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

This review summarizes the role of radiologic tests, especially CT, in the diagnosis and assessment of acute pancreatitis and its complications. Consideration of the underlying pathologic changes of complicated pancreatitis and their radiographic correlates allows identification of the presence, extent, and nature of local complications. This information can be crucial in making appropriate management decisions. Based on these data, general guidelines for the appropriate use of CT in acute pancreatitis can be formulated. Patients with clinically mild pancreatitis in whom the diagnosis is secure probably do not require imaging as long as they respond appropriately to conservative management. In patients with clinically severe pancreatitis, early CT should be performed to evaluate the extent and nature of local complications. If radiographic changes are mild and the patient responds to conservative management, no further imaging is needed. If the patient does not respond appropriately or clinically worsens, follow-up CT should be performed, seeking delayed complications. Patients in whom the initial CT shows severe pancreatitis and peripancreatic inflammatory changes should be followed with serial CT to assess resolution. Initially, serial CT should be performed every 1-2 weeks, or sooner if clinically indicated. If at any time there is clinical suspicion of infection, aggressive use of FNA is indicated. The decision to intervene, whether for infectious or sterile complications of pancreatitis, must still be made on clinical grounds. CT can be helpful in choosing the appropriate means of intervention.
Pancreas 1991
PMID:The radiologic assessment of acute pancreatitis and its complications. 178 47

This overview clearly documents the critical diagnostic and therapeutic role for endoscopic intervention in pancreatitis. Further, although at the forefront of endoscopic development, the new therapeutic techniques discussed offer promise, suggesting cautious optimism. Their ultimate role in treatment of pancreatic disorders must await clarification of appropriate indications, safety, efficacy, and long-term benefit.
Pancreas 1991
PMID:Endoscopic intervention in pancreatitis. 178 49

Accurate predictors of severity in acute pancreatitis are sorely needed. At present, Ranson's scores provide useful information, some of which is recorded too late to be of maximal usefulness. APACHE-II scores on the day of admission and thereafter appear to provide important prognostic information that may enable the clinician to optimize patient care. CT scans, particularly those with bolus injection of i.v. contrast, help enormously in distinguishing interstitial from necrotizing pancreatitis. Most serum markers have not proven to be reliable in making this distinction.
Pancreas 1991
PMID:Predictors of severity in acute pancreatitis. 178 56

Copper and zinc are both secreted by the pancreas but are necessary for pancreatic secretion. We have studied the effects of a 4- or 8-week zinc or copper-deficient diet associated with or without lipid or protein deficiency on rat pancreatic secretion after stimulation by secretin, cerulein, or intraduodenal oleic acid. Twenty animals were in the control group; 40 rats were fed a copper-deficient diet (20 copper-deficient only and 20 copper- plus lipid-deficient). Ninety rats were deprived of zinc (30 of zinc-deficient only, 30 zinc-plus protein-deficient, 30 of zinc- plus lipid-deficient). Only the zinc- plus lipid-deficient diet for 8 weeks decreased basal bicarbonate and basal protein secretion (-42 and -70%, respectively, of the control values). Stimulated secretion was not markedly altered by copper deficiency while zinc deficiency, zinc plus protein deficiencies, and zinc plus lipid deficiencies suppressed almost responses to hormonal stimulation: After 8 weeks, the maximal protein response to oleic acid was reduced to 19.00 +/- 3.40, 18.58 +/- 3.00, and 12.04 +/- 2.91 microgram/30 min/g body weight in zinc- zinc and protein-; and zinc- and lipid-deficient diet, respectively, versus 39.87 +/- 6.33 microgram/30 min/g body weight (p less than 0.05) in controls. In all types of stimulation, lipid deficiency potentiated the deleterious effect of zinc deficiency on pancreatic secretion. This might be paralled with an extremely low level of lipid in the diet of people living in countries in which nutritional pancreatitis is observed and with the relative risk of developing an alcoholic chronic pancreatitis being increased by a low fat diet.
Pancreas 1991 May
PMID:Effects of zinc and copper deficiency associated with protein or lipid deficiency on rat exocrine pancreatic secretion. 186 68

Perfusion of the main pancreatic duct in cats with a dilute solution of bile salts increases ductal permeability. Subsequent perfusion of a permeable duct with activated pancreatic enzymes results in acute edematous pancreatitis. Simultaneous infusion of 16-16 dimethyl-PgE2 converts edematous pancreatitis to acute hemorrhagic pancreatitis (AHP). AHP may be associated with a reduction in pancreatic blood flow; it is certainly associated with increases in microvascular permeability. Low dose dopamine is a splanchnic vasodilator and may also reduce pancreatic microvascular permeability through beta agonist effects. In these studies, we investigated the effect of dopamine in an established feline model of biliary AHP. We also studied its effect on blood flow in both normal pancreas and after induction of AHP. We found that dopamine significantly reduced the degree of pancreatic inflammation, even when administered up to 12 h after onset of biliary AHP. However, the drug had no significant effect on blood flow either in normal pancreas or in the gland affected by hemorrhagic pancreatitis. We concluded that the effect of dopamine was most likely due to its ability to reduce pancreatic microvascular permeability.
Pancreas 1991 Jul
PMID:The effect of dopamine in a model of biliary acute hemorrhagic pancreatitis. 187 97

