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肝实质改变和组织学嗜酸性粒细胞增多作为后续急性肝移植排斥反应的预测指标。

Hepatic parenchymal changes and histologic eosinophilia as predictors of subsequent acute liver allograft rejection.

作者信息

Demirhan Beyhan, Bilezikçi Banu, Haberal A Nihan, Sevmiş Sinasi, Arat Zübeyde, Haberal Mehmet

机构信息

Department of Pathology, Baskent University School of Medicine, Bahçelievler, Ankara, Turkey.

出版信息

Liver Transpl. 2008 Feb;14(2):214-9. doi: 10.1002/lt.21360.

DOI:10.1002/lt.21360
PMID:18236397
Abstract

During the first episode of acute cellular rejection (ACR) after liver transplantation, centrilobular changes in liver biopsy specimens may be possible indicators of subsequent episodes of ACR, early chronic rejection, or acute graft loss. The purpose of this study was to identify differences between the histopathological findings in liver biopsy specimens obtained during the first rejection episode in patients who subsequently developed further episodes of ACR and those who did not. The histopathological findings in 22 patients who had a single episode of acute rejection (group 1) were compared with those in 23 patients who had multiple episodes of acute rejection (group 2). Only the first liver biopsy samples of the latter group were taken into consideration. We assessed the predictive value of centrilobular necrosis, central vein endothelialitis, pericentral inflammation, hepatocellular ballooning, cholestasis, hepatocellular apoptosis, lobular inflammation, the degree of portal eosinophilia, and characteristic portal tract features in poor responders to antirejection treatment. The time to the first episode of ACR and the rejection activity index were similar in patients in both groups. Hepatocellular apoptosis, hepatocellular ballooning, and central vein endothelialitis were common features of both groups. The incidences of pericentral inflammation, centrilobular necrosis, and portal eosinophilia were significantly higher in patients in group 2 than in those in group 1 (P < 0.05). Patients with pericentral inflammation, centrilobular necrosis, and marked portal eosinophilia during an initial episode of acute rejection may be more likely to develop subsequent episodes of ACR.

摘要

在肝移植后的首次急性细胞排斥反应(ACR)期间,肝活检标本中的小叶中心改变可能是后续ACR发作、早期慢性排斥反应或急性移植物丢失的潜在指标。本研究的目的是确定在随后发生进一步ACR发作的患者和未发生进一步ACR发作的患者中,首次排斥反应发作期间获得的肝活检标本的组织病理学发现之间的差异。将22例发生单次急性排斥反应的患者(第1组)的组织病理学发现与23例发生多次急性排斥反应的患者(第2组)的组织病理学发现进行比较。仅考虑后一组的首次肝活检样本。我们评估了小叶中心坏死、中央静脉内皮炎、中央周围炎症、肝细胞气球样变、胆汁淤积、肝细胞凋亡、小叶炎症、门脉嗜酸性粒细胞增多程度以及抗排斥治疗反应不佳者的特征性门管区特征的预测价值。两组患者首次发生ACR的时间和排斥反应活动指数相似。肝细胞凋亡、肝细胞气球样变和中央静脉内皮炎是两组的共同特征。第2组患者中央周围炎症、小叶中心坏死和门脉嗜酸性粒细胞增多的发生率显著高于第1组患者(P < 0.05)。在急性排斥反应初始发作期间出现中央周围炎症、小叶中心坏死和明显门脉嗜酸性粒细胞增多的患者可能更有可能发生后续的ACR发作。

相似文献

1
Hepatic parenchymal changes and histologic eosinophilia as predictors of subsequent acute liver allograft rejection.肝实质改变和组织学嗜酸性粒细胞增多作为后续急性肝移植排斥反应的预测指标。
Liver Transpl. 2008 Feb;14(2):214-9. doi: 10.1002/lt.21360.
2
Relevant histopathologic findings that distinguish acute cellular rejection from cholangitis in hepatic allograft biopsy specimens.在肝移植活检标本中区分急性细胞排斥反应与胆管炎的相关组织病理学发现。
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Acute hepatic allograft rejection: a comparison of patients with and without centrilobular alterations during first rejection episode.急性肝移植排斥反应:首次排斥反应期间有和没有小叶中心改变的患者的比较。
Liver Transpl. 2004 Mar;10(3):369-73. doi: 10.1002/lt.20094.
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Centrilobular necrosis after orthotopic liver transplantation: association with acute cellular rejection and impact on outcome.原位肝移植术后的小叶中心性坏死:与急性细胞排斥反应的关联及其对预后的影响。
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Significance of central perivenulitis in pediatric liver transplantation.儿童肝移植中中央静脉周围炎的意义
Am J Surg Pathol. 2008 Oct;32(10):1479-88. doi: 10.1097/PAS.0b013e31817a8e96.
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Histologic characteristics of late cellular rejection, significance of centrilobular injury, and long-term outcome in pediatric liver transplant recipients.小儿肝移植受者迟发性细胞排斥反应的组织学特征、小叶中心性损伤的意义及长期预后
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Is blood eosinophilia an effective predictor of acute rejection in living donor liver transplantation?血液嗜酸性粒细胞增多是活体肝移植急性排斥反应的有效预测指标吗?
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Can early liver biopsies predict long-term outcome of the graft?早期肝脏活检能否预测移植物的长期预后?
Liver Transpl. 2003 Jan;9(1):99-100. doi: 10.1002/lt.500090116.

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