Li Zong-fang, Zhang Shu, Huang Ying, Xia Xian-ming, Li Ai-min, Pan Dun, Zhang Wei, Wang Juan
Department of General Surgery, Second Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, China.
Chin Med J (Engl). 2008 Mar 20;121(6):561-5.
The pathogenesis of hypersplenism and the immune function of the spleen in patients with portal hypertension (PH) remain obscure. This study aimed to evaluate the morphological changes of blood spleen barrier in spleen with hypersplenism due to PH and provide evidence for an in-depth investigation of the immune function of the spleen with hypersplenism and the mechanism of hypersplenism.
Spleen samples from 12 portal hypertensive patients and 4 patients with traumatic ruptures of spleen were examined. The samples of spleen were made into pathological sections, stained with Masson trichrome stain, Gomori stain, and CD68, CD34 immunohistochemistry, and were examined microscopically for the changes in the distribution of collagen fibers, reticular fibers, macrophages, and vascular endothelial cells. The changes in ultrastructure of macrophages and endothelial cells in marginal zone were also evaluated by transmission electron microscopy.
As compared to the normal spleen, the density of macrophage in the PH spleen was decreased, but the macrophages were mainly located in the marginal zone and distributed around the splenic corpuscle, with many villi and pseudopodium-like protrusion on the cell surface. The accrementition of collagen fibers was obvious around the splenic corpuscle and central artery. The increased reticulate fibers encircled the splenic corpuscle with more connection between the fibers. The vascular endothelial cells were in diffused distribution, without any regionality in PH spleen, but the vessel with enlarged lumina increased in red pulp.
The morphological changes of the blood spleen barrier can be one of the pathological fundaments for the abnormality of the immune function and the increased destruction of blood cells located in the spleens of patients with PH. However, this still entails clarification.
门静脉高压症（PH）患者脾功能亢进的发病机制及脾脏的免疫功能仍不清楚。本研究旨在评估PH所致脾功能亢进患者脾脏血脾屏障的形态学变化，为深入研究脾功能亢进患者脾脏的免疫功能及脾功能亢进的机制提供依据。
对12例门静脉高压患者和4例外伤性脾破裂患者的脾脏样本进行检查。将脾脏样本制成病理切片，用Masson三色染色、Gomori染色以及CD68、CD34免疫组织化学染色，显微镜下观察胶原纤维、网状纤维、巨噬细胞和血管内皮细胞分布的变化。还通过透射电子显微镜评估边缘区巨噬细胞和内皮细胞超微结构的变化。
与正常脾脏相比，PH脾脏中巨噬细胞密度降低，但巨噬细胞主要位于边缘区，围绕脾小体分布，细胞表面有许多绒毛和伪足样突起。脾小体和中央动脉周围胶原纤维增生明显。网状纤维增多，围绕脾小体，纤维间连接增多。血管内皮细胞呈弥漫性分布，在PH脾脏中无任何区域性，但红髓中管腔扩大的血管增多。
血脾屏障的形态学变化可能是PH患者脾脏免疫功能异常及血细胞破坏增加的病理基础之一。然而，这仍有待阐明。
