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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute pancreatitis is an inflammatory disease of the pancreas. Acute abdominal pain is the most common symptom, and increased concentrations of serum amylase and lipase confirm the diagnosis. Pancreatic injury is mild in 80% of patients, who recover without complications. The remaining patients have a severe disease with local and systemic complications. Gallstone migration into the common bile duct and alcohol abuse are the most frequent causes of pancreatitis in adults. About 15-25% of pancreatitis episodes are of unknown origin. Treatment of mild disease is supportive, but severe episodes need management by a multidisciplinary team including gastroenterologists, interventional radiologists, intensivists, and surgeons. Improved understanding of pathophysiology and better assessments of disease severity should ameliorate the management and outcome of this complex disease.
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PMID:Acute pancreatitis. 1837 39

Pancreatitis is a severe and frequently lethal disorder, a major cause of which is alcohol abuse. Parenchymal cell death is a major complication of pancreatitis. In experimental models of acute pancreatitis, acinar cells have been shown to die through both necrosis and apoptosis, the two principal pathways of cell death. The severity of experimental acute pancreatitis correlates directly with the extent of necrosis and inversely with apoptosis. Thus, understanding the regulation of apoptosis and necrosis is becoming exceedingly important in investigations of the pathogenesis and treatment of pancreatitis. Over the past decade, the mitochondria have emerged as a master regulator of cell death in various physiological and pathological processes. Release of mitochondrial cytochrome c into the cytosol is a central event in apoptosis, whereas mitochondrial depolarization resulting in ATP depletion leads to necrosis. The present review focuses on the mitochondrial mechanisms of death responses in pancreatitis, with emphasis on mitochondrial membrane permeabilization and its role in the balance between apoptosis and necrosis in acute pancreatitis, and alcohol's effects on death responses of pancreatitis.
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PMID:Mitochondrial mechanisms of death responses in pancreatitis. 1833 59

Acute pancreatitis (AP) is an acute inflammatory disease of the pancreas. Severe acute pancreatitis (SAP) is the serious forms of AP with high mortality rate. However, the frequency of SAP remains stable over time. Biliary calculi and alcohol abuse are the most common causes of AP. Other causes such as iatrogenic factors, sphincter of Oddi dysfunction (SOD) and eating disorders also cannot be omitted. Blockage of duodenal papilla or ampulla of Vater is common characteristics of AP. Once the blockage appears, the occurrence of pancreatic duct obstruction and bile reflux is inevitable. Obstruction of the pancreatic duct leads to increased intraductal pressure, which results in damage to the integrity of the duct system to a certain extent. Bile reflux can activate trypsin and once trypsin is activated, it activates a variety of injurious pancreatic digestive enzymes with subsequent release of a series of inflammatory mediators. We hypothesized that pancreatic duct obstruction and bile reflux are the key event of AP induced by a variety of other upstream causes. Pancreatic duct obstruction and bile reflux, not a single one can be omitted. Whenever pancreatic duct obstruction and bile reflux are triggered simultaneously, activated digestive enzymes and inflammatory mediators can infiltrate into the parenchyma of the pancreas through impaired pancreatic barrier and induce AP. Blocking the key event of AP is of a great interest with potential therapeutic implications. Endoscopic sphincterotomy (EST) and nasobiliary drainage, which target the cause of AP, may prevent the transformation from AP to SAP and this may be adopted as an essential treatment strategy.
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PMID:The key event of acute pancreatitis: pancreatic duct obstruction and bile reflux, not a single one can be omitted. 1914 95

