Infection recurrence following minimally invasive treatment in patients with infectious pancreatic necrosis.

BACKGROUND: In recent decades, an increasing number of patients have received minimally invasive intervention for infected pancreatic necrosis (IPN) because of the benefits in reducing postoperative multiple organ failure and mortality. However, there are limited published data regarding infection recurrence after treatment of this patient population. AIM: To investigate the incidence and prediction of infection recurrence following successful minimally invasive treatment in IPN patients. METHODS: Medical records for 193 IPN patients, who underwent minimally invasive treatment between February 2014 and October 2018, were retrospectively reviewed. Patients, who survived after the treatment, were divided into two groups: one group with infection after drainage catheter removal and another group without infection. The morphological and clinical data were compared between the two groups. Significantly different variables were introduced into the correlation and multivariate logistic analysis to identify independent predictors for infection recurrence. Sensitivity and specificity for diagnostic performance were determined. RESULTS: Of the 193 IPN patients, 178 were recruited into the study. Of them, 9 (5.06%) patients died and 169 patients survived but infection recurred in 13 of 178 patients (7.30%) at 7 (4-10) d after drainage catheters were removed. White blood cell (WBC) count, serum C-reactive protein (CRP), interleukin-6, and procalcitonin levels measured at the time of catheter removal were significantly higher in patients with infection than in those without (all P < 0.05). In addition, drainage duration and length of the catheter measured by computerized tomography scan were significantly longer in patients with infection (P = 0.025 and P < 0.0001, respectively). Although these parameters all correlated positively with the incidence of infection (all P < 0.05), only WBC, CRP, procalcitonin levels, and catheter length were identified as independent predictors for infection recurrence. The sensitivity and specificity for infection prediction were high in WBC count (≥ 9.95 × 109/L) and serum procalcitonin level (≥ 0.05 ng/mL) but moderate in serum CRP level (cut-off point ≥ 7.37 mg/L). The catheter length (cut-off value ≥ 8.05 cm) had a high sensitivity but low specificity to predict the infection recurrence. CONCLUSION: WBC count, serum procalcitonin, and CRP levels may be valuable for predicting infection recurrence following minimally invasive intervention in IPN patients. These biomarkers should be considered before removing the drainage catheters.

The effect of technical details of percutaneous catheter drainage on the clinical outcomes of infected necrotizing pancreatitis patients

Background/aim: This study aimed to investigate the effect of technical details of percutaneous catheter drainage (PCD) on the clinical outcomes of patients with infected necrotizing pancreatitis (INP). Materials and methods: A total of 44 INP patients treated in our hospital from October 2013 to October 2015 were included. The correlations of the first PCD treatment data and the clinical outcomes were analyzed. Results: The number of catheters was positively correlated with hospital readmission (r = 0.335, P = 0.032). Receiver operating characteristic curve analysis showed that patients with ≥ 3 catheters were more likely to have hospital readmission. Patients with pleural effusion undergoing thoracentesis were more likely to have new intensive care unit admission (P = 0.025) and bleeding in need of intervention (P = 0.032). Patients with more effusion regions had higher incidences of mortality (P = 0.012) and new intensive care unit admissions (2.44 ± 1.03 vs. 1.88 ± 0.80; P = 0.059). Patients with PCD only were less likely to have new intensive care unit admissions (22.22% vs. 54.55%; P = 0.038) than those with PCD + small incision or/and videoscopic assisted retroperitoneal debridement. Conclusion: Number of catheters greater than three was associated with unfavorable outcomes of PCD treatment in INP patients. Patients that received PCD treatment only had better outcomes.

A meta-analysis and systematic review of percutaneous catheter drainage in treating infected pancreatitis necrosis.

