Rapid Recovery from Acute Liver Failure Secondary to Pancreatoduodenectomy-Related Non-Alcoholic Steatohepatitis

Abstract

This report describes a case of liver failure secondary to pancreatoduodenectomy and rapid recovery following treatment. A 68-year-old woman with cancer on the ampulla of Vater underwent surgery for pancreatoduodenectomy. The patient developed liver failure 3 months postsurgically. She was hospitalized after presenting with jaundice, hypoalbuminemia and decreased serum zinc. Computed tomography (CT) of the abdomen showed a reduction in CT attenuation values postoperatively. We suspected fatty liver due to impaired absorption caused by pancreatoduodenectomy. We initiated treatment with branched-chain amino acids and a zinc formulation orally. Trace elements were administered intravenously. Two months after treatment, there was a noticeable improvement in CT findings. The patient’s jaundice and hypoalbuminemia prompted a liver biopsy, which led to a diagnosis of non-alcoholic steatohepatitis.

New onset non‐alcoholic fatty liver disease after resection of pancreatic neuroendocrine tumors

“…After pancreatoduodenectomy (PD), approximately 23‐37% of the patients develop NAFLD/NASH . A significant number of these patients did not suffer from metabolic syndrome preoperatively.…”

“…Some studies suggest that malnutrition or malabsorption of essential nutrients caused by exocrine pancreatic insufficiency (EPI) leads to NAFLD/NASH . Changes in metabolism resulting in hepatic steatosis could lead to sensitivity for hepatocyte damage, inflammation, and fibrosis .…”

“…Pancreatic enzyme administration as treatment of EPI has beneficial impact on hepatic steatosis after PD, indicating that EPI could be the main cause of new onset NAFLD/NASH in these patients . Other evidence for malnutrition in patients with EPI or after PD is the report of increase of taurine serum levels and decrease of methionine, tyrosine, albumin, cholinesterase, zinc, and total cholesterol serum levels . Therefore, other nutrients or mechanism that not yet have been identified could cause the hepatic steatosis.…”

“…After pancreatoduodenectomy (PD), approximately 23-37% of the patients develop NAFLD/NASH. [3][4][5][6][7] A significant number of these patients did not suffer from metabolic syndrome preoperatively. It is likely that mechanisms underlying postoperative NAFLD/NASH differ from mechanisms underlying common metabolic NAFLD/NASH.…”

“…Some studies suggest that malnutrition or malabsorption of essential nutrients caused by exocrine pancreatic insufficiency (EPI) leads to NAFLD/NASH. 3,4,[6][7][8][9] Changes in metabolism resulting in hepatic steatosis could lead to sensitivity for hepatocyte damage, inflammation, and fibrosis. 8,10 Pancreatic enzyme administration as treatment of EPI has beneficial impact on hepatic steatosis after PD, indicating that EPI could be the main cause of new onset NAFLD/ NASH in these patients.…”