Clinical Pathological Analysis of Death from Paraquat Poisoning_West China Medical Journal

Authors：

 ZHUPeng ¹ , LIUYuan ¹ , ZHUHai-biao ¹ , ZIJia-ji ² , CHENXia-meng ¹ , YANGYu ¹ ,  GUANPeng ¹

1. Department of Forensic Pathology, West China School of Preclinical and Forensic Science, Sichuan University, Chengdu, Sichuan 610041, P. R. China;
2. School of Basic Medical Sciences, Dali University, Dali, Yunnan 671000, P. R. China;

Corresponding author：

GUANPeng, Email: guanpengcn@yahoo.com

Keywords：

Paraquat poisoning; Pulmonary fibrosis; Forensic pathology

DOI：

10.7507/1002-0179.20140276

Video：

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Objective To analyze the clinical and pathologic features of paraquat poisoning, discuss the damage mechanism of pulmonary fibrosis caused by paraquat poisoning. Methods We retrospectively analyzed the paraquat poisoning-related cases collected in recent years from January 2010 to December 2013, and compared the clinical features and pathologic changes between acute and chronic paraquat poisoning cases. Results The main clinical and pathologic manifestation of paraquat poisoning was multiple organ damage, especially with lung as its target organ. In acute poisoning deaths, the lung injury was characterized by the pulmonary edema and formation of lung transparent membrane; In chronic poisoning deaths, the injury was characterized by the formation of lung transparent membrane and pulmonary fibrosis. Conclusion In order to make an earlier diagnosis in clinical cases, we should strengthen the cognition of clinical manifestations and damage mechanism of paraquat poisoning. To obtain an accurate conclusion in forensic medicine appraisal, we should draw a comprehensive analysis of the forensic case, the clinical data, the toxicological analysis and the autopsical results.

Citation： ZHUPeng, LIUYuan, ZHUHai-biao, ZIJia-ji, CHENXia-meng, YANGYu, GUANPeng. Clinical Pathological Analysis of Death from Paraquat Poisoning. West China Medical Journal, 2014, 29(5): 910-913. doi: 10.7507/1002-0179.20140276 Copy

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14.	蔡琳, 吴壮, 徐军. 博莱霉素诱导α平滑肌肌动蛋白Cre重组酶转基因小鼠肺纤维化上皮细胞-间质转分化的研究[J]. 中国呼吸与危重监护杂志, 2009, 8(1):52-56.
15.	高振芹, 胡永斌, 彭劲武, 等. ERK信号通路调控二氧化硅诱导的人支气管上皮细胞上皮-间质转化[J]. 中南大学学报·医学版, 2011, 36(11):1085-1089.

1. 李建云, 汪秀兰, 张华, 等. 2例百草枯中毒死亡病例护理讨论报告[J]. 天津护理, 2012, 20(2):75-76.
2. 韦建华, 李航天. 急性百草枯中毒死亡1例报告[J]. 职业与健康, 2006, 22(1):66-67.
3. Hwang KY, Lee EY, Hong SY. Paraquat poisoning in Korea[J]. Arch Environ Health, 2002, 57(2):162-166.
4. 皮丽娟, 祝伟. 百草枯中毒致肺损伤的作用机制及治疗新进展[J]. 内科急危重症杂志, 2013, 19(4):236-238.
5. 黄光照. 法医毒理学[M]. 3版. 北京:人民卫生出版社, 2004:197.
6. 刘鹏, 梁宇光, 何跃忠, 等. 百草枯中毒的基础研究及救治进展[J]. 中国工业医学杂志, 2010, 23(5):364-366.
7. 杨明, 刘莹, 蒋剑峰, 等. 百草枯中毒死亡30例尸解分析[J]. 西部医学, 2008, 20(4):826, 828.
8. 王永进. 百草枯中毒治疗的研究进展[J]. 中国急救医学, 2003, 23(6):49-51.
9. 赖伯才. 百草枯中毒致急性肺损伤的机制及其治疗进展[J]. 基层医学论坛, 2013, 17(28):3772-3774, 3777.
10. 金克炜. 肺癌的肺透明膜形成[J]. 云南医药, 1990, 11(1):54-56.
11. Selman M, King TE, Pardo A, et al. Idiopathic pulmonary fibrosis:prevailing and evolving hypotheses about its pathogenesis and implications for therapy[J]. Ann Intern Med, 2001, 134(2):136-151.
12. Willis BC, Dubois RM, Borok Z. Epithelial origin of myofibroblasts during fibrosis in the lung[J]. Proc Am Thorac Soc, 2006, 3(4):377-382.
13. Rho JK, Choi YJ, Lee JK, et al. Epithelial to mesenchymal transition derived from repeated exposure to gefitinib determines the sensitivity to EGFR inhibitors in A549, a non-small cell lung cancer cell line[J]. Lung Cancer, 2009, 63(2):219-226.
14. 蔡琳, 吴壮, 徐军. 博莱霉素诱导α平滑肌肌动蛋白Cre重组酶转基因小鼠肺纤维化上皮细胞-间质转分化的研究[J]. 中国呼吸与危重监护杂志, 2009, 8(1):52-56.
15. 高振芹, 胡永斌, 彭劲武, 等. ERK信号通路调控二氧化硅诱导的人支气管上皮细胞上皮-间质转化[J]. 中南大学学报·医学版, 2011, 36(11):1085-1089.

West China Medical Journal

Clinical Pathological Analysis of Death from Paraquat Poisoning

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