Obstructive Chronic Pancreatitis Research Articles

Chronic Pancreatitis or Pancreatic Tumor? A Problem-solving Approach

Certain inflammatory pancreatic abnormalities may mimic pancreatic ductal adenocarcinoma at imaging, which precludes accurate preoperative diagnosis and may lead to unnecessary surgery. Inflammatory conditions that may appear masslike include mass-forming chronic pancreatitis, focal autoimmune pancreatitis, and paraduodenal pancreatitis or "groove pancreatitis." In addition, obstructive chronic pancreatitis can mimic an obstructing ampullary mass or main duct intraductal papillary mucinous neoplasm. Secondary imaging features such as the duct-penetrating sign, biliary or main pancreatic duct skip strictures, a capsulelike rim, the pancreatic duct-to-parenchyma ratio, displaced calcifications in patients with chronic calcific pancreatitis, the "double duct" sign, and vessel encasement or displacement can help to suggest the possibility of an inflammatory mass or a neoplastic process. An awareness of the secondary signs that favor a diagnosis of malignant or inflammatory lesions in the pancreas can help the radiologist to perform the differential diagnosis and determine the degree of suspicion for malignancy. Repeat biopsy or surgical resection may be necessary to achieve an accurate diagnosis and prevent unnecessary surgery for inflammatory conditions. Online supplemental material and DICOM image stacksare available for this article. ©RSNA, 2019.

Endoscopic ultrasonography with fine needle aspiration (EUS-FNA) is the diagnosis of choice of metastatic disease of unknwon primary site

and study aims: Chronic pancreatitis is associated with recurrent or persistent abdominal pain over the course of the disease. Ductal hypertension showing obstructed and dilated pancreatic duct has been suggested as a major factor in the mechanism of pain in chronic pancreatitis. Many studies investigating pain relief after endoscopic treatment of pancreatic duct (PD) are available, but the number of studies regarding the morphological changes to pancreas such as changes in PD caliber, pancreatic parenchyma, and especially pancreatic volume is far fewer. As such, we analyzed the changes of ductal caliber and parenchymal volume after endoscopic treatment of PD in patients with obstructive chronic pancreatitis.In this retrospective study, we compared two groups of patients with obstructive chronic pancreatitis that either received endoscopic management of PD or conservative treatment without such endoscopic management. After we obtained age, sex, etiology of chronic pancreatitis, diabetic status, smoking and alcohol abuse status from the database, we compared the incidence for changes in pancreatic parenchymal volume and PD caliber between two groups.In our study population, total of 480 patients was diagnosed with chronic pancreatitis between January 2006 and December 2016, and 166 (34.5%) of these patients were diagnosed with obstructive chronic pancreatitis with obstructed and dilated PD. After reviewing the population with the exclusion criteria, 71 patients were available for the final analysis. 28 of those patient received endoscopic treatment of pancreatic duct and 43 received conservative treatment without any endoscopic treatment of PD. Statistical analysis with Cox proportional hazards models showed that diabetes and endoscopic PD management were significant predictors for progression of PD caliber and in pancreatic parenchyma, and that only PD management influenced the pancreatic volume loss.Endoscopic management of PD in obstructive chronic pancreatitis have advantages on morphologic change such as pancreatic volume loss and progression of PD caliber in long follow-up period.

