Findings Of Chronic Pancreatitis Research Articles

How Are Imaging Findings Associated with Exocrine Insufficiency in Idiopathic Chronic Pancreatitis?

Aim The aim is to study the association between imaging findings in chronic pancreatitis and fecal elastase 1 (FE1) in patients with idiopathic chronic pancreatitis (ICP). Methods In this retrospective study on a prospectively maintained database of patients with ICP, a radiologist blinded to clinical and laboratory findings reviewed CT and/or MRI. Findings were documented according to recommendations of the Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer, October 2018. Low FE1 (<100 μg elastase/g) was considered diagnostic of pancreatic exocrine insufficiency (PEI). Association between imaging findings and FE1 was studied. Results In total, 70 patients (M: F = 37:33) with ICP with mean age of 24.2 (SD 6.5) years, range 10 to 37 years and mean disease duration of 5.6 (SD 4.6) years, range 0 to 20 years were included. Mean FE level was 82.5 (SD 120.1), range 5 to 501 μg elastase/g. Mean main pancreatic duct (MPD) caliber was 7 (SD 4) mm, range 3 to 21 mm and mean pancreatic parenchymal thickness (PPT) was 13.7 (SD 5.5) mm, range 5 to 27 mm. There was a significant association between FE1 and MPD size, PPT, type of pancreatic calcification; presence of intraductal stones, side branch dilatation on magnetic resonance cholangiopancreatography and extent of pancreatic involvement ( p <0.05). In total, 79%, 86%, and 78% with moderate to severe MPD dilatation, pancreatic atrophy, and side branch dilatation had low FE1, respectively. But nearly half of those with no or mild structural abnormality on imaging had low FE1. Conclusion Significant association between FE1 and specific imaging findings demonstrates its potential as a marker of exocrine insufficiency and disease severity in chronic pancreatitis. But imaging and FE1 are complementary rather than supplementary.

Pancreatic fibrosis, acinar atrophy and chronic inflammation in surgical specimens associated with survival in patients with resectable pancreatic ductal adenocarcinoma

BackgroundPancreatic ductal adenocarcinoma (PDAC), one of the most lethal malignancies, is increasing in incidence. However, the stromal reaction pathophysiology and its role in PDAC development remain unknown. We, therefore, investigated the potential role of histological chronic pancreatitis findings and chronic inflammation on surgical PDAC specimens and disease-specific survival (DSS).MethodsBetween 2000 and 2016, we retrospectively enrolled 236 PDAC patients treated with curative-intent pancreatic surgery at Helsinki University Hospital. All pancreatic transection margin slides were re-reviewed and histological findings were evaluated applying international guidelines.ResultsDSS among patients with no fibrosis, acinar atrophy or chronic inflammation identified on pathology slides was significantly better than DSS among patients with fibrosis, acinar atrophy and chronic inflammation [median survival: 41.8 months, 95% confidence interval (CI) 26.0–57.6 vs. 20.6 months, 95% CI 10.3–30.9; log-rank test p = 0.001]. Multivariate analysis revealed that Ca 19–9 > 37 kU/l [hazard ratio (HR) 1.48, 95% CI 1.02–2.16], lymph node metastases N1–2 (HR 1.71, 95% CI 1.16–2.52), tumor size > 30 mm (HR 1.47, 95% CI 1.04–2.08), the combined effect of fibrosis and acinar atrophy (HR 1.91, 95% CI 1.27–2.88) and the combined effect of fibrosis, acinar atrophy and chronic inflammation (HR 1.63, 95% CI 1.03–2.58) independently served as unfavorable prognostic factors for DSS. However, we observed no significant associations between tumor size (> 30 mm) and the degree of perilobular fibrosis (p = 0.655), intralobular fibrosis (p = 0.587), acinar atrophy (p = 0.584) or chronic inflammation (p = 0.453).ConclusionsOur results indicate that the pancreatic stroma is associated with PDAC patients’ DSS. Additionally, the more severe the fibrosis, acinar atrophy and chronic inflammation, the worse the impact on DSS, thereby warranting further studies investigating stroma-targeted therapies.

Healthy pancreatic parenchymal volume and its relationship to exocrine function.

