• acute pancreatitis
• gut microbiota
• gut-pancreas axis
• probiotics

• Probiotics/therapeutic use
• Gastrointestinal Microbiome
• Humans
• Pancreatitis/microbiology
• Pancreatitis/therapy
• Fecal Microbiota Transplantation
• Animals
• Acute Disease

• Acute pancreatitis
• Antibiotics
• Biomarker
• Immune enhancement therapy
• Infected pancreatic necrosis
• Nutrition therapy
• Probiotics
• Scoring system
• Selective digestive decontamination

• Humans
• Pancreatitis, Acute Necrotizing/diagnosis
• Pancreatitis, Acute Necrotizing/prevention & control
• Biomarkers
• C-Reactive Protein
• Treatment Outcome
• Acute Disease
• Necrosis/complications

• Humans
• Pancreatitis/therapy
• Pancreatitis/etiology
• Pancreatitis/diagnosis
• Acute Disease
• Cholangiopancreatography, Endoscopic Retrograde
• United States

• Abdominal pain
• Diet therapy
• Pancreatitis

• Adult
• Humans
• Laparoscopy
• Length of Stay
• Operative Time
• Pancreatectomy/adverse effects
• Postoperative Complications/epidemiology
• Postoperative Complications/etiology
• Prospective Studies
• Retrospective Studies
• Surgical Wound Infection/diagnosis
• Surgical Wound Infection/epidemiology
• Surgical Wound Infection/etiology

Gut–microbiota–brain axis links the relationship between intestinal microbiota and sepsis-associated encephalopathy (SAE). However, the key mediators between them remain unclear.

Memory test was determined by Water maze. Intestinal flora was measured by 16S RNA sequencing. Neurotransmitter was detected by high-performance liquid chromatography (HPLC). Histopathology was determined by H&E, immunofluorescence (IF), and terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) staining. Flow cytometry was employed to determine the proportion of macrophages.

Fecal microbiota transplantation (FMT) relieved hippocampus impairment of SAE rats by inhibiting inflammation cytokine secretion, the expression of IBA-1 and neurotransmitter disturbance, and cell apoptosis and autophagy, accompanied by the reduced M1 polarization and M1 pro-inflammation factors produced by macrophages in mesenteric lymph nodes (MLNs). Actually, M1 polarization in SAE rats depended on intestinal epithelial cell (IEC)-derived exosome. GW4869-initiated inhibition of exosome secretion notably abolished M1 polarization and the secretion of IL-1β. However, GW4869-mediated improvement of hippocampus impairment was counteracted by the delivery of recombinant interleukin (IL)-1β to hippocampus. Mechanistically, IEC-derived exosome induced the excessive circulating IL-1β produced by CP-R048 macrophages, which subsequently induced damage and apoptosis of hippocampal neurons H19-7 in an autophagy-dependent manner. And reactivation of autophagy facilitates intestinal IL-1β-mediated hippocampal neuron injury.

Collectively, intestinal flora disturbance induced the exosome release of IECs, which subsequently caused M1 polarization in MLNs and the accumulation of circulating IL-1β. Circulating IL-1β promoted the damage and apoptosis of neurons in an autophagy-dependent manner. Possibly, targeting intestinal flora or IEC-derived exosome contributes to the treatment of SAE.

• Animals
• Epithelial Cells
• Exosomes
• Fecal Microbiota Transplantation
• Neurons
• Rats
• Sepsis-Associated Encephalopathy

