RT-PCR结果均显示,随心功能障碍持续时间增加,BNP明显升高,而且心功能障碍1h即能观察到BNP mRNA显著升高。结论检测心肌组织中BNP蛋白及BNP mRNA的表达能为法医病理学工作者客观评价心功能状态提供一种新的途径。     

实验性兔羊水栓塞肥大细胞类胰蛋白酶的含量变化

目的观察家兔羊水栓塞 (AFE)后肺组织中肥大细胞类胰蛋白酶 (MCT)含量的变化。方法分别于健康怀孕家兔耳缘静脉注入羊水、制造羊水栓塞的动物模型 ;取肺组织进行HE染色和免疫组织化学MCT染色 ,镜下观察AFE兔肺组织中MCT的变化。结果对照组兔肺组织MCT呈弱阳性反应 (平均阳性细胞计数 11 2 5个 ) ,注入羊水组和注入胎盘提取液与羊水混合液组肺组织中MCT呈强阳性反应 (平均阳性细胞计数分别为 3 2 98和 45 5 3个 )。结论在羊水栓塞时兔肺组织MCT含量增加     

脑钠尿肽的表达调控机制及其法医学应用

脑钠尿肽是主要由心肌细胞分泌的钠尿肽类激素,通常在心肌细胞受到牵拉时产生,具有利钠、利尿、舒张血管、调节血压等功能。临床上BNP是反映心功能的重要指标之一,近年的研究表明,BNP在法医学中对心源性猝死的诊断也具有十分重要的价值。本文综述了BNP的分子结构、表达调控及法医学应用的进展。     

Sudden Death due to Brainstem Leukemic Hemorrhage:A Case Report

Introduction Leukemia is a hematologic neoplasm character- ized by potential infectious and hemorrhagic com- plications. In adult patients with acute leukemia, in- fection is the most common complication. Intracra- nial hemorrhage （ICH） is the second most common complication. However, ICH has been identified as the major cause of morbidity and mortality in pa- tients with leukemia[1-6].     

Sudden Death Due to Undiagnosed Rheumatic Heart Disease in a Child

We report the case of a 5‐year‐old boy who died from complications of rheumatic heart disease with atypical presentation. He was hospitalized for recent inflammatory and neurological symptoms. He was diagnosed with viral encephalitis. He died the day after he was discharged. The macroscopic autopsy findings were unremarkable. Histology revealed typical rheumatic heart disease. Neuropathology showed cerebral infarction due to an embolic event linked with the rheumatic valvulitis. The cause of death was determined as heart failure due to rheumatic heart disease secondary to an undiagnosed acute rheumatic fever. It is related to an autoimmune response to infection with group A streptococcus. It mainly affects children in developing countries. In our case, viral encephalitis was consistent with the medical history and the proper diagnosis was made on histological analysis. Forensic pathologists should consider this diagnosis facing a sudden unexpected death in childhood, even in industrialized countries.     

Eosinophilic Coronary Periarteritis with Arterial Dissection: The Mast Cell Hypothesis

A subset of coronary arterial dissections is associated with eosinophilic coronary periarteritis (ECPA); however, the pathogenesis of the process remains unclear. Mast cells normally reside in coronary arterial adventitia and are known mediators of eosinophilic inflammatory conditions such as type I hypersensitivity reactions. We report two cases in which coronary arterial dissection with ECPA was detected at autopsy. Tryptase, CD68, CD4, CD8, and CD1a immunohistochemical staining was performed to better characterize inflammation. While eosinophils represented a prominent periadventitial inflammatory cell, there were slightly more lymphocytes: CD4/CD8 ratios were within expected reference ranges. There were moderate numbers of macrophages, and few neutrophils or dendritic cells. Numbers of mast cells in dissected versus nondissected sections were compared: adventitial mast cell densities were threefold higher in dissected portions and showed a trend toward increased degranulation. These findings suggest that mast cells may play a role in orchestrating inflammation in cases of ECPA.     

Evaluation of Agonal Cardiac Function for Sudden Cardiac Death in Forensic Medicine with Postmortem Brain Natriuretic Peptide (BNP) and NT-proBNP: A Meta-analysis

Sudden cardiac death (SCD) is an unexpected death caused by a sudden loss of cardiac function, which is currently a global public health problem. Evaluation of the agonal cardiac function of the deceased is a quite important task for the diagnosis of SCD in forensic medicine. Brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) are currently considered as significant biomarkers for the diagnosis of heart failure in both clinical and forensic practices. To investigate the postmortem evaluation roles of postmortem BNP and NT-proBNP levels for SCD, the present study meta-analyzed eight related studies from Embase, Cochrane Library, PubMed, China Biomedical Literature Database, China National Knowledge Infrastructure, and Wanfang Data. Newcastle–Ottawa Quality Assessment Scale was used to assess the quality of the included literature, and the meta-analysis was performed by RevMan 5.3.5 software. Postmortem NT-proBNP in pericardial fluid showed higher levels in the SCD group than that of the non-SCD group with the weighted mean difference = 3665.74, 95% confidence interval: 1812.89–5518.59, and p = 0.0001. However, postmortem levels of BNP in pericardial fluid and NT-proBNP in serum revealed no statistical difference between SCD and non-SCD subjects. The results of present meta-analysis demonstrated that postmortem NT-proBNP in the pericardial fluid could be used as an ancillary indicator for evaluation of agonal cardiac function in forensic medicine.     

