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      Pyrrolizidine alkaloids-induced hepatic sinusoidal obstruction syndrome: Pathogenesis, clinical manifestations, diagnosis, treatment, and outcomes

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          Abstract

          Hepatic sinusoidal obstruction syndrome (HSOS) can be caused by the intake of pyrrolizidine alkaloids (PAs). To date, PAs-induced HSOS has not been extensively studied. In view of the difference in etiology of HSOS between the West and China, clinical profiles, imaging findings, treatment, and outcomes of HSOS associated with hematopoietic stem cell transplantation or oxaliplatin might be hardly extrapolated to PAs-induced HSOS. Reactive metabolites derived from PAs form pyrrole-protein adducts that result in toxic destruction of hepatic sinusoidal endothelial cells. PAs-induced HSOS typically manifests as painful hepatomegaly, ascites, and jaundice. Laboratory tests revealed abnormal liver function tests were observed in most of the patients with PAs-induced HSOS. In addition, contrast computed tomography and magnetic resonance imaging scan show that patients with PAs-induced HSOS have distinct imaging features, which reveal that radiological imaging provides an effective noninvasive method for the diagnosis of PAs-induced HSOS. Liver biopsy and histological examination showed that PAs-induced HSOS displayed distinct features in acute and chronic stages. Therapeutic strategies for PAs-induced HSOS include rigorous fluid management, anticoagulant therapy, glucocorticoids, transjugular intrahepatic portosystemic shunt, liver transplantation, etc. The aim of this review is to describe the pathogenesis, clinical profiles, diagnostic criteria, treatment, and outcomes of PAs-induced HSOS.

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          Most cited references47

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          Vascular disorders of the liver.

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            Venoocclusive disease of the liver following bone marrow transplantation.

            Review of 235 consecutive patients undergoing bone marrow transplantation was performed in order to define the clinical syndrome of venoocclusive disease of the liver (VOD) in these patients. Analysis of all patients with histologically proven VOD revealed a consistent clinical syndrome of liver dysfunction occurring within the first 3 weeks after marrow infusion. This was characterized by hyperbilirubinemia peaking at greater than or equal to 2 mg/dl with at least 2 of 3 other findings: hepatomegaly, ascites, and 5% or greater weight gain. VOD developed in 22% (52 of 235). A persistently elevated aspartate aminotransferase (SGOT) prior to transplant was associated with an increased risk of developing VOD by multivariate analysis (P = 0.0003), and acute leukemia in first remission was associated with a decreased risk (P = 0.02). Neither the preparative regimen (busulfan and cyclophosphamide versus cyclophosphamide and total body irradiation) nor the type of graft (allogeneic versus autologous) influenced the occurrence. Twenty-four of these 52 patients (47%) died with VOD (10% of the entire group). This makes VOD the third leading cause of death in our allogeneic graft recipients, and the second leading cause in our patients receiving autologous transplants. VOD is a common complication of bone marrow transplantation and has a specific clinical presentation, which usually allows diagnosis without the need of liver biopsy.
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              Toxic injury to hepatic sinusoids: sinusoidal obstruction syndrome (veno-occlusive disease).

              The term veno-occlusive disease of the liver refers to a form of toxic liver injury characterized clinically by the development of hepatomegaly, ascites, and jaundice, and histologically by diffuse damage in the centrilobular zone of the liver. The cardinal histologic features of this injury are marked sinusoidal fibrosis, necrosis of pericentral hepatocytes, and narrowing and eventual fibrosis of central veins. Recent studies suggest that the primary site of the toxic injury is sinusoidal endothelial cells, followed by a series of biologic processes that lead to circulatory compromise of centrilobular hepatocytes, fibrosis, and obstruction of liver blood flow. Thus we propose a more appropriate name for this form of liver injury--sinusoidal obstruction syndrome. This review encompasses historical perspectives, clinical manifestations of sinusoidal obstruction syndrome in the setting of hematopoietic cell transplantation, histologic features of centrilobular injury, and a discussion of the pathophysiology of sinusoidal injury, based on both animal and clinical investigations.
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                Author and article information

                Contributors
                Journal
                World J Gastroenterol
                World J. Gastroenterol
                WJG
                World Journal of Gastroenterology
                Baishideng Publishing Group Inc
                1007-9327
                2219-2840
                28 July 2019
                28 July 2019
                : 25
                : 28
                : 3753-3763
                Affiliations
                Division of Gastroenterology, Union Hospital, Tongji Medical college, Huazhong University of Science and Technology, Wuhan 430022, Hubei Province, China
                Division of Gastroenterology, Union Hospital, Tongji Medical college, Huazhong University of Science and Technology, Wuhan 430022, Hubei Province, China
                Department of Radiology, Union Hospital, Tongji Medical college, Huazhong University of Science and technology, Wuhan 430022, Hubei Province, China
                Department of Radiology, Union Hospital, Tongji Medical college, Huazhong University of Science and technology, Wuhan 430022, Hubei Province, China
                Division of Gastroenterology, Union Hospital, Tongji Medical college, Huazhong University of Science and Technology, Wuhan 430022, Hubei Province, China. yuhusong@ 123456163.com
                Author notes

                Author contributions: Yang XQ and Song YH reviewed the literature; Song YH and Ye J established the design and conception of the paper; Li X and Li Q provided the radiological imaging data; all authors contributed to writing and revision of this review.

                Supported by National Natural Science Foundation of China, No. 81570555 and No. 81770582.

                Corresponding author: Yu-Hu Song, MD, PhD, Chief Doctor, Professor, Division of Gastroenterology, Union Hospital, Tongji Medical college, Huazhong University of Science and Technology, No 1277, Jiefang Avenue, Wuhan 430022, Hubei Province, China. yuhusong@ 123456163.com

                Telephone: +86-27-85726678 Fax: +86-27-85726057

                Article
                jWJG.v25.i28.pg3753
                10.3748/wjg.v25.i28.3753
                6676551
                31391770
                11b52dd3-6eaa-4a61-9985-4c8c253025df
                ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.

                This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

                History
                : 17 March 2019
                : 5 June 2019
                : 25 June 2019
                Categories
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                hepatic sinusoidal obstruction syndrome,pyrrolizidine alkaloids,hepatic sinusoidal endothelial cells,pyrrole-protein adducts,diagnostic criteria,symptomatic treatment,anticoagulant therapy

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