Histomonosis in chickens often appears together with colibacillosis in the field. Thus, we have experimentally investigated consequences of the co-infection of birds with Histomonas meleagridis and avian pathogenic Escherichia coli (APEC) on the pathology, host microbiota and bacterial translocation from the gut. Commercial chicken layers were infected via oral and cloacal routes with lux-tagged APEC with or without H. meleagridis whereas negative controls were left uninfected. Except one bird, which died due to colibacillosis, no clinical signs were recorded in birds infected with bioluminescence lux gene tagged E. coli. In co-infected birds, depression and ruffled feathers were observed in 4 birds and average body weight gain significantly decreased. Typhlitis caused by H. meleagridis was present only in co-infected birds, which also had pronounced microscopic lesions in systemic organs such as liver, heart and spleen. The 16S rRNA gene amplicon sequencing showed that in co-infected birds, corresponding to the severity of cecal lesions, microbial species richness and diversity in caeca greatly decreased and the abundance of the Escherichia group, Helicobacter and Bacteroides was relatively higher with a reduction of commensals. Most of the shared Amplicon Sequencing Variants between cecum and blood in co-infected birds belonged to Pseudomonas, Staphylococcus, and members of Enterobacteriaceae while those assigned as Lactobacillus and members of Ruminococcaceae and Lachnospiraceae were found mainly in negative controls. In infected birds, E. coli in the cecal lumen penetrated into deeper layers, a phenomenon noticed with higher incidence in the dead and co-infected birds. Furthermore, numbers of lux-tagged E. coli in caeca were significantly higher at every sampling date in co-infected birds. Altogether, infection of layers with H. meleagridis and E. coli resulted in more severe pathological changes, dramatic shift in the cecal mucosa-associated microbiota, higher tissue colonization of pathogenic bacteria such as avian pathogenic E. coli in the gut and increased penetration of E. coli from the cecal lumen toward peritoneum. This study provides novel insights into the parasite-bacteria interaction in vivo highlighting the role of H. meleagridis to support E. coli in the pathogenesis of colibacillosis in chickens.

• 16S rRNA gene amplicon sequencing
• Escherichia coli
• Histomonas meleagridis
• colibacillosis
• histomonosis
• immunohistochemistry
• microbiota
• translocation

• 16S rDNA
• Bacterial translocation mechanisms
• acute pancreatitis

In acute pancreatitis (AP) gut barrier dysfunction is considered as an important predisposing factor leading to increased intestinal permeability (IP). In this study a pooled analysis of data published in our previous four studies on various aspects of gut permeability and endotoxaemia in patients with AP was attempted to find an association between increased IP and severity of disease and associated complications.

This study was a pooled analysis of data of four previously published prospective studies on AP. Gut permeability, assessed by lactulose/mannitol excretion in urine and endotoxin core antibodies type IgG and IgM (EndoCab IgG and IgM) were measured on days zero and seven (D0 and D7) of admission. All patients received standard treatment of AP. We studied whether IgG and IgM anti-endotoxin titres and lactulose-mannitol ratio (LMR) at admission and D7 were associated with organ failure, infection and mortality.

The titres of anti-endotoxin IgG and IgM were lower in all patients of AP (n=204), both in mild AP (n=24) and severe AP (n=180) in the first week, compared to controls (n=15). There was no significant difference in serum IgG and IgM anti-endotoxin levels and LMR at baseline and at D7 among patients with organ failure, infection and mortality.

Our findings showed that serum IgG and IgM anti-endotoxin titres and LMR at admission and at day 7 were not associated with organ failure, infection, and death of patients with AP.

• Acute pancreatitis
• endotoxaemia
• intestinal permeability
• mortality
• organ failure

Pancreatitis with infected necrosis is a severe complication of acute pancreatitis and carries with it high rates of morbidity and mortality. The management of infected pancreatic necrosis alongside concomitant colorectal cancer has never been described in literature.

A 77 years old gentleman presented to the Emergency Department of our hospital complaining of ongoing abdominal pain for 8 h. The patient had clinical features of pancreatitis with a raised lipase of 3810 U/L, A computed tomography (CT) abdomen confirmed pancreatitis with extensive peri-pancreatic edema. During the course of his admission, the patient had persistent high fevers and delirium thought secondary to infected necrosis, prompting the commencement of broad-spectrum antibiotic therapy with Piperacillin/Tazobactam. Subsequent CT abdomen confirmed extensive pancreatic necrosis (over 70%). Patient was managed with supportive therapy, nutritional support and gut rest initially and improved over the course of his admission and was discharged 42 d post admission. He represented 24 d following his discharge with fever and chills and a repeat CT abdomen scan noted gas bubbles within the necrotic pancreatic tissue thereby confirming infected necrotic pancreatitis. This CT scan also revealed asymmetric thickening of the rectal wall suspicious for malignancy. A rectal cancer was confirmed on flexible sigmoidoscopy. The patient underwent two endoscopic necrosectomies and was treated with intravenous antibiotics and was discharged after 28 d. Within 1 wk post discharge, the patient commenced a course of neoadjuvant radiotherapy and subsequently underwent concomitant chemotherapy prior to undergoing a successful Hartmann’s procedure for treatment of his colorectal cancer.

