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Cirrhosis and hepatopulmonary syndrome Tumgor GWorld J Gastroenterol 2014[Mar]; 20 (10): 2586-94Hepatopulmonary syndrome (HPS) is characterized as a triad: liver disease, intrapulmonary vascular dilatation and arterial hypoxemia. HPS is reported to be present in 4% to 32% of adult patients with end-stage liver disease and in 9%-20% of children. The pathogenesis of HPS has not been clearly identified. Portal hypertension causes impairment in the perfusion of the bowel and increases the enteral translocation of Gram (-) bacteria and endotoxins. This stimulates the release of vasoactive mediators, such as tumor necrosis factor-alpha, heme oxygenase-derived carbon monoxide and nitric oxide. Genetic alterations have not been associated with this syndrome yet; however, cytokines and chemokines have been suggested to play a role. Recently, it was reported that cumulated monocytes lead to the activation of vascular endothelial growth factor-dependent signaling pathways and pulmonary angiogenesis, which plays an important role in HPS pathogenesis. At present, the most effective and only radical treatment is a liver transplant (LT). Cirrhotic patients who are on the waiting list for an LT have a shorter survival period if they develop HPS. Therefore, it is suggested that all cirrhotic cases should be followed closely for HPS and they should have priority in the waiting list.|Animals[MESH]|Hepatopulmonary Syndrome/diagnosis/*etiology/physiopathology/surgery[MESH]|Humans[MESH]|Liver Cirrhosis/*complications/diagnosis/surgery[MESH]|Liver Transplantation[MESH]|Patient Selection[MESH]|Predictive Value of Tests[MESH]|Prognosis[MESH]|Risk Assessment[MESH]|Risk Factors[MESH]|Waiting Lists[MESH] |
