Faulk W P, Labarrere C A, Pitts D, Halbrook H
Center for Reproduction and Transplantation Immunology, Methodist Hospital of Indiana, Indianapolis 46202.
J Heart Lung Transplant. 1993 Mar-Apr;12(2):S125-34.
Ninety cardiac allograft recipients were studied for clinical and functional parameters during a 40-month period. Baseline histologic and immunocytochemical data were obtained from donors' hearts before transplantation, and serial endomyocardial biopsy specimens were studied histologically for cellular infiltrates and immunocytochemically for complement and immunoglobulin deposits and for components of the hemostatic, fibrinolytic, and natural anticoagulant pathways. Results were grouped according to the time from transplantation: the first 3 months, 4 to 21 months, and 22 to 40 months. Each group was evaluated for most frequently obtained immunocytochemical findings and results relevant to clinical-laboratory cooperation in patient management. During the first 3 months, findings of biopsy specimens from allografts that subsequently were going to be problem cases revealed depleted tissue plasminogen activator in arteriolar smooth muscle cells, and recipient IgM that was deposited on donor endothelium of stable grafts was diminished or absent in unstable allografts. In addition, vascular deposits of activated complement components were identified in 50 of 70 allografts. From 4 through 21 months after transplantation, vascular deposits of complement rarely were identified (even in patients who previously had positive biopsy specimens), and the principal vascular lesion was fibrin deposits with impaired anticoagulant pathways and inadequate fibrinolysis, usually without associated cellular infiltrates. From 22 through 40 months after transplantation, the principal vascular lesion was graft-induced atherosclerosis. These immunocytochemically defined qualitative and quantitative changes in unstable or failing allografts form a time-related spectrum of lesions that encompasses the emerging diagnostic entity of vascular rejection.
在40个月的时间里，对90名心脏移植受者的临床和功能参数进行了研究。在移植前从供体心脏获取基线组织学和免疫细胞化学数据，并对系列心内膜活检标本进行组织学研究以检测细胞浸润情况，同时进行免疫细胞化学研究以检测补体和免疫球蛋白沉积情况以及止血、纤维蛋白溶解和天然抗凝途径的成分。结果根据移植后的时间分组：前3个月、4至21个月以及22至40个月。对每组最常见的免疫细胞化学发现以及与患者管理中临床实验室合作相关的结果进行评估。在最初的3个月里，随后将成为问题病例的同种异体移植物活检标本显示小动脉平滑肌细胞中的组织纤溶酶原激活物减少，稳定移植物供体内皮上沉积的受者IgM在不稳定的同种异体移植物中减少或缺失。此外，在70例同种异体移植物中的50例中发现了活化补体成分的血管沉积。移植后4至21个月，很少发现补体的血管沉积（即使在先前活检标本呈阳性的患者中也是如此），主要的血管病变是纤维蛋白沉积，伴有抗凝途径受损和纤维蛋白溶解不足，通常无相关细胞浸润。移植后22至40个月，主要的血管病变是移植物诱导的动脉粥样硬化。这些在不稳定或功能衰竭的同种异体移植物中通过免疫细胞化学定义的定性和定量变化形成了一个与时间相关的病变谱，涵盖了新出现的血管排斥诊断实体。