Pancreatic atrophy as a finding of chronic pancreatitis has largely been a subjective finding. Cross-sectional imaging should provide a means to quantify pancreatic atrophy. The purposes of this study were to: (1) quantify pancreatic volume by magnetic resonance imaging (MRI) in a cohort of children without pancreatic disease, (2) define predictors of pancreatic volume and (3) assess the relationship between pancreatic volume and pancreatic fluid secretion. This study involved further analysis of data collected as part of an institutional review board-approved prospective study of secreted fluid volume in response to secretin in 50 healthy children ages 6-16years. The pancreas was manually segmented on axial MR images to calculate pancreatic volume. Pearson correlation or the Student's t-test were used to define associations between pancreatic volume and patient characteristics and previously calculated secreted fluid volume. Quantile regression was used to define the 5th percentile for pancreatic volume based on body surface area (BSA) [1]. Mean pancreatic volume was 46.0±18.8mL with no significant difference based on sex (boys: 42.4±19mL, girls: 49.1±18.3mL, P=0.21). Pancreatic volume was moderately correlated with age (r=0.51, P=0.002) and strongly correlated with BSA (r=0.75, P<0.0001), with the 5th percentile for pancreatic volume defined by: (24.66×BSA) - 4.97. Pancreatic volume was moderately correlated with volume of fluid secreted after secretin administration (r=0.51, P=0.0002). We report increasing pancreatic volumes by MRI during childhood in a cohort of children without pancreatic disease. We have also shown that pancreatic volume is associated with secreted fluid volume as measured by MRI.

Primary squamous cell carcinoma of head of the pancreas

Primary pancreatic malignancy with pure squamous cell histology is extremely rare and has aggressive behavior with poor prognosis. The management of primary squamous cell carcinoma of the pancreas (SCCP) is poorly defined due to the paucity of data. Preoperative histological diagnosis is difficult in the majority of cases. Curative resection is the main stay of treatment, but most of the cases were found inoperable due to delayed diagnosis and dissemination of the disease at the time of initial diagnosis. Herein, we report a case of primary SCCP in a 44-year-old female located at the head of the pancreas. Her contrast-enhanced computed tomography (CECT) scan image had the findings of pancreatic head mass along with the features of atrophic pancreatitis. Whipple's procedure was performed successfully for the case with the postoperative pathological staging of PT2N0CM0 and chronic pancreatitis. However, the patient died due to sepsis on the 32nd postoperative day. The presence of atrophic pancreatitis on CECT scan and postoperative pathological findings of chronic pancreatitis suggested the development of squamous metaplasia followed by subsequent development of SCCP.

Normal pancreatic parenchymal thickness by CT in healthy children.

Chronic pancreatitis is increasingly recognized in the pediatric population. Atrophy is an important, but qualitative, finding of chronic pancreatitis. To transition to a quantitative measure that can specifically define atrophy requires knowledge of normal pancreatic parenchymal bulk in children. The purpose of this study was to define normal pancreatic thickness (linear measurements) at multiple anatomic locations in the pancreas of healthy children. This was an Institutional Review Board-approved, Health Insurance Portability and Accountability Act (HIPAA)-compliant retrospective study. Three reviewers measured the thickness of the pancreas at four locations (head, neck, body, tail) on computed tomography (CT) examinations performed with intravenous contrast in children without a history of pancreatic disease. Measurements were made on 140 examinations, evenly distributed among 7 age groups (3-16.99years) with 10 males and 10 females in each group. Agreement and bias between reviewers were assessed by intra-class correlation coefficients (ICC) and Bland-Altman analyses. Correlation with age, height and weight were assessed with Spearman's rho (ρ). The mean (for 3 readers) thicknesses of the head, neck, body and tail were 1.3-2cm, 0.7-1cm, 0.9-1.6cm and 1-1.6cm, respectively, depending on patient age. Measurement agreement between reviewers was fair to good (ICC: 0.52-0.7). Bias between reviewers ranged from 0 to 3mm. Pancreatic thickness was weakly to moderately correlated with age (ρ=0.39-0.52), height (ρ=0.44-0.61) and weight (ρ=0.51-0.64). We have defined normal ranges for thickness of the pancreas at four locations, and have shown that these measurements depend on patient age and size. These data may be useful to more objectively define pancreatic atrophy in children with suspected pancreatic disease.

