Absence Of Pancreatic Duct Dilatation Research Articles

S1766 Metastatic Renal Cell Cancer with Pancreatic Mass

Introduction: Pancreas is an uncommon site of metastatic disease. Almost 63% of pancreatic metastasis arise from renal cell cancer. We report a case of metastatic renal cell cancer to pancreas, with contralateral adrenal metastasis 15 years after a radical nephrectomy. Case Description/Methods: 61 years old man with past medical history of renal cell cancer, status post left radical nephrectomy fifteen years ago, presented with dull pain in right lower abdominal for one day. He denied any other abdominal symptoms or weight loss. He smokes up to half a pack of cigarettes daily. His examination was unremarkable but he was noted to have elevated lipase (213U/L) and a bilirubin of 1.1 mg%. On computer tomography abdomen he had bulky, enhancing, soft tissue mass (∼6.7 cm), with dilated pancreatic duct of 1.5 cm with right adrenal mass (Figure). On EUS, the lesion appeared well circumscribed and previously known pancreatic duct dilation was seen. Fine needle biopsy of the mass, which showed numerous atypical cells with round irregular nuclei with prominent nucleoli with clear cytoplasm suggestive of clear cell renal cell carcinoma (Figure). On immune -histochemistry, the tumor was positive for CD10, renal cell carcinoma antigen and PAX 8( Figure) Discussion: Metachronous renal cell cancer to pancreas fifteen years after radial nephrectomy is rare. Our patient had pancreatic metastasis with adrenal involvement and presented with vague abdominal symptoms. .He was noted to have elevated lipase and dilation of main pancreatic duct. Due to a remote history of nephrectomy and the presenting complaints, pancreatic primary was suspected. However, on endoscopic ultrasound the patient was noted to have a well circumscribed lesion in the head of pancreas with dilated pancreatic duct(Figure). Regular borders and absence of pancreatic duct dilation suggested metastatic disease. Our patient had well circumscribed lesion but with a dilated duct. Most pancreatic metastasis are reported to occur within 10 years after treatment of the primary disease but our patient had metastasis fifteen years later without any loco-regional recurrence. Endoscopic ultrasound is extremely important and allows to evaluate the extent of the disease, involvement of portal vein/ superior mesenteric artery, presence of enlarged lymph nodes, which are a must for evaluating the surgical candidature besides providing tissue diagnosis which helped us establish the diagnosis of metastasis.Figure 1.: CT(A,B,C) and EUS(D,E) findings. Image A shows the mass in the Pancreatic head(arrow with red head) with a dilated pancreatic duct seen in imageB( arrow with red head). Adrenal metastasis is seen in image C marked with a red arrow. On EUS, the mass appears well circumscribed( blue arrow, image D) with dilated pancreatic duct seen ( green arrow) in the head of pancreas in E.

A Risk Prediction Model for Post-endoscopic Retrograde Cholangiopancreatography Pancreatitis After Stent Insertion for Malignant Biliary Obstruction: Development and Validation.

Pancreatitis is the most common complication of post-endoscopic retrograde cholangiopancreatography (ERCP). There are currently no prediction models, particularly for post-ERCP pancreatitis (PEP) after biliary stent placement due to malignant biliary obstruction (MBO). To that end, we aim to develop and validate a predictive model for PEP. We retrospectively analyzed the data of patients who underwent ERCP for biliary stent placement due to MBO at the Second Affiliated Hospital of Harbin Medical University from January 1, 2014 to August 31, 2021. The eligible patients were randomly allocated to the development and validation cohorts. A prediction model was built using the development cohort, and the model's effect was validated using a validation cohort. A total of 1524 patients were enrolled, including 1016 in the development cohort and 508 in the validation cohort, with an overall PEP rate of 7.1%. The model's predictors included acute pancreatitis history, the absence of pancreatic duct dilation, nonpancreatic cancer, difficult cannulation, and pancreatic injection. The area under the curve (AUC) in the development cohort was 0.810, and the incidence of PEP in the low-risk, medium-risk, and high-risk groups was 1.53%, 9.12%, and 36.36%, respectively. Meanwhile, the AUC of the validation cohort was 0.781, and the incidence of PEP in the low-risk, medium-risk, and high-risk groups was 4.17%, 8.75%, and 41.67%, respectively. This study was the first to build and validate a risk prediction model, especially for PEP after biliary stent placement due to MBO. Moreover, this model might assist clinicians in identifying high-risk patients and help implement preventive measures in a more timely manner.