Acute pancreatitis is an inflammatory process of the pancreas with variable involvement of regional tissues and remote organs. This review gives a comprehensive overview of the aetiology, pathophysiology, diagnosis and therapy of acute pancreatitis relevant to the intensivist. Recent international guidelines on the management of acute pancreatitis are summarised. Eighty percent of acute pancreatitis episodes are related either to gallstones or to alcohol abuse. Independent of its aetiology, the pathophysiologic hallmark of acute pancreatitis is the premature activation of trypsin, which leads to massive pancreas inflammation, systemic overproduction of pro-inflammatory mediators and ultimately remote organ dysfunction. All guidelines agree that the diagnosis of acute pancreatitis should include clinical symptoms, increased serum amylase or lipase levels and/or characteristic findings on computed tomography. Endoscopic retrograde cholangiopancreatography is recommended as a causative therapy in patients with acute cholangitis or a strong suspicion of gallstones. All guidelines underline the importance of vigorous fluid resuscitation and supplemental oxygen therapy and prefer enteral over parenteral nutrition, with the majority favouring the nasojejunal route. In view of lacking scientific evidence, antibiotic prophylaxis to prevent infection of pancreatic necroses is discouraged by most guidelines. Computed tomography-guided fine needle aspiration is the technique of choice to differentiate between sterile and infected pancreas necrosis. While sterile pancreatic necrosis should be managed conservatively, infected pancreatic necrosis requires debridement and drainage supplemented by antibiotic therapy. Surgical necrosectomy is the traditional approach, but less invasive techniques (retroperitoneal or laparoscopic necrosectomy, computed tomography-guided percutaneous catheter drainage) may be equally effective.
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PMID:Critical care of the patient with acute pancreatitis. 1940 Apr 83

Acute pancreatitis (AP) is an inflammatory disease characterized by steady, acute abdominal pain of varying severity, often radiating from the epigastrium to the back. Its presentation ranges from a self-limiting mild disorder to a more severe and fulminant disease. Severe acute pancreatitis accounts for 30% of all deaths related to pancreatitis. The incidence of AP is increasing progressively with a corresponding increase in the incidence of its risk factors. Alcohol abuse and gallstone migration are the established risk factors for development of AP. In recent years, genetic factors and obesity have also been identified as risk factors responsible for the development of AP. The pathophysiology of AP involves acute inflammation of the acinar cells. Excessive acinar cell injury leads to a condition called systemic inflammatory response syndrome (SIRS). Protracted SIRS is responsible for most of the life-threatening complications associated with AP. Most common AP-related complications include pulmonary, renal, cardiovascular, and central nervous system dysfunction. Thus prompt and accurate diagnosis of AP is of paramount importance. The medical management of AP includes controlling pain, providing adequate nutritional support, and monitoring complications. Endoscopic retrograde cholangiopancreatography and surgery have also shown to reduce the mortality and morbidity associated with AP. Drugs such as resveratrol and rosiglitazone are being investigated as potential candidates for the treatment of AP.
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PMID:Acute pancreatitis: a literature review. 1956 40

Acute pancreatitis is a potentially lethal inflammatory disease with an increased incidence and a decreased mortality rate. The main etiologies are biliary stones and alcohol abuse. The therapeutic approach consists of the elimination of the cause, the hemodynamic and respiratory supports and the treatment of the complications. Moreover, severe acute pancreatitis requires a collaboration between surgeons, radiologists, gastroenterologists and intensive care physicians. The administration of prophylactic antibiotics and the early oral nutritional support are still controversial. In summary, the anticipation in diagnosis, etiology, classification of the severity and early reanimation are needed for an optimal treatment of this complex disease.
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PMID:[Acute pancreatitis or the need of anticipation]. 1971 20

Acute pancreatitis is an inflammatory disorder, that is classically accompanied by abdominal pain and elevated serum lipase and amylase levels. While about 80% of the patients recover without complications, 20% develop severe local and systemic damages. Gallstone migration into the common bile duct and excessive alcohol abuse account for most of the cases, but also drugs have been shown to induce acute pancreatitis. Treatment of acute pancreatitis is only supportive, especially in severe episodes an interdisciplinary cooperation of gastroenterologists, radiologists, intensivists, and surgeons is required. The better understanding of the pathophysiology might merge into more tailored therapeutic procedures and improve the outcome of this disease.
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PMID:[Acute pancreatitis: etiology, diagnosis and therapy]. 1973 51