Role of faecal elastase in predicting echoendoscopic findings in chronic pancreatitis

Role of faecal elastase in predicting echoendoscopic findings in chronic pancreatitis

Annular Pancreas: Endoscopic and Pancreatographic Findings From a Tertiary Referral ERCP Center

Introduction: Annular pancreas is a congenital anomaly whereby pancreatic tissue encircles the duodenum. Current knowledge of endoscopic findings of annular pancreas has been limited to small case series. The aim of this study is to describe the endoscopic and pancreatographic findings of patients with annular pancreas at a large tertiary care ERCP center. Methods: This is a retrospective observational study. Our institutional prospective ERCP database was queried for cases of annular pancreas. The electronic medical record was searched for patient and procedure-related data. Technical success was defined as completion of intended imaging and therapy. Results: From 1/1/94 - 12/31/16, 46 patients with annular pancreas underwent ERCP at our medical center. Indications for ERCP were: chronic abdominal pain (suspicion of sphincter of Oddi dysfunction, n=20, 42.6%), history of acute pancreatitis or recurrent acute pancreatitis (n=16, 34.8%), elevated liver tests (n=10, 21.7%) or other (n=11, 23.9%). The majority of patients were female (n=33, 71.7%) and Caucasian (n=40, 87.0%). The mean age at index ERCP was 46.3 ± 17.2 years. Index ERCP was technically successful in 40 patients (87.0%) and technical success was achieved in 45 patients (97.8%) after two attempts. Pancreatobiliary neoplasia was identified in 7 patients (17.9%). A duodenal narrowing or ring (Fig. 1) was found in the majority of patients (n=39, 84.8%), yet only 2 (4.3%) had retained gastric contents. Pancreas divisum was found in 21 patients (45.7%), 18 being complete divisum. The annular branch was visualized on pancreatogram in 34 patients (73.9%), arising from the ventral pancreatic duct (Fig. 2) in 30 of those 34 patients (88.2%). There were findings of chronic pancreatitis in 15 patients (32.6%) noted at the index ERCP.Figure: Endoscopic image of circumferential narrowing of duodenum in a patient with annular pancreas, with minor papilla noted (yellow arrow) on rim of annulus.Figure: Pancreatogram demonstrating annular ring (yellow arrows), with otherwise normal ductal anatomy (i.e. no pancreas divisum).Conclusion: This is the largest series to date describing the endoscopic and pancreatographic findings of patients with annular pancreas. It demonstrates that patients with annular pancreas who undergo ERCPs are mostly adults. While children with annular pancreas may undergo surgery for upper GI obstructive symptoms, adults appear to present with pancreatobiliary pathology. We found that 45.7% of patients had concurrent pancreas divisum, consistent with prior literature. Nearly one-third of patients had findings of chronic pancreatitis at the time of index ERCP and incidence of pancreatobiliary neoplasia was nearly 18%. It is unclear whether these may be features of the natural history of annular pancreas.

Role of faecal elastase in predicting echoendoscopic findings in chronic pancreatitis

The elevation of insulin-like growth factor 1 (IGF-1) and adipokine retinol-binding protein 4 (RBP-4) is known to be associated with the risk of many cancers. The aim of this study was to evaluate the serum concentrations of IGF-1 and RBP-4 in patients with PDAC and chronic pancreatitis (CP).The study included 43 patients with PDAC, 39 patients with CP and 10 controls. The concentrations of IGF-1 and RBP-4 were obtained using the ELISA method (Corgenix UK Ltd R&D Systems). The study protocol was approved by the Bioethics Committee at the Medical University of Lodz.In PDAC patients the serum IGF-1 level was significantly higher than in patients with CP (107.79 ± 66.40 ng/ml vs 89.91 ± 74.06 ng/ml; P < 0.05). Patients with both CP and diabetes mellitus (DM) were noted to have a significantly lower level of IGF-1 compared with those who only had CP (51.33 ± 24.30 ng/ml vs 108.42 ± 82.39 ng/ml; P = 0.01). The same result was obtained for men with and without DM (58.05 ± 32.44 ng/ml vs 98.79 ± 79.47 ng/ml, P = 0.05). As regards the serum level of RBP-4, the PDAC and CP groups were not significantly different from each other.Diabetes accompanying PDAC does not influence the level of IGF-1 as opposed to diabetes in the course of CP. The IGF-1 level can be useful for early diagnosis of PDAC. High concentration of RBP-4 is not specific to pancreatic cancer, so it does not appear to be a useful biomarker for PDAC.

