Abstract:Acute pancreatitis (AP) is a common disease associated with a substantial medical and financial burden, and with an incidence across Europe ranging from 4.6 to 100 per 100,000 population. Although most cases of AP are caused by gallstones or alcohol abuse, several other causes may be responsible for acute inflammation of the pancreatic gland. Correctly diagnosing AP etiology is a crucial step in the diagnostic and therapeutic work-up of patients to prescribe the most appropriate therapy and to prevent recurren… Show more
“…Chronic pancreatitis is well known to predispose to pancreatic cancer development, the fourth cause of cancer-related deaths worldwide (4). Although alcohol abuse and gallstones are the main causes of AP, idiopathic pancreatitis such as viral pancreatitis represents a fairly high percentage of total cases (5). Type B Coxsackievirus (CVB) infection as a causing factor for AP was first reported in 1958 (6).…”
Coxsackievirus B is a common cause of viral myocarditis and pancreatitis. IL-17A is intensively involved in the pathogenesis of viral myocarditis. Whether IL-17A plays a role in Coxsackievirus B-induced pancreatitis, characterized by acinar cell destruction and immune infiltration, remains largely unknown. We found a significant, but transient, increase of IL-17A expression and gdT influx in the pancreas of C57BL/6J mice within 3 d following CVB3 infection. The pancreatic IL-17A was mainly produced by Vg4 gd T cells, to a lesser extent by CD4 + Th17 cells. IL-17A 2/2 and TCRd 2/2 mice both reduced their susceptibility to CVB3 infection and pancreatitis severity when compared with the wild-type mice, without altering viral load. mAb depletion of Vg4gd T cells significantly improved mice survival and pancreatic pathology via decreasing Th17 expansion and neutrophil influx into the pancreas compared with isotype-treated mice. Transfer of Vg4gd T cells from wild-type, but not IL-17 2/2 , mice reconstituted TCRd 2/2 mice to produce IL-17 and develop pancreatitis to the level of wild-type mice during CVB3 infection, indicating gd T IL-17A is required for the onset of viral pancreatitis. IL-23 was robustly induced in the pancreas within the first day of infection. Administration of exogenous rIL-23 to mice increased CVB3 pancreatitis through in vivo expansion of IL-17 + gdT17 cells at 12 h postinfection. Our findings reveal a key pathogenic role for early-activated gdT17 cells in viral pancreatitis via promoting neutrophil infiltration and Th17 induction. This IL-23/gdT17/neutrophil axis is critically involved in the onset of CVB3 pancreatitis and represents a potential treating target for the disease.
“…Chronic pancreatitis is well known to predispose to pancreatic cancer development, the fourth cause of cancer-related deaths worldwide (4). Although alcohol abuse and gallstones are the main causes of AP, idiopathic pancreatitis such as viral pancreatitis represents a fairly high percentage of total cases (5). Type B Coxsackievirus (CVB) infection as a causing factor for AP was first reported in 1958 (6).…”
Coxsackievirus B is a common cause of viral myocarditis and pancreatitis. IL-17A is intensively involved in the pathogenesis of viral myocarditis. Whether IL-17A plays a role in Coxsackievirus B-induced pancreatitis, characterized by acinar cell destruction and immune infiltration, remains largely unknown. We found a significant, but transient, increase of IL-17A expression and gdT influx in the pancreas of C57BL/6J mice within 3 d following CVB3 infection. The pancreatic IL-17A was mainly produced by Vg4 gd T cells, to a lesser extent by CD4 + Th17 cells. IL-17A 2/2 and TCRd 2/2 mice both reduced their susceptibility to CVB3 infection and pancreatitis severity when compared with the wild-type mice, without altering viral load. mAb depletion of Vg4gd T cells significantly improved mice survival and pancreatic pathology via decreasing Th17 expansion and neutrophil influx into the pancreas compared with isotype-treated mice. Transfer of Vg4gd T cells from wild-type, but not IL-17 2/2 , mice reconstituted TCRd 2/2 mice to produce IL-17 and develop pancreatitis to the level of wild-type mice during CVB3 infection, indicating gd T IL-17A is required for the onset of viral pancreatitis. IL-23 was robustly induced in the pancreas within the first day of infection. Administration of exogenous rIL-23 to mice increased CVB3 pancreatitis through in vivo expansion of IL-17 + gdT17 cells at 12 h postinfection. Our findings reveal a key pathogenic role for early-activated gdT17 cells in viral pancreatitis via promoting neutrophil infiltration and Th17 induction. This IL-23/gdT17/neutrophil axis is critically involved in the onset of CVB3 pancreatitis and represents a potential treating target for the disease.
