Survival rates of patients with acute liver failure (ALF) without transplantation are poor. However, many of them die waiting for a transplant because of donor organ shortage. Supporting these patients until an organ becomes available or until their own liver is able to regenerate itself thus avoiding transplantation is a major goal in their multidisciplinary treatment (1). Animal experimental studies have shown that portal vein arterialization (PVA) enhances the regenerative capacity of the hepatocytes by increasing the oxygen supply to the liver after extended hepatectomy and in toxic-inducedALFmodel(2–4). Furthermore, we have reported a case of PVA performed to rescue a dearterialized liver graft with80%hepatocyte necrosis as a bridge for retransplantation (5). Wepresent here a clinical case of ALF successfully treated with a modified PVA technique. A 25-year-old female was admitted to our hospital for abdominal pain and asthenia. Blood tests revealed severe coagulopathy and hypertransaminasemia (Table 1). Her medical history was unremarkable except for a recent administration of tetracyclines for acne. The viral or autoimmune hepatitis markers were absent. Her liver function deteriorated rapidlyandthe neurological statusworsenedto deepcomarequiring respiratory assistance within 2 days. This dramatic clinical course and the persistent delay of a donor prompted us to attempt, with the informed consent of the family, a PVA procedure by anastomosing the inferior mesenteric artery to the inferior mesenteric vein. At surgery, the liver was macroscopically necrotic and a biopsy showed a severe confluent parenchymal necrosis. In the following days, the neurological conditions improved rapidly as did the hepatic function tests. The coma resolved within 2 days and she was extubated 3 days after arterialization. Ten days later, an angiography demonstrated the shunt patency (Fig. 1 panel A) and only a mild increase in portal pressure(22mmHg).Thepatientliverfunctiontestsprogressivelyimprovedexceptfora marked cholestasis requiring several carbon hemodialysis sessions and a reduced prothrombin activity. A liver biopsy performed 22 days from PVA revealed residual small foci of lobular necrosis and mild inflammation associated, however, with severe cholestasis and collapse of the reticuline fibres. Toavoid long-term complications related to portal hypertension, the arteriovenous shunt was closed with a metal coil during an angiographic procedure (Fig. 1 panel B) leading to a normalization of the portal bloodflow.Thepatientwasdischargedfrom hospital 29 days after PVA and liver tests progressively normalized in the following months. At present, she is in good clinical conditions, back at work and liver tests are normal. Although we cannot rule out the possibility that this patient could have recovered spontaneously, this event is very rare in deeply comatose patients with non-acetaminophen-induced ALF. By bringing the portal vein oxygen saturation up to an arterial blood level, thus likely matching the increased metabolic demand of the regenerating cells, a temporary PVA procedure can represent a new tool in the multidisciplinary approach to ALF. However, clinical trials are needed to validate this positive initial experience before PVA becomes part of clinical practice.
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