Clinical chronic pancreatitis.

To summarize observations in clinical chronic pancreatitis in the past year. A predisposing genetic mutation was identified in 67% of cases of pediatric chronic pancreatitis. A novel susceptibility gene involving a hybrid allele is associated with idiopathic chronic pancreatitis. ABO blood type B and FUT2 nonsecretor status is associated with asymptomatic hyperlipasemia and chronic pancreatitis. Alcohol consumption impairs cystic fibrosis transmembrane conductance regulator (CFTR) activity leading to decreased bicarbonate secretion and patients with susceptible CFTR mutations can develop clinical pancreatitis. Computed tomography imaging findings in chronic pancreatitis correlate poorly with pain patterns. Endoscopic ultrasound features correlate poorly with fibrosis. Circulating epithelial cells are present in chronic pancreatitis patients but not healthy volunteers. Surgery is superior to endoscopic treatment in providing durable pain relief (>5 years). Repetitive pancreatic duct stent placements and chronic narcotic use are preoperative predictors of poor outcome after total pancreatectomy with islet cell auto transplantation. Novel genetic mutations for idiopathic chronic pancreatitis are being identified. Alcohol impairs CFTR activity and may explain a mechanism for pancreatitis. Current imaging modalities correlate poorly with clinical pain presentation and fibrosis in chronic pancreatitis. Novel imaging modalities are needed. As total pancreatectomy with islet cell auto transplantation grows, rigorous outcomes analysis is needed to drive patient selection.

Su1329 Endoscopic Ultrasound (EUS) Findings of Chronic Pancreatitis in Patients Presenting with Diarrhea and Low Fecal Elastase Levels (FE)

Su1329 Endoscopic Ultrasound (EUS) Findings of Chronic Pancreatitis in Patients Presenting with Diarrhea and Low Fecal Elastase Levels (FE)

Association between Smoking and the Progression of Computed Tomography Findings in Chronic Pancreatitis.

Background/AimsSmoking and alcohol intake are two well-known risk factors for chronic pancreatitis. However, there are few studies examining the association between smoking and changes in computed tomography (CT) findings in chronic pancreatitis. The authors evaluated associations between smoking, drinking and the progression of calcification on CT in chronic pancreatitis.MethodsIn this retrospective study, 59 patients with chronic pancreatitis who had undergone initial and follow-up CT between January 2002 and September 2010 were included. Progression of calcification among CT findings was compared according to the amount of alcohol intake and smoking.ResultsThe median duration of follow-up was 51.6 months (range, 17.1 to 112.7 months). At initial CT findings, there was pancreatic calcification in 35 patients (59.3%). In the follow-up CT, progression of calcification was observed in 37 patients (62.7%). Progression of calcification was more common in smokers according to the multivariate analysis (odds ratio [OR], 9.987; p=0.006). The amount of smoking was a significant predictor for progression of calcification in the multivariate analysis (OR, 6.051 in less than 1 pack per day smokers; OR, 36.562 in more than 1 pack per day smokers; p=0.008).ConclusionsContinued smoking accelerates pancreatic calcification, and the amount of smoking is associated with the progression of calcification in chronic pancreatitis.

Pancreatic pain.

Pain is the most common symptom of chronic pancreatitis, with a profound socioeconomic impact. Historical management paradigms failed, as they did not adequately address the fundamental underlying mechanisms. The present article describes the neurobiology of pain and sensitization in this condition, in an effort to explain prior failings and provide future directions for managing pain in chronic pancreatitis. A number of recent advances have been made in understanding the neurobiology of pain for this condition. This has been coupled with clinical advances in assessing sensitization to pain in these patients, which has been shown to predict response to medical and surgical therapy. Pain in chronic pancreatitis is complex. Addressing the mechanical and morphological findings in chronic pancreatitis without addressing the underlying neurobiological mechanisms is destined to fail. New advances in our understanding of the neurobiology of pain in chronic pancreatitis helps to explain prior failings and provides future direction for managing pain in patients afflicted by this disease.

