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

The autotransplant of the left lobe of the pancreas in the latero-cervical region has been successfully performed in 38 adult beagles with a mean cold ischemia time of 52 minutes. Juice volume and amylase, protein and bicarbonate outputs were resumed postoperatively as soon as 6 hours. A single case of thrombosis of the mesenteric vein occurred; all other pancreatic grafts showed good histological vitality at 30 days. This procedure of autografting is proposed as a valid experimental model for the pathophysiologic study of acute pancreatitis.
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PMID:[Functional results of experimental autologous transplantation of the pancreas]. 1044 26

IVR has attracted much attention in Japan over the past decade, and it is expected to be rapidly developed and widely used. Not surprisingly, IVR has already become essential in emergency medicine. This paper addresses IVR of the thoracic and abdominal areas and the pelvis in emergency medicine, in particular the recent IVR focus on the vasculature. CO2-DSA, which enables extravasation and easy detection of a arteriovenous or portal shunt, is also useful in the detection of bleeding in emergency situations. In trauma cases, TAE, originating from an expanded concept of "damage control," is commonly used to stop bleeding in order to perform surgical treatment or used during surgery. Occasionally the two applications are combined when appropriate. TAE is effective in controlling retroperitoneal bleeding resulting from pelvic fracture and parenchymatous organ injuries in the abdominal area. Treatment with stent-grafts, originally used to treat true aneurysms, has recently been used for treatment of injuries of the aorta or arteries and for entry closure due to aortic dissection. Furthermore, stent placement is expected to become an effective cure for organ ischemia, resulting from acute dissections. Is addition, in order to cure rupture of esophagus or gastric varices, such new treatments as TIPS and BRTO have increasingly been used, coupled with the conventional PTO treatment. Continuous regional arterial infusion of protease inhibitor, in an attempt to cure severe acute pancreatitis, significantly reduced the infectious rate at the necrotic lesion, and its resulting mortality rate. It is certain that great progress has been made in emergency medicine. We also should realize that it is desirable to be well versed even in new IVR.
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PMID:[Progress in interventional radiology (IVR) in emergency medicine]. 1048 49

Shock is a biological response associated with hypotension and signs of altered tissue perfusion. Shock can be induced by many different mechanisms. Shock itself induces cytokine production as a result of disturbed microcirculation or ischemia-reperfusion injury. Alternatively, severe inflammatory conditions, such as sepsis and severe acute pancreatitis, are usually associated with prominent mediator production, which often leads to shock. TNF-alpha and IL-1 beta increase the vascular permeability, and nitric oxide reduces systemic vascular resistance. In the management of patients who have experienced clinical insult, we must consider the symptoms of systemic inflammatory response syndrome provoked by inflammatory mediators as a warning sign of the development of shock and organ dysfunction. Early withdrawal from SIRS and avoidance of infectious complications (second attack) should be attempted.
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PMID:[Shock and its mediators]. 1057 Jul 77

In healthy subjects, the 3 known pancreatic trypsinogens, which are endopeptidases belonging to the chymotrypsin superfamily, are activated by enterokinase and partial autoactivation in the duodenum. The premature activation of trypsinogen in the pancreatic interstitium, with the subsequent activation of other pancreatic zymogens, is believed to lead to the autodigestion of the gland, this being the first event in acute pancreatitis. The mechanisms that lead to trypsinogen, activation in acute pancreatitis are largely unknown. However, ischemia, hypercalcemia and the activation of cathepsin B (by cholecystokinin) are thought to be of importance. The easiest and most reliable way to assess trypsinogen activation is the measurement of the activation peptide, TAP, in urine, plasma, pancreatic tissue or ascitic fluid. In the animal model of acute pancreatitis, TAP in ascites and pancreatic tissue has been shown to correlate with the presence and extent of necroses. It has proven to be a good marker for the severity of pancreatitis and is a useful marker in examining the pathophysiology and possible treatment modalities in the animal model of acute pancreatitis. Studies on TAP in human acute pancreatitis were most commonly focused on urinary TAP. Within a 48-hour time frame after the onset of the disease, TAP was a good predictor of the severity of acute pancreatitis. The main advantage over other markers, such as CRP, is that TAP is the earliest marker of necrosis to be increased. Also, increased levels of TAP in ascitic fluid were shown to correlate well with pancreatic necroses. In our experience, plasma TAP was found to have a "diagnostic window" within the first 3 days predicting pancreatic necroses. Positive TAP gave a very good positive prediction and a high specificity towards the development of pancreatic necroses, but did not differ between necrotizing pancreatitis with systemic complications or uncomplicated necrotizing pancreatitis. We therefore think that plasma TAP is a very good marker for local complication in acute pancreatitis and its routine measurements may help to identify patients at a high risk within the first days of the disease.
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PMID:Mechanism and role of trypsinogen activation in acute pancreatitis. 1057 41

Ischaemia is a rare but often lethal aetiology of pancreatitis. A 67-year-old man underwent aortocoronary by-pass. Postoperatively, he developed atrial fibrillation and possibly acute myocardial infarction. Later, he had acute pancreatitis and underwent laparotomy for purulent peritonitis due to a ruptured pancreatic abscess. Cholesterolosis was found but no gallstones. The postoperative period was heavily complicated and the patient eventually died due to multiorgan failure. The occurrence of ischaemic pancreatitis should be more readily suspected in patients with abdominal symptoms following surgery that induces ischaemia of the pancreas. It is possible that delay in diagnosis accounts for the high death rate of such postoperative complication.
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PMID:Ischaemic necrotizing pancreatitis after cardiac surgery. A case report and review of the literature. 1066 96