Sudden Death Due to Hydatid Disease: A Six‐Year Study in the Northern Part of Tunisia

Human ecchinococcosis also known as hydatid disease is a zoonotic infection caused by the tapeworm Ecchinococcus with 2–3 Million cases worldwide. We hereby report a 6 years period study of Sudden death due to hydatidosis aiming to analyze the epidemiological criteria, death circumstances, and autopsy observations attributed to hydatid disease. During the past 6 years, 26 death cases were due to hydatid disease. Our analysis shows that the sex ratio (M/F) was 1.6, the mean age was 31‐year old, and 65% of the subjects lived in rural places. In 17 cases, death occurred in the victim's place, five victims died after a heavy exercise, and in two cases, death occurred immediately after trauma. At autopsy, 91% of the cysts were found in the liver. In three cases, death followed a septic state, and in two cases, it followed an acute respiratory failure. Death was attributed to anaphylaxis in 17 cases.     

Multiple Giant Coronary Artery Aneurysms: A Rare Cause of Sudden Cardiac Death

Multiple giant aneurysms involving the coronary arteries are uncommon and rarely reported. In the presented case, a 63‐year‐old man with poorly controlled hypertension died suddenly. Gross autopsy examination showed multiple giant thrombus‐filled coronary artery aneurysms, atherosclerotic coronary artery disease, and cardiomegaly. Histological sections of the coronary aneurysms showed atherosclerotic changes with both organized and fresh thrombus. Giant coronary aneurysm is defined as a segmental enlargement of a coronary artery with a diameter exceeding 20 mm or more. The main etiology of this nebulous entity is attributed to atherosclerosis and inflammatory or inherited connective tissue disorders with the remainder being congenital, infectious, or idiopathic. Before its cataclysmic presentation, when ruptured or thrombosed, giant coronary aneurysm usually has a silent clinical course. Sudden death owing to giant multiple coronary aneurysms is rare and mandates careful classification of the aneurysms and prudent search for autoimmune‐mediated or genetically based factors for subsequent ancillary autopsy studies.     

Sudden Death Caused by Anomalous Origin of the Coronary Artery During Exercise

Anomalous origin of the coronary artery (AOCA) is a rare, but important cause of sudden cardiac death among young athletes. Nine autopsy cases (8 male, 1 female; mean age, 17.9 years; age range, 11–31 years) of sudden death during or just after exercise caused by AOCA were reviewed. The exercises performed at the time of death were running (4 cases), soccer (2 cases), and baseball, swimming and kendo (Japanese swordsmanship) (1 case each). In 6 cases, the left coronary artery arose from the right sinus of Valsalva, and in 3, the right coronary artery from the left sinus. The coronary arteries passed between the pulmonary artery and the aorta with an acute angle takeoff from the orifice. Three cases had cardiovascular manifestations prior to death. In cases with cardiovascular manifestations, novel imaging methods should be considered to prevent sudden death.     

A Case of Sudden Infant Death Due to Incomplete Kawasaki Disease

Although Kawasaki disease (KD) is a self‐limiting disease, it may cause sudden cardiac death. Diagnosis of KD is principally based on clinical signs; however, some infant cases do not meet the criteria. Such cases are identified as incomplete KD. The sudden death risk in incomplete KD cases is similar to conventional KD. In our 5‐month‐old case, he had been admitted to a hospital for a fever and suppuration at the site of Bacille de Calmette et Guerin (BCG) vaccination. However, after discharge from the hospital, his C‐reactive protein (CRP) levels declined, he got indisposed and died suddenly. A medico‐legal autopsy revealed myocarditis, coronaritis, platelet‐aggregated emboli in coronary arteries, and myocardial degeneration, suggesting that the fatal myocardial infarction was due to thrombus emboli in the coronary arteries. Forensic pathologists therefore should pay attention to the cardiac pathology originated from incomplete KD as a potential cause in cases of sudden infant death.     

病毒性心肌炎猝死心肌MCP-1表达及其法医学意义

目的探讨单核细胞趋化蛋白1（monocyte chemoattractant protein-1,MCP-1）在病毒性心肌炎（viral myocarditis,VMC）所致猝死者心肌组织中的表达及其意义。方法运用改良的免疫组织化学方法,观察VMC猝死组和对照组心肌组织中MCP-1的表达情况,应用统计学处理,比较两组间的表达差异。结果20例VMC猝死组中有17例MCP-1染色阳性;而20例非VMC猝死对照组仅4例局部散在MCP-1弱阳性表达,其余均阴性。VMC组MCP-1阳性表达率明显高于对照组（P〈0.01）。结论MCP-1的免疫组织化学检测可作为法医病理学诊断VMC所致猝死较为客观的病理形态学指标之一。