Postoperative pancreatic fistula (POPF) are major postoperative complications (POCs) following distal pancreatectomy (DP). Notably, POPF may worsen the prognosis of patients with pancreatic cancer. Previously reported risks for POCs include body mass index, pancreatic texture, and albumin levels. Moreover, the C-reactive protein-to-albumin ratio (CAR) is a valuable parameter for prognostication. On the other hand, POCs sometimes lead to a worse prognosis in several cancer types. Thus, we assumed that CAR could be a risk factor for POPFs. This study investigated whether CAR can predict POPF risk in patients with pancreatic cancer following DP. This retrospective study included 72 patients who underwent DP for pancreatic cancer at Ehime University between January 2009 and August 2022. All patients underwent preoperative CAR screening. Risk factors for POPF were analyzed. POPF were observed in 17 of 72 (23.6%) patients. POPF were significantly associated with a higher CAR (p = 0.001). The receiver operating characteristic curve analysis determined the cutoff value for CAR to be 0.05 (sensitivity: 76.5%, specificity: 88.9%, likelihood ratio: 6.88), indicating an increased POPF risk. Univariate and multivariate analysis revealed that CAR ≥ 0.05 was a statistically independent factor for POPF (p < 0.001, p = 0.013). Therefore, CAR has the potential to predict POPF following DP.

Although several prognosticators, such as lymph node metastasis (LNM), were reported for hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), the prognostic impact of intrahepatic lymphatic vessel invasion (LVI) in liver cancer has rarely been reported. We sought to clarify the prognostic impact of intrahepatic lymphatic system involvement in liver cancer. We systematically reviewed retrospective studies that described LVI and clinical outcomes of liver cancer and also included studies that investigated tumor-associated lymphangiogenesis. We conducted a meta-analysis using RevMan software (version 5.4.1; Cochrane Collaboration, Oxford, UK). The prognostic impact of intrahepatic LVI in HCC was not reported previously. However, tumor-associated lymphangiogenesis reportedly correlates with prognosis after HCC resection. The prognostic impact of intrahepatic LVI was reported severally for ICC and a meta-analysis showed that overall survival was poorer in patients with positive LVI than with negative LVI after resection of ICC. Lymphangiogenesis was also reported to predict unfavorable prognosis in ICC. Regarding colorectal liver metastases, LVI was identified as a poor prognosticator in a meta-analysis. A few reports showed correlations between LVI/lymphangiogenesis and LNM in liver cancer. LVI and lymphangiogenesis showed worse prognostic impacts for liver cancer than their absence, but further study is needed.

Proinsulinoma is a subtype of insulinoma that is surgically curable, but localization can be difficult as these tumors are typically too small to be visualized by imaging. We report the case of a 53-year-old woman referred to our hospital with dizziness and headache. Her blood glucose level was 46 mg/dl and Whipple’s triad was present. Although her immunoreactive insulin level during hypoglycemia was in the normal range (5.0 μU/ml), the proinsulin level was elevated (408 pmol/l). Imaging examinations showed no evidence of pancreatic tumor. A preoperative selective arterial calcium injection (SACI) test showed excessive insulin secretion in the splenic artery region, which localized the proinsulinoma to the body or tail of the pancreas, and laparoscopic spleen-preserving distal pancreatectomy was performed. Intraoperative SACI test performed after tumor removal did not show excessive insulin secretion. The intraoperative SACI test appears to be useful for localization and for confirming complete resection of proinsulinoma.

Complete (R0) resection remains the primary surgical objective for colorectal liver metastases (CRLM), but margin width cannot be interpreted independently of tumor anatomy, biology, and the amount of functional liver sacrificed to obtain it. This focused narrative review re-examines surgical margins from the perspective of parenchymal preservation and longitudinal multimodal treatment. We distinguish parenchymal R1 exposure (R1par), an undesirable transection-surface event associated with local recurrence, from planned vascular R1 detachment (R1vasc), which has shown more favorable outcomes than R1par in selected retrospective series but remains dependent on careful anatomical selection. Vessel-skeletonized parenchymal-sparing hepatectomy (VESPAH) is presented as one operative model for achieving complete macroscopic clearance while preserving intrahepatic vascular architecture. We further propose “treatment continuity”—preservation of the physiological and anatomical capacity to receive indicated systemic therapy and repeat local treatment—as a reportable surgical outcome. A four-axis framework integrating technical resectability, functional reserve, tumor biology, and future treatment options is outlined. R0 resection should remain the goal, but the quality of hepatectomy for CRLM may be more comprehensively assessed by considering both the margin achieved at the index operation and the treatments that remain feasible thereafter.

Background/Objectives: Pancreatic ductal adenocarcinoma (PDAC) is characterized by aggressive tumor biology and profound host vulnerability, including pancreatic exocrine insufficiency (PEI), maldigestion, malnutrition, cachexia, sarcopenia, frailty, systemic inflammation, and poor tolerance to multimodal therapy. Gut and intratumoral microbiota have been implicated in pancreatic carcinogenesis, tumor immunity, chemotherapy response, and postoperative outcomes. However, the clinical readiness of microbiome-informed supportive care in PDAC remains uncertain. Results: Current evidence supports plausible mechanistic links among PEI, maldigestion, dysbiosis, microbial metabolites, barrier dysfunction, systemic inflammation, cachexia, sarcopenia, and treatment intolerance. Nevertheless, PDAC microbiome research is limited by major heterogeneity in sampling sites, sequencing platforms, antibiotic exposure, biliary drainage, diet, treatment timing, tumor stage, and analytic pipelines. Evidence is also discordant, particularly regarding alpha diversity and reproducible microbial signatures. Low-biomass tissue contamination and incomplete consideration of fungal and multi-kingdom microbiota further limit interpretation. Conclusions: Microbiome disturbance should currently be viewed as an investigational modifier of nutritional vulnerability and treatment tolerance rather than as a validated clinical biomarker or therapeutic target in PDAC. A clinically responsible framework should distinguish what is actionable now—nutrition screening, PEI management, inflammation and frailty assessment, body-composition evaluation, and treatment-exposure monitoring—from what remains investigational, including microbiome profiling, microbial signatures, probiotics, prebiotics, fecal microbiota transplantation, and metabolite-guided intervention.