Secretin-stimulated Magnetic Resonance Cholangiopancreatography Research Articles

Secretin-Enhanced Magnetic Resonance Cholangiopancreatography - A Reliable Approach to Assess Exocrine Pancreatic Function?

Objectives: To investigate the relation between exocrine pancreatic function and secretin-stimulated magnetic resonance cholangiopancreatography (sMRCP) fluid volumes and its concordance to pancreatic elastase using a case-control approach. Methods: Navigator-triggered T2-weighted 3D-turbo-spin-echo sMRCP was performed on a 1·5-T-system in 977 subjects including volunteers without a history of pancreatitis (group: A n=917) and chronic pancreatic disorder patients without (group: B, n=32) and with diagnosis of exocrine pancreatic insufficiency (EPI) (group: C, n=28). After intravenous administration of 1 unit/kg secretin duodenal filling was graded (0-3) and quantified as sMRCP fluid volume. According to pancreatic elastase ELISA subjects were grouped as severe (<100 μg/g) and moderate (100-200 μg/g) pancreatic elastase insufficiency (PEI). Statistic evaluation comprised Kruskal-Wallis Test, multinomial logistic, linear regression and area-under-the-curve (AUC) analysis. Findings: sMRCP fluid volume was lower in patients with pancreatic disorders compared to controls (P=0·001), but independent of the presence of PEI. The odds ratio of a reduced grading of duodenal filling was higher in patients with EPI (group: C compared to controls) (P=0·001) but not significantly different between controls and patients without EPI (group: B P=0·911) or between both patient groups (group: B versus group: C P=0·059). There was only a small association of sMRCP fluid volume with pancreatic elastase (R2=0·04,P=0·001). AUCs of sMRCP fluid volume were 0·967 (95%CI 0·950-0·985) to detect EPI and 0·581 (95% CI 0·471-0·691) to detect severe PEI. Interpretation: Static sMRCP allows assessment of exocrine pancreatic function and can differentiate patients with diagnosis of EPI from volunteers, but is not suitable for screening of patients with PEI because of its discordance to pancreatic elastase. Funding Statement: The work is part of the Community Medicine Research net, which was funded by following institutions: Federal Ministry of Education and Research (grants 01ZZ9603, 01ZZ0103, 01ZZ0403, 01ZZ0701, 03ZIK012), Ministry of Cultural Affairs as well as the Social Ministry of the Federal State of Mecklenburg-West Pomerania, Federal Ministry of Nutrition, Agriculture and Consumer’s Safety (07HS003), German Research Foundation (projects Gr 1912/5-1, Ko 799/5-1, Vo 955/5-1, Vo 955/6-1, Vo 955/10-1), Competence Network Heart Failure (01GI0205), Competence Network Diabetes (01GI0855), German Asthma and COPD Network (COSYCONET; BMBF 01GI0883), Genopathomik (BMBF FZK 03138010), Alfried Krupp von Bohlen und Halbach Foundation, Alexander v. Humboldt Foundation, Leibniz Society, Siemens AG, Health Care Sector (Erlangen, Germany), Pfizer Pharma GmbH (SBU Endocrinology and Ophthalmology; Berlin Germany), Novo Nordisk (Mainz, Germany), Data Input GmbH (Darmstadt, Germany), GABA International AG (Therwil, Switzerland), Imedos Systems (Jena, Germany) and Heinen and Lowenstein (Bad Ems, Germany). Declaration of Interests: There are no conflicts of financial interest. Ethics Approval Statement: The local ethics committee approved the SHIP study, and written informed consent was obtained from all participating subjects before study inclusion.

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

Pancreatic disease in 2014: Pancreatic fibrosis and standard diagnostics.

In 2014, pancreatic fibrosis has increasingly been recognized as a key determinant of the pathogenesis, therapy response and disease progression of chronic pancreatitis and pancreatic cancer. In addition, secretin-stimulated magnetic resonance cholangiopancreatography has gained increasing importance, especially in visualizing pancreatic duct abnormalities. However, the true imaging capacity has not been fully analysed.

