| 1. |
- Arnelo, Urban, et al.
(författare)
-
Single-operator pancreatoscopy is helpful in the evaluation of suspected intraductal papillary mucinous neoplasms (IPMN)
- 2014
-
Ingår i: Pancreatology (Print). - : Elsevier. - 1424-3903 .- 1424-3911. ; 14:6, s. 510-514
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND OBJECTIVE: Even when advanced cross-sectional imaging modalities have been employed, endoscopic evaluation of intraductal papillary mucinous neoplasms (IPMN) is often required in order to assess the final character and extent of lesions. The current study addresses the use of SpyGlass single-operator peroral pancreatoscopy in suspected IPMN.DESIGN: A prospective, non-randomized exploratory cohort study.SETTING: Single-center.PATIENTS AND INTERVENTION: A prospective study-cohort of 44 consecutive patients in a single tertiary referral center who underwent ERCP and peroral pancreatoscopy, was prospectively collected between July 2007 and March 2013 because of a radiological signs of IPMN. These IPMN-findings were discovered incidentally in 44% of the cases.MAIN OUTCOME MEASUREMENTS: Diagnostic accuracy (specificity & sensitivity) and complications.RESULTS: The targeted region of the pancreatic duct was reached with the SpyGlass system in 41 patients (median age 65 years, 41% female). Three patients were excluded from analysis because of failed deep cannulation of the pancreatic duct. Brush cytology was taken in 88% and direct biopsies in 41%. IPMN with intermediate or high-grade dysplasia was the main final diagnosis (76%) in 22 patients who had surgery. Out of the 17 patients with a final diagnosis of MD-IPMN, 76% were correctly identified by pancreatoscopy. Of the 9 patients with a final diagnosis of BD-IPMN, the pancreatoscopy identified 78% of the cases correctly.The incidence of post-ERCP pancreatitis was 17%. Pancreatoscopy was found to have provided additional diagnostic information in the vast majority of the cases and to affect clinical decision-making in 76%.LIMITATIONS: Single-center study.CONCLUSIONS: Single-operator peroral pancreatoscopy contributed to the clinical evaluation of IPMN lesions and influenced decision-making concerning their clinical management. The problem of post-procedural pancreatitis needs further attention.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
- Del Chiaro, M, et al.
(författare)
-
Enucleation of branch duct-IPMN in a transplant patient
- 2013
-
Ingår i: Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]. - : Elsevier BV. - 1424-3911. ; 13:3, s. 312-313
-
Tidskriftsartikel (refereegranskat)
|
|
| 5. |
|
|
| 6. |
- Larino-Noia, José, et al.
(författare)
-
Early and/or immediately full caloric diet versus standard refeeding in mild acute pancreatitis: A randomized open-label trial
- 2014
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903 .- 1424-3911. ; 14:3, s. 167-173
-
Tidskriftsartikel (refereegranskat)abstract
- Refeeding after acute pancreatitis (AP) is traditionally started in a successively increasing manner when abdominal pain is absent and pancreatic enzymes are decreasing. We aimed to evaluate length of hospital stay (LOHS) and refeeding tolerance for early refeeding and/or immediately full caloric intake in patients recovering from AP. Methods: In this randomized, open-label trial, patients with AP were randomized into four different refeeding protocols. Group 1 and 2 received a stepwise increasing diet during three days while 3 and 4 received an immediately full caloric, low fat diet. Group 2 and 4 started refeeding early (once bowel sounds returned) and 1 and 3 started at standard time (bowel sounds present, no abdominal pain, no fever, leucocytes and pancreatic enzymes decreasing). Main outcomes measurements were LOHS and tolerance (ability to ingest >50% of meals without severe pain, nausea or AP relapse). Results: Eighty patients were evaluated and 72 randomized (median age 60 years, range 24-85, 33 male). LOHS was significantly reduced after early refeeding (median 5 versus 7 days (p = 0.001)) but not in patients receiving immediately full caloric diet, compared to standard management (6 versus 6 days (p = 0.12)). There was no difference in refeeding tolerance comparing immediately full caloric diet versus stepwise increasing diet (31/35 (89%) versus 33/37 (89%) patients tolerating the treatment, p = 1.00) or early versus standard time for refeeding (33/37 (89%) versus 31/35 (89%), (p = 1.00)). Conclusions: Refeeding after AP when bowel sounds are present with immediately full caloric diet is safe and well tolerated. Early refeeding shortens LOHS. Copyright (C) 2014, IAP and EPC. Published by Elsevier India, a division of Reed Elsevier India Pvt. Ltd. All rights reserved.
