Autoimmune pancreatitis (AIP) is a rare type of chronic pancreatitis. However, patients were sometimes misdiagnosed as pancreatic cancer and received unnecessary surgical treatment due to the limited understanding of the clinical doctors and lack of diagnostic and therapeutic experience of AIP. Here, this paper summarizes the related issues of diagnosis and treatment for AIP, thus improving the understanding and the quality of clinical practice.

The incidental detection rate of pancreatic cystic neoplasms continues to rise annually. While precise imaging diagnosis is critical for patient treatment and prognosis, significant challenges persist in current practice. Extensive overlaps in imaging features among different tumor types, coupled with phenomena of "different imaging manifestations for the same disease" and "similar imaging presentations across different diseases," create substantial difficulties in achieving accurate diagnosis. By elucidating the advantages and limitations of various clinically employed imaging modalities for diagnosing pancreatic cystic neoplasms, along with practical challenges encountered in clinical settings, this article explores how to achieve precise differential diagnosis of pancreatic cystic neoplasms based on distinct imaging characteristics, aiming to facilitate individualized precision treatment for patients.

Objective:To explore the prognostic differences and influencing factors between pancreatic cancer originated from intraductal papillary mucinous neoplasm (IPMN)-termed IC-Ds-and pancreatic cancer concomitant with IPMN (C-PDACs).Methods:Clinical data of 382 patients with pathologically confirmed IPMN who underwent surgical resection in the Department of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Naval Medical University from January 2016 to January 2022 were collected. According to pathological diagnosis, patients were divided into the IC-Ds group ( n=288) and the C-PDACs group ( n=94). The IC-Ds group was further divided into the colloid carcinoma subgroup and the ductal adenocarcinoma subgroup based on pathological typing. Data including age, gender, preoperative CA19-9 level, surgical margin status, lymph node metastasis, pathological grade, T stage, postoperative adjuvant chemotherapy, and survival follow-up were recorded. The median follow-up time was 35.00 months for IC-Ds patients and 29.00 months for C-PDACs patients. Clinicopathological characteristics and prognostic factors were compared between the IC-Ds and C-PDACs groups, as well as between the colloid carcinoma and ductal adenocarcinoma subgroups. Kaplan-Meier curves for overall survival were generated. Results:There were no significant differences in age, gender, R1 resection margin between the IC-Ds group and the C-PDACs group. However, in the C-PDACs group, 70 cases (74.47%) had elevated preoperative CA19-9, 40 cases (42.55%) had lymph node metastasis, 25 cases (26.60%) were pathologically confirmed as poorly differentiated carcinoma after surgery, and 54 cases (57.45%) received postoperative adjuvant chemotherapy; the proportions of all these indicators were higher than those in the IC-Ds group (90/288, 31.25%; 72/288, 25.00%; 32/288, 11.11%; 105/288, 36.46%). In contrast, the proportion of T1 stage in the IC-Ds group was higher (40.97% vs 20.21%), and all these differences were statistically significant (all P value <0.05). Among the 288 patients in the IC-Ds group, 97 cases (33.68%) were colloid carcinoma and 191 cases (66.32%) were ductal adenocarcinoma. There were no significant differences in age, gender, R1 resection margin, proportion of poorly differentiated carcinoma between the two subgroups. However, in the ductal adenocarcinoma subgroup, 67 cases (35.08%) had elevated preoperative CA19-9, 56 cases (29.32%) had lymph node metastasis confirmed by postoperative pathology, and 80 cases (41.88%) received postoperative adjuvant chemotherapy; all these proportions were significantly higher than those in the colloid carcinoma subgroup (23/97, 23.71%; 16/97, 17.02%; 25/97, 26.60%). In addition, the ductal adenocarcinoma subgroup had higher proportions of T2 and T3/T4 stages, while the proportion of T1 stage in the colloid carcinoma subgroup (60/97, 61.86%) was significantly higher than that in the ductal adenocarcinoma subgroup (58/191, 30.37%), with all differences being statistically significant (all P value <0.05). The median survival time was 47.00 months (95% CI 42.91-51.09) in the IC-Ds group and 34.00 months (95% CI 29.67-38.33) in the C-PDACs group. For the IC-Ds subgroups, the median survival time was 59.00 months (95% CI 50.79-67.21) in the colloid carcinoma subgroup and 42.00 months (95% CI 35.15-48.85) in the ductal adenocarcinoma subgroup. Significant differences in median survival time were observed between the IC-Ds and C-PDACs groups, between the colloid carcinoma and ductal adenocarcinoma subgroups, and between the ductal adenocarcinoma subgroup and the C-PDACs group (all P value <0.01). Conclusions:IC-Ds has a better prognosis than C-PDACs, and there is significant heterogeneity within IC-Ds, indicating different biological behaviors between the two types, which requires the development of targeted diagnosis and treatment strategies.

