Pathophysiological-based treatments of complications of cirrhosis

被引：8

作者：

Moller, Soren ^{[1
]}

Kimer, Nina ^{[2
,3
]}

Barlose, Mads ^{[1
]}

Bendtsen, Flemming ^{[2
]}

机构：

[1] Copenhagen Univ Hosp, Dept Clin Physiol & Nucl Med, Ctr Funct & Diagnost Imaging & Res, Kettegaard Alle 30, DK-2650 Hvidovre, Denmark

[2] Univ Copenhagen, Gastro Unit, Div Med, Hvidovre Hosp,Fac Hlth Sci, Copenhagen, Denmark

[3] Univ Copenhagen, Novo Nordisk Fdn, Bridge Translat Excellence Programme, Ctr Basic Metab Res, Copenhagen, Denmark

来源：

SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY | 2020年 / 55卷 / 04期

关键词：

Portal hypertension; ascites; oesophageal varices; hyperdynamic circulation; hepatorenal syndrome; hepatopulmonary syndrome; NITRIC-OXIDE SYNTHASE; PORTAL-HYPERTENSION RELATION; HEPATIC STELLATE CELLS; ARGININE METHYL-ESTER; CHRONIC LIVER-FAILURE; NECROSIS-FACTOR-ALPHA; PORTOPULMONARY HYPERTENSION; HEPATOPULMONARY SYNDROME; BETA-BLOCKERS; HYPERDYNAMIC CIRCULATION;

D O I：

10.1080/00365521.2020.1744709

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Detailed knowledge and understanding of the pathophysiological mechanisms and changes in hepatic and splanchnic function leading to the development of haemodynamic changes and portal hypertension in patients with cirrhosis are essential since it guides the search for targets to ameliorate liver-related abnormalities. Recent research has focused on the gut-liver axis, changes in intestinal permeability, translocation of bacterial products, and inflammation as important drivers of haemodynamic alterations and thereby targets for treatment. Additionally, treatment strategies should focus on microbiotic modulation, antiangiogenics, anti-inflammatory strategies, and modulation of bile acid metabolism. This paper aims to review contemporary pathophysiological-based treatment principles of the major complications of cirrhosis and portal hypertension and future targets for treatment.

引用

页码：383 / 394

页数：12

共 149 条

[21] Mechanisms of decompensation and organ failure in cirrhosis: From peripheral arterial vasodilation to systemic inflammation hypothesis [J].