Digestive Disease Department, Marqués de Valdecilla University Hospital, Cantabria University, Av. Valdecilla s/n, 39008 Santander, Spain.
Health Research Institute Marques de Valdeciila, IDIVAL, 39011 Santander, Spain.
Cells. 2019 Nov 24;8(12):1506. doi: 10.3390/cells8121506.
Portal sinusoidal vascular disease is a presinusoidal cause of portal hypertension (PHT) of unknown etiology, characterized by typical manifestations of PHT (esophageal varices, ascites, portosystemic collaterals), plaquetopenia and splenomegaly with a gradient of portal pressure slightly increased, according to the presinusoidal nature of the PHT. A few cases in the literature have shown a relationship between oxaliplatin and the development of presinusoidal portal hypertension, years after the chemotherapy for colorectal cancer (therefore, different to sinusoidal obstruction syndrome). There are three mechanisms through which oxaliplatin can cause sinusoidal damage: 1) damage at the level of endothelial cells and stimulates the release of free radicals and depletion of glutathione transferase, with altering the integrity of the sinusoidal cells. The damage in the endothelial sinusoidal cells allows to erythrocytes to across into the Dissé space and formation of perisinusoidal fibrosis, 2) the appearance of nodular regenerative hyperplasia is favored by the chronic hypoxia of the centrilobular areas and, finally, 3) oxaliplatin can generate an obliteration of the blood capillaries and zones of parenchymal extinction. These three facts can develop, in a minority of cases, the appearance of a presinusoidal increase of portal pressure, which typically appears years after the completion of chemotherapy and sometimes is underdiagnosed until variceal bleeding, ascites or encephalopathy appear. The knowledge of this pathology is essential to be able to perform an early diagnostic and consult to the hepatologist
窦周静脉血管病是一种未知病因的门静脉高压(PHT)的前窦性原因,其特征为典型的 PHT 表现(食管静脉曲张、腹水、门体侧支循环)、血小板减少和脾肿大,门静脉压力梯度略有增加,根据 PHT 的前窦性性质。文献中有少数几例显示奥沙利铂与前窦性门静脉高压的发展之间存在关系,即在结直肠癌的化疗多年后(因此,与窦状阻塞综合征不同)。奥沙利铂可通过三种机制引起窦状损伤:1)损伤内皮细胞水平并刺激自由基释放和谷胱甘肽转移酶耗竭,改变窦状细胞的完整性。内皮窦状细胞的损伤使红细胞穿过 Disse 间隙并形成窦周纤维化,2)结节性再生性增生的出现有利于中心区的慢性缺氧,最后,3)奥沙利铂可导致毛细血管闭塞和实质消失区。在少数情况下,这三个因素会导致门静脉压力的前窦性升高,这种情况通常在化疗完成后数年出现,有时直到出现静脉曲张出血、腹水或肝性脑病才被诊断出来。了解这种病理学对于能够进行早期诊断并咨询肝病学家至关重要。