Journal of gastrointestinal cancer · 2026
Metabolic Dysfunction-Associated Steatotic Liver Disease after Pancreatoduodenectomy: an Underestimated Metabolic Complication Driven by Unique Pathophysiological Mechanisms.
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Tehuitzil-Cordero Andrea, Montalvo-Javé Eduardo, Uribe Misael, Nuño-Lámbarri Natalia
Аннотация
PURPOSE: Pancreatoduodenectomy (PD) remains the cornerstone surgical treatment for resectable periampullary and pancreatic malignancies, with improving survival due to advances in oncologic surgery and perioperative management. Emerging evidence, however, identifies metabolic dysfunction-associated steatotic liver disease (MASLD) as a relevant postoperative complication that may adversely influence long-term outcomes. This review aims to summarizethe incidence, pathophysiology, clinical implications, and management strategies of de novo MASLD following PD in patients with gastrointestinal malignancies.
METHODS: A narrative review of clinical and translational studies was conducted focusing on hepatic steatosis, metabolic derangements, pancreatic exocrine and endocrine insufficiency, and chemotherapy-related liver injury after PD. Particular attention was given to studies evaluating postoperative nutritional status, liver-related morbidity, and implications for oncologic therapy.
RESULTS: De novo MASLD develops in approximately 8-37% of patients within the first year after PD. Unlike classical metabolic MASLD, postoperative disease is predominantly driven by exocrine pancreatic insufficiency, malabsorption, intestinal dysbiosis, and altered gut-liver signaling, leading to hepatic lipotoxicity and inflammation. Progression to metabolic dysfunction-associated steatohepatitis, fibrosis, or cirrhosis has been reported, potentially limiting tolerance to adjuvant chemotherapy. Early pancreatic enzyme replacement therapy improves nutritional parameters and may reduce hepatic steatosis, while duodenum-preserving pancreatic head resection appears to attenuate metabolic sequelae.
CONCLUSION: MASLD represents a distinct and clinically significant postoperative complication following PD with potential impact on oncologic outcomes. Systematic hepatic monitoring and multidisciplinary management should be integrated into postoperative care pathways for patients with gastrointestinal cancers.
METHODS: A narrative review of clinical and translational studies was conducted focusing on hepatic steatosis, metabolic derangements, pancreatic exocrine and endocrine insufficiency, and chemotherapy-related liver injury after PD. Particular attention was given to studies evaluating postoperative nutritional status, liver-related morbidity, and implications for oncologic therapy.
RESULTS: De novo MASLD develops in approximately 8-37% of patients within the first year after PD. Unlike classical metabolic MASLD, postoperative disease is predominantly driven by exocrine pancreatic insufficiency, malabsorption, intestinal dysbiosis, and altered gut-liver signaling, leading to hepatic lipotoxicity and inflammation. Progression to metabolic dysfunction-associated steatohepatitis, fibrosis, or cirrhosis has been reported, potentially limiting tolerance to adjuvant chemotherapy. Early pancreatic enzyme replacement therapy improves nutritional parameters and may reduce hepatic steatosis, while duodenum-preserving pancreatic head resection appears to attenuate metabolic sequelae.
CONCLUSION: MASLD represents a distinct and clinically significant postoperative complication following PD with potential impact on oncologic outcomes. Systematic hepatic monitoring and multidisciplinary management should be integrated into postoperative care pathways for patients with gastrointestinal cancers.