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
- Loizou, L, et al.
(författare)
-
Computed tomography staging of pancreatic cancer : a validation study addressing interobserver agreement
- 2013
-
Ingår i: Pancreatology (Print). - : Elsevier BV. - 1424-3903 .- 1424-3911. ; 13:6, s. 570-575
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND/OBJECTIVES:Ductal adenocarcinoma in the head of the pancreas (PDAC) is usually unresectable at the time of diagnosis due to the involvement of the peripancreatic vessels. Various preoperative classification algorithms have been developed to describe the relationship of the tumor to these vessels, but most of them lack a surgically based approach. We present a CT-based classification algorithm for PDAC based on surgical resectability principles with a focus on interobserver variability.METHODS:Thirty patients with PDAC undergoing pancreaticoduodenectomy were examined by using a standard CT protocol. Nine radiologists, representing three different levels of expertise, evaluated the CT examinations and the tumors were classified into four categories (A-D) according to the proposed system. For the interobserver agreement, the Intraclass Correlation Coefficient (ICC) was estimated.RESULTS:The overall ICC was 0.94 and the ICCs among the trainees, experienced radiologists, and experts were 0.85, 0.76, and 0.92, respectively. All tumors classified as category A1 showed no signs of vascular invasion at surgery. In category A2, 40% of the tumors had corresponding infiltration and required resection of the superior mesenteric vein/portal vein (SMV/PV). One of two tumors in category B2 and two of three in category C required SMV/PV resection. All six patients in category D had both arterial and venous involvement.CONCLUSION:There is almost perfect agreement among radiologists with different levels of expertise in regards to the local staging of PDAC. For tumors in a more advanced preoperative category, an increased risk for vascular involvement was noticed at surgery.
|
|
| 11. |
|
|
| 12. |
|
|
| 13. |
|
|
| 14. |
|
|
| 15. |
- Andersson, Bodil, et al.
(författare)
-
Prediction of Severe Acute Pancreatitis at Admission to Hospital Using Artificial Neural Networks.
- 2011
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 11:3, s. 328-335
-
Tidskriftsartikel (refereegranskat)abstract
- Background/Aims: Artificial neural networks (ANNs) are non-linear pattern recognition techniques, which can be used as a tool in medical decision-making. The aim of this study was to construct and validate an ANN model for early prediction of the severity of acute pancreatitis (AP). Methods: Patients treated for AP from 2002 to 2005 (n = 139) and from 2007 to 2009 (n = 69) were analyzed to develop and validate the ANN model. Severe AP was defined according to the Atlanta criteria. Results: ANNs selected 6 of 23 potential risk variables as relevant for severity prediction, including duration of pain until arrival at the emergency department, creatinine, hemoglobin, alanine aminotransferase, heart rate, and white blood cell count. The discriminatory power for prediction of progression to a severe course, determined from the area under the receiver-operating characteristic curve, was 0.92 for the ANN model, 0.84 for the logistic regression model (p = 0.030), and 0.63 for the APACHE II score (p < 0.001). The numbers of correctly classified patients for a sensitivity of 50 and 75% were significantly higher for the ANN model than for logistic regression (p = 0.002) and APACHE II (p < 0.001). Conclusion: The ANN model identified 6 risk variables available at the time of admission, including duration of pain, a finding not being presented as a risk factor before. The severity classification developed proved to be superior to APACHE II. and IAP.
|
|
| 16. |
- Bartosch-Härlid, Anna, et al.
(författare)
-
Diabetes Mellitus in Pancreatic Cancer and the Need for Diagnosis of Asymptomatic Disease.
