Diagnostic value of magnetic resonance cholangiopancreatography to detect bile duct stones in acute biliary pancreatitis

Objectives

This study aims to evaluate the diagnostic value of magnetic resonance cholangiopancreatography (MRCP) in detecting common bile duct (CBD) stones in acute biliary pancreatitis (ABP).

Delayed common bile duct obstruction in acute pancreatitis

Summary Common bile duct obstruction during acute pancreatitis usually occurs in the early symptomatic phase of the illness, involves only the distal portion of the common bile duct, and subsides with clinical improvement. We present two cases of persistent common bile duct obstruction that developed 2–3 months after complete clinical subsidence of the initial episode of severe acute pancreatitis and involved a long segment of the common bile duct. After surgical decompression, there was no recurrence of common bile duct obstruction or pancreatitis.     

Roux-en-Y drainage of a pancreatic fistula for disconnected pancreatic duct syndrome after acute necrotizing pancreatitis

Background

After acute necrotizing pancreatitis (ANP), a pancreatic fistula may occur from disconnected pancreatic duct syndrome (DPDS) where a segment of the pancreas is no longer in continuity with the main pancreatic duct.

Aim

To study the outcome of patients treated using Roux-Y pancreatic fistula tract-jejunostomy for DPDS after ANP.

Methods

Between 2002 and 2011, patients treated for DPDS in the setting of endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopanreatography (MRCP) documented main pancreatic duct disruption with Roux-Y pancreatic fistula tract-jejunostomy.

Results

In all, seven patients with DPDS were treated. The median age was 62 years (range 49–78) and five were men. The cause of ANP was gallstones (2), alcohol (1), ERCP (1) and idiopathic (3). Pancreatic necrosectomy was done in six patients. Time from onset of pancreatitis to fistula drainage was 270 days (164–365). Pancreatic fistulae arose from DPDS in the head/neck (4) and body/tail (3). Patients had a median fistula output of 140 ml (100–200) per day before surgery. The median operative time was 142 min (75–367) and estimated blood loss was 150 ml (25 to 500). Patients began an oral diet on post-operative day 4 (3–6) and were hospitalized for a median of 7 days (5–12). The median follow-up was 264 days (29–740). Subsequently, one patient required a distal pancreatectomy. After surgery, three patients required oral hypoglycaemics. No patient developed pancreatic exocrine insufficiency.

Conclusion

Internal surgical drainage using Roux-en-Y pancreatic fistula tract-jejunostomy is a safe and definitive treatment for patients with DPDS.     

Pancreatic and bile duct obstruction exacerbates rat caerulein-induced pancreatitis: a new experimental model of acute hemorrhagic pancreatitis

Background Pancreatic duct obstruction induces edematous but not hemorrhagic pancreatitis even when combined with maximal secretory stimulation. The aim of the present study was to test the hypothesis that pancreatic and bile duct obstruction exacerbates edematous pancreatitis induced by supramaximal secretory stimulation by caerulein. Methods In in vivo studies using rats, biliopancreatic duct ligation was combined with supramaximal stimulation of caerulein, and pancreatic histology, serum amylase level, pancreatic edema, and intrapancreatic trypsin activation were evaluated. In in vitro studies, the pancreatic acini were isolated from the rats with biliopancreatic duct ligation, and amylase secretion, intracellular trypsin activation, and acinar cell fragility were evaluated. Results Biliopancreatic duct ligation exacerbated caerulein-induced pancreatitis from edematous to hemorrhagic only when the obstruction preceded caerulein administration. The amylase secretion from the acini was inhibited, and intracellular trypsin activation and the acinar cell fragility on the supramaximal stimulation with cholecystokinin in vitro were enhanced by the preceding in vivo biliopancreatic duct obstruction. Conclusions Preceding biliopancreatic duct obstruction exacerbates caerulein-induced pancreatitis. Enhancement of intracellular trypsin activation is possibly involved in this mechanism.     

Risk factors of recurrent pancreatitis after first acute pancreatitis attack: a retrospective cohort study

Abstract

Background and aims: Few studies have been conducted in Asia on the recurrence of acute pancreatitis (AP). This study was designed to investigate characteristics of the disease to predict recurrence.

