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肝门静脉性硬化症患者循环血管紧张素转换酶水平升高。

Elevated levels of circulating angiotensin converting enzyme in patients with hepatoportal sclerosis.

机构信息

Department of Gastroenterology, Turkiye Yuksek İhtisas Education and Research Hospital, Sihhiye, 06100, Ankara, Turkey.

出版信息

Dig Dis Sci. 2011 Jul;56(7):2160-5. doi: 10.1007/s10620-011-1580-7. Epub 2011 Feb 3.

DOI:10.1007/s10620-011-1580-7
PMID:21290180
Abstract

BACKGROUND AND AIMS

Hepatoportal sclerosis (HPS) is a clinicopathologic condition that is clinically characterized by portal hypertension (varices and portosystemic collateral vessels), splenomegaly and pancytopenia, in the absence of cirrhosis. Although the etiology is obscure, a number of theories such as immunologic and vascular endothelial cellular abnormalities have been put forward to explain the underlying pathophysiology. Angiotensin-converting enzyme (ACE), an important molecule of the renin-angiotensin system (RAS), is also known as a regulatory molecule in systemic and portal circulation in distinct disorders. The aim of the present study was to investigate the possible role of the ACE in the context of RAS in HPS pathogenesis.

MATERIALS AND METHODS

The study was conducted on 30 HPS patients (16 men, 14 women; median age 36 years, range 18-63) and 20 healthy controls. The clinical features of HPS patients including demographics, laboratory, and ultrasonography findings were summarized. Serum ACE levels were measured by using commercially available kits.

RESULTS

Serum median ACE levels were 36 (8-174) U/l and 16 (8-43) U/l for the HPS patients and controls, respectively. Serum ACE levels were significantly higher in patients with HPS compared to the control group (P < 0.05).

CONCLUSION

ACE in the context of RAS may be associated with pathological endothelial occlusive events in the microenvironment of the portal circulation in HPS. Revealing the interactions between circulating and local RAS within the hepatic microenvironment would enlighten the biologic basis and clinical management of liver diseases.

摘要

背景与目的

肝门静脉性硬变(HPS)是一种临床病理状况,其临床特征为门静脉高压(静脉曲张和门体侧支循环)、脾肿大和全血细胞减少,但无肝硬化。尽管病因尚不清楚,但已提出许多理论来解释其潜在的病理生理学,如免疫和血管内皮细胞异常。血管紧张素转换酶(ACE)是肾素-血管紧张素系统(RAS)的一个重要分子,在不同的疾病中也被认为是全身和门脉循环的调节分子。本研究旨在探讨 ACE 在 RAS 中的可能作用及其在 HPS 发病机制中的作用。

材料与方法

本研究共纳入 30 例 HPS 患者(16 名男性,14 名女性;中位年龄 36 岁,范围 18-63 岁)和 20 名健康对照者。总结 HPS 患者的临床特征,包括人口统计学、实验室和超声检查结果。采用商业试剂盒测定血清 ACE 水平。

结果

HPS 患者血清 ACE 中位数为 36(8-174)U/L,对照组为 16(8-43)U/L。HPS 患者血清 ACE 水平明显高于对照组(P<0.05)。

结论

RAS 中的 ACE 可能与 HPS 门静脉循环微环境中的病理性内皮闭塞事件有关。揭示肝内微环境中循环和局部 RAS 之间的相互作用,将阐明肝脏疾病的生物学基础和临床管理。

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