Severe Veno-occlusive Disease/Sinusoidal Obstruction Syndrome After Deceased-donor and Living-donor Liver Transplantation

Takamura, Hiroyuki; Nakanuma, Shinichi; Hayashi, Hironori; Tajima, Hidehiro; Kakinoki, Kaheita; Kitahara, Masaaki; Sakai, Seisho; Makino, Isamu; Nakagawara, Hisatoshi; Miyashita, Tomoharu; Okamoto, Koichi; Nakamura, Keisuke; Oyama, Katsunobu; Inokuchi, Masafumi; Ninomiya, Itasu; Kitagawa, Hirohisa; Fushida, Sachio; Fujimura, Takashi; Onishi, Ichiro; Kayahara, Masato; Tani, Takashi; Arai, Kuniaki; Yamashita, Taro; Yamashita, Tatsuya; Kitamura, Hirotaka; Ikeda, Hiroko; Kaneko, Shuya; Nakanuma, Yasuni; Matsui, Osamu; Ohta, Tetsuo

doi:10.1016/j.transproceed.2014.09.110

Cited by 25 publications

(18 citation statements)

References 59 publications

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“…Platelets can be visualized in rats by immunostaining with antibody to the surface marker, CD41. Clinically, we observed EPA in SOS patients after liver transplantation (32,33) and after oxaliplatin chemotherapy (15). Platelets can be indirectly localized by detection of their surface markers.…”

Section: Discussionmentioning

confidence: 78%

Extravasated platelet aggregation in the livers of rats with drug-induced hepatic sinusoidal obstruction syndrome

Hirata

Tajima

Miyashita

et al. 2017

Molecular Medicine Reports

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Abstract. Oxaliplatin-based chemotherapy plays an important role in the treatment of colorectal liver metastases. Oxaliplatin, however, causes sinusoidal obstruction syndrome (SOS), which is characterized by portal hypertension, splenomegaly, thrombocytopenia, and liver dysfunction. SOS is diagnosed histopathologically by disruption of the sinusoidal endothelium, collagen deposition, fibrosis especially around zone 3, dilatation of the sinusoidal space and congestion. This study assessed the characteristics of a rat model of SOS. SOS was induced in rats by administration of monocrotaline (MCT). Blood chemistries and macroscopic and microscopic findings were compared in rats administered MCT and vehicle (control group). Levels of expression in the liver of CD41, P-selectin, rat endothelial cell antigen-1, CD34, and cleaved caspase-3 were analyzed immunohistochemically. Moreover, livers of these rats were analyzed by electron microscopy. Macroscopically, MCT-treated rats showed accumulation of bloody ascites and blue liver and were diagnosed with SOS histologically. Serum concentrations of aspartate aminotransferase (P=0.003), alanine aminotransferase (P=0.008), total-bilirubin (P=0.012), direct-bilirubin (P=0.007), indirect-bilirubin (P=0.003), lactate dehydrogenase (P<0.001) and hyaluronic acid (P=0.016) were significantly higher, and platelet counts significantly lower (P=0.004), in MCT-treated than in control rats. The livers of MCT-treated rats were immunohistochemically positive for CD41 and P-selectin, suggesting platelet aggregates; for rat endothelial cell antigen-1 and CD34, suggesting sinusoidal endothelial disorder; and for cleaved caspase-3, suggesting hepatocyte apoptosis. Electron microscopic findings revealed platelet aggregation in the space of Disse in the MCT group. Extravasated platelet aggregation in Disse's space may be involved in the development of SOS.

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Section: Discussionmentioning

confidence: 78%

Extravasated platelet aggregation in the livers of rats with drug-induced hepatic sinusoidal obstruction syndrome

Hirata

Tajima

Miyashita

et al. 2017

Molecular Medicine Reports

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“…Hepatic veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome (SOS), is a clinical syndrome occurring after high-dose chemotherapy, hematopoietic stem cell transplantation (HSCT) (1,2), and, less commonly, after ingestion of toxic alkaloids (toxic injury) (3), after high doses of radiotherapy (4) or liver transplantation (5). Clinical diagnosis criteria include hepatomegaly, right-upper quadrant pain, ascites, and jaundice (6), although anicteric forms may occur, particularly, but not exclusively among pediatric population (7).…”

