Fulminant hepatic failure attributed to ackee fruit ingestion in a patient with sickle cell trait

Abstract

We report a case of fulminant liver failure resulting in emergent liver transplantation following 3 weeks of nausea, vomiting, and malaise from Jamaican Vomiting Sickness. Jamaican Vomiting Sickness is caused by ingestion of the unripe arils of the Ackee fruit, its seeds and husks. It is characterized by acute gastrointestinal illness and hypoglycemia. In severe cases, central nervous system depression can occur. In previous studies, histologic sections taken from patients with Jamaican Vomiting Sickness have shown hepatotoxicity similar to that seen in Reye syndrome and/or acetaminophen toxicity. We highlight macroscopic and microscopic changes in the liver secondary to hepatoxicity of Ackee fruit versus those caused by a previously unknown sickle cell trait. We discuss the clinical variables and the synergistic hepatotoxic effect of Ackee fruit and ischemic injury from sickled red blood cells, causing massive hepatic necrosis in this patient.

Figure 1

Gross photograph of the native liver. The specimen weighs 645 g and measures 23 × 15 × 4 cm. Cross section through greatest dimension of the liver shows a shrunken and hemorrhagic liver indicative of parenchymal loss.

Figure 2

Histologic sections from the explanted liver. (a) The portal tracts are close together separated by hemorrhagic areas with hepatocyte loss (H&E, ×20). (b) Trichrome stain highlights a portal tract (P), but pale areas of parenchymal collapse (arrows) are unstained (×100). (c) Hepatocytes with microvesicular steatosis and sickled red blood cells (H&E, ×200). (d) Ductular hepatocytes and inflammatory cells adjacent to an area with hepatocyte loss and sickled cells (H&E, ×200). (e) Periportal ductular hepatocytes in an area of confluent necrosis. Microvesicular steatosis (arrow) and sickled cells of varying ages (arrow heads) are also highlighted in this section (H&E, ×40). (f). Regenerating hepatocytes adjacent to an older area of parenchymal loss. Note multinucleated giant hepatocytes with cholestasis in a largely hypocellular background with some macrophages (H&E, ×200).