Phosphodiesterase III inhibitor attenuates rat sinusoidal obstruction syndrome through inhibition of platelet aggregation in Disse's space

Phosphodiesterase III inhibitor attenuates rat sinusoidal obstruction syndrome through inhibition... IntroductionSinusoidal obstruction syndrome (SOS), previously called veno‐occlusive disease, is a fatal drug‐induced liver injury. Drugs such as busulfan in hematopoietic stem cell transplantation, cyclophosphamide in immunosuppression therapy and bone marrow transplantation, and oxaliplatin in chemotherapy are known to cause SOS. The clinical features of SOS include hyperbilirubinemia, painful hepatomegaly, and weight gain due to ascites. These features decrease the hepatic functional reserve. Prevention and treatment of SOS are necessary to improve complications following liver surgery; however, an effective strategy for SOS remains to be determined.Several studies have reported that initial pathophysiological changes in SOS are possibly the result of drug‐induced injury to liver sinusoidal endothelial cells (LSEC), but mechanisms after LSEC damage remain unclear. We previously immunostained for CD42b, a platelet surface marker, and observed platelets in contact with hepatocytes, especially in zone 3, in the liver tissue of a liver transplant recipient with severe SOS. It was suggested that platelets exist in the extravascular space, the space of Disse, and destruction of hepatocytes were observed. Because of a lack of nuclei, platelets are invisible on histological analysis using hematoxylin and eosin (HE) staining.We considered that LSEC are injured in the liver of SOS patients, and platelets that aggregate http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Gastroenterology and Hepatology Wiley

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Publisher
Wiley Subscription Services, Inc., A Wiley Company
Copyright
© 2018 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd
ISSN
0815-9319
eISSN
1440-1746
D.O.I.
10.1111/jgh.14004
Publisher site
See Article on Publisher Site

Abstract

IntroductionSinusoidal obstruction syndrome (SOS), previously called veno‐occlusive disease, is a fatal drug‐induced liver injury. Drugs such as busulfan in hematopoietic stem cell transplantation, cyclophosphamide in immunosuppression therapy and bone marrow transplantation, and oxaliplatin in chemotherapy are known to cause SOS. The clinical features of SOS include hyperbilirubinemia, painful hepatomegaly, and weight gain due to ascites. These features decrease the hepatic functional reserve. Prevention and treatment of SOS are necessary to improve complications following liver surgery; however, an effective strategy for SOS remains to be determined.Several studies have reported that initial pathophysiological changes in SOS are possibly the result of drug‐induced injury to liver sinusoidal endothelial cells (LSEC), but mechanisms after LSEC damage remain unclear. We previously immunostained for CD42b, a platelet surface marker, and observed platelets in contact with hepatocytes, especially in zone 3, in the liver tissue of a liver transplant recipient with severe SOS. It was suggested that platelets exist in the extravascular space, the space of Disse, and destruction of hepatocytes were observed. Because of a lack of nuclei, platelets are invisible on histological analysis using hematoxylin and eosin (HE) staining.We considered that LSEC are injured in the liver of SOS patients, and platelets that aggregate

Journal

Journal of Gastroenterology and HepatologyWiley

Published: Jan 1, 2018

Keywords: ; ; ; ;

References

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