Porto-Sinusoidal Vascular Disease Associated to Oxaliplatin: An Entity to Think about It

• Published in: Cells (Basel, Switzerland) Switzerland), 2019-11, Vol.8 (12), p.1506
• Main Authors: Puente, Angela, Fortea, Jose Ignacio, Del Pozo, Carmen, Huelin, Patricia, Cagigal, Maria Luisa, Serrano, Marina, Cabezas, Joaquin, Arias Loste, Maria Teresa, Iruzubieta, Paula, Cuadrado, Antonio, Llerena, Susana, Lopez, Carlos, Fábrega, Emilio, Crespo, Javier
• Format: Article
• Language: English
• Subjects: Ascites; Asymptomatic; Capillaries; Chemotherapy; Colorectal carcinoma; Encephalopathy; Endothelial cells; Endothelium; Erythrocytes; Esophagus; Etiology; Fibrosis; Free radicals; Glutathione; Glutathione transferase; Hyperplasia; Hypertension; Hypoxia; Liver diseases; Mortality; Oxaliplatin; Pathogenesis; Peripheral neuropathy; Review; Splenomegaly; Thrombocytopenia; Vascular diseases; Vascular endothelial growth factor
• ISSN: 2073-4409; 2073-4409
• 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