BACKGROUNDAIMS: The bedside index of severity in acute pancreatitis (BISAP) is a new, convenient, prognostic multifactorial scoring system. As more data are needed before clinical application, we compared BISAP, the serum procalcitonin (PCT), and other multifactorial scoring systems simultaneously.Fifty consecutive acute pancreatitis patients were enrolled prospectively. Blood samples were obtained at admission and after 48 hours and imaging studies were performed within 48 hours of admission. The BISAP score was compared with the serum PCT, Ranson's score, and the acute physiology and chronic health examination (APACHE)-II, Glasgow, and Balthazar computed tomography severity index (BCTSI) scores. Acute pancreatitis was graded using the Atlanta criteria. The predictive accuracy of the scoring systems was measured using the area under the receiver-operating curve (AUC).The accuracy of BISAP (≥ 2) at predicting severe acute pancreatitis was 84% and was superior to the serum PCT (≥ 3.29 ng/mL, 76%) which was similar to the APACHE-II score. The best cutoff value of BISAP was 2 (AUC, 0.873; 95% confidence interval, 0.770 to 0.976; p < 0.001). In logistic regression analysis, BISAP had greater statistical significance than serum PCT.BISAP is more accurate for predicting the severity of acute pancreatitis than the serum PCT, APACHE-II, Glasgow, and BCTSI scores.

Pancreatitis is classified into acute (AP) and chronic pancreatitis (CP). Apelin, a small peptide, is the endogenous ligand for the APJ receptor. Apelin and APJ are expressed in the pancreas. The aims of this study were to examine whether apelin influences inflammatory and fibrosis responses to pancreatitis in mice and to identify mechanisms behind apelin's activities. Supra-maximal cerulein-induction of AP or CP caused significant (P<0.05) elevations in pancreatic apelin and APJ expression. Levels declined during the recovery phases. In apelin gene knockout mice (APKO) with pancreatitis, pancreatic neutrophil invasion and myeloperoxidase activity (MPO) were enhanced significantly, apelin treatment suppressed both. Apelin reduced CP-induced elevations of extracellular matrix (ECM)-associated proteins. Apelin inhibited platelet derived growth factor-simulated connective tissue growth factor (CTGF) production and proliferation of pancreatic stellate cells (PSCs). Serum granulocyte colony stimulating factor (G-CSF) and keratinocyte cytokine (KC) levels were higher in APKO mice compared to wild-type (WT) mice with pancreatitis. Apelin reduced AP and CP-induced elevations in pancreatic nuclear factor kappa B (NF-κB) activation. Together, findings imply that the pancreatic apelin-APJ system functions to curb the inflammatory and fibrosis responses during pancreatitis. Furthermore, findings suggest apelin reduces inflammation and fibrosis by reduction of neutrophil recruitment and PSC activity. Inhibition of neutrophil invasion may be mediated by reduced KC and G-CSF secretion. Apelin-induced reductions in PSC proliferation and CTGF production are putative mechanisms underlying apelin's inhibition of ECM production. The apelin-associated changes in NF-κB binding may be linked to apelin's regulation of pancreatic inflammatory and fibrosis responses during pancreatitis.

Acute pancreatitis is a frequent clinical entity in the West. About 80% of patients with acute pancreatitis develop edematous pancreatitis, while 20% develop necrotizing pancreatitis: The latter is a potentially life-threatening disease. In this case, early enteral nutrition has been shown to improve the course of the disease. Usually, gastric enteral nutrition with a polymeric formula via a nasogastric tube is possible; only in a minority of patients is jejunal feeding necessary owing to the high gastric residual volume. An elemental formula is useful for patients with significant intestinal maldigestion. If enteral feeding is not feasible within 5-7 days, (additional) parenteral nutrition has to be considered. Individualized-primary enteral-nutritional support is an essential part of a multimodal therapy in severe acute pancreatitis and it improves clinical outcome.

BACKGROUND:

Acute pancreatitis remains as one of the most difficult and challenging digestive disorder to predict in terms of clinical course and outcome. Every case has an individual course and therefore acute pancreatitis remains challenging and fascinating. Due to this variability, many different scoring systems have evolved during the last decades. Every scoring system has advantages and disadvantages. Not every scoring system is capable of assessing the clinical time course of the disease, some are only suitable for the time of initial presentation.