- 2010
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 10:4, s. 423-428
-
Tidskriftsartikel (refereegranskat)abstract
- Pancreatic cancer is strongly associated with the development of hyperglycemia, peripheral insulin resistance and diabetes mellitus, especially when presented as new-onset diabetes mellitus. Peripheral insulin resistance and hyperinsulinemia have been suggested to promote growth of pancreatic cancer cells, and therefore a relation between long-standing diabetes mellitus type 2 and pancreatic cancer has been implied. Epidemiological studies, though, give incongruent results to this problem. There are data supporting a tumor-derived influence on glucose metabolism, insulin secretion and eventually the development of diabetes mellitus in early stages of pancreatic cancer. The only possibility for curative intent in pancreatic cancer is to diagnose the disease before symptoms occur. Patients with newly diagnosed diabetes mellitus type 2 or hyperglycemia as a risk group have been recommended for primary screening for pancreatic cancer. To date, there is no specific biomarker to identify patients with an asymptomatic pancreatic cancer. The review discuss the relationship between pancreatic cancer and diabetes mellitus and the possibility of secondary screening of patients with newly diagnosed diabetes mellitus type 2 or hyperglycemia in an artificial neural network. PubMed was searched for articles using the Mesh term 'pancreatic neoplasms' combined with 'insulin resistance' and 'glucose metabolism disorders'. Additional articles were retrieved through hyperlinks and by manually searching reference lists in original published articles. In total 36 articles were systematically reviewed. and IAP.
|
|
| 17. |
- Dunér, Siri, et al.
(författare)
-
Pancreatic Cancer: The Role of Pancreatic Stellate Cells in Tumor Progression.
- 2010
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 10:6, s. 673-681
-
Tidskriftsartikel (refereegranskat)abstract
- Pancreatic ductal adenocarcinoma is an aggressive and highly lethal disease frequently characterized by a dense stromal or desmoplastic response. Accumulating evidence exists that tumor desmoplasia plays a central role in disease progression and that e.g. activated pancreatic stellate cells (PSCs) are responsible for the excess matrix production. The mechanisms underlying the tumor versus stroma interplay are complex. Pancreatic cancer cells release mitogenic and fibrogenic stimulants, such as transforming growth factor β(1), platelet-derived growth factor (PDGF), sonic hedgehog, galectin 3, endothelin 1 and serine protease inhibitor nexin 2, all of which may promote the activated PSC phenotype. Stellate cells in turn secrete various factors, including PDGF, stromal-derived factor 1, epidermal growth factor, insulin-like growth factor 1, fibroblast growth factor, secreted protein acidic and rich in cysteine, matrix metalloproteinases, small leucine-rich proteoglycans, periostin and collagen type I that mediate effects on tumor growth, invasion, metastasis and resistance to chemotherapy. This review intends to shed light on the mechanisms by which PSCs in the stroma influence pancreatic cancer development. The increased understanding of this interaction will be of potential value in designing new modalities of targeted therapy. and IAP.
|
|
| 18. |
- Johansen, Dorthe, et al.
(författare)
-
Pre-Diagnostic Levels of Anionic Trypsinogen, Cationic Trypsinogen, and Pancreatic Secretory Trypsin Inhibitor in Relation to Pancreatic Cancer Risk.
- 2010
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 10:2-3, s. 229-237
-
Tidskriftsartikel (refereegranskat)abstract
- Background/Aims: Experimental studies have suggested that trypsinogen may enhance tumor progression and that the ratio between anionic trypsinogen and cationic trypsinogen (HAT/HCT) and between the sum of trypsinogens and pancreatic secretory trypsin inhibitor (PSTI) ((HAT + HCT)/PSTI) are disturbed in patients with pancreatic cancer. The aim of this study was to investigate if pre-diagnostic levels of these parameters are associated with subsequent pancreatic cancer risk. Methods: A total of 33,346 subjects participated in a health screening programme in Malmö, Sweden. Pancreatic cancer cases (n = 84) were matched to three controls each. HAT, HCT and PSTI were analyzed in pre-diagnostic serum samples. Odds ratios for pancreatic cancer were calculated using logistic regression and were then stratified for other risk factors. Results: In the main analysis, a statistically significant association between the ratio between HAT/HCT and pancreatic cancer was observed for all, for the crude OR and for the ORs adjusted for sex, BMI or Helicobacter pylori. When stratified for sex, statistically significant associations were found for females in the crude OR and for the ORs adjusted for time to analysis, BMI, alcohol consumption or H. pylori. There was a positive association between the ratio of HAT/HCT to pancreatic cancer in the intermediate/high alcohol consumption group and subjects with a BMI <25. The sum of trypsinogens showed a similar pattern, but was only of borderline significance in the intermediate/high alcohol consumption group. Conclusion: Our hypothesis predicted an increased risk for pancreatic cancer related to an imbalance between trypsin activity and trypsin inhibition capacity. The findings concerning the ratio of HAT/HCT are in line with this. The results related to analyses stratified for other risk factors should be considered as mainly explorative. and IAP.
|
|
| 19. |
- Lindkvist, Björn, et al.