Anatomic variants of the pancreatic duct and their clinical relevance: an MR-guided study in the general population.

To investigate the frequency of pancreatic duct (PD) variants and their effect on pancreatic exocrine function in a population-based study using non-invasive secretin-stimulated magnetic resonance cholangiopancreatography (sMRCP). Nine hundred and ninety-five volunteers, 457 women and 538 men, aged 51.9 ± 13.4 years, underwent navigator-triggered, T2-weighted, 3D turbo spin echo MRCP on a 1.5 T system after 1 unit/kg secretin administration. Two readers evaluated images for PD variants. Pancreatic exocrine function and morphological signs of chronic pancreatitis such as abnormalities of the main PD, side branch dilatation, and pancreatic cysts were evaluated and related to PD variants using a Kruskal-Wallis test and post hoc analysis. Of all sMRCP, 93.2% were of diagnostic quality. Interobserver reliability for detection of PD variants was found to be kappa 0.752 (95 %CI, 0.733 - 0.771). Normal PD variants were observed in 90.4% (n = 838/927). Variants of pancreas divisum was identified in 9.6% (n = 89/927). Abnormalities of the main PD, side branch dilatation, and pancreatic cysts were observed in 2.4%, 16.6%, and 27.7%, respectively, and were not significantly different between pancreas divisum and non-divisum group (P = 0.122; P = 0.152; P = 0.741). There was no association between PD variants and pancreatic exocrine function (P = 0.367). PD variants including pancreas divisum are not associated with morphological signs of chronic pancreatitis or restriction of pancreatic exocrine function. MRCP allows the evaluation of pancreatic duct variants and morphological change. Pancreatic duct variants are not associated with morphological signs of chronic pancreatitis. Pancreas divisum is not accompanied by restriction of pancreatic exocrine function. Pancreatic duct variants including pancreas divisum are limited in their clinical relevance.

Su1827 Prediction of Islet Yield in Patients Undergoing Total Pancreatectomy With Islet Autotransplantation (TPIAT) for Non-Calcific Chronic Pancreatitis (NCCP) Using Contrast Enhanced MRI and Secretin Stimulated MRCP (sMRCP)

Su1827 Prediction of Islet Yield in Patients Undergoing Total Pancreatectomy With Islet Autotransplantation (TPIAT) for Non-Calcific Chronic Pancreatitis (NCCP) Using Contrast Enhanced MRI and Secretin Stimulated MRCP (sMRCP)

7 Diagnostic Performance of Contrast Enhanced MRI With Secretin-Stimulated MRCP (sMRCP) for Non-Calcific Chronic Pancreatitis (NCCP): A Comparison With Histopathology

7 Diagnostic Performance of Contrast Enhanced MRI With Secretin-Stimulated MRCP (sMRCP) for Non-Calcific Chronic Pancreatitis (NCCP): A Comparison With Histopathology

Secretin-Stimulated MRCP in Volunteers: Assessment of Safety, Duct Visualization, and Pancreatic Exocrine Function

The objective of our study was to investigate secretin-stimulated MRCP in terms of the safety of secretin, improvement of duct visualization, and assessment of pancreatic exocrine function. Eight hundred sixteen volunteers (370 women and 446 men; mean age, 49.7 ± 13.1 [SD] years) underwent 3D MRCP before and after secretin stimulation (1 U/kg of body weight) at 1.5 T. For the first 2 hours after secretin injection, subjects were evaluated for adverse reactions. Improvement of duct visualization after secretin stimulation was subjectively evaluated by two readers and was quantified by duct diameter measurements. Pancreatic exocrine function was evaluated subjectively by two readers according to the duodenal filling and was quantified using calibrated volumetric measurements of total excreted volume and pancreatic flow output. Two subjects (0.2%) showed flushing (minor adverse reaction). Duct visualization after secretin injection was improved for reader 1 in 468 (57.4%) and for reader 2 in 478 (58.6%) subjects, was unchanged for reader 1 in 324 (39.7%) and for reader 2 in 315 (38.6%) subjects, and was worse for reader 1 in 24 (2.9%) and reader 2 in 23 (2.8%) subjects (interrater agreement, κ = 0.925). Main pancreatic duct diameters increased significantly after secretin stimulation: pancreatic head, 10.5% (mean); body, 12.5%; and tail, 7.7%. Pancreatic exocrine function evaluated according to assessment of duodenal filling was as follows: grade 0 (restricted function) in 0.7% of subjects by both readers, grade 1 (reduced function) in 4.8% of subjects by reader 1 and 4.5% of subjects by reader 2, grade 2 (low-grade reduced function) in 31.1% of subjects by reader 1 and 26.5% of subjects by reader 2, and grade 3 (physiologic function) in 63.4% of subjects by reader 1 and 68.3% of subjects by reader 2 (interrater agreement, κ = 0.838). The mean total excreted volume was 111.8 ± 49.8 (SD) mL, and the mean pancreatic flow output was 9.6 ± 4.2 mL/min. Secretin-stimulated MRCP moderately improves main pancreatic duct visualization and allows noninvasive quantification of pancreatic exocrine function with a negligible risk of side effects.

