ArticlePloS one2015
von Willebrand Factor-Rich Platelet Thrombi in the Liver Cause Sinusoidal Obstruction Syndrome following Oxaliplatin-Based Chemotherapy.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Strong association between insufficient plasma exchange and fatal outcomes in Japanese patients with immune-mediated thrombotic thrombocytopenic purpura.International journal of hematology · 2021Article
- Pathological characteristics of liver sinusoidal thrombosis in COVID-19 patients: A series of 43 cases.Hepatology research : the official journal of the Japan Society of Hepatology · 2021Article
- Role of liver sinusoidal endothelial cells in liver diseases.Nature reviews. Gastroenterology & hepatology · 2021Review
- The Provocative Roles of Platelets in Liver Disease and Cancer.Frontiers in oncology · 2021Review
- A predictive value of von Willebrand factor for early response to Bevacizumab therapy in recurrent glioma.Journal of neuro-oncology · 2018Article
- The use of defibrotide in blood and marrow transplantation.Blood advances · 2018Review
- The hepatoprotective role of reduced glutathione and its underlying mechanism in oxaliplatin-induced acute liver injury.Oncology letters · 2018Article
- Persistent Gastrointestinal Angiodysplasia in Heyde's Syndrome after Aortic Valve Replacement.Internal medicine (Tokyo, Japan) · 2017Article
- Effects of heme oxygenase-1-modified bone marrow mesenchymal stem cells on microcirculation and energy metabolism following liver transplantation.World journal of gastroenterology · 2017Article
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Authors and funding
8 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Oxaliplatin-based chemotherapy is widely used to treat advanced colorectal cancer (CRC). Sinusoidal obstruction syndrome (SOS) due to oxaliplatin is a serious type of chemotherapy-associated liver injury (CALI) in CRC patients. SOS is thought to be caused by the sinusoidal endothelial cell damage, which results in the release of unusually-large von Willebrand factor multimers (UL-VWFMs) from endothelial cells. To investigate the pathophysiology of CALI after oxaliplatin-based chemotherapy, we analyzed plasma concentration of von Willebrand factor (VWF) and the distribution of VWFMs in CRC patients. Twenty-three patients with advanced CRC who received oxaliplatin-based chemotherapy with (n = 6) and without (n = 17) bevacizumab were analyzed. CALI (n = 6) and splenomegaly (n = 9) were found only in patients who did not treated with bevacizumab. Plasma VWF antigen (VWF:Ag) and serum aspartate aminotransferase (AST) levels increased after chemotherapy only in patients without bevacizumab. VWFM analysis in patients who did not receive bevacizumab showed the presence of UL-VWFMs and absence of high molecular weight VWFMs during chemotherapy, especially in those with CALI. In addition, plasma VWF:Ag and AST levels increased after chemotherapy in patients with splenomegaly (n = 9), but not in patients without splenomegaly (n = 14). Histological findings in the liver tissue of patients who did not receive bevacizumab included sinusoidal dilatation and microthrombi in the sinusoids. Many microthrombi were positive for both anti-IIb/IIIa and anti-VWF antibodies. Plasma UL-VWFM levels might be increased by damage to endothelial cells as a result of oxaliplatin-based chemotherapy. Bevacizumab could prevent CALI and splenomegaly through inhibition of VWF-rich platelet thrombus formation.
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