Objective:To investigate the causal relationship between biochemical markers and pancreatic cancer using a two-sample Mendelian randomization (MR) approach.Methods:Genome-wide association study (GWAS) data were used to analyze the causal relationship between 35 blood and urine biochemical markers and pancreatic cancer by forward and reverse MR methods. Single nucleotide polymorphism (SNP) associated with exposure variables were used as instrumental variables. The inverse variance weighting method was adopted as the main analytical approach to investigate the causal relationship between exposure factors and outcomes. Meanwhile, MR-Egger method, weighted median method, simple mode method, and weighted mode method were used to enhance the robustness of the results. Additionally, pleiotropy, heterogeneity and sensitivity analyses were conducted to test the reliability of the results.Results:Forward MR screening identified that three blood biochemical markers (cholesterol, cystatin C, and sex hormone-binding globulin) had a positive causal relationship with pancreatic cancer. Cholesterol ( OR=2.361, 95% CI 1.299-4.292, P=0.005), cystatin C( OR=2.108, 95% CI 1.075-4.123, P=0.030), and sex hormone-binding globulin ( OR=1.927, 95% CI 1.031-3.600, P=0.040) were risk factors for pancreatic cancer. Reverse MR screening revealed that three blood biochemical markers (cholesterol, glycated hemoglobin, and sex hormone-binding globulin) had a negative causal relationship with pancreatic cancer. Pancreatic cancer was a protective factor for cholesterol ( OR=0.996, 95% CI 0.992-1.000, P=0.035) and glycated hemoglobin ( OR=0.995, 95% CI 0.991-0.999, P=0.013), while it was a risk factor for sex hormone-binding globulin ( OR=1.005, 95% CI 1.001-1.009, P=0.021). The trends of causal effects obtained by the inverse variance weighting method were basically consistent with those from MR-Egger method, weighted median method, simple mode method and weighted mode method. Pleiotropy, heterogeneity, and sensitivity analyses showed no evidence of pleiotropy or heterogeneity, and no SNP had a significant impact on the overall results. Conclusions:Cholesterol, glycated hemoglobin, and sex hormone-binding globulin are risk factors for pancreatic cancer. Pancreatic cancer is a protective factor for cholesterol and glycated hemoglobin, and a risk factor for sex hormone-binding globulin.

Objective:To explore the effects of magnolol on autophagy in intestinal Cajal cells and intestinal motility in rats with acute necrotizing pancreatitis (ANP).Methods:Forty-five Wistar rats were randomly divided into three groups by a random number table: control group, ANP group and magnolol intervention group, with 15 rats in each group. The ANP model was established by intraperitoneal injection of cerulein. The magnolol intervention group received a tail vein injection of 20 μg/kg magnolol ethanol solution 30 minutes after modeling. After 12 hours, ileal tissues were collected for pathological examination and scoring. Intestinal transit rate was measured using the carbon powder propulsion method, and isolated intestinal muscle strips were prepared to assess amplitude and frequency of spontaneous contraction. Oxidative stress markers in intestinal tissues, including superoxide dismutase (SOD) activity, malondialdehyde (MDA) and nitric oxide (NO) levels, were measured using xanthine oxidase, thiobarbituric acid, and enzymatic reduction assay kits, respectively. Cajal cells were isolated from intestinal smooth muscle tissues, and the expression of autophagy-related proteins (Beclin1, LC3Ⅱ, LC3Ⅰ, p62) and p-Kit was detected by Western blot. Double immunofluorescence staining was used to trace autophagy in Cajal cells.Results:The pathological scores of ileal tissues in the control, ANP, and magnolol intervention groups were (0.33±0.52), (4.83±0.41), and (3.50±0.55), respectively. The score in ANP group was significantly higher than that in the control group, while the score in the magnolol intervention group was lower than that in the ANP group, with statistically significant differences (all P value <0.05). Intestinal transit rate, amplitude and frequency of spontaneous contraction in the ANP group were significantly slower than those in the control group, while these parameters in the magnolol intervention group were significantly improved compared to the ANP group, with statistically significant differences (all P value <0.05). SOD activity in the control, ANP, and magnolol intervention groups were (73.8±8.1), (42.8±7.2), and (71.2±10.4) N/mg prot, respectively; NO levels were (1.72±0.26), (3.19±0.43), and (1.94±0.23) μmol/g prot; and MDA levels were (1.15±0.38), (3.84±0.30), and (1.68±0.33) nmol/mg prot. SOD activity in the ANP group was significantly lower than that in the control group, while NO and MDA contents were significantly higher. In the magnolol intervention group, SOD activity was significantly higher, and NO and MDA contents were significantly lower than those in the ANP group, with statistically significant differences (all P value <0.01). The levels of Beclin1, LC3Ⅱ/Ⅰ ratio, and p-Kit in the intestinal Cajal cells of ANP group were significantly higher than those in the intestinal Cajal cells of control group, while the p62 level was significantly lower. In the intestinal Cajal cells of magnolol intervention group, the levels of Beclin1, LC3Ⅱ/Ⅰ ratio, and p-Kit were significantly lower while the p62 level was significantly higher than those in the intestinal Cajal cells of ANP group, with statistically significant differences (all P value <0.01). The numbers of c-Kit/GFP-LC3 double-positive Cajal cells in the control group, ANP group, and magnolol intervention group were (9.59±5.06), (11.27±8.30), and (10.27±6.30), respectively. The ANP group had significantly more double-positive cells than the control group, while the magnolol intervention group had significantly less double-positive cells than the ANP group, with statistically significant differences (all P value <0.05). Conclusions:Excessive oxidative stress and autophagy in Cajal cells are important mechanisms underlying ANP-induced intestinal motility dysfunction. Magnolol can improve intestinal motility in ANP by antagonizing oxidative stress and reducing autophagy in Cajal cells. p-Kit may play a regulatory role in this process.

Objective:To analyze the effects of low-molecular-weight heparin combined with insulin (LMWH+INS) and double filtration plasmapheresis (DFPP) on lipid profiles and clinical outcomes in patients with hypertriglyceridemic acute pancreatitis (HTG-AP) based on propensity score matching.Methods:The clinical data of 126 patients with HTG-AP from October 2022 to February 2024 in The Third Affiliated Hospital of Nanjing Medical University, Changzhou Traditional Chinese Medicine Hospital Affiliated to Nanjing Traditional Chinese Medicine University and Changzhou First People's Hospital were retrospectively included. Patients were divided into LMWH+INS group ( n=87) and DFPP group ( n=39) according to the treatment. Propensity score matching was applied at a 1∶1 ratio. The repeated measures analysis of variance was conducted to assess dynamic changes of blood lipids within the 5 days of admission between the LMWH+INS and DFPP groups after matching. Clinical symptoms and outcomes were compared between the two matched groups following matching. Results:29 patients were included in both LMWH+INS group and DFPP group after propensity score matching. No statistically significant differences were observed in triglycerides (TG), acute physiology and chronic health evaluation Ⅱ(APACHEⅡ) score, or bedside index for the severity of acute pancreatitis (BISAP) between the two groups (all P value >0.05), indicating comparability. Repeated measures analysis of variance revealed that TG and TC levels in the DFPP group were significantly lower than those in the LMWH+INS group at 2-5 days after admission [TG 2 d: (5.26±2.59) mmol/L vs (10.79±3.81) mmol/L, 3 d: (3.35±1.01) mmol/L vs (7.72±3.64) mmol/L, 4 d: (3.45±0.77) mmol/L vs (6.57±3.17) mmol/L, 5 d: (3.73±1.26) mmol/L vs (5.61±3.07) mmol/L; TC 2 d: (4.83±2.29) mmol/L vs (8.2±2.82) mmol/L, 3 d: (4.23±2.17) mmol/L vs (7.71±2.68) mmol/L, 4 d: (4.28±1.59) mmol/L vs (7.55±2.41) mmol/L, 5 d: (4.1±1.21) mmol/L vs (7.84±2.6) mmol/L], with a more rapid decrease. LDL levels in the LMWH+INS and DFPP groups showed similar trends, with significant decreases at 2 day after admission [(5.41±3.24) mmol/L vs (2.96±1.47) mmol/L, (4.99±3.51) mmol/L vs (2.47±1.53) mmol/L]. The differences mentioned above are all statistically significant (all P value <0.001). No significant changes were observed in HDL levels in either LMWH+INS and DFPP groups at 2-5 days after admission. After matching, the DFPP group had a significantly longer time of resuming feeding [3(2, 3) days vs 4(3, 6) days] and higher hospital cost [12113.87 (9055.31, 14401.84) yuan vs 28025.34 (25388.11, 36335.48) yuan] compared with the LMWH+INS group, with statistically significant differences. Conclusions:DFPP could reduce TG and TC levels more rapidly and effectively than LMWH combined with INS, but does not show an advantage in improving clinical outcomes and reducing hospitalization costs.