(författare)
-
A prospective cohort study on risk of acute pancreatitis related to serum triglycerides, cholesterol and fasting glucose
- 2012
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 12:4, s. 317-324
-
Tidskriftsartikel (refereegranskat)abstract
- Background/objectives: To investigate risk for acute pancreatitis related to moderately elevated triglycerides, cholesterol and fasting glucose. Methods: This was a prospective cohort study in Malmo, Sweden of 33 346 subjects investigated 1974 - 1992 and followed until December 31, 2006. Baseline investigation included a self-administered questionnaire and analysis of serum triglycerides, cholesterol and fasting glucose. Cases of acute pancreatitis (n = 277, median time since baseline investigation 15.6 years) were identified in diagnosis registries and validated retrospectively. Attacks were classified as obstructive or non obstructive (alcohol or non alcohol related). Cox proportional hazards analysis was used to calculate hazard ratios (HR) for acute pancreatitis related to relevant risk factors, adjusting for age, sex, smoking habits and alcohol consumption. Results: Triglycerides were associated with overall, non obstructive and non obstructive non alcohol related acute pancreatitis with adjusted HRs of 1.21 (95% confidence interval (CI), 1.07-1.36), 1.23 (95% CI, 1.06-2.43) and 1.34 (95% Cl, 1.11-1.62) per 1 mmol/l increment, respectively. Corresponding HRs for forth versus first quartile of triglycerides were 1.55 (95% Cl, 1.09-2.21), 1.60 (95% Cl, 1.60-1.01-1.35) and 2.07 (95% Cl, 1.13-3.79). Triglycerides were not associated with obstructive acute pancreatitis and there were no associations between glucose or cholesterol and the risk of acute pancreatitis. Conclusions: We found an association between prediagnostic levels of triglycerides and risk for acute pancreatitis. This association was most pronounced in the non obstructive non alcohol related group. Our findings suggest that triglycerides may be a more important risk factor for acute pancreatitis than what has previously been estimated. Copyright (c) 2012, IAP and EPC. Published by Elsevier India, a division of Reed Elsevier India Pvt. Ltd. All rights reserved.
|
|
| 20. |
- Lindkvist, Björn, et al.
(författare)
-
Serum nutritional markers for prediction of pancreatic exocrine insufficiency in chronic pancreatitis
- 2012
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 12:4, s. 305-310
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Methods for evaluation of pancreatic exocrine insufficiency (PEI) are expensive, labor intensive, and not available at many institutions. The aim of this study was to investigate if PEI in chronic pancreatitis (CP) can by predicted by nutritional markers in blood. Methods: A retrospective analysis of a prospectively collected database of CP patients was performed. Diagnosis of CP was based on endoscopic ultrasonography or magnetic resonance imaging. PEI was investigated by the C-13-mixed triglyceride breath test. Hemoglobin, mean corpuscular volume, lymphocytes, prothrombin time, and serum levels of total protein, albumin, prealbumin, retinol binding protein, cholesterol, triglycerides, amylase, folic acid, vitamin B12, HbA1C, transferrin, ferritin, magnesium and zinc were analyzed. Results: 114 patients were included in the study (97 males, mean age 48.1 years, 54 with alcohol etiology), 38 (33%) suffered from PEI. Magnesium below 2.05 mg/dL, hemoglobin, albumin, prealbumin and retinol binding protein below lower limit of normal and HbA1C above upper limit of normal were associated with PEI in univariate analysis. Magnesium below 2.05 mg/dL detected PEI with a sensitivity, specificity and positive and negative predictive values of 0.88 (95% confidence interval, 0.66-0.97), 0.66 (0.48-0.80), 0.58 (0.39-0.75) and 0.91 (0.73-0.98), respectively. The corresponding values were 1.00 (0.80-1.00), 0.55 (0.38-0.71), 0.52 (0.34-0.69) and 1.00 (0.82-1.00)) if one or more pathological tests among parameters significantly associated with PEI in was used as a positive test for PEI. Conclusion: Serum nutritional markers can be used to predict the probability of PEI in CP and provide guidance in decisions on enzyme replacement therapy. Copyright (c) 2012, IAP and EPC. Published by Elsevier India, a division of Reed Elsevier India Pvt. Ltd. All rights reserved.