Section: Introductionmentioning

confidence: 99%

Diagnosis and Treatment of VOD/SOS After Allogeneic Hematopoietic Stem Cell Transplantation

et al. 2020

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Hepatic veno-occlusive disease (VOD) or sinusoidal obstruction syndrome (SOS) is a rare complication characterized by hepatomegaly, right-upper quadrant pain, jaundice, and ascites, occurring after high-dose chemotherapy, hematopoietic stem cell transplantation (HSCT) and, less commonly, other conditions. We review pathogenesis, clinical appearance and diagnostic criteria, risk factors, prophylaxis, and treatment of the VOD occurring post-HSCT. The injury of the sinusoidal endothelial cells with loss of wall integrity and sinusoidal obstruction is the basis of development of postsinusoidal portal hypertension responsible for clinical syndrome. Risk factors associated with the onset of VOD and diagnostic tools have been recently updated both in the pediatric and adult settings and here are reported. Treatment includes supportive care, intensive management, and specific drug therapy with defibrotide. Because of its severity, particularly in VOD with associated multiorgan disease, prophylaxis approaches are under investigation. During the last years, decreased mortality associated to VOD/SOS has been reported being it attributable to a better intensive and multidisciplinary approach.

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“…Sinusoidal obstruction syndrome, previously called veno-occlusive disease, is a liver disease characterized by damage to liver tissue in zone 3 and is clinically diagnosed by the triad of jaundice, painful hepatomegaly, and ascites/weight gain. 22 Sinusoidal obstruction syndrome is confirmed histologically, including by fibrous obliteration of small hepatic veins by connective tissue and centrilobular hemorrhagic necrosis. 22 Previously, we reported that an allograft parenchyma with EPA in zone 3 progressed from central perivenulitis to centrilobular fibrosis with a finding of SOS.…”

Section: Shinichi Nakanuma Et Al/experimental and Clinical Transplantmentioning

confidence: 99%

“…22 Sinusoidal obstruction syndrome is confirmed histologically, including by fibrous obliteration of small hepatic veins by connective tissue and centrilobular hemorrhagic necrosis. 22 Previously, we reported that an allograft parenchyma with EPA in zone 3 progressed from central perivenulitis to centrilobular fibrosis with a finding of SOS. 4 Extravasated platelet aggregation in zone 3 soon after transplant may be a sign of SOS.…”

Section: Shinichi Nakanuma Et Al/experimental and Clinical Transplantmentioning

confidence: 99%

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2015

Exp Clin Transplant

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Objectives: Continuous thrombocytopenia after liver transplant is associated with a less favorable prognosis, but this pathogenesis remains unclear. We focused on the consumption of platelets in the allograft. We assessed platelet consumption in allografts, and evaluated the pathology of platelet aggregation in an allograft tissue and its involvement in clinical outcomes. Materials and Methods: We took biopsy specimens from 20 patients. To examine the localization of platelet aggregation, CD42b was assayed immunohistochemically, and its level of expression correlated with clinical data and outcomes. Results: Platelet aggregation in zone 3 was 70%, compared with 30% in zone 1 and 50% in zone 2. Platelets were found mainly as extravasated platelet aggregates in local microenvironments. Patients were stratified according to the extent of extravasated platelet aggregates in zone 3 into extravasated platelet aggregate-negative andpositive groups. Graft weight/recipient body weight ratio with the extravasated platelet aggregatepositive group was significantly lower than that of the extravasated platelet aggregate-negative group. Platelet count after surgery was lower, while total bilirubin and prothrombin time/international normalized ratio were higher in the extravasated platelet aggregate-positive than they were in the extravasated platelet aggregate-negative group. Conclusions: Extravasated platelet aggregates in the zone 3 of allograft tissue cause the consumption of platelets and continuous thrombocytopenia after transplant, and may be the clinical marker for deterioration of graft function. Platelet activation and degranulation following the release by platelets of some negative regulators may be involved partially in liver damage.

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Severe Veno-occlusive Disease/Sinusoidal Obstruction Syndrome After Deceased-donor and Living-donor Liver Transplantation

Cited by 25 publications

References 59 publications

Extravasated platelet aggregation in the livers of rats with drug-induced hepatic sinusoidal obstruction syndrome

Extravasated platelet aggregation in the livers of rats with drug-induced hepatic sinusoidal obstruction syndrome

Diagnosis and Treatment of VOD/SOS After Allogeneic Hematopoietic Stem Cell Transplantation

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