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BackgroundCurrently, many nutritional indicators, including controlling nutritional status score (CONUT), can be used to assess a patient’s nutritional status and have been reported as reliable predictors of multiple malignancies. However, the value of CONUT score in predicting postoperative outcomes in patients with hilar cholangiocarcinoma has not been explored. In this study, its predictive value will be discussed and compared with the known predictors the neutrophil lymphocyte ratio (NLR) and prognostic nutritional index (PNI).MethodsPreoperative CONUT scores, PNI and NLR levels of 94 Hilar cholangiocarcinoma (HCCA) patients who underwent radical-intent resection of hepatobiliary surgery in our hospital from March 2010 to April 2019 were retrospectively collected and analyzed. They were grouped according to their optimal cutoff value and the prognostic effects of patients in each group were compared respectively.ResultsCONUThigh was more frequent in patients with Clavien–Dindo classification of ≥IIIa (P = 0.008) and Bile leakage presence (P = 0.011). Kaplan-Meier curves analyzing the relationship between CONUT, PNI, and NLR values and HCCA patient survival (including total survival (OS) and recurrence-free survival (RFS) showed significant differences between groups (P <0.001). Meanwhile, multi-factor analysis found that Degree of cure, PNI, NLR, and preoperative CONUT score were independent prognostic factors for OS and RFS. The predictive power of CONUT score was higher than that of NLR and PNI based on time-dependent receiver operating Characteristic (ROC) analysis and the net reclassification index (NRI) and integrated discriminatory index (IDI) values (P < 0.05).ConclusionCONUT score may be of some clinical reference value in evaluating postoperative prognosis of HCCA patients.

Background Aloin exerts considerable protective effects in various disease models, and its effect on hepatic ischemia-reperfusion (HIR) injury remains unknown. This research is aimed at conducting an in-depth investigation of the antioxidant, anti-inflammatory, and antiapoptosis effects of aloin in HIR injury and explain the underlying molecular mechanisms. Methods In vivo, different concentrations of aloin were intraperitoneally injected 1 h before the establishment of the HIR model in male mice. The hepatic function, pathological status, oxidative stress, and inflammatory and apoptosis markers were measured. In vitro, aloin (AL, C21H22O9) or lipopolysaccharide (LPS) was added to a culture of mouse primary hepatocytes before it underwent hypoxia/reoxygenation (H/R), and the apoptosis in the mouse primary hepatocytes was analyzed. Results We found that 20 mg/kg was the optimum concentration of aloin for mitigating I/R-induced liver tissue damage, characterized by decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Aloin pretreatment substantially suppressed the generation of hepatic malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and IL-6 and enhanced the hepatic superoxide dismutase (SOD) activities as well as glutathione (GSH) and IL-10 levels in the liver tissue of I/R mice; this indicated that aloin ameliorated I/R-induced liver damage by reducing the oxidative stress and inflammatory response. Moreover, aloin inhibited hepatocyte apoptosis and inflammatory response that was caused by the upregulated expression of Bcl-2, the downregulated expression of cleaved caspase3(C-caspase3), Bax, Toll-like receptor 4 (TLR4), FADD, MyD88, TRAF6, phosphorylated IKKα/β (p-IKKα/β), and phosphorylated nuclear factor κB p65 (p-NF-κB p65).

Nonalcoholic fatty liver disease (NAFLD) is a common chronic disease associated with high levels of serum uric acid (SUA). However, whether this relationship applies in obese subjects has been unclear, and no cohort study has previously been conducted in non-obese subjects. We therefore performed a retrospective cohort study among employees of seven companies in China to investigate whether hyperuricemia was independently associated with NAFLD in obese and non-obese subjects, respectively. A total of 2383 initially NAFLD-free subjects were followed up for four years, and 15.2% (363/2383) developed NAFLD. Hyperuricemia subjects had a higher cumulative incidence than did those with normouricemia (29.0% vs. 12.9%, P<0.001). Cox proportional hazard regression analyses showed that baseline hyperuricemia was significantly associated with risk of developing NAFLD in non-obese subjects. This relationship was significantly independent of baseline age, gender, metabolic syndrome components, and other clinical variables (RR = 1.389, 95%CI: 1.051–2.099). However, this association did not exist in obese subjects (RR = 1.010, 95%CI: 0.649–1.571). The independent effect of hyperuricemia on NAFLD was stronger in females (RR = 2.138, 95%CI: 1.050–4.355) than in males (RR = 1.435, 95%CI: 1.021–2.018). In conclusion, further studies are needed to explore the different mechanisms between obese and non-obese subjects, and the reason hyperuricemia raises NAFLD risk in females more than in males.