蜡样芽孢杆菌食物中毒后肝功能衰竭,这是一种未得到充分认识的病症:病例报告。

IF 2.5 Q2 GASTROENTEROLOGY & HEPATOLOGY
Olivier Chatelanat, Mikaël de Lorenzi-Tognon, Laurent Spahr, Abdessalam Cherkaoui, Roger Stephan, Marie Ongaro, Laurent Kaiser, Nicolas Goossens
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引用次数: 0

摘要

背景:已知蜡样芽孢杆菌(B. cereus)可引起两种食源性疾病:腹泻综合症和呕吐综合症。由于这两种疾病的病程通常是自限性的,因此报告率很低。据报道,肝功能衰竭、肺出血和脑水肿等罕见病例(有时甚至是致命病例)主要发生在儿童和青壮年身上。病例摘要:一名 48 岁的女性患者因进食米饭沙拉后不到 30 分钟出现呕吐、腹泻、寒战(无发热)、气喘和腹部弥漫性绞痛而到急诊科就诊。她的既往病史与胆囊切除术和治愈的桥本氏病有关。她没有服用任何药物,并宣称每周只喝一杯酒。在急诊科,她接受了对乙酰氨基酚、甲氧氯普胺、昂丹司琼治疗,并静脉输注了生理盐水。血气分析显示她患有代谢性酸中毒和高乳酸血症,凝血功能显示她的凝血酶原活性较低[32%;正常值(N):70-140],因子V活性较低(15%;正常值:>70)。转氨酶升高,伴有高胆红素血症、脂肪酶升高和横纹肌溶解症。患者接受了 N-乙酰半胱氨酸治疗。腹部超声波检查未发现慢性肝病或肝肿大的迹象。入院第二天,精神运动活动有所改善,转氨酶和脂肪酶开始下降。横纹肌溶解症逐渐恶化,第3天达到高峰。肝病筛查结果显示,病毒性和自身免疫性肝衰竭的病因均为阴性。粪便培养对蜡样芽孢杆菌菌落呈阳性,在处理的米饭沙拉样本中也发现了这种菌落,而血液培养呈阴性。患者的病情逐渐好转,包括肝功能指标和精神运动能力,第 9 天即可出院回家:我们描述了一例成年患者因食源性蜡样芽孢杆菌中毒而导致肝细胞功能障碍的罕见病例。尽管该病例并不常见,但所报告的肝功能障碍的严重程度和麦角毒素对肝脏的毒性机制表明,在发生食源性中毒时应避免使用对乙酰氨基酚,而正乙酰半胱氨酸可能是一种潜在的治疗方法,有助于防止线粒体功能障碍引起的氧化应激导致肝细胞坏死。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Liver failure after Bacillus cereus food poisoning, an under-recognized entity: A case report.

Background: Bacillus cereus (B. cereus) is known to cause 2 types of foodborne diseases; the diarrheal and emetic syndromes. They are largely underreported due to their usually self-limiting course. Rare and sometimes fatal cases of liver failure, pulmonary hemorrhage and cerebral oedema have been reported mainly in children and young adults. We present here a case of liver failure associated with B. cereus food poisoning in a middle-aged patient.

Case summary: A 48-year-old female patient presented to the emergency department for emesis, diarrhea, chills without fever, asthenia and diffuse abdominal cramps that started less than 30 minutes after eating a rice salad. Her past medical history was relevant for cholecystectomy and a cured Hashimoto's disease. She did not take any medication, drugs and declared a consumption of one glass of wine per week. In the emergency department, she was treated with acetaminophen, metoclopramide, ondansetron, and an intravenous normal saline infusion. Blood gas analysis revealed a metabolic acidosis with hyperlactatemia, coagulation revealed a low prothrombin activity [32 %; normal values (N): 70-140] and a low Factor V activity (15%; N: > 70). Transaminases were elevated with hyperbilirubinemia, elevated lipase and rhabdomyolysis. N-acetylcysteine treatment was introduced. Abdominal echography revealed no signs of chronic hepatopathy or hepatomegaly. Day after the admission, psychomotor activity improved, transaminases and lipase started decreasing. Rhabdomyolysis gradually worsened to peak on day 3. Screening tests for liver disease were negative for viral and autoimmune cause of liver failure. Stools cultures were positive for colonies of the B. cereus group which were also identified in the rice salad samples processed whereas blood cultures were negative. The patient's condition improved gradually including her liver function parameters and psychomotor activity which allowed her discharged home on day 9.

Conclusion: We describe a rare case of hepatocellular dysfunction due to a foodborne B. cereus intoxication in an adult patient. Even if it is uncommon, the severity of liver dysfunction reported and mechanism of the cereulide toxin toxicity on liver suggest that acetaminophen should be avoided in case of a foodborne intoxication and n-acetylcysteine could be a potential therapy helping to prevent hepatocytes necrosis due to the oxidative stress induced by mitochondrial dysfunction.

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来源期刊
World Journal of Hepatology
World Journal of Hepatology GASTROENTEROLOGY & HEPATOLOGY-
CiteScore
4.10
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