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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute pancreatitis is a frequent inflammatory and necrotic process of pancreas and peripancreatic field. To detect the presence of infected or sterile necrotic components and hemorrhage of the pancreatic paranchyma is important for therapeutic approach. Chronic pancreatitis is characterized by irreversible exocrine dysfunction, progressive loss of pancreatic tissue and morphological changes of the pancreatic canal. Imaging modalities play a primary role in the management of both acute and cronic pancreatitis. CT and MR imaging confirm the diagnosis and detect the severity of disease. In chronic pancreatitis, MRCP after Secretin administration, Spiral CT and endoscopic US seems to replace diagnostic ERCP. However differentiation of pseudotumor of chronic pancreatitis from the pancreatic carcinoma is difficult with either imaging modalities.
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PMID:The role of diagnostic radiology in pancreatitis. 1133 94

The objective of the study was to assess by means of magnetic resonance cholangiopancreatography whether acute biliary pancreatitis leads to alterations in pancreatic morphology and the main pancreatic duct; to establish whether such alterations are related to the severity of the acute episode and if they are to be considered as sequelae of the illness or on the contrary the findings constitute diagnostic morphological criteria of chronic pancreatitis. Forty patients with acute biliary pancreatitis were prospectively and consecutively studied, 15 female (37.5%) and 25 male (62.5%). During the acute phase the severity was assessed according to the Atlanta criteria. During subsequent follow-up,we assessed the morphology of the gland and the main pancreatic duct with magnetic resonance cholangiopancreatography 5 years after the episode of pancreatitis, and compared the findings with the findings from a control group. We administered secretin in 16 of the study group cases when visualization of the duct was incomplete or absent. The statistical study of diameter and length showed significant differences in the main pancreatic duct of the case and control groups. No relationship was found between the severity of the illness and morphological alterations of the pancreas after pancreatitis. The statistical analysis, which compared the diameter and the length of the main pancreatic duct before and after the injection of secretin in the study group showed significant differences. We conclude that after acute biliary pancreatitis, in the long term, scarring lesions are detected, which are considered to be sequelae of the acute episode, unrelated to its severity. Secretin stimulation improved visualization of the main pancreatic duct in the magnetic resonance cholangiopancreatography.
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PMID:Acute biliary pancreatitis: does the pancreas change morphologically in the long term? 1577

Endoscopic retrograde cholangiopancreatography (ERCP) is highly sensitive for detecting chronic pancreatitis, even when mild, but it is invasive. Magnetic resonance cholangiopancreatography (MRCP), a noninvasive modality, well demonstrates dilatation, stricture, and irregularity of the main pancreatic duct as well as filling defects due to pancreatic stones and protein plugs in chronic pancreatitis. MRCP well visualizes the pancreatic ducts distal to the sites of complete obstruction and noncommunicating pseudocysts, in contrast to ERCP. MRCP is sensitive for detecting moderate to severe pancreatitis but not for mild pancreatitis. However, secretin-stimulated MRCP and technological innovations in magnetic resonance may improve diagnostic accuracy. A recently developed technique, secretin-stimulated diffusion-weighted magnetic resonance imaging (DW-MRI), noninvasively and accurately evaluates pancreatic exocrine function. In conclusion, MRCP can most likely replace ERCP for evaluation of moderate to severe chronic pancreatitis. Secretin-stimulated DW-MRI may help to detect mild or early pancreatitis.
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PMID:Magnetic resonance imaging for diagnosing chronic pancreatitis. 1723 38

High-quality magnetic resonance (MR) cholangiopancreatographic images are difficult to obtain in children due to the small caliber of the pediatric bile ducts and to motion artifacts. However, there has been ongoing improvement in image quality, thanks to better coil technology, increased speed of acquisition, refinement in respiratory compensation techniques, and newer sequences. Heavily T2-weighted fast spin-echo (FSE) and single-shot FSE MR imaging sequences with long echo times are used to image the biliary and pancreatic ducts. Secretin has been shown to improve the visualization of the pancreatic duct and pancreaticobiliary junction. Factors that affect image quality in pediatric MR cholangiopancreatography include sedation, negative oral contrast material, radiofrequency coil selection, respiratory compensation techniques, echo time, echo train length, section-slab thickness, planes of scanning, field of view, and number of signals acquired. However, giving proper attention to these factors and tailoring the study to the body size of the patient (which varies considerably) can lead to high-quality diagnostic MR cholangiopancreatographic images. Use of MR cholangiopancreatography in children is limited by the need for sedation or anesthesia, high cost, limited availability, and long scanning times. Nonetheless, this modality can be a viable alternative to endoscopic retrograde cholangiopancreatography (ERCP) in the evaluation of various entities such as choledochal cyst, recurrent pancreatitis, primary sclerosing cholangitis, and a transplanted liver, and may obviate ERCP.
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PMID:Pediatric MR cholangiopancreatography: principles, technique, and clinical applications. 1900 51

In a small number of patients with pancreas divisum (with stenotic minor papilla) a relative obstruction to pancreatic exocrine secretory flow results in pancreatitis. We report a 2-year-old boy presenting with recurrent bouts of abdominal pain. The diagnosis of acute pancreatitis was made based on blood biochemistry results. Ultrasound, computed tomography and magnetic resonance imaging showed several abdominal pseudocysts, peritoneal exsudate and confirmed pancreatitis but initially failed to reveal the aetiology. Ascites and cysts contained pancreatic enzymes. After weeks of combined conservative and surgical treatment, a magnetic resonance cholangiopancreaticography with secretin, showed a pancreas divisum with a cyst between the ducts of Santorini and Wirsung. Based on these findings, two endoscopic papillotomies (minor and major papilla) were performed. Three years follow-up was uneventful. In a child with recurrent pancreatitis or pancreatitis with chronic recurrent abdominal pain it is crucial to search aggressively for congenital abnormalities, including pancreas divisum. Secretin-enhanced magnetic resonance cholangiopancreaticography or diffusion-weighted magnetic resonance imaging is a valuable diagnostic tool for visualizing pancreatic duct anatomy.
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PMID:A two-year old boy with recurrent bouts of acute abdominal pain. 2129 65