Pancreas Proapoptotic Proteases in Patients with Chronic Pancreatitis

Aim. To study features of localization of the DNA-ase I and endonuclease-G proapoptotic proteases in the pancreas in chronic pancreatitis (CP). Materials and methods. Histological pancreas preparations from 60 patients with various CP forms were studied: group I — 10 patients with obstructive CP; group II — 21 patients with calcific CP; group III — 13 patients with fibroparenchymal CP; group IV — 16 patients with CP complicated by pseudocyst. Pancreas biopsies were obtained during planned organ operations, as well as using a fine-needle biopsy under ultrasound control. Tissue material was fixed in Bowen medium. Microscopic tissue sections were prepared and subsequently stained with hematoxylin-eosin and by Mallory-Slinchenko. Immunohistochemical typing of proapoptotic proteases was performed according to the indirect avidin-streptavidin-peroxidase reaction (“Elite”, USA) using rabbit antibodies to DNA-I and endonuclease-G (“Chemicon”, USA, 1: 500 dilution — 1: 2000, incubation 12:00, + 4 °С).Results. Patients in all the groups demonstrated signs of chronic inflammation, with 31.7 % of cases showing signs of its exacerbation. Atrophic changes were found in most patients (96.7 %). No significant differences were observed with regard to the severity and frequency of fibrosis of various degrees in the groups: mild, moderate, severe and full fibrosis was detected in 6.7 %, 20.0 %, 16.7 % and 56.6 %, respectively. The study of the localization of proapoptotic nucleases in the structures of the pancreas showed proapoptotic nucleases of DNA-ase I to be exclusively located in the cytoplasm of pancreatic acinar cells. At all stages of CP fibrosis, single acinar cells with translocation of the nuclease from the cytoplasm into the cell nucleus were found in the lobes of the pancreas. Endonuclease-G was found in large numbers in the cytoplasm of pancreatic islets, with it lower number being detected in the cytoplasm of the epithelial cells of the ducts. Conclusions. In CP, proapoptotic proteases of DNase I and endonuclease G are expressed in the cytoplasm of cells located in different pancreas zones. Thus, DNase I is expressed in the cytoplasm of acinar cells, while endonuclease G is most typical for insular cells and those in the epithelium of the ducts. This proves the existence of various apoptosis mechanisms in the exo- and endocrine portions of the pancreas.

Low Serum Trypsin Levels Predict Deep Pancreatic Cannulation Failure During Endoscopic Retrograde Cholangiopancreatography in Patients With Symptomatic Obstructive Chronic Pancreatitis

Deep pancreatic cannulation (DPC) failure during endoscopic retrograde cholangiopancreatography (ERCP) in patients with chronic pancreatitis (CP) can occur in the presence of ductal obstruction due to strictures and/or stones. There are currently no simple preprocedure clinical or laboratory tests that can predict DPC failure during ERCP. All adult patients with definite CP by M-ANNHEIM criteria referred to the pancreatitis clinic between 2010 and 2017 were evaluated. Serum trypsin levels were obtained to assess the morphologic severity of disease and/or exocrine insufficiency. Univariable and multivariable logistic regression analyses were performed to identify factors associated with DPC failure. There were 346 patients, of whom 100 underwent trypsin measurements and ERCP for symptomatic CP. Deep pancreatic cannulation failure occurred in 32 (32%). There were no significant differences with regard to age, sex, etiology, smoking, and alcohol use. Deep pancreatic cannulation failure was more likely to occur in patients with low trypsin levels (53.1% vs 25%, P = 0.007) compared with those with successful DPC. Low trypsin levels were independently associated with DPC failure in adjusted analysis (odds ratio, 3.7; 95% confidence interval, 1.2-11; P = 0.02). Low serum trypsin levels independently predict DPC failure during ERCP in patients with symptomatic obstructive CP.

Smoking as a factor of immune deficiency deepening in patients with chronic obstructive pulmonary disease and chronic pancreatitis