Su1465 Association Between Smoking and the Change of Computed Tomography Findings in Chronic Pancreatitis

Su1465 Association Between Smoking and the Change of Computed Tomography Findings in Chronic Pancreatitis

Relationship between Patient Symptoms and Endosonographic Findings in Chronic Pancreatitis

Background/Aims: The endoscopic ultrasound (EUS) diagnosis of chronic pancreatitis (CP) relies on the presence of up to nine distinct pancreatic parenchymal and ductal abnormalities, without considering other factors such as age, duration of disease or clinical symptoms. Our goal was to examine the impact of patient symptoms on EUS findings in patients with CP. Methods: All patients with previously suspected CP who had symptomatic disease referred to our medical center for pancreatic EUS were identified. Patients were stratified into two groups based on their clinical symptoms — pain only and steatorrhea ± pain. Groups were compared using two-tailed comparative testing. Results: 53 patients (group 1) with pain only and 27 patients with steatorrhea ± pain (group 2) were identified. Patients in group 1 were younger and more likely female. Compared to group 1 (pain only), group 2 (steatorrhea ± pain) had more total (5.37 vs. 3.28, p < 0.01) and ductal abnormalities (2.56 vs. 0.83, p < 0.01), although the number of parenchymal abnormalities between groups 1 and 2 (2.45 vs. 2.88, p = 0.07) was not different. Conclusion: The presence of steatorrhea ± pain in patients with CP undergoing pancreatic EUS examination is associated with more total and ductal abnormalities. Stratification based on underlying patient symptoms may be valuable as an adjunct to endosonographic findings in making or excluding the diagnosis of CP.

Normal Pancreatic Exocrine Function Does Not Exclude MRI/MRCP Chronic Pancreatitis Findings

Abnormal pancreatic function tests have been reported to precede the imaging findings of chronic pancreatitis. Magnetic resonance imaging (MRI) with magnetic resonance cholangiopancreatography (MRCP) is increasingly accepted as the primary imaging modality for the detection of structural changes of early mild chronic pancreatitis. The aim of this study was to evaluate MRI/MRCP findings in patients with symptoms consistent with chronic pancreatitis who have normal Secretin Endoscopic Pancreatic Function test. A retrospective study of 32 patients referred for evaluation of chronic abdominal pain consistent with chronic pancreatitis and reported normal standard abdominal imaging (ultrasound, computed tomography, or MRI). All patients underwent Secretin Endoscopic Pancreatic Function testing and pancreatic MRI/MRCP at our institution. We reviewed the MRI/MRCP images in patients who had normal Secretin Endoscopic Pancreatic Function testing. MRI/MRCP images were assessed for pancreatic duct morphology, gland size, parenchymal signal and morphology, and arterial contrast enhancement. Of the 32 patients, 23 had normal Secretin Endoscopic Pancreatic Function testing, and 8 of them had mild to marked spectrum of abnormal MRI/MRCP findings that were predominantly focal. Frequencies of the findings were as follows: pancreatic duct stricture (n=3), pancreatic duct dilatation (n=3), side branch ectasia (n=4), atrophy (n=5), decreased arterial enhancement (n=5), decreased parenchymal signal (n=1), and cavity formation (n=1). The remaining15 patients had normal pancreatic structure on MRI/MRCP. Normal pancreatic function testing cannot exclude abnormal MRI/MRCP especially focal findings of chronic pancreatitis. Further studies needed to verify significance of these findings and establish MRI/MRCP imaging criteria for the diagnosis of chronic pancreatitis.

Does Endoscopic Ultrasonography Influence the Management of Patients with Acute Pancreatitis?

