Causes and predictors of unplanned reoperations within 30 days post laparoscopic pancreaticoduodenectomy: a comprehensive analysis.

Objective: To delineate the risk factors and causes of unplanned reoperations within 30 days following laparoscopic pancreaticoduodenectomy (LPD). Methods: A retrospective study reviewed 311 LPD patients at Ningbo Medical Center Li Huili Hospital from 2017 to 2024. Demographic and clinical parameters were analyzed using univariate and multivariate analyses, with P < 0.05 indicating statistical significance. Results: Out of 311 patients, 23 (7.4%) required unplanned reoperations within 30 days post-LPD, primarily due to postoperative bleeding (82.6%). Other causes included anastomotic leakage, abdominal infection, and afferent loop obstruction. The reoperation intervals varied, with the majority occurring within 0 to 14 days post-surgery. Univariate analysis identified significant risk factors: diabetes, liver cirrhosis, elevated CRP on POD-3 and POD-7, pre-operative serum prealbumin < 0.15 g/L, prolonged operation time, intraoperative bleeding > 120 ml, vascular reconstruction, soft pancreatic texture, and a main pancreatic duct diameter ≤3 mm (all P < 0.05). Multivariate analysis confirmed independent risk factors: pre-operative serum prealbumin < 0.15 g/L (OR = 3.519, 95% CI 1.167-10.613), CRP on POD-7 (OR = 1.013, 95% CI 1.001-1.026), vascular reconstruction (OR = 9.897, 95% CI 2.405-40.733), soft pancreatic texture (OR = 5.243, 95% CI 1.628-16.885), and a main pancreatic duct diameter ≤3 mm (OR = 3.462, 95% CI 1.049-11.423), all associated with unplanned reoperation within 30 days post-LPD (all P < 0.05). Conclusion: Postoperative bleeding is the primary cause of unplanned reoperations after LPD. Independent risk factors, confirmed by multivariate analysis, include low pre-operative serum prealbumin, elevated CRP on POD-7, vascular reconstruction, soft pancreatic texture, and a main pancreatic duct diameter of ≤3 mm. Comprehensive peri-operative management focusing on these risk factors can reduce the likelihood of unplanned reoperations and improve patient outcomes.

Macrotrabecular-massive subtype-based nomogram to predict early recurrence of hepatocellular carcinoma after surgery.

OBJECTIVES: To analyze the predictive factors on early postoperative recurrence of hepatocellular carcinoma (HCC) and to establish a new nomogram to predict early postoperative recurrence of HCC. METHODS: A retrospective analysis of 383 patients who had undergone curative resection between February 2012 and September 2020 in our center was performed. The Kaplan-Meier method was used for survival curve analysis. Univariate and multivariate Cox regression were performed to identify independent risk factors associated with early recurrence, and a nomogram for predicting early recurrence of HCC was established. RESULTS: A total of 152/383 patients developed recurrence after surgery, of which 83 had recurrence within 1 year. Multivariate Cox regression analysis showed that preoperative alpha-fetoprotein level ≥400 ng/ml (P = 0.001), tumor diameter ≥5 cm (P = 0.009) and MVI (P = 0.007 and macrotrabecular-massive HCC (P = 0.003) were independent risk factors for early postoperative recurrence of HCC. The macrotrabecular-massive-based nomogram obtained a good C-index (0.74) for predicting early recurrence of HCC, and the area under the curve for predicting early recurrence was 0.767, which was better than the single American Joint Committee on Cancer T stage and Barcelona Clinic Liver Cancer stage. CONCLUSIONS: The nomogram based on macrotrabecular-massive HCC can effectively predict early postoperative recurrence of HCC.

CircFOXM1 promotes proliferation and metastasis of hepatocellular carcinoma via regulating miR-1179/SPAG5 axis.

Hepatocellular carcinoma (HCC) predominantly occurs in patients with chronic liver disease, accounting for 70-90% of all liver cancer cases. The role of circFOXM1/miR-1179/SPAG5 axis in HCC has not been reported. This study aimed to explore the regulatory mechanism of circFOXM1 in HCC proliferation and metastasis. RNA polymerase inhibitor actinomycin D and RNase R exonuclease were used to identify circFOXM1 in HCC cells. The qRT-PCR was used to detect circFOXM1 expression. Specific siRNA for circFOXM1 was designed, and the sequence of circFOXM1 was inserted in pLCDH-ciR to overexpress circFOXM. Cell proliferation was detected by CCK8 in vitro, by tumor volume and tumor weight of HCC xenograft in vivo. Cell migration was detected by transwell test. Binding status of circFOXM1 with miR-1179 was detected by luciferase reporter gene assay. Rescue experiments were applied to identify the oncogenic mechanism of circFOXM1 in HCC cells. Actinomycin D assay confirmed the cyclization of circFOXM1. RNase R treatment showed that circFOXM1 was not affected by RNase R exonuclease. CCK8 assay, tumor volume and tumor weight showed that circFOXM1 effectively promoted HCC cell proliferation. Transwell assay showed that circFOXM effectively promoted migration and invasion abilities of HCC cells. Luciferase reporter gene activity assay showed that miR-1179 had complementary binding sites with circFOXM1 and SPAG5. CircFOXM1 silencing inhibited malignant phenotypes in HCC cells were partly rescued by either miR-1179 silencing or SPAG5 overexpression. CircFOXM1 promoted HCC cell proliferation and metastasis by regulating miR-1179/SPAG5 axis.

Vitamin C Intake and Pancreatic Cancer Risk: A Meta-Analysis of Published Case-Control and Cohort Studies.

BACKGROUND: Observational studies inconsistently reported the relationship between vitamin C intake and risk of pancreatic cancer. We conducted a meta-analysis of published case-control and cohort studies to quantify the association. METHODS: Potentially eligible studies were found on PubMed and EMBASE databases through May 31, 2015. A random-effects model was assigned to compute summary point estimates with corresponding 95% confidence intervals (CIs). Subgroup and meta-regression analyses were also performed to explore sources of heterogeneity. RESULTS: Our final analyses included 20 observational studies comprising nearly 5 thousand cases of pancreatic cancer. When comparing the highest with the lowest categories of vitamin C intake, the summary odds ratio/relative risk for case-control studies (14 studies), cohort studies (6 studies) and all studies combined was 0.58 (95% CI: 0.52-0.66), 0.93 (95% CI: 0.78-1.11) and 0.66 (95% CI: 0.58-0.75), respectively. The difference in the findings between case-control and cohort studies was statistically significant (P < .001). Possible publication bias was shown in the meta-analysis of case-control studies. CONCLUSION: There is insufficient evidence to conclude any relationship between vitamin C intake and risk of pancreatic cancer. The strong inverse association observed in case-control studies may be affected by biases (eg, recall and selection biases) that particularly affect case-control studies and/or potential publication bias. Future prospective studies of vitamin C intake and pancreatic cancer are needed.