Methods: We retrospectively analyzed 617 patients that experienced a first AP attack between January 2009 and December 2014. Based on reviews of clinical and follow-up data, we attempted to identify risk factors of recurrence using Cox regression analysis.

Results: During a median follow-up of 3.2?years (range 3–72?months), 100(16.2%) of the 617 study subjects experienced one or more episodes of recurrent acute pancreatitis (RAP). Of these 100 patients, 75(75%) experienced one relapse, 12(12%) two relapses, and 13(13%) three or more relapses. The etiologies of RAP were an alcohol (48%), gallstone (31%), idiopathic (14%), and others (7%). Univariate analysis showed that an age of <60?years, male gender, smoking, an alcohol-associated etiology, and a local complication at index admission were significant risk factors of RAP. Cox regression analysis showed that an age of <60?years (HR = 1.602, 95% CI: 1.029–2.493), male gender (HR = 1.927, 95% CI: 1.127–3.295), and the presence of a local complication (HR = 3.334, 95% CI: 2.211–5.026) were significant risk factors of RAP development.

Conclusion: A local complication at index admission was found to be the strongest risk factor of RAP, and a male gender and an age of <60?years were significantly associated with RAP. Special attention and close follow-up should be afforded to patients with a local complication at index admission or male patients <60?years old.     

Progression to recurrent acute pancreatitis after a first attack of acute pancreatitis in adults

PurposePatients with a first attack of acute pancreatitis (AP) can develop recurrent acute pancreatitis (RAP). Hence, this study aimed to investigate the clinical features of the disease and the risk factors for RAP.MethodsWe performed a retrospective study of 522 patients from Jan 1 to Dec 31, 2006. All patients with AP were followed for 36 months. The primary end point was the rate of RAP. The secondary end points were the risk factors that were evaluated by Cox regression analysis. The cumulative risk of RAP was assessed using Kaplan-Meier analysis.Results56 of the 522 patients (10.7%) developed RAP. Among those RAP patients, 37 (7.1%) experienced one relapse, 10 (1.9%) experienced two relapses, and 9 (1.7%) experienced three or more relapses. Univariate analysis indicated that age (p = 0.016), male sex, etiology of AP (p = 0.001), local complications (p = 0.001) and Length of stay (LOS) (p = 0.007) were associated with RAP. Multivariate analysis with the Cox proportional hazards model showed that male sex (HR = 2.486, 95% CI, 0.169–0.960, p = 0.04), HTG-associated etiology (HR = 5.690, 95% CI, 2.138–15.146, p = 0.001), alcohol-associated etiology (HR = 5.867, 95% CI, 1.446–23.803, p = 0.013) and current local complications at index admission (HR = 8.917, 95% CI, 3.650–21.789, p = 0.001) were significant independent risk factors for RAP.ConclusionsA first attack of AP led to RAP in 10.7% of patients within 3 years. Male sex was significantly associated with RAP. The etiologies of alcohol and HTG and local complications were the strongest risk factors for recurrent disease. Patients with these characteristics should be given special attention and followed-up closely.     

Secretin-stimulated magnetic resonance imaging/magnetic resonance cholangiopancreatography for the detection of chronic pancreatitis: A meta-analysis

ObjectiveTo evaluate the diagnostic accuracy of secretin-stimulated magnetic resonance imaging/magnetic resonance cholangiopancreatography (S-MRI/MRCP) as noninvasive modalities in detecting chronic pancreatitis (CP).MethodsA systematic literature search in the PubMed, EMBASE, Web of Science, Cochrane, and Chinese Biomedical Literature Databases to identify relevant original studies. Study quality was assessed using the Quality Assessment of Diagnostic Accuracy Studies (version 2). Study data were independently extracted to calculate sensitivity and specificity, as well as areas under summary receiver operating characteristic curves (AUCs), and to test for heterogeneity and the threshold effect.ResultsThe sample comprised 11 studies including 180 patients with CP and 340 patients without CP. Pooled sensitivity and specificity were 0.72 (95% confidence interval [CI] 0.65–0.78) and 0.87 (95% CI 0.83–0.90), respectively. Pooled positive and negative likelihood ratios were 4.99 (95% CI 2.59–9.61) and 0.32 (95% CI 0.19–0.54), respectively. The diagnostic odds ratio was 23.31 (95% CI 7.50–72.44). The AUC and Q¹ index were 0.8631 and 0.7937, respectively. Publication bias was absent (P = 0.64).ConclusionsS-MRI/MRCP had low sensitivity and moderately high specificity for the detection of CP. Large-scale, quality-controlled, prospective studies are needed to verify the diagnostic accuracy of these modalities.     