Objective:To explore the effects and possible mechanism of intestinal microbiota on lung injury in mice with acute necrotizing pancreatitis (ANP).Methods:The experimental mice were randomly assigned to normal control group (CON group), ANP model group (ANP group) and intestinal germ-free group (ABX group), with 6 mice in each group. The ANP mouse model was constructed by intraperitoneal injection of caerulein (100 μg/kg, for 10 times) at an interval of 1 hour each time, followed by 10 mg/kg lipopolysaccharide injection. Mice in ABX group were treated by Abx solution (0.5 g/L vancomycin, 1 g/L neomycin, 1 g/L metronidazole, and 1 g/L ampicillin), 1 ml/100 g gavage for 28 days before preparation of the ANP model. The CON group was injected intraperitoneally with an equal volume of PBS. Histopathologic examination of the pancreas, lungs, and terminal ileum was routinely performed. Serum amylase levels were measured using enzymatic kinetic chemistry, and serum diamine oxidase (DAO) and lung tissue myeloperoxidase (MPO) activities were measured using ELISA assay. Expression of inflammatory factors, pyroptosis-related molecules in lung tissue and intestinal epithelial tight junction proteins was detected by fluorescence quantitative PCR. Western blotting was used to detect the expression of the pyroptosis molecules caspase-1 and GSDMD in lung tissue, and intestinal epithelial tight junction proteins. Changes of bacterial distribution in lung tissue were measured by fluorescence in situ hybridization. Results:The pathological scores of pancreatic tissue of CON, ANP, and ABX group were (0.67±0.26), (7.33±0.82), and (5.67±0.81); the pathological scores of lung tissue were (1.67±0.41), (5.67±0.41), and (3.58±0.58); the pathological scores of ileal tissue were (0.58±0.52), (3.83±0.75), and (4.33±0.82); the serum amylase levels were (403.95±93.11), (1037.24±126.77), and (647.32±145.90)U/L; the MPO levels in lung tissue were (0.23±0.03), (0.63±0.09), and (0.48±0.05)U/g. ABX group had significantly lower scores in pancreatic and lung tissues, serum amylase levels, and MPO levels in lung tissue compared to ANP group, and all the differences were statistically significant (all P value <0.05). The expression level in pancreatis tissue from CON, ANP and ABX group of IL-1β mRNA was 1.84±0.90, 36.26±5.56 and 16.65±6.43, IL-6 mRNA was 1.07±0.15, 2.90±0.42 and 1.34±0.62, TNF-α mRNA was 0.47±0.11, 0.76±0.11 and 0.46±0.07, HMGB1 mRNA was 0.38±0.02, 0.72±0.22 and 0.44±0.08, caspase-1 mRNA was 1.07±0.18, 2.04±0.31 and 0.85±0.54, ASC mRNA was 1.24±0.19, 5.68±0.41 and 3.89±1.47, GSDMD mRNA was 0.79±0.17, 0.94±0.14 and 0.61±0.08, IL-18 mRNA was 0.83±0.27, 4.17±0.79 and 3.57±0.03, respectively. The expression of IL-1β, IL-6, TNF-α, HMGB1, caspase-1, ASC, and IL-18 mRNA in lung tissue was significantly increased in ANP group compared to the CON group; conversely, ABX group showed a significant decrease in the expression of these markers compared to ANP group; and all the differences were statistically significant (all P values <0.05). The protein level of caspase-1 in lung tissue of CON, ANP and ABX group was 1.59±0.51, 2.28±0.13, 1.38±0.47, and that of GSDMD was 1.90±0.09, 2.20±0.07 and 1.76±0.27, respectively, which in ANP group were significantly higher than in CON group, but in ABX group was significantly lower than in ANP group, and all the differences were statistically significant (all P values <0.05). The serum DAO levels of CON, ANP, and ABX group were (0.06±0.15), (0.52±0.11) and (0.58±0.11) ng/ml; the expression level of ileum tissue of claudin1 mRNA and protein was 0.98±0.26, 0.42±0.18, 0.32±0.24 and 1.05±0.08, 0.82±0.09, 0.19±0.04; occludin mRNA and protein was 0.91±0.07, 0.31±0.05, 0.32±0.14 and 1.03±0.07, 0.61±0.04, 0.64±0.11; ZO-1 mRNA and protein was 1.01±0.08, 0.80±0.28, 0.60±0.28, and 0.86±0.10, 0.99±0.30, 0.62±0.30. The serum DAO level was significantly elevated in both ANP and ABX groups compared to the CON group. The mRNA and protein expression of claudin-1 and occludin in both ANP and ABX groups were significantly lower than those in CON group; the expression of claudin-1 in ABX group was significantly downregulated compared to ANP group; and all the differences were statistically significant (all P values <0.05). The relative fluorescence intensities of lung tissue in CON, ANP, and ABX groups were 0.03±0.01, 0.06±0.01, and 0.04±0.01, respectively, which in ANP group was significantly higher compared to CON group, but in ABX group was significantly lower than ANP group; all the differences were statistically significant (all P values <0.05). Conclusions:Intestinal microbiota may attenuate acute pancreatitis-associated acute lung injury by inhibiting the pyroptosis pathway in lung tissue.

