Extended survival in 3 cases of orthotopic homotransplantation of the human liver.

Extended survival in 3 cases of orthotopic homotransplantation of the human liver.
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3例同种人肝脏原位移植延长生存期。

DOI:
10.1097/00007890-196810000-00022
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发表时间:
1968
期刊:
影响因子:
3.8
通讯作者:
K. Porter
K. Porter
中科院分区:
医学2区
文献类型:
--
作者:
T. Starzl;C. Groth;L. Brettschneider;J. B. Moon;V. Fulginiti;E. Cotton;K. Porter

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为治疗原发性肝细胞癌或肝外胆道闭锁,对3例13 ~ 20个半月的儿童进行了同种异体尸体肝原位移植。供受体淋巴细胞抗原相容性从好到差不等。免疫抑制治疗采用硫唑嘌呤、泼尼松和异源抗淋巴细胞球蛋白(ALG)。 在所有3例受体中,术中右膈神经麻痹,可能是由于应用于肝上下腔静脉的血管夹压碎了右膈神经。术后2 ~ 10周恢复正常关节活动。在手术的无肝期,发现没有必要使用外部旁路对闭塞的腔静脉和门静脉系统进行减压。 在移植过程中,同种异体移植物持续轻度至中度缺血性损伤。缺氧可能导致血运重建后中度严重的术中代谢性酸中毒,但肝脏提供了令人满意的术后早期功能。随后,感染性肝梗死和随后的革兰氏阴性败血症的发展,在每个病人。在一个明显是由于技术并发症,导致血栓形成的部分肝动脉供应,但在其他两个梗死发生后超过3周。在后一种情况下,可能是由于临床上不明显的排斥反应或其他未知因素引起的血流减少。在适当的抗生素覆盖下切除或清创脓毒性梗死。在所有3例患者中,这一过程的组织学证据支持了排斥反应的可能病因作用。再生随后促成了一个变量填充的肝内缺损。 晚期功能从完全满意到低于正常,这是通过合成和排泄的多功能试验来判断的。只有一名患者有肝衰竭的临床证据,表现为持续性黄疸和腹水。所有3名儿童在94天、86天和49天后都还活着,第四名患者现在已经术后2周。
Orthotopic homotransplantation of cadaver livers was carried out in 3 children, aged 13 to 20½ months, for the treatment of primary liver-cell carcinoma or extrahepatic biliary atresia. The donor-recipient lymphocyte antigen compatibility ranged from good to poor. Immunosuppressive therapy was with azathioprine, prednisone, and heterologous antilymphocyte globulin (ALG). In all 3 recipients, the right phrenic nerve was paralyzed during operation, probably by crushing it with the vascular clamp that was applied to the suprahepatic inferior vena cava. Normal diaphragmatic movement returned from 2 to 10 weeks later. During the anhepatic phase of the procedure, it was found that decompression of the occluded vena caval and portal venous systems with external bypasses was not necessary. In the process of transplantation, the homografts sustained from minor to moderate ischemic injury. The anoxia probably contributed to a moderately severe intraoperative metabolic acidosis following revascularization, but the livers provided satisfactory early postoperative function. Subsequently, infected liver infarctions and consequent gram-negative septicemia developed in each patient. In one this was evidently due to a technical complication with resultant thrombosis of part of the hepatic arterial supply, but in the other two the infarctions occurred after more than 3 weeks. In the latter cases, a blood flow reduction caused by clinically inevident rejection or other unknown factors may have been responsible. The septic infarcts were excised or debrided under appropriate antibiotic coverage. The possible etiologic role of rejection was supported by histologic evidence of this process in all 3 of the patients. Regeneration subsequently contributed to a variable filling in of the intrahepatic defects. Late function has ranged from completely satisfactory to subnormal, as judged by multiple function tests of synthesis and excretion. Only one patient has clinical evidence of liver failure, manifested by persistent jaundice and ascites. All 3 children are alive after 94, 86, and 49 days, as well as a fourth patient, who is now 2 weeks postoperative.