BACKGROUND: In the current meta-analysis, we focus on the exploration of percutaneous catheter drainage (PCD) in terms of its overall safety as well as efficacy in the treatment of infected pancreatitis necrosis based on qualified studies. METHODS: The following electronic databases were searched to identify eligible studies through the use of index words updated to May 2018: PubMed, Cochrane, and Embase. Relative risk (RR) or mean difference (MD) along with 95% confidence interval (95% CI) were utilized for the main outcomes. RESULTS: A total of 622 patients in the PCD group and 650 patients in the control group from 13 studies were included in the present meta-analysis. The aggregated results indicated that the incidence of bleeding was decreased significantly (RR: 0.42, 95% CI: 0.25-0.70) in the PCD group as compared with the control group. In addition, PCD decreased the mortality (RR: 0.76, 95% CI: 0.41-1.42), hospital duration (SMD: -0.22, 95% CI: -0.77 to -0.33), duration in intensive care unit (ICU) (SMD: -0.13, 95% CI: -0.30 to -0.04), pancreatic fistula (RR: 0.73, 95% CI: 0.46-1.17), and organ failure (RR: 0.91, 95% CI: 0.45-1.82) in comparison with the control group, but without statistical significance. CONCLUSION: Our findings provide evidence for the treatment effect of PCD in the decrease of bleeding, mortality, duration in hospital and ICU, pancreatic fistula, organ failure as compared with the surgical treatment. In conclusion, further studies based on high-quality RCTs with larger sample size and long-term follow-ups are warranted for the confirmation of PCD efficacy in treating infected pancreatitis necrosis.

Silencing pancreatic adenocarcinoma upregulated factor (PAUF) increases the sensitivity of pancreatic cancer cells to gemcitabine.

Pancreatic adenocarcinoma upregulated factor (PAUF) is a new oncogene that activates signaling pathways that play a critical role in resistance to gemcitabine. We thus speculated that PAUF also plays a role in resistance to gemcitabine of pancreatic cancer cells. We established BxPC-3 cell lines with stable PAUF knockdown (BxPC-3_shPAUF) and controls (BxPC-3_shCtrl) and evaluated sensitivity to gemcitabine in vitro by MTT and flow cytometry. We established a xenograft model of human pancreatic cancer to examine PAUF function in gemcitabine resistance in vivo. Gene chip microarrays were performed to identify differentially expressed genes in BxPC-3_shPAUF and BxPC-3_shCtrl cells. Silencing PAUF increased the sensitivity of BxPC-3 cells to gemcitabine in vitro and in vivo. PAUF-knockdown BxPC-3 cell lines treated with gemcitabine showed increased proliferation inhibition and apoptosis compared with controls. Gemcitabine exhibited a more pronounced effect on reduction of BxPC-3_shPAUF tumors than BxPC-3_shCtrl tumors. Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) assays confirmed a significantly higher apoptotic rate of BXPC-3_shPAUF tumors compared with BXPC-3_shCtrl tumors. Gene array showed that PAUF function in gemcitabine sensitivity might involve MRP2, MRP3, MDR1, PIK3R1, and NFkB2 genes. PAUF could be considered as a key molecular target for sensitizing pancreatic cancer cells to gemcitabine.

MMI-166, a selective matrix metalloproteinase inhibitor, promotes apoptosis in human pancreatic cancer.

MMI-166 is a third-generation selective matrix metalloproteinase (MMP) inhibitor that prevents tumor invasion and metastasis by downregulating the activity of MMP-2 and MMP-9. However, MMI-166's effect in pancreatic cancer cells has not been widely studied. Initially, we treated SW1990, human pancreatic cancer cells, with 0, 50 or 100 µg/ml of MMI-166 for 24 h. Apoptosis in the cells was then observed by inverted fluorescence microscope and flow cytometry; the apoptosis rate was dependent on MMI-166 concentration. We then injected nude mice with SW1990 cells. Volume of the resulting xenograft tumors in nude mice treated with MMI-166 was far less than that of the control group, whereas their apoptotic index was much greater. Expression of MMP-2, MMP-9, c-myc and survivin were markedly lower in tumors from the treated mice than in the control group. In cell experiments, MMP-2 and MMP-9 activities were downregulated by MMI-166 compared with controls, as were both mRNA and protein levels of MMP-2, MMP-9 and c-myc, although survivin expression did not differ. These results show that MMI-166 can induce apoptosis of pancreatic cancer cells in vitro and in vivo. The mechanism may be related to downregulation of c-myc by MMI-166.