Pancreatic Morphological Changes in Long-Term Follow-Up after Initial Episode of Acute Alcoholic Pancreatitis

ObjectiveThe long-term morphological changes induced by a single episode of alcoholic pancreatitis are not known. Our aim was to study these morphological changes in secretin-stimulated magnetic resonance cholangiopancreatography (S-MRCP) after the first episode of alcohol-associated acute pancreatitis and to evaluate the risk factors and possible protective factors potentially associated with later chronic findings. We have previously reported 2-year follow-up results in pancreatic morphology. This study extends the follow-up to 9 years. Patients and MethodsIn this prospective follow-up study, S-MRCP imaging was performed for 44 (41 M, 3 F; mean age, 46 (25–68) years) patients after their first episode of alcohol-associated pancreatitis. Pancreatic morphology was evaluated at 3 months and at 2, 7, and 9 years after hospitalization. Recurrent attacks of pancreatitis were studied and pancreatic function was monitored by laboratory tests. Patients’ alcohol consumption was evaluated with questionnaires, laboratory markers, and self-estimated alcohol consumption via interview. Smoking and body mass index were annually recorded. ResultsAt 3 months, 32 % of the patients had normal findings in S-MRCP, 52 % had acute, and 16 % had chronic changes. At 7 years, S-MRCP was performed on 36 patients with normal findings in 53 %, the rest (47 %) having chronic findings. Pancreatic cyst was present in 36 %, parenchymal changes in 28 %, and atrophy in 28 % of the cases. There were no new changes in the pancreas in the attending patients between 7 and 9 years (18 patients). Of the patients with only acute findings at 3 months, 60 % resolved to normal in 7 years, but the rest (40 %) showed chronic changes later on. The initial attack was mild in 65 %, moderate in 25 %, and severe in 10 % of the patients. Patients with mild first attack had fewer chronic changes at 7 years compared to patients with moderate or moderate and severe together (p = 0.03, p = 0.01). Of the patients in the seventh year of S-MRCP, 22 % had suffered a recurrent episode of acute pancreatitis (mean, 22 (2–60) months) and 11 % had a clinical diagnosis of chronic pancreatitis. At 7 years, 88 % of the patients with recurrences had chronic findings in S-MRCP versus 36 % with nonrecurrent pancreatitis (p = 0.02). Six (17 %) patients abstained from alcohol throughout follow-up (mean, 8.7 (7–9.1) years), but even one of these developed pancreatic atrophy. Out of the non-abstinent patients who did not suffer recurrences, 4/22 (18 %) had developed new findings during at follow-up S-MRCP (NS). In univariate analysis, heavy smoking showed no correlation with increased chronic changes compared to nonsmoking. ConclusionsMorphological pancreatic changes increase with recurrent episodes of acute pancreatitis. Patients with mild first attack have fewer chronic changes in the pancreas in the long term. However, even a single episode of acute alcoholic pancreatitis may induce chronic morphological changes in long-term follow-up.

