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BackgroundInfected pancreatic necrosis (IPN) is a serious local complication of acute pancreatitis, with high mortality. Minimally invasive therapy including percutaneous catheter drainage (PCD) has become the preferred method for IPN instead of traditional open necrosectomy. However, the efficacy of double-catheter lavage in combination with percutaneous flexible endoscopic debridement after PCD failure is unknown compared with surgical necrosectomy.MethodsA total of 27 cases of IPN patients with failure PCD between Jan 2014 and Dec 2015 were enrolled in this retrospective cohort study. Fifteen patients received double-catheter lavage in combination with percutaneous flexible endoscopic debridement, and 12 patients underwent open necrosectomy. The primary endpoint was the composite end point of major complications or death. The secondary endpoint included mortality, major complication rate, ICU admission length of stay, and overall length of stay.ResultsThe primary endpoint occurrence rate in double-catheter lavage in combination with percutaneous flexible endoscopic debridement group (8/15, 53%) was significantly lower than that in open necrosectomy group (11/12, 92%) (RR = 1.71, 95% CI = 1.04 – 2.84, P < 0.05). Though the mortality between two groups showed no statistical significance (0% vs. 17%, P = 0.19), the rate of new-onset multiple organ failure and ICU admission length of stay in the experimental group was significantly lower than that in open necrosectomy group (13% vs. 58%, P = 0.04; 0 vs. 17, P = 0.02, respectively). Only 40% of patients required ICU admission after percutaneous debridement, which was markedly lower than the patients who underwent surgery (83%; P < 0.05).ConclusionsDouble-catheter lavage in combination with percutaneous flexible endoscopic debridement showed superior effectiveness, safety, and convenience in patients with IPN after PCD failure as compared to open necrosectomy.Electronic supplementary materialThe online version of this article (10.1186/s12876-017-0717-3) contains supplementary material, which is available to authorized users.

Background Intra-abdominal hypertension (IAH) in acute pancreatitis (AP) is associated with deterioration in organ function. This trial aimed to assess the efficacy of neostigmine for IAH in patients with AP. Methods In this single-center, randomized trial, consenting patients with IAH within 2 weeks of AP onset received conventional treatment for 24 h. Patients with sustained intra-abdominal pressure (IAP) ≥ 12 mmHg were randomized to receive intramuscular neostigmine (1 mg every 12 h increased to every 8 h or every 6 h, depending on response) or continue conventional treatment for 7 days. The primary outcome was the percent change of IAP at 24 h after randomization. Results A total of 80 patients were recruited to neostigmine (n = 40) or conventional treatment (n = 40). There was no significant difference in baseline parameters. The rate of decrease in IAP was significantly faster in the neostigmine group compared to the conventional group by 24 h (median with 25th–75th percentile: −18.7% [− 28.4 to − 4.7%] vs. − 5.4% [− 18.0% to 0], P = 0.017). This effect was more pronounced in patients with baseline IAP ≥ 15 mmHg (P = 0.018). Per-protocol analysis confirmed these results (P = 0.03). Stool volume was consistently higher in the neostigmine group during the 7-day observational period (all P < 0.05). Other secondary outcomes were not significantly different between neostigmine and conventional treatment groups. Conclusion Neostigmine reduced IAP and promoted defecation in patients with AP and IAH. These results warrant a larger, placebo-controlled, double-blind phase III trial. Trial registration Clinical Trial No: NCT02543658 (registered August /27, 2015).

ObjectivesTo investigate the dynamic changes in gastric varices in patients with acute pancreatitis (AP) and to develop a novel nomogram for the early prediction of sinistral portal hypertension (SPH).MethodsThis was a retrospective, case-control study with an analysis of the quantitative, dynamic computed tomography imaging results of SPH in patients with moderate and severe AP with a long-term follow-up. Multivariate logistic regression analysis and nomogram were employed.ResultsThe SPH group (n = 94) and non-SPH group (n = 94) were matched. The dynamic changes showed an increasing trend in the diameter of gastric fundus, short gastric, gastric coronary, and gastroepiploic veins, which did not recover during the one-year follow-up. Multivariate analysis showed that male (adjusted odds ratio (adjOR), 8.71; 95% confidence interval (CI), 2.86–26.53; P &lt; 0.001), body mass index ≥27.5 kg/m2 (adjOR, 5.49; 95% CI, 1.85–16.29; P = 0.002), prothrombin time ≥12.6 s (adjOR, 2.82; 95% CI, 1.11–7.17; P = 0.03), and the patency of splenic vein [stenosis (adjOR, 8.48; 95% CI, 2.13–33.71; P = 0.002), and occlusion (adjOR, 34.57; 95% CI, 10.87–110.00; P &lt; 0.001)] were independently associated with the development of SPH. The nomogram incorporating these factors demonstrated good discrimination, calibration and clinical utility. The area under the curve was as high as 0.92 (95% CI, 0.87–0.95).ConclusionThe dynamic changes in varices in SPH are long-term and slowly progressing. Males and obese patients with abnormal splenic veins and coagulopathies are at high risk for developing SPH. A simple nomogram tool helps in the early, accurate prediction of SPH.