Pancreatitis and pancreatic cancer represent two major diseases of the exocrine pancreas. Pancreatitis exhibits both acute and chronic manifestations. The commonest causes of acute pancreatitis are gallstones and alcohol abuse; the latter is also the predominant cause of chronic pancreatitis. Recent evidence indicates that endotoxinemia, which occurs in alcoholics due to increased gut permeability, may trigger overt necroinflammation of the pancreas in alcoholics and one that may also play a critical role in progression to chronic pancreatitis (acinar atrophy and fibrosis) via activation of pancreatic stellate cells (PSCs). Chronic pancreatitis is a major risk factor for the development of pancreatic cancer, which is the fourth leading cause of cancer-related deaths in humans. Increasing attention has been paid in recent years to the role of the stroma in pancreatic cancer progression. It is now well established that PSCs play a key role in the production of cancer stroma and that they interact closely with cancer cells to create a tumor facilitatory environment that stimulates local tumor growth and distant metastasis. This review summarizes recent advances in our understanding of the pathogenesis of alcoholic pancreatitis and pancreatic cancer, with particular reference to the central role played by PSCs in both diseases. An improved knowledge of PSC biology has the potential to provide an insight into pathways that may be therapeutically targeted to inhibit PSC activation, thereby inhibiting the development of fibrosis in chronic pancreatitis and interrupting stellate cell-cancer cell interactions so as to retard cancer progression.
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PMID:New insights into alcoholic pancreatitis and pancreatic cancer. 1979 99

Pathologic responses arising from the pancreatic acinar cell appear to have a central role in initiating acute pancreatitis. Environmental factors that sensitize the acinar cell to harmful stimuli likely have a critical role in many forms of pancreatitis, including that induced by alcohol abuse. Activation of zymogens within the acinar cell and an inhibition of secretion are critical, but poorly understood, early pancreatitis events. While there is firm evidence relating trypsinogen activation to pancreatitis, the importance of other zymogens has been less studied. Preliminary studies suggest that trypsin may be activated by mechanisms that are distinct from other zymogens. Further, unlike the small intestine, it may not catalyze the activation of other zymogens. These features could affect strategies aimed at inhibiting proteases to treat pancreatitis. Specific intracellular signals are required to activate pancreatitis pathways in the acinar cell. The most important is calcium. Recent studies have suggested that calcium release through specific calcium channels in the endoplasmic reticulum is the means by which pathological elevations in cytosolic calcium occur. Although the targets of abnormal calcium signaling are unknown, calcineurin, a calcium-dependent phosphatase, may serve such a role. Finally, recent work suggests that an acute acid load might sensitize the acinar cell to pancreatitis responses. Therapies aimed at preventing or reversing the effects of an acid load on the pancreas may be important for treatment.
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PMID:The acinar cell and early pancreatitis responses. 1989 90

Acute pancreatitis occasionally presents as pancreatic abscess with complications like pleural effusion and ascites. There are several pre-disposing factors, the most common being cholelithiaisis, alcohol abuse, infective causes, trauma, and metabolic causes such as diabetic ketoacidosis, while some cases are idiopathic. Here, we report a rare case of acute necrotizing pancreatitis in a 40-year-old male who presented with pain in the abdomen, ascites and left basal pleural effusion. A computerized tomography (CT) scan showed findings suggestive of pancreatic necrosis, with abscess formation and free-fluid surrounding area. The aspirated pus sample was processed for Gram staining and culture, which yielded growth of Prevotella species in an anaerobic culture. Exploratory laparotomy was performed and intra-abdominal collection drained. Necrosectomy of the distal tail and body of the pancreas was performed. The patient was started on antibiotics and along with supportive treatment, responded well.
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PMID:Acute necrotizing pancreatitis with pancreatic abscess due to Prevotella species in a diabetic. 2006 70


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