Assessment of exocrine pancreatic function by secretin‐stimulated magnetic resonance cholangiopancreaticography and diffusion‐weighted imaging in healthy controls

To characterize and quantify exocrine pancreatic function by secretin-stimulated magnetic resonance cholangiopancreaticography (s-MRCP) and diffusion-weighted imaging (DWI) in healthy subjects and compare these findings to morphological features, ie, pancreatic volume and secretin-stimulated peak bicarbonate concentration measured in pancreatic juice. Pancreatic magnetic resonance imaging (MRI) (1.5 T) was performed in 20 healthy volunteers among which 10 underwent gastroscopy with duodenal intubation. MRI included T2-weighted imaging and DWI acquired before and 1, 5, 9, and 13 minutes after secretin administration. Secreted pancreatic juice volumes were calculated based on the sequential T2-weighted images and pancreatic volumes and apparent diffusion coefficient (ADC) values were estimated. The mean pancreatic secretion rate declined from 9.5 mL/min at 1-5 minutes (postsecretin) to 2.9 mL/min at 9-13 minutes. Pancreatic head ADC values significantly increased from baseline (1.29 × 10(-3) mm(2) /s) to 1 minute postsecretin (1.48 × 10(-3) mm(2) /s) (P = 0.003). Secreted pancreatic juice volume at 1 minute after secretin correlated positively with peak bicarbonate concentration (n = 10, P = 0.05). Secretin-stimulated MRCP and DWI can characterize and quantify exocrine pancreatic function in healthy subjects. These imaging methods may prove relevant for patients with exocrine pancreatic dysfunction.

Morphological and functional evaluation of chronic pancreatitis with magnetic resonance imaging

Magnetic resonance imaging (MRI) techniques for assessment of morphology and function of the pancreas have been improved dramatically the recent years and MRI is very often used in diagnosing and follow-up of chronic pancreatitis (CP) patients. Standard MRI including fat-suppressed T1-weighted and T2-weighted imaging techniques reveal decreased signal and glandular atrophy of the pancreas in CP. In contrast-enhanced MRI of the pancreas in CP the pancreatic signal is usually reduced and delayed due to decreased perfusion as a result of chronic inflammation and fibrosis. Thus, morphological changes of the ductal system can be assessed by magnetic resonance cholangiopancreatography (MRCP). Furthermore, secretin-stimulated MRCP is a valuable technique to evaluate side branch pathology and the exocrine function of the pancreas and diffusion weighted imaging can be used to quantify both parenchymal fibrotic changes and the exocrine function of the pancreas. These standard and advanced MRI techniques are supplementary techniques to reveal morphological and functional changes of the pancreas in CP. Recently, spectroscopy has been used for assessment of metabolite concentrations in-vivo in different tissues and may have the potential to offer better tissue characterization of the pancreas. Hence, the purpose of the present review is to provide an update on standard and advanced MRI techniques of the pancreas in CP.

Sa1206 Post Secretin-Stimulated MRCP Pancreatitis: A New Cause of Acute Pancreatitis

Sa1206 Post Secretin-Stimulated MRCP Pancreatitis: A New Cause of Acute Pancreatitis

Magnetic resonance cholangiopancreatography: the ABC of MRCP

Magnetic resonance cholangiopancreatography (MRCP) is a technique that has evolved over the past two decades. It continues to have a fundamental role in the non-invasive investigation of many pancreatico-biliary disorders. The purpose of this review is to summarise the key concepts behind MRCP, the different techniques that are currently employed (including functional and secretin-stimulated MRCP), the pitfalls the reader should be aware of, and the main clinical indications for its use.

