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

Dorsal column stimulators (DCS) have been implanted in 130 patients with various chronic pain syndromes at the University of California, San Francisco, between 1969 and 1973. Preoperative psychiatric evaluation and percutaneous dorsal column stimulation testing were of value in rejecting those patients most likely to have unsatisfactory long-term results with DCS. Best results occurred in patients with phantom limb or peripheral nerve pain and worst results in patients with paraplegic pain, documented arachnoiditis, pancreatitis and arthritis. The need is stressed for careful preoperative selection and for close, prolonged postoperative care in a situation permitting access to multidisciplinary facilities for patient care.
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PMID:Experience with dorsal column stimulation for relief of chronic intractable pain: 1968-1973. 108 Aug 99

Balb/C weanling mice were inoculated intraperitoneally with a myocarditic variant of coxsackie-virus B3, with the aim of characterizing more fully the cell damage induced in the heart as well as in other organs. During the first week postinfection (pi), all animals developed acinar pancreatitis, followed by focal myocarditis. In accordance with the increasing infectivity titers, such progressive histopathological changes correlated with local viral replication. From day 4 pi, acinar degeneration accompanied by diffuse inflammatory exudate was observed in the pancreas, followed by fatty tissue replacement by day 8. In the heart, focal necrosis rather than inflammatory reaction first appeared at 4 days pi and became widespread by 6-8 days pi. Necrotic foci usually presented calcium deposits, with absence of myofibrils in the affected fibers. The fact that both periodic acid Schiff (PAS) and Best carmine staining remained positive even after diastase treatment ruled out basophilic necrosis. In summary, the pancreas appeared to be the site of primary viral replication leading to viremia.
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PMID:Murine acinar pancreatitis preceding necrotizing myocarditis after Coxsackievirus B3 inoculation. 166 7

A simple, rapid screening procedure for determining the relative amounts of pancreatic (P)- and salivary (S)-type amylase in serum is presented, involving incorporation of a selective inhibitor (from wheat-germ) into commercially available BMD Single-Vial Amylase and Beckman Enzymatic Amylase-DS procedures for manual and automated isoamylase measurements. Optimal concentrations of inhibitor inhibit the S-type amylase fraction by 87-88%. In contrast, the pancreatic fraction is inhibited by only 19% in either the manual or automated methods. The degree of inhibition is constant for amylase activities up to at least 520 U/L. Use of the ratio (P-amylase/total amylase activity) X 100 helps differentiate between hyperamylasemia caused by S-type or P-type amylase. In preliminary studies, patients with pancreatitis showed a ratio greater than 70%.
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PMID:Determinations of amylase isoenzymes in serum by use of a selective inhibitor. 617 45

The pancreas was generally ignored in antiquity, both as an organ and as a seat of disease. The first description of the pancreas is attributed to Herophilus. It was in the 17th century that the main duct of the organ was described and its significance demonstrated. At that time, Brunner thought that the pancreas was not essential to digestion, and he failed to associate the pancreas with diabetes. Claude Bernard discovered the function of the pancreas in digestion. In 1922, Banting and Best obtained isletin and demonstrated the capacity of the substance to cause a dog to recover from diabetic coma. In 1889, Reginald Fitz firmly established pancreatitis as a disease entity. In 1927, the first case of hyperinsulinism due to a tumor of the islet cells was reported. Twenty-eight years later, Zollinger and Ellison described two patients with unusually severe peptic ulcer disease, both of whom had noninsulin-secreting tumors of the pancreatic islets. Subsequently, gastrin was isolated as the hormone responsible for this syndrome. In March 1940, Dr. O. Whipple performed the first recorded one-stage pancreaticoduodenectomy. Much progress has been made since then and today transplantation of isolated islets and portions of whole pancreas is a reality.
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PMID:History of the pancreas. 635 46

Studies using experimental models indicate that the earliest changes in acute pancreatitis involve intra-acinar cell events including the co-localization of lysosomal hydrolases with digestive enzyme zymogens. This co-localization phenomenon leads to trypsinogen activation and subsequent cell injury. Following acinar cell injury, a series of extra-acinar cell changes determine the severity of pancreatitis by promoting or reducing the inflammatory response and by influencing cell death events. Most patients with pancreatitis are diagnosed when acinar cell injury has already occurred. Therapies designed to modify the subsequent extra-acinar cell inflammatory process may prove useful in the management of clinical pancreatitis.
Baillieres Best Pract Res Clin Gastroenterol 1999 Jul
PMID:Early events in acute pancreatitis. 1103 Jun 2

The pancreatic acinar cell is potentially the initial site of injury that begins the series of events leading to acute pancreatitis. Pathological intrapancreatic zymogen activation occurs in experimental pancreatitis in animals and in human pancreatitis. Intracellular activation has been clearly linked to aberrant zymogen processing in one form of hereditary pancreatitis; in this genetic disease a mutation in cationic trypsinogen may eliminate the degradation of any trypsin activated in the acinar cell. Recent studies have also provided the first direct evidence that trypsinogen activation takes place early in the course of caerulein-induced pancreatitis; parallel studies have used isolated pancreatic acini and conditions that simulate those that cause pancreatitis in vivo to demonstrate that zymogens can be pathologically activated in isolated cells. A unique acinar cell pathway regulates the intracellular proteinase processing of zymogens to their active forms. Stimulating the acinar cell with supramaximal concentrations of cholecystokinin (CCK) or carbamylcholine can activate this pathway. The activation depends on a low pH compartment within the acinar cell and activation of an intracellular serine protease. A marker of trypsinogen processing, the trypsinogen activation peptide (TAP), is generated in acinar cell compartments that do not overlap with secretory granules. This compartment overlaps with a marker of recycling endosomes and lysosomes. Thus, zymogen processing within the acinar cell proceeds in a distinct subcellular compartment and is dependent on a low pH environment and activation of serine proteases.
Baillieres Best Pract Res Clin Gastroenterol 1999 Jul
PMID:Mechanisms of intracellular zymogen activation. 1103 Jun 3