|
|
| 21. |
- Rosendahl, Ann, et al.
(författare)
-
Celecoxib synergizes human pancreatic ductal adenocarcinoma cells to sorafenib-induced growth inhibition.
- 2012
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 12:3, s. 219-226
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Pancreatic ductal adenocarcinoma is frequently associated with aberrant activation of the Ras/Raf/MAPK pathway and cyclooxygenase-2 (COX-2) overexpression. This study evaluated the potential for combining the multikinase inhibitor sorafenib and the specific COX-2 inhibitor celecoxib as therapy in pancreatic ductal adenocarcinoma cells. METHODS: BxPC-3, MIAPaCa-2, PANC-1 and AsPC-1 pancreatic adenocarcinoma cells were exposed to sorafenib and celecoxib combined treatment in vitro. Cell viability and various growth promoting and survival signaling pathways were monitored by MTT, flow cytometry and Western blotting. RESULTS: Combined treatment with sorafenib and celecoxib synergistically inhibited pancreatic adenocarcinoma cell proliferation. This regimen produced combination index (CI) values between 0.67 and 0.92 for the various cell lines, indicating significant synergistic interactions between sorafenib and celecoxib, which also markedly inhibited the migratory capacity. The growth inhibition was associated with an accumulation of cells in the G(0)/G(1) phase of the cell cycle and induction of apoptosis. These changes were accompanied by a significant reduction of p21(WAF1/Cip1) levels, where celecoxib sensitized the cells to sorafenib-mediated p21(WAF1/Cip1) suppression. CONCLUSION: These results suggest that combined treatment with sorafenib and celecoxib synergistically induce growth inhibition and apoptosis in pancreatic adenocarcinoma cells through a process involving p21(WAF1/Cip1) suppression
|
|
| 22. |
- Rosendahl, Ann, et al.
(författare)
-
Polysaccharide-K (PSK) increases p21(WAF/Cip1) and promotes apoptosis in pancreatic cancer cells.
- 2012
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 12:6, s. 467-474
-
Tidskriftsartikel (refereegranskat)abstract
- Polysaccharide-K (PSK, Krestin(®)) is a natural remedy and one of the most commonly used medicinal mushroom extracts. It has been used as oral adjuvant treatment in cancer therapy in Japan and other Asian countries for more than 40 years. PSK is thought to be an immune modulator, however, its antitumor actions remain undefined. The aim of the present study was to investigate underlying mechanisms by which PSK exerts its antitumor effects on malignant epithelial cells.
|
|
| 23. |
- Shan, Yun-feng, et al.
(författare)
-
Experimental studies on treatment of pancreatic cancer with double-regulated duplicative adenovirus AdTPHre-hEndo carrying human endostatin gene
- 2013
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 13:4, s. 393-400
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Gene-virus targeted therapy is a promising new method of treating pancreatic cancer. To increase the efficacy and decrease the side-effect, we constructed a conditionally replicative adenovirus (CRAd) expressing human endostatin, with a human Telomoerase Reverse Transcriptase (hTERT) promoter for the regulation of the early stage of adenovirus expression of gene E1a and a Hypoxia Response Element (HRE) promoter to regulate the gene E1b. Methods: A gene recombination technique was adopted to construct and generate the adenovirus AdTPHre-hEndo. Pancreatic cancer cells were studied both in vitro and in vivo. Western blotting was adopted to observe the expressions of protein E1A and E1B; duplication assay was applied to observe the selective duplication capability of recombinant cells. MTT assay was applied to measure the lethal effects of virus on pancreatic cancer cells, and ELISA was adopted to detect the human endostatin gene expression. A pancreatic cancer transplantation tumor model of nude mice was constructed to observe the antitumor effects of the virus. Results: Double-regulated duplicative adenovirus AdTPHre-hEndo genes were successfully constructed. Duplication and lethal assays proved that AdTPHre-hEndo could replicate specifically in pancreatic cancer cells and kill them. The endostatin expression in a cultured supernatant from tumor cells was significantly higher than that obtained from non-duplicative adenovirus vectors carrying that gene. The animal experiment demonstrated that AdTPHre-hEndo has a high capability to limit pancreatic cancer growth. Conclusions: AdTPHre-hEndo has a special ability to duplicate and kill pancreatic cancer cells in in vitro and in vivo experiments, thus providing a new gene-virus-based treatment system for pancreatic cancer. Copyright (C) 2013, IAP and EPC. Published by Elsevier India, a division of Reed Elsevier India Pvt. Ltd. All rights reserved.