The Effects of Morphine–Neostigmine and Secretin Provocation on Pancreaticobiliary Morphology in Healthy Subjects: A Randomized, Double‐blind Crossover Study Using Serial MRCP

Secretin-stimulated magnetic resonance cholangiopancreatography (MRCP) is used for the diagnosis of sphincter of Oddi dysfunction (SOD), but it does not correlate well with sphincter of Oddi manometry. Serial MRCP following morphine-neostigmine provocation may be of value in the assessment of SOD, but the effects of these pharmacological agents on pancreaticobiliary morphology in healthy subjects have not been studied. The aim of the present study was to use serial MRCP to characterize the effects of morphine-neostigmine and secretin provocation on serum pancreatic enzyme responses and pancreaticobiliary ductal morphology in healthy subjects. Following a baseline scan and serum lipase and amylase assays, 10 healthy subjects were randomized in a double-blind manner to receive morphine (10 mg intramuscularly [IM]), neostigmine (1 mg IM) and saline (intravenously [IV]); OR saline (IM), saline (IM) and secretin (1 U/kg IV). A MRCP study was performed at 5, 30, 60, 90, 120, 150, and 180 min thereafter, with blood samples taken every 60 min for 4 h. Pancreatic duct (PD) diameter, visible PD length, common bile duct (CBD) diameter, and gallbladder volume were recorded. Crossover studies were performed 10 days later. Serum pancreatic enzyme concentrations were significantly greater (amylase, P = 0.003; lipase, P = 0.04) after morphine-neostigmine than after secretin. Following morphine-neostigmine and secretin provocation, the mean (SEM) percentage increase in PD diameter was 28.7 (7.2) versus 12.9 (3.3); P < 0.0001, and visible PD length was 49.4 (11.5) versus 28.1 (8.2); P < 0.0001, respectively. The effects of morphine-neostigmine were more pronounced than those of secretin in healthy subjects. The diagnostic utility of morphine-neostigmine stimulated serial MRCP for SOD merits further evaluation.

Erratum to: Secretin-stimulated MRCP

Erratum to: Secretin-stimulated MRCP N. J. Lee, K. W. Kim, T. K. Kim, M. H. Kim, S. Y. Kim, M.-S. Park, A. Y. Kim, H. K. Ha, P. N. Kim, M.-G. Lee Department of Radiology, Asan Medical Center, University of Ulsan College of Medicine, 388-1, Pungnap 2-dong, Songpa-gu, Seoul 138-736, Korea Department of Radiology, Eulgi Medical Center, 280-1, Hagye-dong, Nowon-gu, Seoul 139-711, Korea Department of Medical Imaging, Toronto General Hospital, 200 Elizabeth St, Toronto, Ontario, Canada M5G2C4 Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1, Pungnap 2-dong, Songpa-gu, Seoul 138-736, Korea Department of Radiology, Yong Dong Severance Hospital, 146-92 Dokok-dong, Kangnam-ku, Seoul 137-270, Korea

肝外胆管に拡張のない膵・胆管合流異常での胆道内における膵液逆流, うっ滞の検討 : セクレチン負荷MRCPからみた考察

肝外胆管に拡張のない膵・胆管合流異常での胆道内における膵液逆流, うっ滞の検討 : セクレチン負荷MRCPからみた考察

Pancreatic function and morphology in Sjögren's syndrome

Objective. Sjögren's syndrome (SS) is considered to be a universal exocrinopathy most likely based on autoimmune mechanisms. The degree of exocrine involvement in SS with the exception of salivary and lachrymal glands is, however, not yet established. Material and methods. We therefore examined the morphology, the exocrine and endocrine functions of the pancreas in 12 healthy consecutively included levolunteers with established SS, but without known pancreatic disease, using secretin-stimulated magnetic resonance cholangiopancreatography (MRCP), a Lundh test, oral glucose tolerance test, and blood sampling. Results. Twenty-five percent of the patients had morphological changes of pancreas as evaluated by secretin-stimulated MRCP, and two patients had chronic pancreatitis-like changes. Four patients had reduced exocrine function of the pancreas with either significantly reduced amylase and/or lipase in the pancreatic juice. Conclusions. The prevalence of pancreatic dysfunction was increased to 25–33% in the study population which is much higher than in the background population. Thus, pancreatic dysfunction and chronic pancreatitis should be considered in SS.

