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缺血性肝炎:临床表现与发病机制

Ischemic hepatitis: clinical presentation and pathogenesis.

作者信息

Seeto R K, Fenn B, Rockey D C

机构信息

Department of Medicine (RKS, BF), Division of Gastroenterology, University of California, San Francisco, San Francisco, California, USA.

出版信息

Am J Med. 2000 Aug 1;109(2):109-13. doi: 10.1016/s0002-9343(00)00461-7.

Abstract

BACKGROUND

The pathophysiology of ischemic hepatitis, otherwise known as "shock liver," is poorly understood, although it is believed to be the result of a reduction in systemic blood flow as typically occurs in shock. The aim of this study was to investigate the importance of this phenomenon as well as other clinical features in patients with ischemic hepatitis.

METHODS

We identified a cohort of 31 patients (case group) who met the most commonly accepted definition of ischemic hepatitis (an acute reversible elevation in either the serum alanine or aspartate aminotransferase level of at least 20 times the upper limit of normal, excluding known causes of acute hepatitis or hepatocellular injury, in an appropriate clinical setting). We also evaluated the clinical features and serum aminotransferase levels in a cohort (the control group) of 31 previously healthy patients who sustained major nonhepatic trauma at San Francisco General Hospital, a major trauma center. Both groups of patients had documented systolic blood pressures <75 mm Hg for at least 15 minutes. Clinical and hemodynamic (invasive and noninvasive) data were recorded.

RESULTS

Despite the marked reduction in blood pressure, no patient in the control group developed ischemic hepatitis. The mean (+/- SD) peak serum aspartate aminotransferase level in the control group was only 78 +/- 72 IU, in contrast with a mean peak of 2,088 +/- 2,165 IU in the case group. All 31 patients with ischemic hepatitis had evidence of underlying organic heart disease, 29 (94%) of whom had right-sided heart failure.

CONCLUSIONS

Systemic hypotension or shock alone did not lead to ischemic hepatitis in any patient. The vast majority of patients with ischemic hepatitis had severe underlying cardiac disease that had often led to passive congestion of the liver. These data lead us to propose that right-sided heart failure, with resultant hepatic venous congestion, may predispose the liver to hepatic injury induced by a hypotensive event.

摘要

背景

缺血性肝炎,又称“休克肝”,其病理生理学机制尚不清楚,不过人们认为它是休克时典型出现的全身血流减少的结果。本研究的目的是调查缺血性肝炎患者中这一现象以及其他临床特征的重要性。

方法

我们确定了一组31例患者(病例组),他们符合缺血性肝炎最普遍接受的定义(在适当的临床环境中,血清丙氨酸或天冬氨酸转氨酶水平急性可逆性升高至少为正常上限的20倍,排除急性肝炎或肝细胞损伤的已知病因)。我们还评估了一组31例先前健康的患者(对照组)的临床特征和血清转氨酶水平,这些患者在一家主要创伤中心——旧金山总医院遭受了严重的非肝脏创伤。两组患者均记录到收缩压<75 mmHg至少15分钟。记录临床和血流动力学(有创和无创)数据。

结果

尽管血压显著降低,但对照组中没有患者发生缺血性肝炎。对照组血清天冬氨酸转氨酶水平的平均(±标准差)峰值仅为78±72 IU,而病例组的平均峰值为2088±2165 IU。所有31例缺血性肝炎患者均有潜在器质性心脏病的证据,其中29例(94%)有右心衰竭。

结论

单纯的系统性低血压或休克不会导致任何患者发生缺血性肝炎。绝大多数缺血性肝炎患者有严重的潜在心脏病,常导致肝脏被动性充血。这些数据使我们提出,右心衰竭导致肝静脉充血,可能使肝脏易受低血压事件引起的肝损伤。

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