Purpose: Endoscopic ultrasonography (EUS) is useful in detecting biliopancreatic diseases. This study is designed to evaluate the usefulness of EUS in detecting the cause of acute pancreatitis. Methods: In this study, we retrospectively analyzed 80 available cases, which were diagnosed as acute pancreatitis by computed tomography (CT) at our hospital between April 2000 and September 2007. Cases with obstructive pancreatitis due to pancreatic ductal carcinoma were excluded. Final diagnoses were determined by endoscopic retrograde cholangiopancreatography and/or surgical exploration, and all cases diagnosed as idiopathic were followed up at least 12 months after the initial diagnosis. As choledocholithiasis and occult intraductal pancreatic tumor (IPT) are thought as determinant factors for the management of acute pancreatitis, we evaluate the diagnostic accuracy of detecting these diseases in the following diagnostic processes. First, we tried to diagnose these factors only using CT in all cases. If choledocholithiasis were detected, we performed endoscopic treatment without performing EUS. Second, we performed EUS additionally for further examination, and reconsidered the management according to EUS findings. All cause was classified into 5 groups: choledocholithiasis including debris, alcoholic, spontaneous stones pass, IPT and idiopathic. Results: The number of each group was as follows: choledocholithiasis, 41; alcoholic, 21; spontaneous stones pass, 4; IPT, 3; idiopathic, 11. Only using CT, 16 of 41 cases with choledocholithiasis and 2 of 3 cases with IPT were missed. So 18 cases were incorrectly diagnosed in total, and the over all accuracy was 77.5% (62/80). EUS was additionally performed in 55 cases, and 16 cases with choledocholithiasis and 2 cases with IPT were correctly diagnosed. Therefore, additional EUS correctly influenced 16 of 16 misdiagnosed cases correctly. Neither another CT nor MRI could detect any abnormal findings in 2 cases with IPT (intraductal acinar cell carcinoma and non invasive minute ampullary carcinoma). Furthermore, findings of chronic pancreatitis (hyperechoic foci, hyperechoic strands, lobularity) were detected in 7 of 21 alcoholic cases. The over all accuracy of EUS was 100% (54/54), and was statistically higher than that of using only CT (p < 0.0005). Conclusions: EUS is very useful in detecting not only choledocholithiasis but also minute intraductal pancreatic tumor. We recommend EUS for all cases which are diagnosed as acute pancreatitis without choledocholithiasis by CT.

A Clinical and Economic Evaluation of Endoscopic Ultrasound for Patients at Risk for Familial Pancreatic Adenocarcinoma

Background and Aims: Approximately 10% of pancreatic adenocarcinoma is familial. Approximately 50% of Ist-degree relatives (FDRs) have endoscopic ultrasound (EUS) findings of chronic pancreatitis. We modeled the natural history of these patients to compare 4 management strategies. Methods: We performed a systematic review, and created a Markov model for 45-year-old male FDRs, with findings of chronic pancreatitis on screening EUS. We compared 4 strategies: doing nothing, prophylactic total pancreatectomy (PTP), annual surveillance by EUS, and annual surveillance with EUS and fine needle aspiration (EUS/FNA). Outcomes incorporated mortality, quality of life, procedural complications, and costs. Results: In the Do Nothing strategy, the lifetime risk of cancer was 20%. Doing nothing provided the greatest remaining years of life, the lowest cost, and the greatest remaining quality-adjusted life years (QALYs). PTP provided the fewest remaining years of life, and the fewest remaining QALYs. Screening with EUS provided nearly identical results to PTP, and screening with EUS/FNA provided intermediate results between PTP and doing nothing. PTP provided the longest life expectancy if the lifetime risk of pancreatic cancer was at least 46%, and provided the most QALYs if the risk was at least 68%. Conclusions: FDRs from familial pancreatic cancer kindreds, who have EUS findings of chronic pancreatitis, have increased risk for cancer, but their precise risk is unknown. Without the ability to further quantify that risk, the most effective strategy is to do nothing.