Influence of fully covered metal stenting on the risk of post‐endoscopic retrograde cholangiopancreatography pancreatitis: A large multicenter study·

Fully covered self-expandable metal stents (FCSEMSs) have been increasingly used in the management of benign or malignant biliary disorders. However, the risk of post-endoscopic retrograde cholangiopancreatography pancreatitis (PEP) with transpapillary placement of the FCSEMS remains controversial. This study therefore aimed to investigate the risk of PEP in patients who received FCSEMS implantation. In total, 602 patients who underwent endoscopic transpapillary FCSEMS placement at five Chinese medical centers, between 2011 and 2018, were included in this retrospective study. Patients who were younger than 18years and with stent placement above the papilla were excluded from the study. PEP and the risk factors were reviewed. PEP occurred in 56 (9.3%) patients, and eight (1.3%) of them experienced moderate-to-severe PEP. The incidence of PEP rose to 14.6% (51/349) when patients had no pancreatic duct (PD) dilation, and even to 18.6% if no prophylactic approaches were adopted. Prophylactic PD stenting showed better efficacy in reducing the incidence of PEP than did rectal use of indomethacin (3.5% vs 10.8%, P=0.023). Multivariate logistic regression revealed that difficult cannulation (OR 2.837, 95% CI 1.245-6.465, P=0.013), PD dilation (OR 0.145, 95% CI 0.05-0.422, P<0.001), and PD stenting (OR 0.247, 95% CI 0.089-0.686, P=0.007) were significantly associated with PEP risk. Post-procedure cholecystitis was found in 4.0% of patients. The risk of post-procedure pancreatitis is modestly increased in patients receiving transpapillary FCSEMS placement, particularly when there is absence of PD dilation. Thus, prophylactic pancreatic stenting is recommended in such a condition.

Nonhypervascular pancreatic neuroendocrine tumors: Spectrum of MDCT imaging findings and differentiation from pancreatic ductal adenocarcinoma

PurposeThe purpose of our study was to determine contrast-enhanced MDCT features to differentiate nonhypervascular pancreatic neuroendocrine tumors (PNETs) from pancreatic ductal adenocarcinomas (PDACs). Methodsand materials: We included 74 patients with PNETs and 80 patients with PDACs who underwent preoperative MDCT. Two radiologists evaluated the morphologic characteristic and enhancement patterns of the tumors. Quantitative and qualitative analysis was performed, including evaluation of tumor size, homogeneity, contrast enhancement pattern, presence of pancreatic duct dilatation and tumor invasion to the adjacent vessels and peripancreatic infiltration. Tumor-to-pancreas enhancement ratio was defined as the Hounsfield units (HU) value of the tumor divided by the HU value of the pancreas. the first group was hypervascular PNETs showing hyperenhancement on arterial phase images and nonhypervascular PNETs, showing iso- or hypoenhancement on arterial phase images. After that, two radiologists estimated the possibilities of PNET or PDAC were for nonhypervascular PNETs. ResultsOn the basis of arterial enhancement, 43 PNETs were hypervascular and 31 were nonhypervascular. When compared to PDAC, nonhypervascular PNETs more frequently had well-defined tumor margins, intratumoral cystic components, calcifications and blood vessels and less frequently had main pancreatic duct dilatation, peripancreatic infiltration and vascular invasion (p < 0.01 for all). Nonhypervascular PNETs had higher tumor-to-pancreas enhancement ratio in venous phase (1.02 vs. 0.78, p = 0.012). Nonhypervascular PNETs more often had portal-venous hyperenhancement or persistent isoenhancement, while PDAC more often had persistent hypoenhancement or gradual delayed enhancement (p < 0.001). The absence of pancreatic duct dilatation and portal-venous hyperenhancement or persistent isoenhancement were the independent predictors for nonhypervascular PNETs.(The most accurate MDCT-findings to predict nonhypervascular PNET were the absence of pancreatic duct dilatation and peripancreatic infiltration (79% and 92% accuracy), portal-venous phase hyperenhancement or persistent isoenhancement (77%), the presence of intratumoral blood vessels (77%) and relative enhancement intensity in venous phase >0.9 (76%). Using these criteria, the area under curve for differentiation of PNET from PDAC was 0.906–0.846. ConclusionCombined assessment of the enhancement and morphologic characteristics can improve the differentiation between nonhypervascular PNETs and PDAC at contrast-enhanced MDCT.

