Development of de novo nonalcoholic fatty liver disease following pancreatectomy

Abstract

De novo non-alcoholic fatty liver disease (NAFLD) after pancreatectomy is a recognized phenomenon; however, its pathophysiology is poorly understood. This study aimed to determine the incidence and identify peri-operative risk factors for the development of de novo NAFLD within various pancreatectomy groups. This single-center retrospective cohort study included patients who underwent pancreatectomy between 2000 and 2020. The incidence rate of de novo NAFLD and time to diagnosis were recorded across patients with malignant versus benign indications for pancreatectomy. The overall incidence of de novo NAFLD after pancreatectomy was 17.5% (24/136). Twenty-one percent (20/94) of patients with malignant indications for surgery developed NAFLD compared to 9.5% (4/42) with benign indications (P = .09). Time to development of hepatic steatosis in the malignant group was 26.4 months and was significantly shorter by an average of 6 months when compared to the benign group (32.8 months, P = .03). Higher pre-operative body mass index was associated with new-onset NAFLD (P = .03). Pre-operative body mass index is a significant predictor for de novo NAFLD and highlights a group that should be closely monitored post-operatively, especially after resections for pancreatic malignancy.

Cross-sectional imaging after pancreatic surgery: The dialogue between the radiologist and the surgeon

“…About 2.2% of patients who undergo pancreatic resection may have a postoperative increase in liver enzymes, which is considered a normal postoperative finding if serum aminotransferases show only a mild increase and a peak in levels on the first day after surgery followed by a slow decrease until normal values are reached usually within 5 days [104] . De novo development of non-alcoholic fatty liver disease (NAFLD) after pancreatic surgery has been increasingly observed, with a reported incidence of up to 37% occurring 4 to 12 months postoperatively [105] , [106] , [107] , [108] , [109] , [110] , [111] . The two main possible causative mechanisms for the development of hepatic steatosis after pancreatic surgery include metabolic syndrome and insulin resistance leading to increased circulating free fatty acid in the blood, liver uptake of free fatty acid, and lipogenesis in the liver and malnutrition, malabsorption of amino acids, decreased insulin secretion, decreased carnitine, and choline levels, and upregulated levels of peroxisome proliferator-activated receptors.…”

Novel Insights into Postoperative Surveillance in Resected Pancreatic Cystic Neoplasms—A Review

“…In addition to the resection type, other risk factors for NAFLD occurrence were residual pancreatic volume, pancreatic exocrine and endocrine dysfunction and post-operative nutritional management [99]. Patel V. et al also investigated the incidence, time to diagnosis and perioperative risk factors of de novo NAFLD in a single-center retrospective cohort study including patients who underwent pancreatectomy for both benign and malignant pathologies between 2000 and 2020 [100]. The overall incidence of de novo NAFLD was 17.5%, with a two-fold higher incidence in patients with malignant compared to benign pancreatic disease (21.3% vs. 9.5%) and a significantly shorter (by an average of 6 months) time to diagnosis compared to the benign group (26.4 vs. 32.8 months, p = 0.03).…”