Objective:To investigate lipid metabolism gene mutations and pathogenicity of hypertriglyceridemia acute pancreatitis (HTG-AP) patients.Methods:Clinical data of 495 HTG-AP patients admitted from June 2018 to June 2020 in the center for severe acute pancreatitis of Eastern Theater General Hospital were retrospectively analyzed. Whole-exome sequencing and mutation verification were performed by next-generation sequencing technology and Sanger sequencing. The pathogenicity of gene mutation was analyzed by population mutation ratio, pathogenicity prediction software, conservation scoring software, protein structure prediction, and in vitro experiments. Results:The mutation ratio of lipid metabolism-related genes, namely LPL, APOA5, LMF1, GPIHBP1, and APOC2, were 14.81%, 55.78%, 43.61%, 1.62%, and 0.61%, respectively. Among them, 44 heterozygous mutations in LPL gene were detected including 36 missense mutations, 5 nonsense mutations and 3 frameshift mutations, which were all rarely carried in single patient. Six HTG-AP patients carried the LPL gene heterozygous mutation c.835C>G (p.Leu279Val). The mean level of serum triglyceride at the onset of HTG-AP was 27.4 mmol/L. All of them had a history of recurrent HTG-AP, and most of them had severe acute pancreatitis. The serum LPL concentration and activity were lower than the normal level. The pathogenicity analysis results suggested that the LPL p.Leu279Val was a rare, highly possible pathogenic and highly conserved gene mutation. The in vitro results showed that the LPL p.Leu279Val could significantly reduce the synthesis and secretion ability of LPL as well as its enzymatic activity. Conclusions:The mutation ratio of lipid metabolism-related genes, including LPL, APOA5, LMF1, GPIHBP1, and APOC2, are relatively high in the HTG-AP patients. The LPL p.Leu279Val is a rare and highly possible pathogenic gene mutation, which may lead to recurrent episodes of HTG-AP.

Objective:To investigate the therapeutic effects of adeno-associated virus vector 5 (AAV5)-mediated hepatic lipoprotein lipase (LPL) expression on serum triglyceride (TG) metabolism and hypertriglyceridemic acute pancreatitis (HTG-AP) in mice.Methods:Ten male C57BL/6 Lpl+/- mice were randomly divided into two groups by a random number table: the Lpl+/- control group and the Lpl+/- gene therapy group, with five mice in each group. The Lpl+/- control group received a tail vein injection of AAV5 vector carrying the enhanced green fluorescent protein (EGFP) gene (AAV5-EGFP), while the Lpl+/- gene therapy group received a tail vein injection of AAV5 vector carrying the human LPLS447X gene (AAV5-LPLS447X). Oral fat tolerance tests were performed at 14, 28, and 56 days post-injection. Twenty wild-type ICR mice were randomly divided into a control group and a gene therapy group, with ten mice in each group. The ICR control group was injected with AAV5-EGFP, and the ICR gene therapy group was injected with AAV5-LPLS447X. Fourteen days after injection, the mice underwent intraperitoneal injection of P407 solution (0.5 g/kg) and caerulein (200 μg/kg) to induce HTG-AP. Serum TG, total cholesterol (TC), amylase, lipase levels, and plasma LPL activity after heparin injection were measured by microplate reader. Plasma LPL concentration was measured using an enzyme-linked immunosorbent assay (ELISA). LPL mRNA expression levels in the liver, heart, and adipose tissue of Lpl+/- mice were determined by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). LPL protein expression in the liver tissue of ICR mice was detected by immunohistochemistry at 28 days after gene therapy. Histopathological changes in the pancreas were observed using hematoxylin-eosin staining. Results:Compared to the Lpl+/- control group, the Lpl+/- gene therapy group showed a significant decrease in serum TG levels starting from day 21. After oral administration of olive oil, the increase and peak of serum TG levels were significantly lower than those in the control group. Furthermore, hepatic LPL