致命性AMANITA中毒引起的肝衰竭死亡率很高,中国没有有效的解毒剂。2020年7月30日,云南省第一人民医院传染病和肝病科收治了一名67岁的女性患者,因致命的茴香中毒导致肝功能衰竭。患者因腹痛到急诊科治疗,吃了350-400克的Amanita蘑菇2天后呕吐和腹泻,伴有疲劳1天。体检无异常。实验室指标:丙氨酸转氨酶(ALT)4798U/L,天冬氨酸氨基转移酶(AST)10030U/L,活化部分凝血活酶时间(APTT)57.5s,凝血酶原时间(PT)72.1s,国际标准化比率(INR)8.66,凝血酶原活性(PA)10%。根据病人的病史,临床表现和实验室数据,诊断为土豆子肽蘑菇中毒和急性肝功能衰竭。根据安氏毒素中毒的机制作为肝肠循环,采用内镜逆行胰胆管造影术和超声引导下胆囊穿刺引流术进行胆汁引流以排出毒素,以阻断毒素的肝肠循环.然而,两种方法都失败了,所以进行了开放性胆囊造口术。因为病人的凝血功能很差,开腹胆囊造口术前给予人工肝血浆置换改善凝血功能,最终成功排出胆汁。经过总共19天的综合治疗,病人痊愈出院,随访1年后未发现后遗症。对于这样的患者,需要早期识别疾病,根据毒素的特点和毒理机制,尽快阻断毒素的肝肠循环,可能是抢救安氏毒素中毒肝衰竭患者的关键治疗方法,有必要结合积极补液和血液净化等综合治疗,以进一步提高生存率。
The fatality rate of liver failure caused by fatal
amanita poisoning is high, and there are no effective antidote drugs in China. On July 30, 2020, the department of infectious diseases and liver diseases of the First People\'s Hospital of Yunnan Province admitted a 67-year-old female patient with liver failure caused by fatal
amanita poisoning. The patient went to the emergency department for treatment due to abdominal pain, vomiting and diarrhea after eating 350-400 g of
amanita mushroom for 2 days, accompanied by fatigue for 1 day. There was no abnormality in physical examination. Laboratory indexes: alanine aminotransferase (ALT) 4 798 U/L, aspartate aminotransferase (AST) 10 030 U/L, activated partial thromboplastin time (APTT) 57.5 s, prothrombin time (PT) 72.1 s, international normalized ratio (INR) 8.66, prothrombinactivity (PA) 10%. Based on the patient\'s medical history, clinical manifestations and laboratory data, the diagnosis was
amanita peptide mushroom poisoning and acute liver failure. According to the mechanism of
amanita toxin poisoning as enterohepatic circulation, endoscopic retrograde cholangiopancreatography and ultrasound-guided gallbladder puncture and drainage for drainage of bile to discharge toxins were performed to interrupt the enterohepatic circulation of toxins. However, both methods failed, so open cholecystostomy was performed. Because the patient\'s coagulation function was very poor, artificial hepatic plasma exchange was given to improve coagulation function before open cholecystostomy, and eventually bile was drained successfully. After a total of 19 days of comprehensive medical treatment, the patient was cured and discharged from the hospital, and no sequelae was found after 1 year of follow-up. For such patients, early identification of the disease is required, and blocking the enterohepatic circulation of toxins as soon as possible according to the characteristics and toxicological mechanism of toxins may be the key treatment for rescuing patients with liver failure poisoned by amanita toxin, and it is necessary to combine comprehensive treatments such as active fluid replacement and blood purification to further improve the survival rate.