Development of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) after pancreaticoduodenectomy: proposal of a postoperative NAFLD scoring system
Abstract:In conclusion, NAFLD develops frequently in patients who undergo PD, and some patients even progress to NASH. A postoperative NAFLD scoring system makes it possible to predict the occurrence of NAFLD after PD, and aggressive nutrition support is needed for patients with high scores.
“…Similar to our results, in the previous randomized control trial between PPPD and conventional PD, the nutritional status including the postoperative weight loss was comparable between PPPD and conventional PD groups [13,14]. On the other hand, Kato et al [35] reported eating disorders other than pancreatic dysfunction after pancreatectomy were an important risk factor for NAFLD after pancreatectomy, and postoperative malnutrition associated with DGE and digestive disturbance due to complicated reconstruction leads to the development of NAFLD. Previous studies have revealed that the decrease in the hepatic CT value reflects the degree of fat deposition within the liver [23,36].…”
Background: There are a few reports that compare the rate of postoperative complications between subtotal stomach-preserving pancreatoduodenectomy (SSPPD) and antrectomy-combined pancreatoduodenectomy (ACPD), especially with respect to delayed gastric emptying (DGE) after pancreatoduodenectomy (PD). Methods: From 2002 to 2013, 628 patients who underwent SSPPD (n = 78) or ACPD (n = 550) were enrolled in this study. The rate of DGE and the nutritional status were compared between patients receiving ACPD and SSPPD. Results: The overall morbidity rate (p = 0.830) was comparable between both groups; however, the incidence of DGE grade B or C was significantly higher in the SSPPD group than that in the ACPD group (16 vs. 7%, p = 0.007). A multivariate analysis identified SSPPD rather than ACPD (p = 0.007) and portal vein resection and reconstruction (p = 0.028) to be independent risk factors for DGE grade B or C. The changes in the body weight and nutritional parameters 3, 6, and 12 months after surgery were comparable between 2 groups. Conclusions: SSPPD and not ACPD was an independent risk factor for grade B or C DGE, but the postoperative nutritional status was comparable between the 2 groups based on the limited nutritional data. Combined resection of antrum will help reduce the risk of DGE after PD.
“…Similar to our results, in the previous randomized control trial between PPPD and conventional PD, the nutritional status including the postoperative weight loss was comparable between PPPD and conventional PD groups [13,14]. On the other hand, Kato et al [35] reported eating disorders other than pancreatic dysfunction after pancreatectomy were an important risk factor for NAFLD after pancreatectomy, and postoperative malnutrition associated with DGE and digestive disturbance due to complicated reconstruction leads to the development of NAFLD. Previous studies have revealed that the decrease in the hepatic CT value reflects the degree of fat deposition within the liver [23,36].…”
Background: There are a few reports that compare the rate of postoperative complications between subtotal stomach-preserving pancreatoduodenectomy (SSPPD) and antrectomy-combined pancreatoduodenectomy (ACPD), especially with respect to delayed gastric emptying (DGE) after pancreatoduodenectomy (PD). Methods: From 2002 to 2013, 628 patients who underwent SSPPD (n = 78) or ACPD (n = 550) were enrolled in this study. The rate of DGE and the nutritional status were compared between patients receiving ACPD and SSPPD. Results: The overall morbidity rate (p = 0.830) was comparable between both groups; however, the incidence of DGE grade B or C was significantly higher in the SSPPD group than that in the ACPD group (16 vs. 7%, p = 0.007). A multivariate analysis identified SSPPD rather than ACPD (p = 0.007) and portal vein resection and reconstruction (p = 0.028) to be independent risk factors for DGE grade B or C. The changes in the body weight and nutritional parameters 3, 6, and 12 months after surgery were comparable between 2 groups. Conclusions: SSPPD and not ACPD was an independent risk factor for grade B or C DGE, but the postoperative nutritional status was comparable between the 2 groups based on the limited nutritional data. Combined resection of antrum will help reduce the risk of DGE after PD.
“…These findings suggest that the mechanisms underlying NAFLD after PD differ from those causing NAFLD associated with metabolic syndrome. Recent studies have also suggested that pancreatic exocrine insufficiency may cause NAFLD after PD [8,9] . Although only univariate analyses were examined in our study, pancreatic cancer was associated with the development of NAFLD, which is considered to lead to impaired pancreatic exocrine functions due to obstruction of the MPD, in turn resulting in obstructive distal pancreatic atrophy and fibrosis.…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, several studies have shown strong relationships among NAFLD associated with metabolic syndrome, hepatic insulin resistance and type 2 diabetes mellitus [5][6][7] . On the other hand, NAFLD sometimes develops after pancreatoduodenectomy (PD) [8] . Tanaka et al [9] recently reported that NAFLD after PD was characterized by non-obesity and a lack of both hyperlipidemia and insulin resistance.…”
AIM:To investigate the pathogenesis of non-alcoholic fatty liver disease (NAFLD) after pancreatoduodenectomy (PD).
