Pathophysiology after pancreaticoduodenectomy

Kang, Chang Moo; Lee, Jin Ho

doi:10.3748/wjg.v21.i19.5794

Cited by 48 publications

(47 citation statements)

References 87 publications

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“…It is likely that mechanisms underlying postoperative NAFLD/NASH differ from mechanisms underlying common metabolic NAFLD/NASH. Remarkably, hepatic steatosis following PD was related to non‐obesity, lack of hyperlipidaemia or insulin resistance, indicating another cause for NAFLD/NASH than metabolic syndrome . Still, the process leading to the NAFLD/NASH in these postoperative patients is unclear.…”

Section: Introductionmentioning

confidence: 99%

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

Mackay

Genc

Takkenberg

et al. 2018

Journal of Surgical Oncology

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Background and ObjectivesNon‐alcoholic fatty liver disease (NAFLD) and non‐alcoholic steatohepatis (NASH) may occur after pancreatic resection due to exocrine pancreatic insufficiency (EPI). Patients with long‐term survival, such as after pancreatic neuroendocrine tumor (pNET) resection, are at risk of NAFLD/NASH. We aimed to determine the incidence and risk factors for new onset NAFLD/NASH and EPI after pNET resection.MethodsRetrospective monocenter cohort study. Patients who underwent pNET resection (1992‐2016) were assessed for new onset NAFLD/NASH and EPI. Postoperative NAFLD/NASH was determined by a blinded abdominal radiologist, who compared pre‐ and postoperative imaging.ResultsOut of 235 patients with pNET, a total of 112 patients underwent resection and were included with a median follow‐up of 54 months. New onset NAFLD/NASH occurred in 20% and EPI in 49% of patients. Multivariate analysis showed that the only risk factor for new onset NAFLD/NASH was recurrent disease (OR 4.4, 95% CI 1.1‐16.8, P = 0.031), but not EPI (OR 0.94, 95% CI 0.3‐2.8, P = 0.911). The only risk factor for EPI was pancreatoduodenectomy (OR 4.3, 95% CI 1.4‐13.7, P = 0.012).ConclusionsNew onset NAFLD/NASH is occasionally found after pNET resection, especially in patients with recurrent disease, but is not related to EPI.

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Section: Introductionmentioning

confidence: 99%

“…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 .…”

Section: Introductionmentioning

confidence: 99%

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

Mackay

Genc

Takkenberg

et al. 2018

Journal of Surgical Oncology

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“…After pancreatic resection, patients may experience similar issues as those with chronic pancreatitis or cystic fibrosis, who also experience pancreatic enzyme insufficiency and its sequelae. After pancreatic resection, patients may experience nutrition consequences similar to those of patients who have undergone bariatric surgery, specifically Roux‐en‐Y gastric bypass 20 . In the absence of appropriate research to support recommendations for the long‐term survivor of pancreatic cancer after surgery, clinicians may consider borrowing from the literature for these other conditions to inform their interventions, with careful follow‐up for safety and response to therapy.…”

Section: Resultsmentioning

confidence: 99%

“…Many of the nutrition consequences for long‐term survivors of pancreatic cancer are due to the removal of the duodenum and/or stomach 13 , 20 , 21 . Not only are these required for nutrient breakdown and absorption, but these structures also secrete gastrointestinal hormones influencing gut motility, so disruption in their hormone production can cause gastrointestinal asynchrony 3 , 20 , 22 . Much of the absorption of vitamins and minerals (most notably iron and calcium) is in this first part of the small intestine 21 , 23 .…”

Section: Anatomic Influencesmentioning

confidence: 99%

“…When groups were stratified into those with and without PEI, there were no significant differences between them 54 . Because literature on this subject is sparse but the theoretical concern is high, we looked beyond the pancreatic cancer and PEI literature to that of Roux‐en‐Y gastric bypass, as the anatomic changes are similar to those after PD and PPPD 20 . A small longitudinal study of women having undergone Roux‐en‐Y gastric bypass evaluated bone density.…”

Section: Bone Densitymentioning

confidence: 99%

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Nutrition Implications for Long‐Term Survivors of Pancreatic Cancer Surgery

Petzel

Hoffman

2017

Nut in Clin Prac

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With slowly increasing survival rates in pancreatic cancer and international consensus guidelines recommending surgical resection of premalignant lesions, survival post-pancreatic resection is increasing. With longer survival time, the significant comorbidities of such major surgery have far-reaching effects on the nutrition status of the survivor of pancreatic cancer. This review describes the many nutrition-related side effects of pancreatic surgery, including the development of pancreatic enzyme insufficiency, micronutrient deficiencies, diabetes, fatty liver, and metabolic bone disease. Beyond causing additional medical problems, each of these can have significant effects on quality of life and functional status. The potential mechanisms, diagnosis criteria, and potential treatments of these conditions are described. Overall, little literature exists to fully describe the effects of these comorbidities, and even less is able to guide effective treatments for this population. Clinicians caring for these patients should begin incorporating goals for promotion of long-term health and reduction of these known and reported comorbidities in patients who have undergone pancreatic surgery. Treatment plans in this population remain understudied, and clinicians may need to consider recommendations for similar disease states when developing interventions for these patients.

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Are transmembrane 6 superfamily member 2 gene polymorphisms associated with steatohepatitis after pancreaticoduodenectomy?

Mori,

Ozawa,

Sasaki

et al. 2024

JGH Open

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AimAfter pancreaticoduodenectomy, 20–40% of patients develop steatotic liver disease (SLD), and steatohepatitis can be a problem. Although patatin‐like phospholipase domain‐containing 3 protein (PNPLA3) and transmembrane 6 superfamily member 2 (TM6SF2) polymorphisms are involved in SLD and steatohepatitis development, whether this is the case after pancreaticoduodenectomy is unclear.Methods and ResultsForty‐three patients with pancreatic cancer who underwent pancreaticoduodenectomy at our hospital between April 1, 2018, and March 31, 2021, were included. We extracted DNA from noncancerous areas of residual specimens after pancreaticoduodenectomy and determined PNPLA3 and TM6SF2 gene polymorphisms using real‐time polymerase chain reaction. SLD was defined as a liver with an attenuation value of ≤40 HU or a liver‐to‐spleen ratio of ≤0.9 on computed tomography. We defined high hepatic fibrosis indexes (HFI) instead of steatohepatitis as a Fibrosis‐4 index of ≥2.67 or nonalcoholic fatty liver disease fibrosis score of ≥0.675 in patients with SLD. The cumulative incidence of SLD (P = 0.299) and high HFI (P = 0.987) after pancreaticoduodenectomy were not significantly different between the PNPLA3 homozygous and minor allele groups. The incidences of high HFI at 1 year after pancreaticoduodenectomy were 16.8% and 27.0% in the TM6SF2 major homozygous and minor allele groups, respectively, with a significant difference in the cumulative incidence (P = 0.046).ConclusionThe TM6SF2 minor allele may contribute to steatohepatitis development after pancreaticoduodenectomy.

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Pathophysiology after pancreaticoduodenectomy

Cited by 48 publications

References 87 publications

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

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

Nutrition Implications for Long‐Term Survivors of Pancreatic Cancer Surgery

Are transmembrane 6 superfamily member 2 gene polymorphisms associated with steatohepatitis after pancreaticoduodenectomy?

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