Differentiating Autoimmune Pancreatitis From Pancreatic Adenocarcinoma Using Dual-Phase Computed Tomography

This article aimed to study features on dual-phase computed tomography (CT) that help differentiate autoimmune pancreatitis (AIP) from pancreatic adenocarcinoma (PA). The CTs of 32 patients with AIP were matched with equal number of PA and were independently evaluated by 3 radiologists who assigned a diagnosis of AIP, PA, or unsure. Interobserver agreement between radiologists was evaluated using κ statistics. The mean accuracies for diagnosing AIP and PA were 68% and 83%, respectively. There was moderate agreement between radiologists (κ, 0.58; P < 0.0001). The most common findings for AIP were common bile duct (CBD) stricture (63%), bile duct wall hyperenhancement (47%), and diffuse parenchymal enlargement (41%). The most common findings for PA were focal mass (78%; κ, 0.58; P < 0.0001) and pancreatic ductal dilatation (69%; κ, 0.7; P < 0.0001). Findings helpful for diagnosing AIP were diffuse enlargement, parenchymal atrophy as well as absence of pancreatic duct dilatation and focal mass. Findings helpful for diagnosing PA were focal mass and pancreatic ductal dilatation. Misdiagnosis of PA in patients with AIP was due to focal mass, pancreatic duct dilatation, and pancreatic atrophy, whereas misdiagnosis of AIP in patients with PA was due to absence of atrophy, presence of diffuse enlargement, and peripancreatic halo. Diffuse enlargement, hypoenhancement, and characteristic peripancreatic halo are strong indicators for a diagnosis of AIP. Radiologists demonstrated moderate agreement in distinguishing AIP from PA on the basis of CT imaging.

RESULT OF SURGICAL TREATMENT FOR CHRONIC PANCREATITIS

Of 32 patients with chronic pancreatitis who could be followed for more than six months postoperatively, those showing no dilatation of the pancreatic duct, defined as having a main pancreatic duct less than 6mm in diameter, underwent an analysis of their clinical pictures and operative results to investigate a desirable method of surgical treatment for this condition. Of eight patients with an absence of pancreatic duct dilatation, localized lesions were found in five. These were disorders of pancreatic endocrine and exocrine functions and pancreatic fibrosis, the dogree being mild in most cases. In one patient with lesions in the head of the pancreas, plastic surgery of the papillopancreatic duct orifice for the purpose of removing pain seemed to be sufficient because there was no stenosis of the main pancreatic duct or other accessory lesions. In four patients with lesions in the caudal area, which were accompanied by accessory lesions such as stenosis of the main pancreatic duct at that area, cyst, and abscess, pain removal procedure or partial pancreatectomy on the caudal side for the accessory lesions was considered necessary. Diffuse lesions were found in three patients, who also showed moderate or severe disorders of pancreatic endocrine and exocrine functions and pancreatic fibrosis. In such cases, extensive pancreatectomy including total pancreatectomy, is usually indicated. However, there are some doubts about the propriety of extensive pancreatectomy only for the purpose of removing pain. In this regard, we consider infusion of a sclerosing agent into the main pancreatic duct and total excision of the pancreatic plexus. The former method, however, has various problems to solve before its clinical application, requiring development of a new sclerosing agent. As for total excision of the pancreatic plexus, we have so far experienced only one patient, who has been followed up for a relatively short period of three months, with an extremely favorable course of postoperative conditions. It seems that this technique is a nromising surgical method for this condition.