Clinical findings of chronic pancreatitis associated with gene mutations (GM)

Clinical findings of chronic pancreatitis associated with gene mutations (GM)

A rare cause of massive pleural effusion

Pleural effusions commonly complicate pancreatitis and are usually reactive. Massive pleural effusions are a rare but recognised complication of pancreatitis, the management of which may require surgical intervention. Bishop et al. [1] reported massive pleural effusion secondary to pancreaticopleural fistula in a 4-year-old girl who, following failure of medical management, underwent surgery. Namazi and Mowla [2] also reported a patient with massive pleural effusion secondary to pancreatitis, who underwent drainage of a pancreatic cyst following failure of conservative management. Medical management of massive pleural effusion secondary to pancreatitis is reported to be successful in approximately 40% of adult cases [3]. We report successful resolution following medical management in a 12-year-old girl who presented with a massive right pleural effusion secondary to chronic pancreatitis. A 12-yearold girl presented with poor weight gain, and abdominal and retrosternal chest pain. She underwent a barium meal and an upper and lower gastrointestinal endoscopy. Apart from Enterobius vermicularis infestation resulting in a mild nonspecific proctitis, these investigations were normal. Empirical treatment with Gaviscon and mebendazole resulted in weight gain and symptom resolution. Six months later, she presented with a 2-month history of progressive shortness of breath and poor exercise tolerance. She was noted to be pyrexial and complained of right upper quadrant abdominal and chest pain. Clinical examination revealed no signs of respiratory distress, normal pulse oximetry and respiratory rate. However, there were absent breath sounds over the right lung and a chest X-ray film demonstrated a right pleural effusion (Fig. 1). An ultrasound scan and a chest CT scan confirmed a hyper-echoic fluid collection, total collapse of the right lung with no evidence of septation, mediastinal mass or lymphadenopathy. A Mantoux test was negative. Analysis of pleural fluid obtained after drainage revealed a white cell count of 1.05·10/l, raised amylase of 24777 U/l with a protein content of 32 g/l. Simultaneous serum analysis revealed a serum albumin of 31 g/l and an amylase of 304 U/l. The patient was treated conservatively with chest tube drainage, intravenous antibiotics, and intravenous octreotide (1 lg/kg/h), omeprazole and parentral nutrition. Within 2 weeks her pleural effusion resolved, her plasma amylase normalised and enteral nutrition was reintroduced. A magnetic resonance cholangiopancreatography delineated the pancreas and confirmed a dilated tortuous and beaded pancreatic duct with no evidence of pancreatopleural fistula or pseudocyst (Fig. 2). Further investigation confirmed that the patient and her father both carry the N291 mutation in the PRSS1 hereditary pancreatitis gene explaining her findings of chronic pancreatitis. The patient has remained symptom free with normal plasma amylase levels for 12 months following presentation, and her father has never had symptoms suggestive of pancreatitis. Pleural effusions commonly complicate acute pancreatitis and are usually small, left-sided and reactive. They arise from inflammation of the diaphragm and pleura, the amylase concentration of which may be moderately elevated. Pleural effusions arising from chronic pancreatitis are rare in children and result from either posterior disruption of the pancreatic duct into the retroperitoneal space leading to the formation of a fistulous tract between the pancreas and the pleural cavity through the aortic or oesophageal hiatus, or direct extension of a pancreatic pseudocyst [3]. These effusions tend to be large and recurrent with a dramatically elevated amylase content. M. Lawson (&) AE A. M. Dalzell Department of Paediatric Gastroenterology, Royal Liverpool Children’s Hospital NHS Trust Alder Hey, Eaton Road, L12 2AP Liverpool, UK E-mail: maureenlawson@doctors.org.uk Tel.: +44-151-2525373 Fax: +44-151-2525928

Differentiating a chronic hyperplastic mass from pancreatic cancer: a challenge remaining in multidetector CT of the pancreas

A multitude of clinical symptoms originate from pancreatic inflammatory or neoplastic processes due to their highly complex composition, function, and anatomic relationships to adjacent organs as well as the heterogeneous patterns of vascular perfusion and neural innervation of the pancreatic gland which complicate an early and precise diagnosis. Whereas early assessment of inflammatory or neoplastic pancreatic processes is a prerequisite for a successful curative approach, the classical radiologic signs of chronic pancreatitis and pancreatic carcinoma show significant similarities. This article provides an overview of the pathogenesis and imaging findings in chronic pancreatitis and pancreatic cancer, including some new approaches for visualizing the subtle but distinct differences between these two entities.