This case highlights the efficacy of endoscopic necrosectomy, early enteral feeding and targeted antibiotic therapy for timely management of infected necrotic pancreatitis. The prompt resolution of pancreatitis permitted the patient to undergo neoadjuvant treatment and resection for his concomitant colorectal cancer.

• Necrotizing pancreatitis
• Rectal cancer
• Enteral nutrition
• Endoscopy
• Case report

• biofilm constituents
• indication of stenting
• micro-organisms profile
• pancreatic stents
• predisposing factors

• Acute pancreatitis
• Bacterial translocation
• Colonic cleansing
• Intestinal flora

• acute pancreatitis
• bacterial translocation
• infection
• probiotics

AIM: To investigate effects of perirenal space blocking (PSB) on gastrointestinal function in patients with severe acute pancreatitis (SAP).

METHODS: Forty patients with SAP were randomly allocated to receive PSB or no PSB (NPSB). All the SAP patients received specialized medical therapy (SMT). Patients in the PSB group received PSB + SMT when hospitalized and after diagnosis, whereas patients in the NPSB group only received SMT. A modified gastrointestinal failure (GIF) scoring system was used to assess the gastrointestinal function in SAP patients after admission. Pain severity (visual analog scale, 0 to 100) was monitored every 24 h for 72 h.

RESULTS: Modified GIF score decreased in both groups during the 10-d study period. The median score decrease was initially significantly greater in the PSB group than in the NPSB group after PSB was performed. During the 72-h study period, pain intensity decreased in both groups. The median pain decrease was significantly greater in the PSB group than in the NPSB group at single time points. Patients in the PSB group had significantly lower incidences of hospital mortality, multiple organ dysfunction syndrome, systemic inflammatory response syndrome, and pancreatic infection, and stayed in the intensive care unit for a shorter duration. However, no difference in terms of operation incidence was found between the two groups.

CONCLUSION: PSB could ameliorate gastrointestinal dysfunction or failure during the early stage of SAP. Moreover, PSB administration could improve prognosis and decrease the mortality of SAP patients.

• Perirenal space blocking
• Therapeutics
• Severe acute pancreatitis
• Gastrointestinal function
• Prognosis

• Abdominal Pain/etiology
• Abdominal Pain/therapy
• Acute Disease
• Adult
• Anesthetics, Local/administration & dosage
• Celiac Plexus/physiopathology
• China
• Female
• Gastrointestinal Diseases/diagnosis
• Gastrointestinal Diseases/etiology
• Gastrointestinal Diseases/mortality
• Gastrointestinal Diseases/physiopathology
• Gastrointestinal Diseases/therapy
• Gastrointestinal Motility
• Hospital Mortality
• Humans
• Lidocaine/administration & dosage
• Male
• Middle Aged
• Nerve Block/methods
• Pancreatitis/complications
• Pancreatitis/diagnosis
• Pancreatitis/mortality
• Pancreatitis/physiopathology
• Pancreatitis/therapy
• Prospective Studies
• Recovery of Function
• Severity of Illness Index
• Time Factors
• Treatment Outcome

• Hepatic failure
• Immunonutrition
• Nutrition
• Obesity
• Pulmonary failure
• Renal failure

Amelioration of intestinal dysmotility and stasis during the early period of acute necrotizing pancreatitis (ANP) appears to be important to reduce the risks of secondary pancreatic infection. We aimed to characterize the association between the neuropathy of the enteric nervous system and gut dysfunction and to examine the effect of octreotide on motor innervation in the early stage of ANP.

The rats were randomly divided into eight groups: control+saline; control+octreotide; ANP+saline and ANP+octreotide (24 h, 48 h, 72 h). The spontaneous activity of ileal segments and the response to ACh, l-NNA were recorded. The alterations of myenteric neuronal nitric oxide synthase (nNOS), choline acetyltransferase (CHAT), PGP9.5 and somatostatin receptor 2 (SSTR₂) immunoreactive cells were evaluated by immunofluorescence and the protein expression of nNOS and CHAT were evaluated by western blot. We found the amplitude of spontaneous contractions at 48 h and the response to ACh at 24 h declined in the ANP+saline rats. A higher contractile response to both ACh and to l-NNA was observed in the ANP+octreotide group, compared with the ANP+saline rats at 24 h. A significant reduction in the nNOS and cholinergic neurons was observed in ANP+saline rats at the three time points. However, this reduction was greatly ameliorated in the presence of octreotide at 24 h and 48 h. The protein expression of CHAT neurons at 24 h and the nNOS neurons at 48 h in the ANP+octreotide rats was much higher than the ANP+saline rats.