Sphincter of Oddi Dysfunction

Sphincter of Oddi dysfunction (SOD) is a poorly-understood disorder, typically presenting as postcholecystectomy, "biliary-type," right-sided abdominal and/or chest wall pain. Most patients referred to specialist clinics for work-up of presumed SOD do not, in fact, have anything wrong with their bile ducts or biliary sphincter mechanisms. A careful history and focused physical examination will often identify the true source of the pain syndrome, ranging from chest wall costochondritis and nerve injury at surgical trochar sites, to gastroparesis and visceral hypersensitivity ("irritable bowel"). The Rome III classification of functional gallbladder and biliary disorders defines SOD as episodic (not daily) pain lasting more than 30 min, which is disruptive of normal activities and not associated with bowel upset. It is not relieved by gastric acid suppression or antispasmodics. Other causes of abdominal pain must be excluded. Standard work-up includes endoscopic retrograde cholangiopancreatography (ERCP) with biliary manometry, which risks post-ERCP pancreatitis, especially in young women with normal bile ducts and liver serology. Noninvasive tests for SOD, such as timed ("gated") cholecystokinin (CCK)-stimulated hepatobiliary iminodiacetic acid (HIDA) scans and secretin-stimulated magnetic resonance cholangiopancreatography, are imperfect and still evolving. Although many doubt the very existence of SOD, a multidisciplinary approach to the management of pre- and postcholecystectomy abdominal pain syndromes is long overdue.

MRI and S‐MRCP findings in patients with suspected chronic pancreatitis: Correlation with endoscopic pancreatic function testing (ePFT)

To review magnetic resonance imaging (MRI) and secretin stimulated magnetic resonance cholangiopancreatography (S-MRCP) findings of patients with suspected chronic pancreatitis and compare them with endoscopic pancreatic function testing (ePFT). MRI and S-MRCP findings of 36 patients with clinically suspected chronic pancreatitis were reviewed. Baseline ductal changes, duodenal filling grades, and pancreatic duct caliber change (PDC) on S-MRCP, mean values of pancreatic anteroposterior (AP) diameter, signal intensity ratio (SIR) between pancreas and the spleen on T1-weighted fat saturated images, and arterial to venous (A/V) enhancement ratios were compared between groups of normal and abnormal pancreatic exocrine function determined by ePFT. All patients (n = 24) with normal ePFT (HCO(3) >80 mEq/L) had grade 3 normal duodenal filling. Patients with abnormal ePFT (HCO(3) <80 mEq/L) (n = 12) had grade 1 (n = 1) and grade 2 (n = 11) diminished duodenal filling (P < 0.0001). PDC was 1.51 in the normal ePFT group versus 1.27 in the abnormal ePFT group (P = 0.01). No significant differences were found in terms of mean pancreatic AP diameter (21.8 vs. 19.8 cm), SIR (1.59 vs. 1.44), and A/V (1.08 vs. 1.01) between groups of normal/abnormal pancreatic exocrine function. Despite discrepancies between pancreatic exocrine function and the findings on standard MRI/MRCP, the S-MRCP findings are comparable to ePFT in the evaluation of chronic pancreatitis.

Secretin-stimulated MR cholangio-pancreatography in the evaluation of asymptomatic patients with non-specific pancreatic hyperenzymemia

Purpose To assess the diagnostic value of secretin-stimulated MRCP (SS-MRCP) compared with conventional MRCP in asymptomatic patients with mild elevations of pancreatic enzymes. Materials and methods Eighty asymptomatic patients with pancreatic hyperenzymemia underwent MR imaging at 1.5 T-device (Signa EXCITE, GE Healthcare). After the acquisition of axial T1w,T2w sequences, and conventional MRCP, SS-MRCP was performed using a single-slice coronal breath-hold, thick-slab, SSFSE T2w sequence, repeated every 30 s up to 15 min following intravenous injection of secretin (Secrelux ®, Sanochemia). Results On the basis of the standards of reference, our final diagnoses were: negative findings ( n = 23), pancreas divisum ( n = 22), mild chronic pancreatitis ( n = 14), inflammatory ampullary stenosis ( n = 3), juxtapapillary duodenal diverticulum ( n = 1), small cystic lesions (<1 cm) ( n = 22; 5/22 cases associated with pancreas divisum). The image quality of SS-MRCP was significantly higher than that of conventional MRCP ( p < 0.0001). Standards of reference did not differ significantly from of SS-MRCP findings ( p = 0.5), while was statistically different from those of conventional MRCP ( p < 0.0001). A significant difference was found between conventional MRCP and SS-MRCP findings ( p < 0.0001). Conclusion In asymptomatic patients with non-specific pancreatic hyperenzymemia SS-MRCP may represent the best non-invasive diagnostic technique, since it gives morphological and functional information.