Absence of Pancreatic Duct Dilation in Chronic Pancreatitis

Of 22 patients treated surgically for intractable pain from chronic alcoholic pancreatitis, eight did not show notable dilation of the main pancreatic duct by endoscopic retrograde cholangiopancreatography (ERCP), operative pancreatography, and/or operative and microscopical studies of the pancreas after subtotal pancreatectomy. In all patients, far advanced parenchymal pancreatitis was evident at operation and by microscopical study of the removed portion of the pancreas. These findings indicate that the basic problem in a considerable number of patients with symptomatic alcoholic chronic pancreatitis is not related primarily to obstruction with dilation of the major pancreatic duct, but to intrinsic changes in the parenchymal pancreas. The preoperative use of ERCP and individualization of operative procedures with a preference for subtotal or partial pancreatectomy for symptomatic chronic alcoholic pancreatitis are supported.

The political-economic dynamics of California's farm labor market-a highly specific model of international factor flows

The purpose of our study was to determine contrast-enhanced MDCT features to differentiate nonhypervascular pancreatic neuroendocrine tumors (PNETs) from pancreatic ductal adenocarcinomas (PDACs).and materials: We included 74 patients with PNETs and 80 patients with PDACs who underwent preoperative MDCT. Two radiologists evaluated the morphologic characteristic and enhancement patterns of the tumors. Quantitative and qualitative analysis was performed, including evaluation of tumor size, homogeneity, contrast enhancement pattern, presence of pancreatic duct dilatation and tumor invasion to the adjacent vessels and peripancreatic infiltration. Tumor-to-pancreas enhancement ratio was defined as the Hounsfield units (HU) value of the tumor divided by the HU value of the pancreas. the first group was hypervascular PNETs showing hyperenhancement on arterial phase images and nonhypervascular PNETs, showing iso- or hypoenhancement on arterial phase images. After that, two radiologists estimated the possibilities of PNET or PDAC were for nonhypervascular PNETs.On the basis of arterial enhancement, 43 PNETs were hypervascular and 31 were nonhypervascular. When compared to PDAC, nonhypervascular PNETs more frequently had well-defined tumor margins, intratumoral cystic components, calcifications and blood vessels and less frequently had main pancreatic duct dilatation, peripancreatic infiltration and vascular invasion (p < 0.01 for all). Nonhypervascular PNETs had higher tumor-to-pancreas enhancement ratio in venous phase (1.02 vs. 0.78, p = 0.012). Nonhypervascular PNETs more often had portal-venous hyperenhancement or persistent isoenhancement, while PDAC more often had persistent hypoenhancement or gradual delayed enhancement (p < 0.001). The absence of pancreatic duct dilatation and portal-venous hyperenhancement or persistent isoenhancement were the independent predictors for nonhypervascular PNETs.(The most accurate MDCT-findings to predict nonhypervascular PNET were the absence of pancreatic duct dilatation and peripancreatic infiltration (79% and 92% accuracy), portal-venous phase hyperenhancement or persistent isoenhancement (77%), the presence of intratumoral blood vessels (77%) and relative enhancement intensity in venous phase >0.9 (76%). Using these criteria, the area under curve for differentiation of PNET from PDAC was 0.906–0.846.Combined assessment of the enhancement and morphologic characteristics can improve the differentiation between nonhypervascular PNETs and PDAC at contrast-enhanced MDCT.