Acute pancreatitis is a common, often severe disease with multiple causes. Many of the aetiological factors responsible for triggering acute pancreatitis have been identified but the pathophysiological mechanism by which they do so is still poorly understood. Free calcium ions within the cytosol of the acinar cell ([Ca2+]i) act as a key intracellular second messenger in the processes of stimulus-secretion coupling and may be crucial in the pathogenesis of acute pancreatitis. [Ca2+]i signals have been shown to be disrupted early in experimental pancreatitis, and it is known that an abnormal rise in [Ca2+]i is toxic by a variety of mechanisms. It has been demonstrated that abnormal, prolonged elevations in [Ca2+]i result from caerulein hyperstimulation and ethanol treatment, and it is likely that all the known causes of acute pancreatitis can cause similar disruptions. Elevations in [Ca2+]i have also been shown to be associated with both acinar cell vacuolization and intracellular enzyme activation, both of which are key steps in the pathogenesis of acute pancreatitis. A disturbance of intracellular Ca2+ signalling and the generation of an abnormal elevation in [Ca2+]i appears to be the common factor linking all the known triggers for acute pancreatitis and initiating the further sequence of pathological events leading to clinical disease.
Baillieres Best Pract Res Clin Gastroenterol 1999 Jul
PMID:Intracellular free ionized calcium in the pathogenesis of acute pancreatitis. 1103 Jun 4

Hereditary pancreatitis is an unusual form of acute and chronic pancreatitis with a familial predisposition. Recently, the gene mutations causing most cases of hereditary pancreatitis have been identified in the cationic trypsinogen gene. The known mutations are trypsinogen R117H and N211. These may predispose to acute pancreatitis by eliminating one of the fail-safe mechanisms used by the pancreas to eliminate prematurely activated trypsin. Accumulation of active trypsin mutants are hypothesized to initiate a digestive enzyme activation cascade in the pancreatic acinar cells leading to autodigestion, an intense inflammatory response, and acute pancreatitis. The observation that these patients also develop typical chronic pancreatitis and may later develop pancreatic cancer provides strong evidence that these conditions are linked. Knowledge of the pathophysiological conditions leading to acute and chronic pancreatitis and the development of a transgenic mouse expressing the mutant human trypsinogen genes will provide directions and tools necessary for the effective treatment or prevention of this human disease.
Baillieres Best Pract Res Clin Gastroenterol 1999 Jul
PMID:Hereditary pancreatitis: new insights, new directions. 1103 Jun 5

Cytokines have been shown to play a pivotal role in multiple organ dysfunction, a major cause of death in severe acute pancreatitis. Moreover, the two-hit hypothesis of the cytokine-induced systemic inflammatory response syndrome explains the variable individual response to severe acute pancreatitis and the impact of secondary events such as sepsis or therapeutic intervention. Many experimental anti-cytokine therapies have been administered following induction of experimental pancreatitis, and have proved to be therapeutic. Patients with severe pancreatitis present early because of pain. Clearly then a window for therapeutic intervention is available between onset of symptoms and peak pro-inflammatory cytokine expression. It is this fundamental observation that convinces many in the field that the treatment of AP will be one of the first clinical successes for novel drugs or therapy that seek to modulate the inflammatory response.
Baillieres Best Pract Res Clin Gastroenterol 1999 Jul
PMID:Cytokines and acute pancreatitis. 1103 Jun 6

Bacterial infection of pancreatic necrotic tissue is a frequent complication of severe acute pancreatitis. Infected pancreatic necrotic tissue is observed in 30-70% of all patients suffering from necrotizing pancreatitis. It is the leading cause of deaths in severe acute pancreatitis, with mortality rates ranging from 15 to 30%. The incidence of infection increases with the extent of the necrotic areas and with the time after onset of pancreatitis. Compared to patients with sterile necrosis, those with infection of the necrotic areas have an increased mortality, and systemic complications occur more frequently. Standard treatment for infected pancreatic necrotic tissue is surgical debridement, whereas conservative management is feasible in approximately 30% of the patients with sterile necrosis. As bacterial infection of pancreatic necrotic tissue has a tremendous impact on the prognosis of the disease and on the patient's clinical course, efforts have been made to prevent it. Although clinical and experimental data provide evidence that prophylactic antibiotics have beneficial effects on the outcome and course of patients with severe acute pancreatitis, this topic has to be investigated further. General recommendations concerning the early use of antibiotics have to await the results of larger, double-blind studies.
Baillieres Best Pract Res Clin Gastroenterol 1999 Jul
PMID:Natural history of acute pancreatitis and the role of infection. 1103 Jun 7


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