Wiest Reiner, Weiss Thomas S, Danielyan Lusine, Buechler Christa
Department of Visceral Surgery and Medicine, University Inselspital, 3010 Bern, Switzerland.
Children's University Hospital (KUNO), Regensburg University Hospital, 93053 Regensburg, Germany.
J Clin Med. 2021 Jun 17;10(12):2669. doi: 10.3390/jcm10122669.
Amyloid-beta (Aβ) deposition in the brain is the main pathological hallmark of Alzheimer disease. Peripheral clearance of Aβ may possibly also lower brain levels. Recent evidence suggested that hepatic clearance of Aβ42 is impaired in liver cirrhosis. To further test this hypothesis, serum Aβ42 was measured by ELISA in portal venous serum (PVS), systemic venous serum (SVS), and hepatic venous serum (HVS) of 20 patients with liver cirrhosis. Mean Aβ42 level was 24.7 ± 20.4 pg/mL in PVS, 21.2 ± 16.7 pg/mL in HVS, and 19.2 ± 11.7 pg/mL in SVS. Similar levels in the three blood compartments suggested that the cirrhotic liver does not clear Aβ42. Aβ42 was neither associated with the model of end-stage liver disease score nor the Child-Pugh score. Patients with abnormal creatinine or bilirubin levels or prolonged prothrombin time did not display higher Aβ42 levels. Patients with massive ascites and patients with large varices had serum Aβ42 levels similar to patients without these complications. Serum Aβ42 was negatively associated with connective tissue growth factor levels (r = -0.580, = 0.007) and a protective role of Aβ42 in fibrogenesis was already described. Diabetic patients with liver cirrhosis had higher Aβ42 levels ( = 0.069 for PVS, = 0.047 for HVS and = 0.181 for SVS), which is in accordance with previous reports. Present analysis showed that the cirrhotic liver does not eliminate Aβ42. Further studies are needed to explore the association of liver cirrhosis, Aβ42 levels, and cognitive dysfunction.
β淀粉样蛋白（Aβ）在大脑中的沉积是阿尔茨海默病的主要病理标志。Aβ的外周清除可能也会降低大脑中的水平。最近的证据表明，肝硬化患者肝脏对Aβ42的清除受损。为了进一步验证这一假设，采用酶联免疫吸附测定法（ELISA）检测了20例肝硬化患者门静脉血清（PVS）、体静脉血清（SVS）和肝静脉血清（HVS）中的Aβ42水平。PVS中Aβ42的平均水平为24.7±20.4 pg/mL，HVS中为21.2±16.7 pg/mL，SVS中为19.2±11.7 pg/mL。三个血腔中的水平相似，表明肝硬化肝脏不能清除Aβ42。Aβ42水平与终末期肝病评分模型及Child-Pugh评分均无关联。肌酐或胆红素水平异常或凝血酶原时间延长的患者，其Aβ42水平并未升高。有大量腹水的患者和有大静脉曲张的患者，其血清Aβ42水平与无这些并发症的患者相似。血清Aβ42水平与结缔组织生长因子水平呈负相关（r = -0.580，P = 0.007），且已有研究描述了Aβ42在纤维生成中的保护作用。肝硬化合并糖尿病的患者Aβ42水平较高（PVS中P = 0.069，HVS中P = 0.047，SVS中P = 0.181），这与之前的报道一致。目前的分析表明，肝硬化肝脏不能清除Aβ42。需要进一步研究来探讨肝硬化、Aβ42水平与认知功能障碍之间的关联。