|
|
| 24. |
- Sun, Chen, et al.
(författare)
-
The Role of Phosphatidylinositol 3-Kinase Signaling Pathways in Pancreatic Cancer
- 2011
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 11:2, s. 252-260
-
Forskningsöversikt (refereegranskat)abstract
- Background: Pancreatic cancer is a highly malignant cancer and the fourth leading cause of cancer-related death. It is characterized by a rapid disease progression, a highly invasive tumor phenotype, and frequently resistance to chemotherapy. Despite significant advances in diagnosis, staging, and surgical management of the disease during the past decade, prognosis of pancreatic cancer is still dismal. Methods and Results: The phosphatidylinositol 3-kinase (PI3K) signaling pathways regulate cellular growth, metabolism, survival, and motility in pancreatic cancer. Pancreatic cancer is associated with a high degree of genetic alterations that can result in aberrant activation of the PI3K signaling pathway. Elucidating the role of the PI3K signaling pathway in pancreatic cancer may thus be both meaningful and necessary. Conclusion: Improved knowledge of the PI3K signaling pathway in pancreatic cancer would furthermore be helpful in understanding mechanisms of tumor initiation and progression, and in identifying appropriate targeted anticancer treatment in pancreatic cancer. Copyright (C) 2011 S. Karger AG, Basel and IAP
|
|
| 25. |
- Zhou, Mengtao, et al.
(författare)
-
The efficiency of continuous regional intra-arterial infusion in the treatment of infected pancreatic necrosis
- 2013
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 13:3, s. 212-215
-
Tidskriftsartikel (refereegranskat)abstract
- Objective: Our aim was to investigate the efficiency of continuous regional intra-arterial infusion (CRAI) with antisecretory agents and antibiotics in the treatment of infected pancreatic necrosis. Materials and methods: CRAI was used as a new clinical technique to treat acute pancreatitis patients during a 4-year period at the First Affiliated Hospital, Wenzhou Medical College, China. In this retrospective study, thirty-four patients with proven infected pancreatic necrosis were included. Twelve patients were treated with CRAL and were matched according to age, sex, APACHE II scores, Ranson scores and remote organ dysfunction, with 22 patients with IPN treated surgically. The clinical outcome following surgery and CRAI were compared. Results: No difference was found between the two groups when comparing age, gender, APACHE II scores, Ranson scores and remote organ dysfunction (p > 0.05). The patients treated with CRAI had a lower incidence of complications (33.3% vs 72.7%), duration of hospitalization (27.1 +/- 4.7 days vs 43.0 +/- 12.0 days) and cost of hospitalization (4.09 +/- 1.64 thousand RMB vs 8.77 +/- 3.74 thousand RMB) as compared to patients treated with surgery (p < 0.05). The survival rate was significantly higher in the CRAI group as compared to the surgical group (91.7% vs 63.6%; p < 0.01). However, the two groups had similar rates of concomitant operative treatment and incidence of remote organ dysfunction (p > 0.05). Conclusions: CRAI or CRAI in combination with abscess drainage seemingly improve the clinical outcome in patients with infected pancreatic necrosis. Further confirmative prospective randomized multicenter studies are warranted prior to broad introduction of the CRAI concept. Copyright (C) 2013, IAP and EPC. Published by Elsevier India, a division of Reed Elsevier India Pvt. Ltd. All rights reserved.
|
|