The effect on endogenous beta-endorphins of a new synthetic protease inhibitor was studied in acute pancreatitis. Pancreatitis was induced by the injection of autologous bile mixed with trypsin into the main pancreatic duct after ligation of the accessory duct. Plasma beta-endorphin concentrations and cardiovascular function were measured. Ten dogs (control group) were given 10 ml/kg/h of lactate Ringer's solution intravenously beginning 1 h before the induction of pancreatitis and continuing throughout the experiments. Six dogs received an intravenous infusion of 3 mg/kg/h of a new synthetic protease inhibitor, E-3123 (4-(2-succinimidoethylthio)4-geranidinobenzoate methanesuLfonate), in lactate Ringer's solution soon after the induction of pancreatitis. Plasma beta-endorphin concentrations in the control group increased significantly. However, plasma beta-endorphin levels in the protease inhibitor group did not increase as in the control group. The protease inhibitor infusion improved hypotension, myocardial depression, and plasma lactate, suggesting that the inhibitory effect of the protease inhibitor on beta-endorphin release contributed to the improvement.
Pancreas 1991 Jul
PMID:Effect of a new synthetic protease inhibitor on beta-endorphin release during acute pancreatitis in dogs. 187

Acute pancreatitis may result from viral infections, including mumps, coxsackie B, Epstein-Barr, and varicella. However, viral pancreatitis has not been reported after immunization with viral vaccines. We report the occurrence of acute pancreatitis in an adult who had received measles, mumps, and rubella II vaccine (MMR II).
Pancreas 1991 Jul
PMID:Pancreatitis caused by measles, mumps, and rubella vaccine. 187 5

A new kit for radioimmunoassay of serum phospholipase A2 (PLA2) with monoclonal antibody (S-0932, Shionogi, Osaka, Japan) was used to examine PLA2 levels in patients with various diseases. Patients with acute pancreatitis showed significantly increased serum PLA2 levels. In patients with chronic pancreatitis, significant correlations were observed between the levels of factors evaluated by the secretin test and serum PLA2 levels. In patients with pancreatic cancer, serum PLA2 levels varied with disease severity. Serum PLA2 concentrations were within the normal range in patients with other malignant tumors, diabetes mellitus, and chronic liver diseases but were increased in patients with chronic renal failure. S-Sepharose column analysis of sera showed a small peak of pro-PLA2 and a large peak of PLA2 in sera from patients with severe acute pancreatitis, but a large peak of pro-PLA2 in healthy controls and patients with other diseases. On G-100 gel filtration, high-molecular-weight PLA2 immunoreactivity was detected in sera of patients with chronic renal failure, whereas a single peak of PLA2 immunoreactivity coinciding with that of standard PLA2 was detected in sera of patients with acute pancreatitis. These results suggest that (a) measurement of serum PLA2 is clinically useful for diagnosis and monitoring of pancreatitis, (b) active PLA2 in the circulation is dominant in severe acute pancreatitis, and (c) the kidney may be the main site of PLA2 degradation or excretion.
Pancreas 1991 Sep
PMID:Clinical usefulness of serum phospholipase A2 determination in patients with pancreatic diseases. 194 16

During the 1965-9 period, we studied the consequences of acute pancreatitis in a group of 53 patients (1). Using the 1963 Marseille classification of pancreatitis (2), we pointed, inter alia, to the incidence of changes in exocrine and endocrine functions of the pancreas in some patients (something that we would refer to as residua after acute pancreatitis, today), and emphasized the need for a detailed examination of patients, following an attack of acute pancreatitis. In this article we wish to reemphasize the need for such detailed examination, this time in connection with new classifications of pancreatitis, i.e., the Revised Classification of Pancreatitis--Marseille, 1984 (3), and the Pancreatitis Classification of Marseille-Rome 1988 (4,5). The latter classification, based on studies of lesions and causes of pancreatitis, constitutes yet another attempt to integrate pathology into the prerequisites for clear-cut definition of the disease. However, a definition of pancreatitis, based on pathological findings, remains an aim yet to be attained in everyday clinical practice. That is why the clinician will rely on the Marseille classification (1984), taking into account the Marseille-Rome classification (1988).
Pancreas 1991 Sep
PMID:Why a detailed examination after acute pancreatitis? 194 17

In an attempt to study the mechanisms leading to fibrosis in chronic pancreatitis, an in situ immunohistochemical investigation of lymphocytes and of class II major histocompatibility complex expression (HLA-DR) by epithelial cells has been designed. Samples of normal pancreas (n = 8), chronic calcifying pancreatitis (n = 4), chronic obstructive pancreatitis (n = 6), and diffuse fibrosing pancreatitis (n = 6) have been studied. In normal pancreas, T-lymphocytes were rare and were located in the epithelial layer of pancreatic ducts and in the periductal connective tissue. Duct cells were constantly HLA-DR negative. In chronic calcifying pancreatitis and chronic obstructive pancreatitis, T cells were numerous and were located around ducts and in the spreading areas of fibrous septa. In chronic obstructive pancreatitis, the duct cells strongly expressed the HLA-DR antigen. In diffuse fibrosing pancreatitis, fibrous tissue was devoid of lymphocytes and duct cells never expressed the HLA class II antigen. These results suggest that lymphocytes are involved in the fibrosing process occurring in chronic calcifying pancreatitis and chronic obstructive pancreatitis but not in diffuse fibrosing pancreatitis. The significance of de novo expression of HLA-DR antigen by duct cells is discussed.
Pancreas 1990 Jul
PMID:Lymphocyte subsets and HLA-DR expression in normal pancreas and chronic pancreatitis. 197 51


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