Somatostatin prevents acute pancreatitis after pancreatic duct sphincter hydrostatic balloon dilation in patients with idiopathic recurrent pancreatitis.

The purpose of this study was to determine whether prophylactic somatostatin infusion can prevent pancreatitis after hydrostatic balloon dilation of the pancreatic duct sphincter segment in 16 patients with idiopathic recurrent pancreatitis. This study demonstrated that prophylactic administration of somatostatin before, during, and after the procedure diminished the incidence and severity of acute pancreatitis. We recommend consideration of such prophylaxis in patients undergoing this procedure.     

Effects of tetraprenylacetone on pancreatic exocrine secretion and acute pancreatitis in two experimental models in rats

Summary The effects of tetraprenylacetone (TPN), an acyclic polyisoprenoid with antiulcer actions, on pancreatic exocrine secretion, and its preventive and therapeutic effects on acute pancreatitis in two experimental models were studied in rats. Intraduodenal administration of TPN (0, 100, 200 and 400 mg/kg/h) caused dose-dependent increases in pancreatic juice and bicarbonate output without increasing protein output and plasma cholecystokinin (CCK) concentrations. TPN-stimulated pancreatic exocrine secretion was completely abolished by antisecretin serum but it was not by CCK receptor antagonist loxiglumide (50 mg/kg/h). In acute pancreatitis induced by four subcutaneous injections of 20 μg/kg cerulein at hourly intervals over, 3 h, TPN (400 mg/kg) given by an oral route either 1 h before the first cerulein injection or immediately after the last injection significantly reduced the increases in serum amylase and lipase activities and pancreatic wet wt. Pretreatment with TPN caused histologic improvements, whereas posttreatment failed to ameliorate histologic alterations. In severe type of acute pancreatitis induced by retrograde intraductal injection of 1.0 mL/kg of 4% sodium taurocholate, TPN exerted no apparent beneficial effects on biochemical and histologic alterations of acute pancreatitis. It is concluded that TPN given by an oral route stimulates pancreatic exocrine secretion through an increase in endogenous secretin release and causes beneficial effects on the experimental model of mild acute pancreatitis in rats.     

Sphincter of Oddi dysfunction and bile duct microlithiasis in acute idiopathic pancreatitis

Although there are numerous causes of acute panc-reatitis, an etiology cannot always be found. Two potential etiologies, microlithiasis and sphincter of Oddi dysfunction, are discussed in this review. Gallbladder microlithiasis, missed on transcutaneous ultrasound, is reported as the cause of idiopathic acute pancreatitis in a wide frequency range of 6%-80%. The best diagnostic technique for gallbladder microlithiasis is endoscopic ultrasound although biliary crystal analysis and empiric cholecystectomy remain as reasonable options. In contrast, in patients who are post-cholecystectomy, bile duct microlithiasis does not appear to have a role in the pathogenesis of acute pancreatitis. Sphincter of Oddi dysfunction is present in 30%-65% of patients with idiopathic acute recurrent pancreatitis in whom other diagnoses have been excluded. It is unclear if this sphincter dysfunction was the original etiology of the first episode of pancreatitis although it appears to have a causative role in recurring episodes since sphincter ablation decreases the frequency of recurrent attacks. Unfortunately, this conclusion is primarily based on small retrospective case series; larger prospective studies of the outcome of pancreatic sphincterotomy for SOD-associated acute pancreatitis are sorely needed. Another problem with this diagnosis and its treatment is the concern over potential procedure related complications from endoscopic retrograde cholangiopancreatography （ERCP）, manometry and pancreatic sphincterotomy. For these reasons, patients should have recurrent acute pancreatitis, not a single episode, and have a careful informed consent before assessment of the sphincter of Oddi is undertaken.     

