Li Y S, Bao J, Xu Y, Wang T L
Department of Gastroenterology and Hepatology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Pathology Department, the China-Japan Friendship Hospital, Beijing 100020, China.
Zhonghua Gan Zang Bing Za Zhi. 2020 Apr 20;28(4):332-337. doi: 10.3760/cma.j.cn501113-20190724-00269.
To observe the histopathological manifestations of liver biopsy in patients with hepatic sinusoidal obstruction syndrome (HSOS) induced by pyrrolizidine alkaloid (PA). Patients diagnosed with PA-HSOS from 2012 to 2017 were selected, and the general conditions, liver function indexes, medication history, liver biopsy time, histopathological slides of liver biopsy, and follow-up data of clinical prognosis after 6 months of onset were collected. Clinical staging with clinical data was used to observe the histopathological manifestations of patients at different clinical stages. Wilcoxon rank-sum test, unpaired t-test and univariate linear regression analysis were used for data analysis. A total of 16 cases were collected. Alanine transaminase and aspartate transaminase was 59.25 U/L and 25.50 U/L, 108 U/L and 45 U/L, respectively, after 6 months of onset and follow-up, and the differences were statistically significant. Moreover, total bile acids and albumin was 35 μmol/L and 36.15 μmol/L, and 32.45 g/L and 31 g/L, respectively, and the differences were not statistically significant. PA-HSOS pathological development process was divided into early, middle and late stages. In the early stage, the central lobular sinusoidal endothelium integrity was impaired and the entry of erythrocytes had interspersed thin reticular fibers and perisinusoidal space. In the middle stage (hemorrhagic zone), erythrocytes, reticular fibers and collagen fibers were lysed, densely collapsed and deposited. The cavity of the bloodstream was hyperemic and dilated, and the cavity was covered with sinus endothelial cells. The hepatic plate regenerated around the hemorrhagic zone and some of the hepatic sinuses were decompensated. In the late stage, deposited collagen in the hemorrhagic zone had formed a large fibrous scar, and most of the dilated cavity in the bloodstream was covered with vascular endothelium. The marginal zone hepatic cells were regenerated in two rows and gradually inserted into the fibrous septum. Different hepatic lobular lesions obtained from the same patients liver biopsy tissues were changed at different stages. Hepatic lobule injury proportion with severe internal bleeding in liver biopsy tissue had no relation with the prognosis of patients. In the early stage of PA-HSOS, erythrocytes in the central zone of lobules enter the perisinusoidal space through the damaged sinus endothelium, which is manifested as hepatic plate hemorrhagic necrosis. In the middle and late stage, liver plate regeneration and vascular remodeling occurred, so most of the patients' clinical course was self-limited. Pathological staging and liver biopsy time have an apparent correlation, but the prognosis of patients cannot be judged based on the extent of hemorrhage and injury of biopsy samples.
观察吡咯烷生物碱（PA）所致肝窦阻塞综合征（HSOS）患者肝脏活检的组织病理学表现。选取2012年至2017年诊断为PA-HSOS的患者，收集其一般情况、肝功能指标、用药史、肝脏活检时间、肝脏活检组织病理学切片以及发病6个月后临床预后的随访资料。结合临床资料进行临床分期，观察不同临床分期患者的组织病理学表现。采用Wilcoxon秩和检验、非配对t检验及单因素线性回归分析进行数据分析。共收集16例患者。发病6个月及随访时丙氨酸转氨酶和天冬氨酸转氨酶分别为59.25 U/L和25.50 U/L、108 U/L和45 U/L，差异有统计学意义。此外，总胆汁酸和白蛋白分别为35 μmol/L和36.15 μmol/L、32.45 g/L和31 g/L，差异无统计学意义。PA-HSOS的病理发展过程分为早、中、晚三期。早期，中央小叶窦内皮完整性受损，红细胞进入有散在细网状纤维和窦周间隙。中期（出血区），红细胞、网状纤维和胶原纤维溶解、密集塌陷和沉积。血腔充血扩张，腔内覆盖窦内皮细胞。肝板在出血区周围再生，部分肝窦失代偿。晚期，出血区沉积的胶原形成大的纤维瘢痕，血腔中大部分扩张腔被血管内皮覆盖。边缘区肝细胞呈双排再生并逐渐插入纤维间隔。同一患者肝脏活检组织不同肝小叶病变在不同阶段发生变化。肝脏活检组织严重内出血的肝小叶损伤比例与患者预后无关。在PA-HSOS早期，小叶中央区红细胞通过受损的窦内皮进入窦周间隙，表现为肝板出血坏死。在中晚期，肝板再生和血管重塑发生，因此大多数患者的临床病程是自限性的。病理分期与肝脏活检时间有明显相关性，但不能根据活检样本的出血和损伤程度判断患者预后。
