Extravasated platelet aggregation in liver zone 3 may correlate with the progression of sinusoidal obstruction syndrome following living donor liver transplantation: A case report.

Extravasated platelet aggregation in liver zone 3 may correlate with the progression of sinusoidal obstruction syndrome following living donor liver transplantation: A case report.
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DOI:
10.3892/etm.2015.2245
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发表时间:
2015-04
影响因子:
2.7
通讯作者:
Ohta T
Ohta T
中科院分区:
医学4区
文献类型:
--
作者:
Nakanuma S;Miyashita T;Hayashi H;Tajima H;Takamura H;Tsukada T;Okamoto K;Sakai S;Makino I;Kinoshita J;Nakamura K;Oyama K;Inokuchi M;Nakagawara H;Ninomiya I;Kitagawa H;Fushida S;Fujimura T;Ohta T

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肝窦阻塞综合征(SOS),以前被称为静脉闭塞性疾病,在肝移植(LT)后相对罕见。然而,药物治疗无效的SOS可导致小叶中心纤维化、门脉高压和肝功能衰竭。虽然在SOS发生早期,中央静脉(3区)周围的血窦状内皮细胞损伤就已经发生,但SOS发生的详细机制及其与血小板减少的关系尚不完全清楚。本报告描述了一例活体供体肝移植术后出现不明原因的血小板减少的SOS患者。SOS的进展导致移植物功能障碍,患者死亡。用抗血小板分化标志簇42b(血小板膜糖蛋白Ib)的抗体用免疫组织化学方法检测移植肝中血小板的存在。血小板聚集物沿肝窦和肝细胞胞浆内附着,特别是在3区,而在1区未见染色。这些结果表明,免疫抑制剂他克莫司或皮质类固醇脉冲的毒性引起的肝窦内皮细胞损伤是肝窦内皮细胞聚集和吞噬血小板的始动因素,而血小板的活化和脱颗粒可能至少部分参与了SOS的发病机制。
Sinusoidal obstruction syndrome (SOS), previously known as veno-occlusive disease, is relatively rare subsequent to liver transplantation (LT). SOS refractory to medical therapy, however, can result in centrilobular fibrosis, portal hypertension and liver failure. Although sinusoidal endothelial cell damage around central venules (zone 3) occurs early in the development of SOS, the detailed mechanism of SOS development and its association with thrombocytopenia are not yet completely understood. The present report describes a patient who experienced SOS with unexplained thrombocytopenia following living donor LT. The progression of SOS resulted in graft dysfunction and the patient succumbed. The presence of platelets in the liver allograft was assayed immunohistochemically using antibody to the platelet marker cluster of differentiation 42b (platelet glycoprotein Ib). Platelet aggregates were found attached to hepatocytes along the sinusoid and within the cytoplasm of hepatocytes, particularly in zone 3. By contrast, no staining was observed in zone 1. These findings suggested that extravasated platelet aggregation in the space of Disse and the phagocytosis of platelets by hepatocytes were initiated by sinusoidal endothelial cell damage due to the toxicity of the immunosuppressant tacrolimus or a corticosteroid pulse, and that platelet activation and degranulation may be at least partially involved in the mechanism responsible for SOS.
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