The objective of the work – to study the state of humoral link of the immune system in patients with chronic pancreatitis with concomitant COPD and without it. There were examined 90 patients with COPD in combination with chronic pancreatitis (45 women and 45 men) aged 35–86 years, mean age – (56.42 ± 4.11 years) and 43 – with chronic pancreatitis. Among the examined individuals there were 32 persons with chronic pancreatitis and COPD I st. (35.5 %), and 58 persons with chronic pancreatitis and COPD II st. (64.5 %). Duration of the disease – from 1 to 25 years, the combination of diseases – from 1 to 10 years. There were 20 (22.2 %) active smokers among surveyed patients. The duration of the smoking 10–30 years, middle duration – (22.75 ± 1.20) years. The smoking experience of 9 patients was 10–20 packs/years, 11 – more than 20 pack/years. Methods of examination: general clinical, laboratory, instrumental, questioning, testing, statistical methods. In patients with chronic pancreatitis without COPD, the level of all studied classes of Ig was significantly increased (IgG 10.4 %, IgA 13.1 %, IgM 45.9 %; P < 0.05). Disbalance in immunoglobulines level was detected in patients with COPD with a significant decrease (P < 0.05) in IgG and IgA levels (by 7.9 % and 27.3 % respectively) and IgM increased (by 76.7 %). This indicates an imbalance in the functioning of the cellular immune system with the formation of a secondary immune deficiency. The increase in the level of immune complexes in both groups (2.6 and 3.2 times, respectively) showed the presence of torpid inflammatory process in COPD. The presence of tobacco smoking in patients with chronic pancreatitis and COPD significantly deepened the changes in the immune system in comparison with non-smokers.

СORRECTION OF MALNUTRITION IN PATIENTS WITH CHRONIC PANCREATITIS

Aim:To estimate the frequency of occurrence malnutrition and efficacy its correction in chronic pancreatitis (CP).Materials and methods:148 patients were examined. Group I included 71 people with chronic alcoholic pancreatitis (CAP); group II — 77 patients with chronic obstructive pancreatitis (COP). Trophological status (TS) was investigated by criteria of V.M. Luft. Lymphocytes, pancreatic amylase, lipase, total protein, albumin, urine diastase and faecal elastase-1 were investigated before and after treatment. Two treatment options were used: combination therapy (CT, (Mezym-forte 10500 USP/day and pharmaconutrient Ensure 2 200 ml/day)) and high-dose pancreatic enzyme replacement therapy ((HD PERT), Kreon 120000 USP/day) for 10 weeks. 62 patients received HD PERT: 24 patients with CAP and 38 patients with COP; CT — 86 patients: 47 and 39, respectively.Results:The prevalence of malnutrition in patients with CP was 92% (n=136). Lymphopenia was determined in 44%, hypoproteinemia-in 11,5%, hypoalbuminemia-in 54%. 12 (8%) patients did not have malnutrition. In the group CAP: mild malnutrion was established in44, moderate — in 20, severe — 2, eutrophia — 6; in the group COP: mild malnutrion — in 33, moderate — in 37, severe — 0, eutrophia — 6. Aftertreatment in the group CAP: malnutrion moderate — in 7, mild — 58, eutrophia — 7, in the COP: malnutrion moderate — 37, mind — 31, eutrophy — 8.Conclusions:Malnutrition is frequent symptom complex in patients with CP. The severity of malnutrition is more severy in CAP. The most effective treatment malnutrition was CT in patients with CAP. HD PERT is indicated to correct exocrine pancreatic insufficiency.

Differential Cell Susceptibilities to KrasG12D in the Setting of Obstructive Chronic Pancreatitis.

Background & AimsActivating mutation of the KRAS gene is common in some cancers, such as pancreatic cancer, but rare in other cancers. Chronic pancreatitis is a predisposing condition for pancreatic ductal adenocarcinoma (PDAC), but how it synergizes with KRAS mutation is not known.MethodsWe used a mouse model to express an activating mutation of Kras in conjunction with obstruction of the main pancreatic duct to recapitulate a common etiology of human chronic pancreatitis. Because the cell of origin of PDAC is not clear, Kras mutation was introduced into either duct cells or acinar cells.ResultsAlthough KrasG12D expression in both cell types was protective against damage-associated cell death, chronic pancreatitis induced p53, p21, and growth arrest only in acinar-derived cells. Mutant duct cells did not elevate p53 or p21 expression and exhibited increased proliferation driving the appearance of PDAC over time.ConclusionsOne mechanism by which tissues may be susceptible or resistant to KRASG12D-initiated tumorigenesis is whether they undergo a p53-mediated damage response. In summary, we have uncovered a mechanism by which inflammation and intrinsic cellular programming synergize for the development of PDAC.