The pathogenesis of ileus in the early stage of ANP may be related to the neuropathy of the enteric nervous system. Octreotide may reduce the severity of ileus by lessening the damage to enteric motor innervation.

• Animals
• Blotting, Western
• Cell Movement/drug effects
• Choline O-Acetyltransferase/metabolism
• Enteric Nervous System/drug effects
• Enteric Nervous System/metabolism
• Enteric Nervous System/pathology
• Gastrointestinal Agents/pharmacology
• Immunoenzyme Techniques
• Intestine, Small/drug effects
• Intestine, Small/metabolism
• Intestine, Small/pathology
• Male
• Motor Neurons/drug effects
• Motor Neurons/metabolism
• Motor Neurons/pathology
• Nitric Oxide Synthase Type I/metabolism
• Octreotide/pharmacology
• Pancreatitis, Acute Necrotizing/drug therapy
• Pancreatitis, Acute Necrotizing/metabolism
• Pancreatitis, Acute Necrotizing/pathology
• Rats
• Rats, Sprague-Dawley
• Receptors, Somatostatin/metabolism
• Ubiquitin Thiolesterase/metabolism

• Adult
• Catheterization
• Cohort Studies
• Drainage/methods
• Female
• Humans
• Male
• Middle Aged
• Minimally Invasive Surgical Procedures
• Pancreatitis, Acute Necrotizing/complications
• Pancreatitis, Acute Necrotizing/mortality
• Pancreatitis, Acute Necrotizing/surgery
• Pancreatitis, Acute Necrotizing/therapy
• Retrospective Studies
• Sepsis/etiology
• Sepsis/therapy
• Treatment Outcome

• Acute Disease
• Body Fluids
• Humans
• Necrosis
• Needles
• Pancreas/pathology
• Pancreatitis/surgery
• Randomized Controlled Trials as Topic
• Severity of Illness Index
• Suction/instrumentation
• Suction/methods

• Acute Disease
• Enteral Nutrition
• Humans
• Pancreatitis/mortality
• Pancreatitis/therapy
• Parenteral Nutrition
• Randomized Controlled Trials as Topic

• Acute Disease
• Adult
• Aged
• Biopsy, Fine-Needle/methods
• Catheterization/methods
• Drainage/methods
• Exudates and Transudates
• Female
• Humans
• Longevity
• Male
• Middle Aged
• Pancreatitis/surgery
• Treatment Outcome
• Ultrasonography, Interventional

• Adult
• Aged
• Bacterial Infections/complications
• Bacterial Infections/microbiology
• Female
• Fungi/isolation & purification
• Gram-Negative Bacteria/isolation & purification
• Gram-Positive Bacteria/isolation & purification
• Humans
• Male
• Middle Aged
• Mycoses/complications
• Mycoses/microbiology
• Pancreatitis, Acute Necrotizing/complications
• Pancreatitis, Acute Necrotizing/mortality
• Pancreatitis, Acute Necrotizing/therapy
• Retrospective Studies
• Survival Analysis
• Survival Rate
• Time Factors
• Young Adult

AIM: To study retrospectively the influence of intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) in patients with early acute pancreatitis (AP) (during the first week after admission) on physiological functions, and the association of the presence of IAH/ACS and outcome.

METHODS: Patients (n = 74) with AP recruited in this study were divided into two groups according to intra-abdominal pressure (IAP) determined by indirect measurement using the transvesical route via Foley bladder catheter during the first week after admission. Patients (n = 44) with IAP ≥ 12 mmHg were assigned in IAH group, and the remaining patients (n = 30) with IAP < 12 mmHg in normal IAP group. For analysis of the influence of IAH/ACS on organ function and outcome, the physiological parameters and the occurrence of organ dysfunction during intensive care unit (ICU) stay were recorded, as were the incidences of pancreatic infection and in-hospital mortality.