AIM:

This paper will give an overview on the development of different widely used scoring systems and their performance in assessing severity and prognosis of acute pancreatitis.

CONCLUSION:

Severity assessment means objective quantification of overall severity of illness. Early and reliable stratification of severity is required to decide best treatment of the individual patient, preparation for possible evolving complications or for referral to specialist centers. No single scoring system is able to cover the entire range of problems associated with treatment and assessment of acute pancreatitis. In our clinical experience, we recommend hematocrit upon admission, daily sequential organ failure assessment score and procalcitonin, C-reactive protein on day 3 and CT severity index beyond the first week. These scoring tools together with close clinical follow-up of the patient ultimately lead to an optimized treatment of this challenging disease.

Severe acute pancreatitis is one of the critical conditions that may develop in children with cancer. The leading cause of death due to acute pancreatitis is infectious pancreatitis or circulation collapse. Therefore, patients who develop acute pancreatitis while undergoing chemotherapy or after hematopoietic transplantation are at risk for a life-threatening and fatal course. We treated 140 patients with malignancy from April 2002 to March 2009 at our hospital and encountered 3 patients under neutropenia who developed severe acute pancreatitis. Two of them were successfully treated with continuous regional arterial infusion of a protease inhibitor and antibiotic even under agranulocytosis. Another patient was treated with conventional therapy with intravenous antibiotics plus a protease inhibitor and total or partial parenteral nutrition. Even though the two patients treated with continuous regional arterial infusion presented much more severe conditions, their symptoms resolved earlier. In conclusion, acute pancreatitis is one of the severe complications of childhood malignancy. Even under agranulocytosis, continuous regional arterial infusion of a protease inhibitor and antibiotic was well tolerated and effective among our cases and might reduce early death due to pancreatitis.

The efficacy of lawsone against L-arginine induced acute pancreatitis was determined at 24 h by determination of serum levels of amylase, lipase and proinflammatory cytokines [tumor necrosis factor (TNF)-alpha, C-reactive proteins and interleukin (IL)], pancreatic myeloperoxidase (MPO) activity, lipid peroxidation (thiobarbituric acid reactive substances (TBARS)], nitrate/nitrite levels, and the wet weight/body weight ratio. Lawsone and methylprednisolone treatments significantly attenuated the L-arginine- induced increases in pancreatic wet weight/body weight ratio, and decreased the serum levels of amylase and lipase, and TNF-alpha and IL-6 and significantly lowered pancreatic levels of MPO, TBARS, and nitrate/nitrite. The histoimmunological findings further proved the amelioration of pancreatic injury by lawsone and further proved anti-inflammatory and antioxidant agent property of lawsone.