Early surgery versus current step-up practice for chronic pancreatitis: a multicenter randomized controlled trial

Background: Surgical intervention for patients with chronic pancreatitis is currently used as last resort treatment when both medical and endoscopic treatment have failed. We conducted a randomized controlled trial to compare early surgery with the current step-up approach. Methods: We included patients with obstructive chronic pancreatitis and severe pain, who recently started using opioids. Patients with strong opioids for >2 months or weak opioids for >6 months were excluded. Patients were randomized to early surgery (i.e. within 6 weeks) or to the step-up approach (medical treatment, endoscopy if needed, surgery if needed). Primary endpoint was the mean Izbicki pain score. Results: Eighty-eight patients were randomized, 44 to early surgery (41 underwent surgery) and 44 to the step-up approach. Patients in the early surgery group had a lower Izbicki pain score during follow-up compared to patients in the step-up approach (35 vs. 48, P= 0.018). Pain relief during follow-up was achieved in 54% of patients in early surgery and in 33% of patients in the step-up approach (P< 0.001). Fewer interventions were performed in the early surgery group (median 1 vs. 3, P< 0.001). Complications, mortality (0%), hospital admissions, pancreatic function and quality of life were comparable among groups. Conclusions: The preferred treatment strategy for patients with chronic pancreatitis and a dilated pancreatic duct is early surgery within the first months of opioid use, because this provides better pain control with less interventions than the current step-up approach.

Low serum trypsin levels predict deep pancreatic cannulation failure during ERCP in patients with symptomatic obstructive chronic pancreatitis

Advances in cell and molecular biology studies have revolutionized the diagnosis and treatment of many different diseases. Cell and molecular diagnostics (CMD) have become an essential part of investigations required in providing optimal care and has become an important tool for the health care providers for better treatment. CMD gives insights into the pathogenesis and prognosis of various diseases. Rapid technological advances have helped to increase the speed and performance of various molecular assays thereby reducing turnaround time, in turn translating to providing better clinical services. With the increase in CMD applications to clinical services, entire world has seen a sudden spurt of cellular and molecular labs. However, this has highlighted an acute shortage of trained laboratory personnel who can carry out cellular or molecular assays in a diagnostic mode. Understanding the mechanisms of disease at the molecular and genetic levels can now be translated into diagnostic, prognostic, and therapeutic applications in modern medicine. Molecules at abnormal levels (quantitative or qualitative) provide not only a signature for the presence of a disease, but also the indication for a drug targeting the specific abnormal function. Concurrently, the role of CMD has expanded from mere study observations to constantly translating new discoveries and novel technologies into useful clinical tests that provide a molecular fingerprint of diseases and that are predictive of the response. In the introductory chapter we will cover the importance of biological sample collection from different methods; cell-based diagnostic methods, cellular pathway diagnostic targets, and molecular-based methods.

Mo1324 - Is Obstructive Chronic Pancreatitis Due to Necrotizing Pacreatitis Different from other Obstructive Chronic Pancreatitis? A Large Recent Series of 176 Patients with this Uncommon Entity

Mo1324 - Is Obstructive Chronic Pancreatitis Due to Necrotizing Pacreatitis Different from other Obstructive Chronic Pancreatitis? A Large Recent Series of 176 Patients with this Uncommon Entity

P.04.6: Endoscopic vs Surgical for the Management of Pain for Obstructive Chronic Pancreatitis: A Systematic Review and Meta-Analysis

P.04.6: Endoscopic vs Surgical for the Management of Pain for Obstructive Chronic Pancreatitis: A Systematic Review and Meta-Analysis

Clinical response to dorsal duct drainage via the minor papilla in refractory obstructing chronic calcific pancreatitis.

