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Background/Aims: The operative management of groove pancreatitis (GP) is still a matter of controversy and pancreaticoduodenectomy (PD) can be a high-risk procedure for patients. The aim of this study was to report our 9-year experience of surgical resection for GP and to review relevant literature. Methods: A retrospective review of patients undergoing pancreatectomy for GP from August 1, 2008, through May 31, 2017 was performed. Patients with clinical, radiologic, and final pathologic confirmation of GP were included. Literature on the current understanding of GP was reviewed. Results: Eight patients from total 449 pancreatectomies met inclusion criteria. Four male and 4 female patients (mean age, 51.9 years; mean body mass index, 25.3) underwent pylorus-preserving pancreatoduodenectomy (3 by laparoscopy and 5 by open approach). Mean (range) operative time and blood loss was 343 (167–525) min and 218 (40–500) mL respectively. Pancreatic fistula and delayed gastric emptying were noted in one patient each. No major complications occurred, but minor complications occurred in 5 (62%) patients. Mean hospital stay was 6.1 (range 3–14) days. At median follow-up of 18.15 (interquartile range 7.25–33.8) months, all patients experienced a resolution of pancreatitis and improvement in symptoms. Conclusions: PD is a safe procedure for GP. Short-term surgical outcomes are acceptable and long-term outcomes are associated with improved symptom control. [ABSTRACT FROM AUTHOR]

Chronic pancreatitis has long been thought to be mainly associated with immoderate alcohol consumption. The observation that only ∼10% of heavy drinkers develop chronic pancreatitis not only suggests that other environmental factors, such as tobacco smoke, are potent additional risk factors, but also that the genetic component of pancreatitis is more common than previously presumed. Either disease-causing or protective traits have been indentified for mutations in different trypsinogen genes, the gene for the trypsin inhibitor SPINK1, chymotrypsinogen C, and the cystic fibrosis transmembane conductance regulator (CFTR). Other factors that have been proposed to contribute to pancreatitis are obesity, diets high in animal protein and fat, as well as antioxidant deficiencies. For the development of pancreatic cancer, preexisting chronic pancreatitis, more prominently hereditary pancreatitis, is a risk factor. The data on environmental risk factors for pancreatic cancer are, with the notable exception of tobacco smoke, either sparse, unconfirmed or controversial. Obesity appears to increase the risk of pancreatic cancer in the West but not in Japan. Diets high in processed or red meat, diets low in fruits and vegetables, phytochemicals such as lycopene and flavonols, have been proposed and refuted as risk or protective factors in different trials. The best established and single most important risk factor for cancer as well as pancreatitis and the one to clearly avoid is tobacco smoke. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Groove pancreatitis is a segmental chronic pancreatitis that affects the anatomical area between the pancreatic head, the duodenum, and the common bile duct, referred to as the groove area. Most patients with groove pancreatitis are males aged 40–50 years with a history of alcohol abuse. In about 20% of patients undergoing pancreaticoduodenectomy to treat chronic pancreatitis, groove pancreatitis is detected. The clinical symptoms are weight loss, upper abdominal pain, postprandial vomiting, and nausea due to duodenal stenosis. The pathogenesis of groove pancreatitis is thought to be anatomical or functional obstruction of the minor papilla. The viscosity of pancreatic juice increases due to excessive alcohol consumption and/or smoking, leading to calcification of the pancreatic duct. According to these conditions, pancreatitis in the groove area might arise due to impaired pancreatic juice outflow. The descending part of the duodenum is usually stenotic. Severe fibrosis and scarring are evident in the groove area. Characteristic pathological findings are cystic lesions in the duodenal wall, Brunner gland hyperplasia, dilation of Santorini’s duct and protein plaques in the pancreatic duct. A differential diagnosis of groove pancreatitis from peripancreatic cancer is clinically important. Cystic lesions in the duodenal wall and smooth stenosis of the bile duct are important findings of groove pancreatitis revealed by endoscopic ultrasonography, computed tomography and magnetic resonance imaging. Biopsy through the duodenum is also useful for diagnosis. Conservative treatment options include endoscopic stenting of the minor papilla, but long-term outcomes remain unclear. Pancreatoduodenectomy is a rational treatment for symptomatic groove pancreatitis. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background/Aims: Hereditary pancreatitis (HP) is a rare cause of chronic pancreatitis (CP; 1%) and more than 25 mutations in the PRSS1 gene have been detected. HP patients with the p.R122H mutation have a 35% lifetime risk of developing pancreatic cancer, but the oncogenetic process remains unknown. We have investigated the histopathological features and frequency of BRAF and KRAS2 mutations in 2 patients with PRSS1 mutations (p.A121T, p.R122H) and patients with CP (n = 11). Methods: Pancreatic tissue was stained with hematoxylin-eosin and examined by light microscopy. Mutational analysis of the BRAF (exon 5, 11) and KRAS2 (exon 1) genes was performed using PCR and direct DNA sequencing. Results: Histopathological features revealed similar results in both patients, pancreata showed strong fibrosis and ducts with signs of distortion, irregular size and noticeable dilatations. We identified one BRAF mutation (p.V600E) in the p.R122H patient and two KRAS2 (p.G12D; p.G12C) mutations in CP controls. Conclusions: Our results sustain the knowledge about the clinical phenotype of patients with PRSS1 mutations who have a high risk of pancreatic cancer. Whether the histopathological picture or the BRAF mutation is specific for patients with PRSS1 mutations or plays a specific role in the tumorigenesis of patients with HP needs to be further evaluated. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]