Induction of acute pancreatitis follows a uniform mechanism independent of the different etiologic factors such as gallstones, alcohol, ischemia, hyperlipidemia, hypercalcemia, hereditary and others. Each cause seems to affect primarily the acinar cell, resulting in premature intracellular activation of trypsinogen and other digestive enzymes. Activated enzymes and oxygen free radicals injure the acinar cell and cause a release of cytokines and vasoactive mediators, attract inflammatory cells and activate the vascular endothelium as well as the expression of adhesion molecules. The disturbance of the pancreatic microcirculation induces a progression from edematous to necrotizing pancreatitis independent of the early intracellular events, including protease activation. Specific therapy must be directed towards microperfusion failure as a secondary pathogenetic step, since the initial enzyme activation and cytokine release is irreversible by the time of clinical presentation. In experimental designs comparable to the clinical situation the following therapeutic principles have proven beneficial: increase of blood fluidity by dextran, inhibition of leukocyte-endothelium interaction by ICAM-1 antibodies, and blockade of local vasoconstriction by endothelin-receptor antagonists.
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PMID:[New pathophysiologic knowledge about acute pancreatitis]. 1078 41

We herein describe a 70-year-old male patient who developed colonic necrosis following severe acute pancreatitis. He was referred to our hospital with a diagnosis of acute pancreatitis. In the course of the disease, he developed sudden and massive hematochezia and died. The autopsy findings revealed large bowel ischemia with transmural infarction. The possible pathogenic mechanisms of colonic ischemia are also discussed.
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PMID:Development of colonic necrosis following severe acute pancreatitis. 1080 Nov 38

Acute pancreatitis is a disorder that has numerous causes and an obscure pathogenesis. Bile duct stones and alcohol abuse together account for about 80% of acute pancreatitis. Most episodes of biliary pancreatitis are associated with transient impaction of the stone in the ampulla (that causes obstruction of the pancreatic duct, with ductal hypertension) or passage of the stone though and into the duodenum. Other causes of acute pancreatitis are various toxins, drugs, other obstructive causes (such as malignancy or fibrotic sphincter of Oddi), metabolic abnormalities, trauma, ischemia, infection, autoimmune diseases, etc. In 10% of cases of acute pancreatitis, no underlying cause can be identified; this is idiopathic pancreatitis. Occult biliary microlithiasis may be the cause of two thirds of the cases of "idiopathic" acute pancreatitis. Intra-acinar activation of trypsinogen plays a central role in the pathogenesis of acute pancreatitis, resulting in subsequent activation of other proteases causing the subsequent cell damage. Ischemia/reperfusion injury is increasingly recognized as a common and important mechanism in the pathogenesis of acute pancreatitis and especially in the progression from mild edematous to severe necrotizing form. Increased intracellular calcium concentration also mediates acinar cell damage. Oxygen-derived free radicals and many cytokines (e.g., interleukin [IL]-1, IL-6, IL-8, tumor necrosis factor-alpha, platelet activating factor) are considered to be principal mediators in the transformation of acute pancreatitis from a local inflammatory process into a multiorgan illness.
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PMID:Etiology and pathogenesis of acute pancreatitis: current concepts. 1087 61

Induction of NF-kappaB-dependent gene expression plays an important role in a number of biological processes including inflammation and ischemia-reperfusion injury. However, few attempts aimed at selective regulation of this transcription factor have been successful. We report here that a naturally occurring antibacterial peptide PR39 reversibly binds to the alpha 7 subunit of the 26S proteasome and blocks degradation of NF-kappa B inhibitor I kappa B alpha by the ubiquitin-proteasome pathway without affecting overall proteasome activity. I kappa B alpha phosphorylation and ubiquitination occur normally after PR39 treatment, and binding of valosin-containing proteins is not impaired. The inhibition of I kappa B alpha degradation abolishes induction of NF-kappa B-dependent gene expression in cell culture and in mouse models of acute pancreatitis and myocardial infarction, including upregulation of endothelial adhesion proteins VCAM-1 and ICAM-1. In the latter model, sustained infusion of PR39 peptide resulted in significant reduction of myocardial infarct size. PR39 and related peptides may provide novel means to regulate cellular function and to control of NF-kappa B-dependent gene expression for therapeutic purposes.
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PMID:Inhibition of ubiquitin-proteasome pathway-mediated I kappa B alpha degradation by a naturally occurring antibacterial peptide. 1093 Apr 47

An ischemic origin of acute pancreatitis has been considered for a long time, at least as an aiding factor: ischemia has a fundamental role in the development of necrotizing pancreatitis from an oedematous one. Shock, heart condition and celiac-mesenteric ischemia can determine the onset of an acute pancreatitis through local ischemic lesions. Personal experience with a case of acute pancreatitis following an intestinal ischemic failure is reported. The duration of ischemia and, in particular, the free radicals formation during the organ reperfusion have been considered as the main pathogenetic factors. In the observed case, the ischemic hypothesis seems to be supported from the lack of other known factors and from the intestinal ischemic failure episode.
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PMID:[Ischemic pathogenesis of acute pancreatitis. A case report]. 1105 41


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