Background and study aims Complete stone removal from the main pancreatic duct might not be achieved in all patients with obstructive chronic calcific pancreatitis. We report our results for endoscopic dorsal pancreatic duct (DPD) bypass of obstructing stones in the ventral pancreatic duct (VPD). Patients and methods 16 patients with obstructive chronic calcific pancreatitis were treated with a DPD bypass. Clinical success was defined as significant pain relief and no hospital admissions for pain management during the ongoing treatment period. Results Among 16 patients meeting entry criteria, 10 (62.5 %) had a history of unsuccessful endoscopic therapy, and 8 had failed extracorporeal shockwave lithotripsy (ESWL). Clinical success was achieved in 12 patients (75 %). Among these responders, 10 patients (83.3 %) had markedly improved or complete pain relief after the first stent placement, which persisted throughout the follow-up period; 11 patients (91.7 %) were able to discontinue their daily analgesics. Conclusions In selected patients with obstructive chronic calcific pancreatitis, the DPD bypass may be considered as a rescue endoscopic therapy, potentially obviating the need for surgery when standard endoscopic methods and ESWL fail.

Abstract B19: Kras mutation imparts neoplastic potential on duct cells but not acinar cells in a mouse model of obstructive chronic pancreatitis

Abstract Understanding the progression of human pancreatic cancer is difficult due to the late stage of diagnosis of this deadly disease. We must therefore rely upon robust model systems to understand how pancreatic cancer arises, how its acute and chronic phases of progression are regulated, and how best to identify and treat it, hopefully still in the early stage. Models of pancreatic ductal adenocarcinoma (PDAC) that accurately reflect human disease are still being developed. To mimic human disease, PDAC must arise from mutations occurring in adult animals and with etiologies relevant to humans. We developed a new mouse model that incorporates obstructive chronic pancreatitis with tissue-specific, adult-onset expression of mutant Kras. We found that KrasG12D expression in duct cells but not in acinar cells led to progression of metaplastic ducts to eventual dysplasia and cancer. In early-stage disease, Kras mutation in acinar cells led to increased acinar-to-ductal metaplasia but did not downregulate p53, thus leading to reduced cell survival. Ducts naturally express much lower p53 levels, however, and there was increased survival of KrasG12D-mediated, duct-derived metaplastic cells. Furthermore, acinar cells upregulated Pdx1 during acinar-to-ductal metaplasia while duct cells did not do so during their metaplastic transition. Without chronic pancreatitis, Kras mutation in acinar cells causes abundant Pancreatic Intraepithelial Neoplasm (PanIN)-like lesions. However, overexpression of Pdx1 in acinar cells in this context permitted acinar-to-ductal metaplasia but prevented PanIN-like lesion formation, suggesting that Pdx1 can repress neoplastic progression. In summary, in the setting of obstructive chronic pancreatitis, ducts are the principal source of cancer development via reduced Pdx1 and p53 levels and increased cell survival. Citation Format: Fong C. Pan, Jessica N. Kim, Chanjuan Shi, Mary K. Washington, Maike Sander, Maureen Gannon, Robert D. Beauchamp, Christopher V. Wright, Anna L. Means.{Authors}. Kras mutation imparts neoplastic potential on duct cells but not acinar cells in a mouse model of obstructive chronic pancreatitis. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; 2016 May 12-15; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2016;76(24 Suppl):Abstract nr B19.

How do outcomes compare after endoscopic or surgical intervention in people with painful obstructive chronic pancreatitis?

How do outcomes compare after endoscopic or surgical intervention in people with painful obstructive chronic pancreatitis?

Channel Gating Regulation by the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) First Cytosolic Loop