mRNA expression levels were significantly higher (1.96±0.11 vs 1.02±0.12) with statistical significance ( P<0.05). Compared to the ICR control group, the ICR gene therapy group showed a significant decrease in serum TG and TC levels, and plasma LPL activity (0.17±0.05 mEq/L·h -1vs 0.06±0.02 mEq/L·h -1) was significantly higher at 28 days after heparin injection with statistical significance (all P value <0.05). Immunohistochemical results showed high expression of LPL protein on the hepatocyte membrane in the liver of ICR gene therapy group mice. Moreover, pancreatic edema, inflammatory infiltration, and acinar cell necrosis were significantly alleviated compared to the control group. Conclusions:LPLS447X treatment can promote LPL expression in the liver of mice, significantly reduce TG levels, and alleviate the severity of HTG-AP.

Objective:To identify independent risk factors for early recurrence following curative resection of resectable pancreatic cancer and establish a nomogram prediction model.Methods:Clinical data from 405 patients with resectable pancreatic cancer treated at Renji Hospital, Shanghai Jiao Tong University School of Medicine from February 2010 to December 2020 were retrospectively reviewed. Patients were stratified into a training cohort (265 patients form February 2010 to December 2018) and a validation cohort (140 patients from January 2019 to December 2020) based on surgery dates. Optimal cutoff values for clinical variables were determined using X-tile software. Independent risk factors were identified through univariate and multivariate Cox proportional hazards regression analyses. Kaplan-Meier curves for recurrence-free survival (RFS) were generated across subgroups, and a nomogram was developed to predict early recurrence (within 1 year post-surgery). Time-dependent receiver operating characteristic (tROC) curves was drawn and area under the curve (AUC) metrics were utilized to evaluate predictive accuracy, while model reliability was assessed by calibration curves. Individualized risk scores derived from the nomogram were stratified into high- and low-risk groups using X-tile-derived cutoff values. Survival differences between groups were analyzed via log-rank tests. The clinical application value was judged by decision curve analysis (DCA) compared to TNM staging. Results:In the training cohort, 139 patients (52.45%) experienced early recurrence, with a median RFS of 11.1 months [interquartile range ( IQR): 6.0-26.0]. The validation cohort reported 70 early recurrences (50.00%) and a median RFS of 11.8 months ( IQR: 4.9-21.4). Univariate analysis revealed significant associations between early recurrence and tumor diameter, carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), carbohydrate antigen 125 (CA125), systemic immune-inflammation index (SⅡ), and prognostic nutritional index (PNI). Multivariate analysis identified tumor diameter ≥3.75 cm ( HR=1.718, 95% CI 1.223-2.412, P=0.002), CA19-9≥218 U/ml ( HR=1.567, 95% CI 1.107-2.220, P=0.011), CA125≥20.98 U/ml ( HR=2.501, 95% CI 1.768-3.539, P<0.001), SⅡ≥388.28 ( HR=1.708, 95% CI 1.096-2.662, P=0.018), and PNI<53.18 ( HR=0.596, 95% CI 0.404-0.879, P=0.009) as independent risk factors for early recurrence. The nomogram achieved AUC values of 0.771 and 0.708 in the training and validation cohorts, respectively. Calibration curves demonstrated strong agreement between predicted and observed survival probabilities. Kaplan-Meier analysis revealed significantly lower 1-year RFS rates in high-risk versus low-risk groups for both cohorts (training: HR=3.65, 95% CI 2.45-5.44, P<0.001; validation: HR=2.37, 95% CI 1.39-4.06, P=0.001). DCA indicated superior net benefit of the nomogram over TNM staging across threshold probabilities of 0.2-0.9. Conclusions:The proposed nomogram effectively integrates clinical and serological biomarkers to preoperatively assess early recurrence risk in resectable pancreatic cancer patients, offering enhanced precision for clinical decision-making.