This review provides some aspects on the physiology of stimulation and inhibition of pancreatic digestive enzyme secretion and the pathophysiology of pancreatic acinar cell function leading to pancreatitis. Cholecystokinin (CCK) stimulates both directly via CCK-A receptors on acinar cells and indirectly via CCK-B receptors on nerves, followed by acetylcholine release, pancreatic enzyme secretion. It is still not known whether CCK-A receptors exist in human acinar cells, in contrast to acinar cells of rodents where CCK-A receptors have been well described. CCK has numerous actions both in the periphery and in the central nervous systems. CCK inhibits gastric motility and regulates satiety. Another major function of CCK is stimulation of gallbladder contraction. This function enables that bile acids act simultaneously with pancreatic lipolytic enzymes. Secretin is a major stimulator of bicarbonate secretion. Trypsinogen is activated by the gut mucosal enzyme enterokinase. The other pancreatic proenzymes are activated by trypsin. Termination of enzyme secretion may be regulated by negative feedback mechanisms via destruction of CCK-releasing peptides by trypsin. Furthermore, the ileum may act as a brake by release of inhibitory hormones such as PYY and somatostatin. In the pathophysiology of acute pancreatitis, fusion of zymogen granules with lysosomes leading to intracellular activation of trypsinogen is regarded as an initiation step. This activation of trypsinogen may be caused by the lysosomal enzyme cathepsin B. However, autoactivation of trypsinogen itself may be a possibility in pathogenesis. Autoactivation is enhanced in certain mutations of trypsinogen. Furthermore, an imbalance of protease inhibitors and active proteases may be involved. The role of pancreatic lipolytic enzymes, the role of bicarbonate secretion, and toxic Ca(2+) signals by excessive liberation from the endoplasmic reticulum have to be discussed in the pathogenesis of acute pancreatitis.
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PMID:New advances in cell physiology and pathophysiology of the exocrine pancreas. 2152 56

Rat pancreatic acinar cells possess only the p21-activated kinase (PAKs), PAK4 of the group II PAK, and it is activated by gastrointestinal hormones/neurotransmitters stimulating PLC and by a number of growth factors. However, little is known generally of cAMP agents causing PAK4 activation, and there are no studies with gastrointestinal hormones/neurotransmitters activating cAMP cascades. In the present study, we examined the ability of VIP and secretin, which stimulate cAMP generation in pancreatic acini, to stimulate PAK4 activation, the signaling cascades involved, and their possible role in activating sodium-potassium adenosine triphosphatase (Na+,K+-ATPase). PAK4 activation was compared with activation of the well-established cAMP target, cyclic AMP response element binding protein (CREB). Secretin-stimulated PAK4 activation was inhibited by KT-5720 and PKA Type II inhibitor (PKI), protein kinase A (PKA) inhibitors, whereas VIP activation was inhibited by ESI-09 and HJC0197, exchange protein directly activated by cAMP (EPAC) inhibitors. In contrast, both VIP/secretin-stimulated phosphorylation of CREB (pCREB) via EPAC activation; however, it was inhibited by the p44/42 inhibitor PD98059 and the p38 inhibitor SB202190. The specific EPAC agonist 8-CPT-2- O-Me-cAMP as well 8-Br-cAMP and forskolin stimulated PAK4 activation. Secretin/VIP activation of Na+,K+-ATPase, was inhibited by PAK4 inhibitors (PF-3758309, LCH-7749944). These results demonstrate PAK4 is activated in pancreatic acini by stimulation of both VIP-/secretin-preferring receptors, as is CREB. However, they differ in their signaling cascades. Furthermore, PAK4 activation is needed for Na+,K+ATPase activation, which mediates pancreatic fluid secretion. These results, coupled with recent studies reporting PAKs are involved in both pancreatitis/pancreatic cancer growth/enzyme secretion, show that PAK4, similar to PAK2, likely plays an important role in both pancreatic physiological/pathological responses. NEW & NOTEWORTHY Pancreatic acini possess only the group II p21-activated kinase, PAK4, which is activated by PLC-stimulating agents/growth factors and is important in enzyme-secretion/growth/pancreatitis. Little information exists on cAMP-activating agents stimulating group II PAKs. We studied ability/effect of cyclic AMP-stimulating agents [vasoactive intestinal polypeptide (VIP), secretin] on PAK4 activity in rat pancreatic-acini. Both VIP/secretin activated PAK4/CREB, but the cAMP signaling cascades differed for EPAC, MAPK, and PKA pathways. Both hormones require PAK4 activation to stimulate sodium-potassium adenosine triphosphatase activity. This study shows PAK4 plays an important role in VIP-/secretin-stimulated pancreatic fluid secretion and suggests it plays important roles in pancreatic acinar physiological/pathophysiological responses mediated by cAMP-activating agents.
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PMID:Cyclic AMP-dependent protein kinase A and EPAC mediate VIP and secretin stimulation of PAK4 and activation of Na+,K+-ATPase in pancreatic acinar cells. 3052 Jun 94


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