Secretin MRCP and endoscopic pancreatic manometry in the evaluation of sphincter of Oddi function: a comparative pilot study in patients with idiopathic recurrent pancreatitis

BACKGROUND: Sphincter of Oddi dysfunction plays an important etiologic role in idiopathic acute recurrent pancreatitis. Sphincter of Oddi manometry is the most accurate test of sphincter of Oddi function, but it is associated with an increased risk of post-procedure pancreatitis and is non-diagnostic in about a third of cases. Secretin MRCP has a diagnostic efficacy comparable to ERCP, but data on its sensitivity with regard to sphincter of Oddi function are lacking. The aim of this study was to compare secretin MRCP and pancreatic sphincter of Oddi manometry for evaluation of sphincter of Oddi function in patients with idiopathic acute recurrent pancreatitis. METHODS: Eighteen consecutive patients with idiopathic acute recurrent pancreatitis underwent secretin MRCP and pancreatic sphincter of Oddi manometry/ERCP. Data from 15 patients were suitable for analysis. Fifteen subjects with asymptomatic, non-pancreatic hyperamylasemia matched for age and gender underwent secretin MRCP and served as a control group. RESULTS: Sphincter of Oddi manometry documented sphincter dysfunction in 6/15 patients (40%) and secretin MRCP, in 4/15 patients (26.7%). Sphincter of Oddi manometry confirmed the presence of elevated basal sphincter of Oddi pressure in two of the 4 patients with abnormal and other forms of sphincter of Oddi dyskinesia in the other two. None of the control subjects had an abnormal secretin MRCP. Secretin MRCP and sphincter of Oddi manometry were concordant in 13/15 patients (86.7%); positive and negative diagnoses for sphincter of Oddi dysfunction agreed in, respectively, 81.8% and 100% (kappa value 0.706). CONCLUSIONS: Secretin MRCP seems to be a useful noninvasive procedure for investigation of pancreatic sphincter of Oddi function, but evaluation in larger series is needed.     

PRSS1 and SPINK1 mutations in idiopathic chronic and recurrent acute pancreatitis

AIM: To identify gene mutations in PRSS1 and SPINK1 in individuals with early onset idiopathic chronic or recurrent acute pancreatitis.METHODS: The cationic trypsinogen gene (PRSS1; exons 2 and 3) and the serine protease inhibitor Kazal 1 gene (SPINK1; exon 3) were selectively amplified and sequenced from blood samples of 19 patients admitted to the Pancreas Clinic at our institution with chronic pancreatitis and/or idiopathic recurrent acute pancreatitis that were diagnosed or with onset before age 35. Fifty healthy volunteers served as controls. Whole blood samples were collected and gene specific sequences were amplified by polymerase chain reaction (PCR). All PCR products were subsequently sequenced in order to identify the presence of any mutations.RESULTS: Nineteen patients with pancreatitis (14 males; median age 24 years, range 15-48 years) were included in this study, of which five showed the presence of gene mutations. Direct sequencing results indicated the presence of two previously unidentified mutations in exon 2 of PRSS1 (V39E and N42S) in two patients with recurrent acute pancreatitis. Two cases had the N34S SPINK1 mutation. Analysis of the relatives of one patient homozygous for this mutation showed that five of the six family members carried the N34S SPINK1 mutation. Of these members, three were healthy heterozygous carriers and two were homozygotes (one sibling had diabetes, the other was healthy). Another patient was heterozygous for a novel SPINK1 mutation located on exon 3 (V46D). All members from this patient’s family had normal genotypes, indicating that it was a de novo mutation. No mutations in either gene were present in the control subjects.CONCLUSION: Two novel PRSS1 mutations and one novel SPINK1 mutation were identified in Mexican patients with early onset idiopathic recurrent acute pancreatitis.     