In this study, we present data indicating a robust and specific domain interaction between the cystic fibrosis transmembrane conductance regulator (CFTR) first cytosolic loop (CL1) and nucleotide binding domain 1 (NBD1) that allows ion transport to proceed in a regulated fashion. We used co-precipitation and ELISA to establish the molecular contact and showed that binding kinetics were not altered by the common clinical mutation F508del. Both intrinsic ATPase activity and CFTR channel gating were inhibited severely by CL1 peptide, suggesting that NBD1/CL1 binding is a crucial requirement for ATP hydrolysis and channel function. In addition to cystic fibrosis, CFTR dysregulation has been implicated in the pathogenesis of prevalent diseases such as chronic obstructive pulmonary disease, acquired rhinosinusitis, pancreatitis, and lethal secretory diarrhea (e.g. cholera). On the basis of clinical relevance of the CFTR as a therapeutic target, a cell-free drug screen was established to identify modulators of NBD1/CL1 channel activity independent of F508del CFTR and pharmacologic rescue. Our findings support a targetable mechanism of CFTR regulation in which conformational changes in the NBDs cause reorientation of transmembrane domains via interactions with CL1 and result in channel gating.

Epithelial Anion Transport as Modulator of Chemokine Signaling.

The pivotal role of epithelial cells is to secrete and absorb ions and water in order to allow the formation of a luminal fluid compartment that is fundamental for the epithelial function as a barrier against environmental factors. Importantly, epithelial cells also take part in the innate immune system. As a first line of defense they detect pathogens and react by secreting and responding to chemokines and cytokines, thus aggravating immune responses or resolving inflammatory states. Loss of epithelial anion transport is well documented in a variety of diseases including cystic fibrosis, chronic obstructive pulmonary disease, asthma, pancreatitis, and cholestatic liver disease. Here we review the effect of aberrant anion secretion with focus on the release of inflammatory mediators by epithelial cells and discuss putative mechanisms linking these transport defects to the augmented epithelial release of chemokines and cytokines. These mechanisms may contribute to the excessive and persistent inflammation in many respiratory and gastrointestinal diseases.

Diffusion-weighted MR imaging of pancreatic cancer and inflammation: Prognostic significance of pancreatic inflammation in pancreatic cancer patients.

Pancreatic cancer often accompanies chronic obstructive pancreatitis (COP) due to obstruction of the main pancreatic duct, and the inflammatory environment may enhance cancer progression. The purpose of this study is to evaluate COP using the apparent diffusion coefficient (ADC) value measured by diffusion-weighted MR imaging (DWI), and to assess its prognostic significance in pancreatic cancer. Twenty-eight patients (16 men, 12 women; mean age 67.1 years) with pancreatic cancers who underwent DWI followed by curative surgery were evaluated. The ADC value of pancreatic parenchyma upstream to the tumor (upstream pancreas) was measured and compared with the upstream pancreatic duct dilatation to assess whether DWI could reflect COP. The ADC values of tumor and upstream portion were compared with overall survival (OS) using Cox regression and Kaplan-Meier analysis. The ADC value of upstream pancreas was significantly lower in patients with greater dilated pancreatic duct than those with less (P = 0.03). In univariate Cox regression analysis, the ADC value of upstream pancreas showed a significant association with OS (P = 0.01), but that of tumor did not (P = 0.06). In Kaplan-Meier analysis, patients with lower ADC value of upstream pancreas (<1.36 × 10(-3) mm(2)/s) were significantly associated with poor OS (P = 0.0006). In multivariate analysis, the ADC value of upstream pancreas was identified as an independent prognostic factor (P = 0.01; hazards ratio, 0.05; 95% CI, 0.004-0.59). The ADC value of upstream pancreas was an independent prognostic factor for OS in pancreatic cancer patients. Inflammatory environment may play an important role in pancreatic cancer progression.

Influence of exogenous glutathione on the system of antioxidant protection of the body in case of comorbid course of chronic obstructive pulmonary disease and chronic pancreatitis

Aim. To study the condition of oxidant-antioxidant system in patients with comorbid course of chronic obstructive pulmonary disease (COPD) and chronic pancreatitis (CP) with oral administration of glutathione. Methods and results. 60 patients with COPD (GOLD1-2, В stage) were examined in the phase of non-infectious exacerbation with comorbid CP in the phase of exacerbation were divided into 2 groups. The main group (2, M) received therapy with hepaval (reduced glutathione per 250 mg twice a day) during 30 days. A tendency to increased activity of reduced glutathione in 1,2 and 1,6 times in the control and main groups was observed (р<0,05). Conclusion. Treatment with hepaval promotes intensity of LPO processes decrease and restoration of the main factor of the antioxidant protective system in the blood – reduced glutathione.

