Bogomolets National Medical University, Ministry of Health of Ukraine, Kiev, Ukraine.
Institute of Biology and Medicine, Taras Shevchenko National University of Kyiv, Kiev, Ukraine.
Dig Dis. 2022;40(2):232-238. doi: 10.1159/000516412. Epub 2021 Apr 9.
The pathophysiology of hepatic encephalopathy (HE) is incompletely understood. It remains elusive how the contributing factors of neuronal ammonia accumulation, cell swelling, and inflammation interact.
The objective of this study was to find the correlation between neuronal autoantibody levels and the degree of HE as first indication of immune-mediated pathogenesis.
We investigated serum autoantibody levels of representative brain proteins in patients with HE as well as in an experimental rat model with cirrhosis and HE after carbon tetrachloride exposure. They were examined in relation to presence of HE and the degree of neurological impairment evaluated by quantitative scores.
In HE, an increase in all of the examined antibodies was observed in serum. The grade of antibody elevation correlated to the degree of encephalopathy registered by quantitative evaluation of brain dysfunction.
The degree of HE parallels neuronal autoantibody elevation. In case a causal relationship could finally be established, it adds to the understanding of HE and may open a new perspective for treatment of this handicapping condition by immunosuppressive strategies.
肝性脑病（HE）的病理生理学尚未完全阐明。导致神经元氨积聚、细胞肿胀和炎症的因素如何相互作用仍然难以捉摸。
本研究的目的是寻找神经元自身抗体水平与 HE 严重程度之间的相关性，作为免疫介导发病机制的初步迹象。
我们研究了 HE 患者以及四氯化碳暴露后肝硬化和 HE 实验大鼠模型血清中代表性脑蛋白的自身抗体水平。它们与 HE 的存在以及通过定量评分评估的神经功能障碍程度有关。
在 HE 中，所有检测到的抗体在血清中均升高。抗体升高的程度与脑功能障碍的定量评估所记录的脑病严重程度相关。
HE 的严重程度与神经元自身抗体的升高平行。如果最终能够确立因果关系，这将有助于我们理解 HE，并可能为这种致残疾病的免疫抑制治疗策略开辟新的视角。