RESULTS: IAH within the first week after admission was found in 44 patients (59.46%). Although the APACHE II scores on admission and the Ranson scores within 48 h after hospitalization were elevated in IAH patients in early stage, they did not show the statistically significant differences from patients with normal IAP within a week after admission (16.18 ± 3.90 vs 15.70 ± 4.25, P = 0.616; 3.70 ± 0.93 vs 3.47 ± 0.94, P = 0.285, respectively). ACS in early AP was recorded in 20 patients (27.03%). During any 24-h period of the first week after admission, the recorded mean IAP correlated significantly with the Marshall score calculated at the same time interval in IAH group (r = 0.635, P < 0.001). Although ACS patients had obvious amelioration in physiological variables within 24 h after decompression, the incidences of pancreatitic infection, septic shock, multiple organ dysfunction syndrome (MODS) and death in the patients with ACS were significantly higher than that in other patients without ACS (pancreatitic infection: 60.0% vs 7.4%, P < 0.001; septic shock: 70.0% vs 11.1%, P < 0.001; MODS: 90.0% vs 31.5%, P < 0.001; mortality: 75.0% vs 3.7%, P < 0.001).

CONCLUSION: IAH/ACS is a frequent finding in patients admitted to the ICU because of AP. Patients with IAP at approximately 10-12 mmHg and early signs of changes in physiologic variables should be seriously considered for urgent decompression to improve survival.

• Acute pancreatitis
• Abdominal compartment syndrome
• Intra-abdominal pressure
• Intra-abdominal hypertension
• Organ dysfunction

Approximately 20% of patients with acute pancreatitis develop a severe disease associated with complications and high risk of mortality. The purpose of this study is to review pathogenesis and prognostic factors of severe acute pancreatitis (SAP). An extensive medline search was undertaken with focusing on pathogenesis, complications and prognostic evaluation of SAP. Cytokines and other inflammatory markers play a major role in the pathogenesis and course of SAP and can be used as prognostic markers in its early phase. Other markers such as simple prognostic scores have been found to be as effective as multifactorial scoring systems (MFSS) at 48 h with the advantage of simplicity, efficacy, low cost, accuracy and early prediction of SAP. Recently, several laboratory markers including hematocrit, blood urea nitrogen (BUN), creatinine, matrix metalloproteinase-9 (MMP-9) and serum amyloid A (SAA) have been used as early predictors of severity within the first 24 h. The last few years have witnessed a tremendous progress in understanding the pathogenesis and predicting the outcome of SAP. In this review we classified the prognostic markers into predictors of severity, pancreatic necrosis (PN), infected PN (IPN) and mortality.

• Acute pancreatitis
• Pathogenesis
• Prediction
• Severity
• Necrosis
• Infected necrosis
• Mortality

• Animals
• Colon/drug effects
• Colon/pathology
• Disease Models, Animal
• Female
• Gastrointestinal Motility/drug effects
• Indoles/therapeutic use
• Intestine, Small/drug effects
• Intestine, Small/enzymology
• Intestine, Small/pathology
• Mice
• Pancreatitis, Acute Necrotizing/drug therapy
• Pancreatitis, Acute Necrotizing/enzymology
• Pancreatitis, Acute Necrotizing/pathology
• Peroxidase/metabolism
• Serotonin Receptor Agonists/therapeutic use

• Anti-Bacterial Agents/administration & dosage
• Disinfection/methods
• Enteral Nutrition/methods
• Female
• Humans
• Japan
• Lymphocyte Count
• Male
• Middle Aged
• Pancreatitis, Acute Necrotizing/complications
• Pancreatitis, Acute Necrotizing/mortality
• Pancreatitis, Acute Necrotizing/surgery
• Retrospective Studies
• Sepsis/etiology
• Sepsis/prevention & control
• Severity of Illness Index
• Survival Rate
• Time Factors
• Treatment Outcome

• Acute Disease
• Animals
• Apoptosis
• Bacterial Translocation
• Female
• Mice
• Mice, Inbred C3H
• Multiple Organ Failure/physiopathology
• Pancreatitis/physiopathology
• Risk Factors
• Signal Transduction
• Toll-Like Receptor 4/physiology

• Anti-Infective Agents/therapeutic use
• Bacterial Infections/epidemiology
• Bacterial Infections/etiology
• Bacterial Infections/prevention & control
• Double-Blind Method
• Enteral Nutrition/methods
• Female
• Follow-Up Studies
• Humans
• Incidence
• Male
• Middle Aged
• Pancreaticoduodenectomy/methods
• Postoperative Care/methods
• Probiotics/therapeutic use
• Prospective Studies
• Pylorus/surgery
• Survival Rate
• Treatment Outcome