Emond Jean C, Fisher Robert A, Everson Gregory, Samstein Benjamin, Pomposelli James J, Zhao Binsheng, Forney Sarah, Olthoff Kim M, Baker Talia B, Gillespie Brenda W, Merion Robert M
Center for Liver Disease and Transplantation, Columbia University, New York, NY.
Liver Transpl. 2015 Feb;21(2):151-61. doi: 10.1002/lt.24062.
Previous reports have drawn attention to persistently decreased platelet counts among liver donors. We hypothesized an etiologic association between altered platelet counts and postdonation splenomegaly and sought to explore this relationship. This study analyzed de-identified computed tomography/magnetic resonance scans of 388 donors from 9 Adult-to-Adult Living Donor Liver Transplantation Cohort Study centers read at a central computational image analysis laboratory. Resulting liver and spleen volumes were correlated with time-matched clinical laboratory values. Predonation liver volumes varied 2-fold in healthy subjects, even when they were normalized by the body surface area (BSA; range = 522-1887 cc/m(2) , n = 346). At month 3 (M3), postdonation liver volumes were, on average, 79% of predonation volumes [interquartile range (IQR) = 73%-86%, n = 165] and approached 88% at year 1 (Y1; IQR = 80%-93%, n = 75). The mean spleen volume before donation was 245 cc (n = 346). Spleen volumes greater than 100% of the predonation volume occurred in 92% of donors at M3 (n = 165) and in 88% at Y1 after donation (n = 75). We sought to develop a standard spleen volume (SSV) model to predict normal spleen volumes in donors before donation and found that decreased platelet counts, a younger age, a higher predonation liver volume, higher hemoglobin levels, and a higher BSA predicted a larger spleen volume (n = 344, R(2) = 0.52). When this was applied to postdonation values, some large volumes were underpredicted by the SSV model. Models developed on the basis of the reduced sample of postdonation volumes yielded smaller underpredictions. These findings confirm previous observations of thrombocytopenia being associated with splenomegaly after donation. The results of the SSV model suggest that the biology of this phenomenon is complex. This merits further long-term mechanistic studies of liver donors with an investigation of the role of other factors such as thrombopoietin and exposure to viral infections to better understand the evolution of the spleen volume after liver donation.
先前的报告已提请注意活体肝供者血小板计数持续下降的情况。我们推测血小板计数改变与供肝后脾肿大之间存在病因学关联,并试图探究这种关系。本研究分析了来自9个成人对成人生存活体肝移植队列研究中心的388名供者的匿名计算机断层扫描/磁共振扫描图像,这些图像在一个中央计算机图像分析实验室进行解读。由此得出的肝脏和脾脏体积与时间匹配的临床实验室值相关。在健康受试者中,供肝前肝脏体积变化达2倍,即使按体表面积(BSA;范围 = 522 - 1887 cc/m²,n = 346)进行标准化后也是如此。在术后3个月(M3),供肝后肝脏体积平均为供肝前体积的79%[四分位间距(IQR)= 73% - 86%,n = 165],在术后1年(Y1)接近88%(IQR = 80% - 93%,n = 75)。供肝前脾脏平均体积为245 cc(n = 346)。术后3个月时,92%的供者(n = 165)脾脏体积大于供肝前体积的100%,术后1年时这一比例为88%(n = 75)。我们试图建立一个标准脾脏体积(SSV)模型来预测供者供肝前的正常脾脏体积,发现血小板计数降低、年龄较小、供肝前肝脏体积较大、血红蛋白水平较高以及BSA较高可预测脾脏体积较大(n = 344,R² = 0.52)。当将此模型应用于供肝后的值时,一些较大体积被SSV模型低估。基于供肝后体积的减少样本建立的模型低估程度较小。这些发现证实了先前关于血小板减少与供肝后脾肿大相关的观察结果。SSV模型的结果表明这一现象的生物学机制较为复杂。这值得对活体肝供者进行进一步的长期机制研究,调查其他因素如血小板生成素和病毒感染暴露的作用,以更好地理解供肝后脾脏体积的演变。