METHODS:A cohort of 82 patients who underwent PD at Okayama University Hospital between 2003 and 2009 was enrolled and the clinicopathological features were compared between patients with and without NAFLD after PD. Computed tomography (CT) images were evaluated every 6 mo after PD for follow-up. Hepatic steatosis was diagnosed on CT when hepatic attenuation values were 40 Hounsfield units. Liver biopsy was performed for 4 of 30 patients with NAFLD after PD who consented to undergo biopsies. To compare NAFLD after PD with NAFLD associated with metabolic syndrome, liver samples were obtained from 10 patients with NAFLD associated with metabolic syndrome [fatty liver, n = 5; non-alcoholic steatohepatitis (NASH), n = 5] by percutaneous ultrasonography-guided liver biopsy. Double-fluorescence immunohistochemistry was applied to examine CD14 expression as a marker of lipopolysaccharide (LPS)-sensitized macrophage cells (Kupffer cells) in liver biopsy specimens.
RESULTS:The incidence of postoperative NAFLD was 36.6% (30/82). Univariate analysis identified cancer of the pancreatic head, sex, diameter of the main pancreatic duct, and dissection of the nerve plexus as factors associated with the development of NAFLD after PD. Those patients who developed NAFLD after PD demonstrated significantly decreased levels of serum albumin, total protein, cholesterol and triglycerides compared to patients without NAFLD after PD, but no glucose intolerance or insulin resistance. Liver biopsy was performed in four patients with NAFLD after PD. All four patients showed moderate-to-severe steatosis and NASH was diagnosed in two. Numbers of cells positive for CD68 (a marker of Kupffer cells) and CD14 (a marker of LPSsensitized Kupffer cells) were counted in all biopsy specimens. The number of CD68+ cells in specimens of NAFLD after PD was significantly increased from that in specimens of NAFLD associated with metabolic syndrome specimens, which indicated the presence of significantly more Kupffer cells in NAFLD after PD than in NAFLD associated with metabolic syndrome. Similarly, more CD14+ cells, namely, LPS-sensitized Kupffer cells, were observed in NAFLD after PD than in NAFLD associated with metabolic syndrome. Regarding NASH, more CD68+ cells and CD14+ cells were observed in NASH after PD specimens than in NASH associated with metabolic syndrome. This showed that more Kupffer cells and more LPS-sensitized Kupffer cells were present in NASH after PD than in NASH associated with metabolic syndrome. These observations suggest that after PD, Kupffer cells and LPS-sensitized Kupffer cells were significantly upregulated, not only in NASH, but also in simple fatty liver.
ORIGINAL ARTICLECONCLUSION: NAFLD after PD is characterized by both malnutrition and the up-regulation of CD14 on Kupffer cells. Gut-derived endotoxin appears central to the development of NAFLD after PD.
“…A Japanese group proposed a scoring system to predict the development of NAFLD using data of 54 cases, which included 5 components of pancreatic carcinoma, extent of pancreatic resection, pancreatic texture, postoperative diarrhea, and postoperative eating disorder. The authors suggested that their scoring system makes it possible to predict the occurrence of NAFLD after pancreaticoduodenectomy, and aggressive nutrition support is needed for patients with high scores [27]. Postoperative malnutrition associated with delayed gastric emptying and digestive disturbance due to complicated reconstruction, postoperative insulin resistance and other various risk factors leads to the development of NAFLD.…”
Background: Prevalence of hepatic steatosis following pylorus-preserving pancreaticoduodenectomy (PPPD) is high. This study intended to reveal the prevalence and patterns of de novo hepatic steatosis following PPPD. Methods: We investigated postoperative de novo hepatic steatosis following PPPD (n = 101) with a control group of bile duct resection (BDR) (n = 54). Results: At postoperative 1 year, hepatic steatosis occurred in 21 of 82 patients (25.6%) of PPPD group and in 2 of 47 patients (4.3%) of BDR group (p = 0.001). Thereafter, at 2 to 5 years, a high prevalence of hepatic steatosis persisted in the PPPD group, but no further occurrence developed in BDR group. Once steatosis developed, it persisted until the end of the study period or patient death. Five-year cumulative incidence of hepatic steatosis was 26.7% in the PPPD group and 3.7% in BDR group (p < 0.001). Univariate analyses showed that patient sex, age, body mass index, blood lipid profile, recurrence of tumor, and diabetes did not have significant influence on the development of hepatic steatosis following PPPD. Conclusions: De novo hepatic steatosis may develop in a not negligible proportion of patients undergone PPPD. Multicenter studies with a high number of patients are needed to elucidate its pathogenesis and to find effective treatment for pancreaticoduodenectomy-associated hepatic steatosis. i 2014 S. Karger AG, Basel
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