Pentoxifylline for slow to resolve hepatopulmonary syndrome post liver transplantation: Helpful or Unnecessary?

摘要

Hepatopulmonary syndrome (HPS), characterized by hypoxia due to intrapulmonary vasodilation and shunting usually in the setting of cirrhotic portal hypertension, affects at least 20% of cirrhotic patients (3). While liver transplantation (LT) is the only effective treatment for HPS, depending on the severity, recipients may experience protracted hypoxia post-LT (1). Hypoxia following LT imposes risks to the recipient such as graft ischemia. Although patients with HPS receive priority for LT, these patients have inferior outcomes, with 1 year recipient survival rates approximating just 70% as compared to 90% in age-matched controls (1,2). Furthermore, patients transplanted with HPS may suffer psychological hardship in the postoperative setting with residual HPS, and there are no reliable means to predict the duration of the resolution after transplant. Nitric oxide and tumor necrosis alpha (TNF-alpha) are potent vasodilators implicated in the pathogenesis of HPS (4,5). The degree of severity of HPS is determined by the recipient's P02 on a room air arterial blood gas ; patients with P02 < 60 mm Hg have severe HPS and the worst survival. Following LT, subjects with advanced HPS may require prolongation of invasive or non-invasive ventilation. There is limited data on the epidemiology and natural history of severe HPS post-LT. The mean duration of residual HPS in subjects transplanted with severe HPS that required pre-operative non-invasive ventilation was 40 days in a report of 5 subjects (6).