Histopathological study of pancreatic duct in acute fulminant pancreatitis

AIM: To study the pathological changes in the pancreas of acute fulminant pancreatitis patients suffering from sudden death. METHODS: Pancreatic duct specimens taken at autopsy from 30 patients with acute fulminant pancreatitis were examined under a light microscope for histopathological changes, with those of 30 other patients who died of other diseases as controls. RESULTS: Among the 30 cases of acute fulminant pancreatitis, 29 (96.7%) were non-inflammatory including hemorrhagic necrotic type (2 cases) and one were inflammatory. The pathological findings showed that all the above types had pancreatic ductal changes, including the accumulation of shed ductal epithelial cells, eosinophilic materials in the ductal lumen and the presence of ductules in the wall of the pancreatic duct. In the control group, except for 1 case presenting ductules, there were no other changes observed. CONCLUSION: Abnormal structural changes can cause damage to the ductal system of the pancreas, leading to an escape of activated proteolytic and lipolytic enzymes into the interstitial tissues and resulting in edema, ischemia, hemorrhage, necrosis and development of acute fulminant pancreatitis, which is an important cause of sudden death.     

Main pancreatic duct: morphlogy after acute biliary pancreatitis with magnetic resonance cholangiopancreatography after secretin stimulation.

OBJECTIVE: to assess whether a magnetic resonance cholangiopancreatography performed after an acute biliary pancreatitis leads to pancreatic morphological alterations and if secretin stimulation influences the visualization of the pancreatic tree. METHOD: forty patients with acute biliary pancreatitis, 25 female (62,5/) and 15 male (37,5/), 27 mild and 13 severe, were prospectively and consecutively studied. All patients had undergone cholecystectomy. No altered pancreatic functions were observed. Morphology of the pancreas and of the main pancreatic duct were assessed by magnetic resonance cholangiopancreatography five years after the episode of pancreatitis and a comparative study between patients and case controls was carried out. Secretin was given in 16 cases in whom the visualization of the duct was incomplete or absent. Ductal morphology before and after secretin stimulation was compared. RESUTLS: significant differences were observed when the diameter and length of the main pancreatic duct were compared in patients and control cases and was completely visualized in 60% of the cases, and could be seen in all patients after secretin stimulation. The comparative statistical analysis of the length and diameter of the pancreatic duct before and after the secretin stimulation showed significant differences. CONCLUSION: acute biliary pancreatitis leads to morphological alterations, regarded as scar lesions which do not become chronic. Secretin stimulation improves the visualization of the main pancreatic duct.     

急性胰腺炎后胰腺外分泌功能研究概况

近年来,急性胰腺炎发病率日益增高,而对于急性期后胰腺外分泌功能的恢复情况研究甚少。本文回顾分析相关国内外文献,对急性胰腺炎后胰腺外分泌功能的情况做一综述。     

杂种狗主胰管的解剖学及胰腺炎模型制作

目的了解杂种狗主胰管的长度和直径大小,复制狗水肿型和坏死型胰腺炎模型．方法杂种狗２３只,分对照组（ｎ＝７）和实验组（ｎ＝１６）,实验组经主胰管注入牛磺胆酸钠和胰蛋白酶分别复制水肿型（ＡＰ,ｎ＝８）和坏死型（ＡＮＰ,ｎ＝８）胰腺炎模型,测量主胰管的长度、直径,检测血中淀粉酶（Ａｍｙ）活性,并取胰腺作病理学观察．结果♀杂种狗主胰管长度１４５６ｍｍ±１７８ｍｍ,直径２２３ｍｍ±０１６ｍｍ;♂则分别为１４１９ｍｍ±２０１ｍｍ,２３１ｍｍ±０１８ｍｍ;实验组Ａｍｙ显著高于对照组,尤以ＡＮＰ组最为显著（ｍｍｏｌ／ｓ,ＡＰ：ｄ１,３７±１ｖｓ１４±１,ｄ２,３２±１ｖｓ１３±１;ＡＮＰ：ｄ１,１２３±２３ｖｓ１４±１,１１８±１９ｖｓ１３±１）;ＡＰ组胰腺腺泡可见充血、水肿,ＡＮＰ组胰腺腺泡大片出血、坏死．结论杂种狗主胰管的解剖特点适合用于复制理想的胰腺炎动物模型