“…5 Pancreatic trauma might trigger several consequences including pancreatic leaks, abscesses, pseudocysts, pancreatitis and pancreatic necrosis. [6][7][8][9][10] The risk of complications and mortality should be considered with extensive parenchymal and ductal injuries as well as when the diagnosis is delayed. 11,12 Evaluation of the extent of pancreatic injury by various imaging techniques in the setting of abdominal trauma might be demanding.…”
Background: Management of pancreatic trauma remains challenging due to difficulty in diagnosis and complexity of surgical interventions. In Egypt, reports on pancreatic trauma are scarce.Methods: Medical records of adult patients with pancreatic trauma who were admitted at Sohag University Hospital (2012-2019) were retrospectively studied. Patients were categorized into group A of non-operative management (NOM), group B which required upfront exploratory laparotomy due to hemodynamic instability and group C in which surgical management was implemented after thorough preoperative assessment. Pancreatic injuries were ranked by the pancreas injury scale (PIS).Results: Thirty-two patients (25 males and 7 females) were enrolled, and median age of 36 (range: 23-68) years. Twenty-eight patients (87.5%) had blunt trauma whereas penetrating injury occurred in 4 (12.5%). There were 9 patients in group A, 7 in group B and 16 in group C. High grades of pancreatic injury ≥3 occurred in 4 patients from group B and 5 from group C. Distal pancreatectomy was performed in 7 patients while central resection and panceatico-gastrostomy in one. Grade IV injury occurred only in one patient who received damage-control laparotomy. Post-operative complication were significantly increased in group B compared with C, in correlation worse hemodynamic status and increased severity of PIS. Post-operative mortality occurred in 2 patients (6%), both from group B. Late consequences included pancreatic pseudocyst (4 cases) and walled off pancreatic necrosis (2 cases).Conclusions: High grades of pancreatic injury and hemodynamic instability correlate with worse outcome after surgery for pancreatic trauma.
“…Acute pancreatitis continues to be one of the most common gastrointestinal (GI) conditions requiring hospitalization. The term "idiopathic acute pancreatitis" (IAP) is used when the most common causes of acute pancreatitis, like alcohol and gallstones, have been ruled out, with there also being no discernible etiology after extensive evaluation of patient history, physical examination, laboratory tests, and conventional imaging studies [1,2]. Transabdominal ultrasound and computed tomography (CT) are the usual initial imaging modalities and are indicated after causes such as drugs, infections, genetic mutations, and metabolic disorders, such as hypercalcemia and hypertriglyceridemia, have been ruled out.…”
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confidence: 99%
“…Despite the above work-up, an etiology is not established in approximately 10 % -30 % of acute pancreatitis cases [4]. In such cases, current recommendations suggest at least two GI imaging techniques be performed that include endoscopic ultrasonography (EUS) and magnetic resonance cholangiopancreatography (MRCP) to further evaluate a cause for the acute pancreatitis [1,2]. Undetected microlithiasis and/or biliary sludge has been considered as one of the major undiagnosed causes of IAP accounting for 30 % -80 % of cases.…”
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confidence: 99%
“…Undetected microlithiasis and/or biliary sludge has been considered as one of the major undiagnosed causes of IAP accounting for 30 % -80 % of cases. Other causes that could potentially be diagnosed by GI imaging modalities are pancreas divisum, sphincter of Oddi dysfunction, a choledochocele, an anomalous pancreaticobiliary junction, an annular pancreas, and pancreatic and/or ampullary neoplasms [1,2].…”
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