Secretin-stimulated MR cholangio-pancreatography and pathological correlative study in a swine obstructive chronic pancreatitis model

Objective To investigate the correlativity between secretin-stimulated magnetic resonance cholangiopancreatography (sMRCP) findings and pathological severity in a swine chronic pancreatitis (CP) model. Methods Thirty-nine swine were divided randomly into control group (n= 12) and experimental group (n= 27). In experimental group, the main pancreatic duct (MPD) was incompletely ligated to establish the model of obstructive CP. In control group, laparotomy was performed but without ligating the MPD. At the 4th, 8th and 12th week after modeling, one third swine of each group were undergone a series of dynamic sMRCP scans before (0 min) and at 1, 3, 5, 7, 9, 11 min after administration of secretin (0.6 μg/kg). And the MPD diameter and duodenum filling (DF) degree were measured. All survivals were sacrificed to pathological examination including HE and Van Gieson staining for histopathological grading. According to pathological severity, swine were divided into normal group, mild CP group and moderate to severe CP group. MRI features and indexes, including baselined diameter (BD), end diameter (ED), maximum diameter (MD), the largest expansion rate (LER), time to peak (Tpeak) and end change rate of pancreatic duct and duodenal filling (DF) scores were measured. The relationships between pathological grading and sMPCP indexes were analysed. The comparison of sMRCP data among the 3 groups were used ariance analysis, χ2 test and U test. Correlations between sMPCP indexes and pathological severity were tested using Spearman rank correlation coefficients. The diagnostic efficiency of sMRCP indexes were evaluated by ROC method. Results (1) In experimental group, 22 CP models were established and 19 CP swine (mild CP, n= 8; moderate and severe CP, n=11) were performed sMRCP successfully. Eleven swine in normal group were obtained satisfactory MRCP images. (2) sMRCP results: BD of 3 groups were (1.56±0.46),(2.95±1.17),(7.41±1.91) mm, respectively. ED were (1.49±0.31),(2.96±1.17) and (7.37±1.90) mm, respectively. MD were (2.39±0.43),(3.91±1.27) and (7.86±1.87)mm, respectively. The median of LER were 42.10%, 34.85% and 6.58%, respectively. The median of DF scores were 3, 3, 2, respectively. The differences of above indexes have statistically significance (P values were all 0.05) ,and no correlation with pathological severity(P values were all>0.05) .For differential diagnosis between normal and mild CP, the area under ROC of BD, ED, MD, LER and DFscores were 0.915, 0.977, 0.926, 0.778 and 0.472, respectively and differential diagnosis between mild CP and moderate to severe CP group, the area under ROC were 0.966,0.966,0.960,1.000 and 0.915, respectively. Conclusions sMRCP findings of CP have characteristics and could be used for in vivo evaluation on the CP pathologic grades. Key words: Pancreatitis, chronic; Models, animal; Magnetic resonance imaging

Obstructive chronic pancreatitis secondary to a duodenal duplication cyst containing the ampulla

s / Pancreatology 15 (2015) e1ee17 e10 brush cytology of the common bile duct was negative for malignancy. Tumor markers were negative and IgG4 levels were not measured. Results: A cephalic pancreaticoduodenectomy was performed and a pancreatic head tumor was found. Histology revealed plasmacytic infiltration of the pancreatic parenchyma, gallbladder and bile and cystic ducts with a predominance of IgG4-positive plasma cells (90/high-power field). Final diagnosis was a lymphoplasmacytic sclerosing pancreatitis with biliary involvement. Discussion: IgG4-associated cholangitis is a rare type of AIP associated with bile duct involvement with or without pancreatic affection that responds well to steroids therapy, so it is important to rule out AIP in the diagnostic work-up of an EC to avoid unnecessary surgeries.