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本文引用的文献

1
Procalcitonin as a marker of sepsis in alcoholic hepatitis.降钙素原作为酒精性肝炎中脓毒症的标志物。
Hepatol Int. 2014 Jul;8(3):436-42. doi: 10.1007/s12072-014-9540-x. Epub 2014 Jun 3.
2
Inflammation and portal hypertension - the undiscovered country.炎症和门静脉高压——未被发现的领域。
J Hepatol. 2014 Jul;61(1):155-63. doi: 10.1016/j.jhep.2014.03.014. Epub 2014 Mar 18.
3
A histologic scoring system for prognosis of patients with alcoholic hepatitis.酒精性肝炎患者预后的组织学评分系统。
Gastroenterology. 2014 May;146(5):1231-9.e1-6. doi: 10.1053/j.gastro.2014.01.018. Epub 2014 Jan 15.
4
Interactions between the intestinal microbiome and liver diseases.肠道微生物组与肝脏疾病的相互作用。
Gastroenterology. 2014 May;146(6):1513-24. doi: 10.1053/j.gastro.2014.01.020. Epub 2014 Jan 15.
5
CCL20 mediates lipopolysaccharide induced liver injury and is a potential driver of inflammation and fibrosis in alcoholic hepatitis.CCL20介导脂多糖诱导的肝损伤,是酒精性肝炎炎症和纤维化的潜在驱动因素。
Gut. 2014 Nov;63(11):1782-92. doi: 10.1136/gutjnl-2013-306098. Epub 2014 Jan 10.
6
Altered profile of human gut microbiome is associated with cirrhosis and its complications.人类肠道微生物群的改变与肝硬化及其并发症相关。
J Hepatol. 2014 May;60(5):940-7. doi: 10.1016/j.jhep.2013.12.019. Epub 2013 Dec 25.
7
Invasive aspergillosis in patients with severe alcoholic hepatitis.严重酒精性肝炎患者的侵袭性曲霉病。
J Hepatol. 2014 Feb;60(2):267-74. doi: 10.1016/j.jhep.2013.09.011. Epub 2013 Sep 17.
8
Type-1 hepatorenal syndrome associated with infections in cirrhosis: natural history, outcome of kidney function, and survival.1 型肝性肾病综合征与肝硬化感染相关:肾功能的自然病史、结局和生存。
Hepatology. 2014 Apr;59(4):1505-13. doi: 10.1002/hep.26687. Epub 2014 Feb 25.
9
Sterile inflammation in the liver and pancreas.肝脏和胰腺的无菌性炎症。
J Gastroenterol Hepatol. 2013 Aug;28 Suppl 1(0 1):61-7. doi: 10.1111/jgh.12018.
10
Acute phase proteins for the diagnosis of bacterial infection and prediction of mortality in acute complications of cirrhosis.用于诊断细菌感染和预测肝硬化急性并发症患者死亡率的急性期蛋白。
Ann Hepatol. 2013 Jul-Aug;12(4):599-607.

全身炎症反应和血清脂多糖水平可预测酒精性肝炎患者的多器官功能衰竭和死亡。

Systemic inflammatory response and serum lipopolysaccharide levels predict multiple organ failure and death in alcoholic hepatitis.

作者信息

Michelena Javier, Altamirano José, Abraldes Juan G, Affò Silvia, Morales-Ibanez Oriol, Sancho-Bru Pau, Dominguez Marlene, García-Pagán Juan Carlos, Fernández Javier, Arroyo Vicente, Ginès Pere, Louvet Alexandre, Mathurin Philippe, Mehal Wajahat Z, Caballería Juan, Bataller Ramón

机构信息

Liver Unit, Hospital Clínic, Barcelona, Spain.

Institut d'Investigacions Biomèdiques August-Pi-Sunyer, University of Barcelona, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas, Barcelona, Spain.

出版信息

Hepatology. 2015 Sep;62(3):762-72. doi: 10.1002/hep.27779. Epub 2015 Apr 13.

DOI:10.1002/hep.27779
PMID:25761863
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4549175/
Abstract

UNLABELLED

Alcoholic hepatitis (AH) frequently progresses to multiple organ failure (MOF) and death. However, the driving factors are largely unknown. At admission, patients with AH often show criteria of systemic inflammatory response syndrome (SIRS) even in the absence of an infection. We hypothesize that the presence of SIRS may predispose to MOF and death. To test this hypothesis, we studied a cohort including 162 patients with biopsy-proven AH. The presence of SIRS and infections was assessed in all patients, and multivariate analyses identified variables independently associated with MOF and 90-day mortality. At admission, 32 (19.8%) patients were diagnosed with a bacterial infection, while 75 (46.3%) fulfilled SIRS criteria; 58 patients (35.8%) developed MOF during hospitalization. Short-term mortality was significantly higher among patients who developed MOF (62.1% versus 3.8%, P < 0.001). The presence of SIRS was a major predictor of MOF (odds ratio = 2.69, P = 0.025) and strongly correlated with mortality. Importantly, the course of patients with SIRS with and without infection was similar in terms of MOF development and short-term mortality. Finally, we sought to identify serum markers that differentiate SIRS with and without infection. We studied serum levels of high-sensitivity C-reactive protein, procalcitonin, and lipopolysaccharide at admission. All of them predicted mortality. Procalcitonin, but not high-sensitivity C-reactive protein, serum levels identified those patients with SIRS and infection. Lipopolysaccharide serum levels predicted MOF and the response to prednisolone.

CONCLUSION

In the presence or absence of infections, SIRS is a major determinant of MOF and mortality in AH, and the mechanisms involved in the development of SIRS should be investigated; procalcitonin serum levels can help to identify patients with infection, and lipopolysaccharide levels may help to predict mortality and the response to steroids.

摘要

未标注

酒精性肝炎(AH)常进展为多器官功能衰竭(MOF)并导致死亡。然而,其驱动因素在很大程度上尚不清楚。入院时,AH患者即使没有感染也常表现出全身炎症反应综合征(SIRS)的标准。我们假设SIRS的存在可能易导致MOF和死亡。为验证这一假设,我们研究了一个队列,其中包括162例经活检证实为AH的患者。评估了所有患者SIRS和感染的存在情况,并通过多变量分析确定了与MOF和90天死亡率独立相关的变量。入院时,32例(19.8%)患者被诊断为细菌感染,而75例(46.3%)符合SIRS标准;58例患者(35.8%)在住院期间发生了MOF。发生MOF的患者短期死亡率显著更高(62.1%对3.8%,P < 0.001)。SIRS的存在是MOF的主要预测因素(优势比=2.69,P = 0.025),且与死亡率密切相关。重要的是,有无感染的SIRS患者在MOF发生和短期死亡率方面病程相似。最后,我们试图确定区分有无感染的SIRS的血清标志物。我们研究了入院时高敏C反应蛋白、降钙素原和脂多糖的血清水平。所有这些都可预测死亡率。降钙素原而非高敏C反应蛋白的血清水平可识别有SIRS和感染的患者。脂多糖血清水平可预测MOF及对泼尼松龙的反应。

结论

无论有无感染,SIRS都是AH中MOF和死亡率的主要决定因素,应研究SIRS发生发展的机制;降钙素原血清水平有助于识别感染患者,脂多糖水平可能有助于预测死亡率及对类固醇的反应。