PurposeThis study aimed to elucidate the molecular mechanisms of the anti-pancreatic fibrosis effects of matrine in rats.Materials and MethodsTrinitrobenzene sulfonic acid was administrated to rats to establish a pancreatic fibrosis model. Rats were divided into four groups: Control, Sham, Model, and Matrine (n=8). Hematoxylin-eosin staining, Masson staining, and Azan staining were performed to evaluate pancreatic fibrosis. Expression of transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA), and collagen I in pancreatic tissues was evaluated by immunohistochemical staining. mRNA and protein levels of TGF-β receptor 1 (TβR1), TβR2, and Smad2 in pancreatic tissues were determined by RT-PCR and Western blot, respectively.ResultsIn the model group, hyperplasia of glandules around the glandular ducts, mitochondrial swelling of acinous cells, and severe fibrosis were found. Interestingly, in the Matrine group, mitochondrial swelling was only found in a small number of acinous cells, and the fundamental structures of pancreatic tissues were intact. Moreover, pancreatic fibrosis was markedly alleviated. Comparing to the Sham group, expression of α-SMA, TGF-β1, and collagen I was sharply elevated in the Model group (p<0.05); however, their expressions were much lower in the Matrine group, compared to the Model group (p<0.05). Compared with the Sham group, mRNA and protein levels of Smad2, TβR1, and TβR2 in the Model group were notably raised (p<0.05). However, their high expression was significantly downregulated in the Matrine group (p<0.05).ConclusionMatrine suppressed pancreatic fibrosis by regulating TGF-β/Smad signaling in rats.

MicroRNAs (miRNAs/miRs) have aroused increasing attention in colorectal cancer (CRC) therapy. This study is designed for a detailed analysis of the roles of miR-16-5p and forkhead box K1 (FOXK1) in cell angiogenesis and proliferation during CRC in addition to their underlying mechanisms. CRC tissues and colon cancer cell lines (SW620 and HCT8) were investigated. qRT-PCR and Western blot were utilized to evaluate miR-16-5p and FOXK1 expression. Following gain- and loss-of-function assays on miR-16-5p or FOXK1, the effects of miR-16-5p and FOXK1 were assessed on cell angiogenesis and proliferation in CRC cells. A dual-luciferase reporter assay was employed to evaluate the binding relationship of miR-16-5p and FOXK1. Western blot was used to determine the effects of miR-16-5p and FOXK1 on key molecules of the PI3K/Akt/mTOR pathway. Highly expressed FOXK1 and lowly expressed miR-16-5p were observed in CRC cells and tissues. miR-16-5p overexpression or FOXK1 knockdown reduced CRC cell proliferation and angiogenesis of human umbilical vein endothelial cells co-cultured with the supernatant of CRC cells, whereas miR-16-5p silencing or FOXK1 upregulation caused opposite trends. Additionally, miR-16-5p negatively modulated FOXK1 expression. The blockade of the PI3K/Akt/mTOR pathway was triggered by miR-16-5p overexpression or FOXK1 silencing. In conclusion, miR-16-5p hampers cell angiogenesis and proliferation during CRC by targeting FOXK1 to block the PI3K/Akt/mTOR pathway.

Aims: We investigated whether faecal microbiota transplantation (FMT) decreases intra-abdominal pressure (IAP) and improves gastrointestinal (GI) dysfunction and infectious complications in acute pancreatitis (AP).Methods: In this first randomised, single-blind, parallel-group, controlled study, we recruited and enrolled consecutive patients with AP complicated with GI dysfunction. Eligible participants were randomly assigned to receive faecal transplant (n = 30) or normal saline (n = 30) via a nasoduodenal tube once and then again 2 days later. The primary endpoint was the rate of IAP decline; secondary endpoints were GI function, infectious complications, organ failure, hospital stay and mortality. Analyses were based on intention to treat.Results: We enrolled 60 participants and randomly assigned them to the FMT (n = 30) or control (n = 30) group. Baseline characteristics and disease severity were similar for both groups. IAP decreased significantly 1 week after intervention in both groups, with no difference in the IAP decline rate between FMT and Control group [0.1 (−0.6, 0.5) vs. 0.2 (−0.2, 0.6); P = 0.27]. Normal gastrointestinal failure (GIF) scores were achieved in 12 (40%) patients in the FMT group and 14 (47%) in the control group, with no significant difference (P = 0.60). However, D-lactate was significantly elevated in the FMT group compared to the control group, as calculated by the rate of decline [−0.3 (−3.7, 0.8) vs. 0.4 (−1.1, 0.9); P = 0.01]. Infectious complications occurred in 15 (50%) and 16 (53.33%) patients in the FMT and control groups, respectively (P = 0.80). However, interleukin-6 (IL-6) was significantly elevated in the FMT group compared to the control group, as calculated by the rate of decline [0.4 (−3.6, 0.9) vs. 0.8 (−1.7, 1.0); P = 0.03]. One participant experienced transient nausea immediately after FMT, but no serious adverse events were attributed to FMT.Conclusion: FMT had no obvious effect on IAP and infectious complications in AP patients, though GI barrier indictors might be adversely affected. Further multi-centre studies are needed to confirm our findings. The study was registered at https://clinicaltrials.gov (NCT02318134).

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