Pancreas Divisum: Beyond the Apparent

Acute recurrent pancreatitis is a common clinical problem. The etiology and clinical management vary widely. Pancreas divisum is the most common congenital anomaly of the pancreas. However, only a small percentage of individuals with pancreas divisum develop acute or recurrent pancreatitis. Clinical manifestations range from isolated episodes of acute recurrent pancreatitis to chronic pancreatitis, and in some cases unexplained pain without any recognizable inflammation. The variations in clinical presentation, clinical progression of the disease, and responses to endoscopic or nonendoscopic treatments are not entirely predictable. 1 These facts have led to substantial controversy about the association of pancreas divisum with pancreatic disease. They lead us to believe that mere presence of an anatomic anomaly is not in itself sufficient and there have to be other disease modifiers or cofactors that are responsible for pancreatic injury. Environmental insults such as oxidative stresses could play a role, however, these do not seem to be universally reproducible. A key may lie in the genetic make up of the individual. In this issue of the journal, Garg and colleagues 2 have investigated the association of genetic mutations and acute recurrent pancreatitis in individuals with pancreas divisum. They have tested for genetic mutations known to be associated with pancreatitis: cystic fibrosis transmembrane conductance regulator gene (CFTR), cationic trypsinogen (PRSS1), and serine protease inhibitor Kazal type 1 (SPINK1) gene. This study was conducted in a tertiary referral center in Northern India. They studied 12 subjects with pancreas divisum and acute recurrent pancreatitis. Their control group included patients with acute recurrent pancreatitis but no pancreas divisum, patients with chronic pancreatitis due to other causes, and healthy volunteers. Mutations in individuals with asymptomatic pancreas divisum were not evaluated. Detailed work-up was carried out including analysis for the presence of microcrystals in the bile before considering etiology of pancreatitis to be idiopathic. All subjects with pancreas divisum and acute recurrent pancreatitis underwent endoscopic retrograde cholangiopancreatography with minor papillotomy and temporary stenting of the dorsal duct. Response to endoscopic therapy was defined as reduction in >50% of acute pancreatitis episodes/year. Prevalence of SPINK1 gene mutations was found to be similar in patients with recurrent acute pancreatitis with or without pancreas divisum and those with chronic pancreatitis. However, only 1 in 50 of the control group had SPINK1 gene mutation. Polymorphism in the CFTR gene was seen at a higher frequency in those with pancreas divisum. One could argue that the ideal control should be those with pancreas divisum but without symptoms. From clinical practice, we know that these controls would be hard to identify without the use of secretin-stimulated magnetic resonance cholangiopancreatography or other expensive noninvasive imaging. SPINK1 gene mutations along with mutations in CFTR have been previously shown to occur at a higher frequency in patients with idiopathic chronic and acute recurrent pancreatitis. 3,4 Some animal studies have demonstrated that genetic mutations in CFTR might be responsible for an increased inflammatory response in mice. 5 SPINK1 gene mutations were previously found in a Finnish study to occur at a higher rate in those with acute pancreatitis, suggesting that the SPINK1 gene mutation probably enhances the susceptibility to acute pancreatitis. 6 This study of Garg and colleagues raises a very thought-provoking question: is pancreatitis in patients with pancreas divisum related to the outflow obstruction at the minor papilla? From previous studies we know that only a minority of those with pancreas divisum are symptomatic and the responses to therapy are not uniformly the same despite minor papillotomy, which should relieve any obstruction. The findings of this and other studies suggest an etiology other than a simple mechanical obstruction alone. In this study, responses to endoscopic therapy were similar to those already reported, with significant improvement in approximately 70% of patients. 7 This study involved numbers that were too small to examine whether the response to therapy is predictable based on the genetic mutations. Despite the