Reichenbach A, Fuchs U, Kasper M, el-Hifnawi E, Eckstein A K
Paul Flechsig Institute for Brain Research, Leipzig University, Germany.
Acta Neuropathol. 1995;90(3):273-81. doi: 10.1007/BF00296511.
More than 80 years ago, Alzheimer described changes in the brains of patients who had suffered hepatic failure. Astrocytes are primarily affected; their nuclei become swollen, their intermediate filament protein composition is altered and their cytoplasm becomes vacuolated. Cells with these features are called Alzheimer type II astrocytes and these changes have been attributed to the toxic effects of elevated ammonia levels. The present study investigates whether the dominant glia of another part of the central nervous system, the Müller cells of the retina, undergo similar changes. Retinae of patients who had died with symptoms of hepatic failure were processed for histology, histochemistry, and immunocytochemistry. Cell nuclei were measured from brain astrocytes (insula cortex), Müller cells, and retinal bipolar neurons. Hepatic failure resulted in the enlargement of nuclei in astrocytes and Müller cells, and the enhanced expression in Müller cells of glial fibrillary acidic protein, cathepsin D, and the beta-subunit of prolyl 4-hydroxylase (glial-p55). In some retinae, signs of gliosis were also observed. We conclude that increased levels of serum ammonia resulting from hepatic insufficiency cause changes in Müller cells that are similar to those seen in brain astrocytes. We term this condition hepatic retinopathy.
80多年前，阿尔茨海默描述了肝功能衰竭患者大脑中的变化。星形胶质细胞受到主要影响；它们的细胞核肿胀，中间丝蛋白组成改变，细胞质出现空泡化。具有这些特征的细胞被称为II型阿尔茨海默星形胶质细胞，这些变化被认为是氨水平升高的毒性作用所致。本研究调查中枢神经系统另一部分的主要神经胶质细胞，即视网膜的米勒细胞，是否会发生类似变化。对死于肝功能衰竭症状的患者的视网膜进行组织学、组织化学和免疫细胞化学处理。对脑星形胶质细胞（岛叶皮质）、米勒细胞和视网膜双极神经元的细胞核进行测量。肝功能衰竭导致星形胶质细胞和米勒细胞的细胞核增大，以及米勒细胞中胶质纤维酸性蛋白、组织蛋白酶D和脯氨酰4-羟化酶β亚基（胶质-p55）的表达增强。在一些视网膜中，还观察到了胶质增生的迹象。我们得出结论，肝功能不全导致的血清氨水平升高会引起米勒细胞的变化，这些变化与脑星形胶质细胞中的变化相似。我们将这种情况称为肝性视网膜病变。
