Canto A L, Sesso A, De Brito T
J Pathol. 1977 Sep;123(1):35-44. doi: 10.1002/path.1711230105.
A morphometric, light and electron-microscopy study of the sinusoids in human Mansonian schistosomiasis with and without portal hypertension showed a sequence of events beginning with an increased number of cell nuclei, particularly evident at the centrolobular region. This is followed by deposition of reticulin fibres along the perisinusoidal space. Later, increased numbers of cells and reticulin fibres are seen throughout the lobule. Other findings, such as reduplication of the sinusoidal lining and the focal appearance beneath the cell layer of the thin discontinuous membrane, were also reported. This perisinusoidal fibrosis probably adds an element of heightened intrasinusoidal pressure to the perisinusoidal hypertension already described in this disease. Its pathogenic mechanism is obscure. The hepatic sinusoids in Mansonian schistosomiasis receive mainly arterial blood. High intraluminal pressure could be one explanation of the perisinusoidal fibrosis in these cases. However, as possibly occurs in primary sinusoidal portal hypertension, chronic immunological stimulation leading to proliferation of Küpffer cells and lipocytes could be an alternative mechanism.
一项针对伴有和不伴有门静脉高压的曼氏血吸虫病患者肝血窦的形态测量、光镜和电镜研究显示了一系列事件,始于细胞核数量增加,在小叶中央区尤为明显。随后是网状纤维沿肝血窦周隙沉积。之后,整个小叶可见细胞和网状纤维数量增加。还报告了其他发现,如肝血窦内衬的重复以及薄的不连续膜在细胞层下方的局灶性表现。这种肝血窦周纤维化可能会给该疾病中已描述的肝血窦周高压增加窦内压升高这一因素。其致病机制尚不清楚。曼氏血吸虫病中的肝血窦主要接受动脉血。管腔内高压可能是这些病例中肝血窦周纤维化的一种解释。然而,正如在原发性肝血窦门静脉高压中可能发生的那样,导致库普弗细胞和脂肪细胞增殖的慢性免疫刺激可能是另一种机制。