To examine fibrinogen-like protein 2 (fgl2) expression during taurocholate-induced acute pancreatitis progression in rats and its correlation with pancreatic injury severity.Forty-eight male Sprague-Dawley rats were randomly divided into the severe acute pancreatitis (SAP) group (n = 24) and the sham operation (SO) group (n = 24). Sodium taurocholate (4% at doses of 1 mL/kg body weight) was retrogradely injected into the biliopancreatic ducts of the rats to induce SAP. Pancreatic tissues were prepared immediately after sacrifice. At the time of sacrifice, blood was obtained for determination of serum amylase activity and isolation of peripheral blood mononuclear cells (PBMCs). Pancreatic tissue specimens were obtained for routine light microscopy including hematoxylin and eosin staining, and the severity of pancreatic injury was evaluated 1, 4 and 8 h after induction. Expression of fgl2 mRNA was measured in the pancreas and PBMCs using reverse transcription polymerase chain reaction. Expression of fgl2 protein was evaluated in pancreatic tissues using Western blotting and immunohistochemical staining. Masson staining was also performed to observe microthrombosis.At each time point, levels of fgl2 mRNAs in pancreatic tissues and PBMCs were higher (P < 0.05) in the SAP group than in the SO group. For pancreatic tissue in SAP vs SO, the levels were: after 1 h, 3.911 ± 1.277 vs 1.000 ± 0.673; after 4 h, 9.850 ± 3.095 vs 1.136 ± 0.609; and after 8 h, 12.870 ± 3.046 vs 1.177 ± 0.458. For PBMCs in SAP vs SO, the levels were: after 1 h, 2.678 ± 1.509 vs 1.000 ± 0.965; after 4 h, 6.922 ± 1.984 vs 1.051 ± 0.781; and after 8 h, 13.533 ± 6.575 vs 1.306 ± 1.179. Levels of fgl2 protein expression as determined by Western blotting and immunohistochemical staining were markedly up-regulated (P < 0.001) in the SAP group compared with those in the SO group. For Western blotting in SAP vs SO, the results were: after 1 h, 2.183 ± 0.115 vs 1.110 ± 0.158; after 4 h, 2.697 ± 0.090 vs 0.947 ± 0.361; and after 8 h, 3.258 ± 0.094 vs 1.208 ± 0.082. For immunohistochemical staining in SAP vs SO, the results were: after 1 h, 1.793 ± 0.463 vs 0.808 ± 0.252; after 4 h, 4.535 ± 0.550 vs 0.871 ± 0.318; and after 8 h, 6.071 ± 0.941 vs 1.020 ± 0.406. Moreover, we observed a positive correlation in the pancreas (r = 0.852, P < 0.001) and PBMCs (r = 0.735, P < 0.001) between fgl2 expression and the severity of pancreatic injury. Masson staining showed that microthrombosis (%) in rats with SAP was increased (P < 0.001) compared with that in the SO group and it was closely correlated with fgl2 expression in the pancreas (r = 0.842, P < 0.001). For Masson staining in SAP vs SO, the results were: after 1 h, 26.880 ± 9.031 vs 8.630 ± 3.739; after 4 h, 53.750 ± 19.039 vs 8.500 ± 4.472; and after 8 h, 80.250 ± 12.915 vs 10.630 ± 7.003.Microthrombosis due to fgl2 overexpression contributes to pancreatic impairment in rats with SAP, and fgl2 level may serve as a biomarker during early stages of disease.

BACKGROUND:

To investigate the effects of early enteral nutrition (EEN) on intra-abdominal pressure (IAP) and disease severity in patients with severe acute pancreatitis (SAP).

METHODS:

Enteral nutrition (EN) was started within 48 h after admission in the EEN group and from the 8th day in the delayed enteral nutrition (DEN) group. The IAP and intra-abdominal hypertension (IAH) incidence were recorded for 2 weeks. The caloric intake and feeding intolerance (FI) incidence were recorded daily after EN was started. The severity markers and clinical outcome variables were also recorded.

RESULTS:

Sixty patients were enrolled to this study. No difference about IAP was found. The IAH incidence of the EEN group was significantly lower than that of the DEN group from the 9th day (8/30 versus 18/30; P = 0.009) after admission. The FI incidence of the EEN group was higher than that of the DEN group during the initial 3 days of feeding (25/30 versus 12/30; P = 0.001; 22/30 versus 9/30; P = 0.001; 15/30 versus 4/30; P = 0.002). Patients with an IAP <15 mmHg had lower FI incidence than those with an IAP ≥15 mmHg on the 1st day (20/22 versus 17/38; P < 0.001), the 3rd day (11/13 versus 8/47; P < 0.001), and the 7th day (3/5 versus 3/55; P = 0.005) of feeding. The severity markers and clinical outcome variables of the EEN group were significantly improved.

CONCLUSIONS:

Early enteral nutrition did not increase IAP. In contrast, it might prevent the development of IAH. In addition, EEN might be not appropriate during the initial 3-4 days of SAP onset. Moreover, EN might be of benefit to patients with an IAP <15 mmHg. Early enteral nutrition could improve disease severity and clinical outcome, but did not decrease mortality of SAP.

We report on three patients who developed four episodes of acute pancreatitis while their systemic lupus erythematosus was active and being treated with prednisolone. In all three, gastritis was first considered and treated due to abdominal pain, vomiting, and epigastric tenderness, but their symptoms did not improve. Then pancreatic enzymes were measured, which confirmed pancreatitis. Imaging studies showed an enlarged pancreas in one case, a normal pancreas in two cases, and a focal hypodense nonenhancing parenchyma in one case. Corticosteroids were prescribed for both active SLE and SLE-related pancreatitis. Pulse methylprednisolone was prescribed in one episode, increasing oral prednisolone in one episode, and the same dose of prednisolone continued in the other two episodes. All cases recovered without complications. SLE-related pancreatitis should be considered in SLE patients when the SLE is active and a patient develops abdominal pain and vomiting.